BRCSU

2017 Endodontic Board Review and Scientific Update
Schedule
Virginia Commonwealth University
DAY 1: Friday, February 10, 2017
7 a.m. Registration and Breakfast
7:45 a.m. Welcome

David C. Sarett, D.M.D., M.S., Dean, VCU School of Dentistry; Clara Spatafore, D.D.S., M.S.,
Chair, VCUSOD Department of Endodontics; Garry Myers, D.D.S., AAE President-Elect; and
Raphael Garofalo, D.D.S., B.Sc., College of Diplomates Director
8 a.m. Top 20 Questions on the Top 20 Prescribed Drugs

B. Ellen Byrne, D.D.S., Ph.D.
Our patients are living longer and taking more medications. This clinical relevant
presentation will review to top 20 drugs prescribed, including indications,
contraindications, oral side effects and drug interactions. Familiarity with these drugs will
provide the practitioner with a better appreciation for over health of the patient and
implications for prescribing additional medications.
Learning Objectives:
Name the top 20 drugs prescribed.
Identify clinically relevant drug interactions involving the top 20 drugs.
Identify side effects.
Disclosure: Dr. Byrne has no past or present proprietary or relevant financial relationship
or receive gifts in kind (including soft intangible remuneration), consulting position or
affiliation, or other personal interest of any nature or kind in any product, service, course
and/or company, or in any firm beneficially associated therewith.
9:30 a.m. Break
10 a.m. Radiology in Endodontics

Sonali A. Rathore, D.D.S., M.S.
To understand appropriate use of radiographs in endodontic practice.
To establish a differential diagnosis based on a systematic approach.
To understand the use and limitations of 2D vs 3D (cone beam CT) technology.
To understand radiation dose of different radiographic modalities.
To understand principles of selection criteria and guidelines based on the AAE and
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AAOMR.
Disclosure: Dr. Rathore has no past or present proprietary or relevant financial
relationship or receive gifts in kind (including soft intangible remuneration), consulting
position or affiliation, or other personal interest of any nature or kind in any product,
service, course and/or company, or in any firm beneficially associated therewith.
11 a.m. Pathology and Endodontics

John Svirsky, D.D.S., M.Ed.
Demonstrate a logical approach to the diagnosis and treatment of common
radiolucent lesions found on radiographs.
Recognize the common radiographic lesion found in endodontic practices.
Recognize the histologic appearance of the lesions commonly found in endodontic
practices.
Disclosure: Dr. Svirsky has no past or present proprietary or relevant financial relationship
12:30 p.m. Lunch
1:30 p.m. Risk Assessment and Management of the Medically Complex Endodontic Patient
Bradford Johnson, D.D.S.
The goal of this presentation is to serve as a brief overview of common medical conditions
that may require modification of the standard treatment protocol to ensure safe
endodontic treatment. The intended audience is candidates preparing for the written and
oral parts of the American Board of Endodontics certification exam and other
endodontists.
Describe a risk assessment strategy for medically complex patients and know
when to modify your standard treatment protocol and/or seek medical
consultation prior to treatment.
Discuss common drug:drug interactions and allergies relevant to endodontic
practice.
Explain appropriate treatment modifications for patients with cardiovascular
disease, diabetes, pulmonary diseases, kidney and liver disease,
immunosuppression, history of bisphosphonate therapy and prosthetic joint
replacement.
Disclosure: Dr. Johnson has a past or present consulting position or affiliation with
DENTSPLY Sirona and has received honorarium from the College of Diplomates and the
Chicago Dental Society.
3 p.m. Break
3:15 p.m. Microbiology of Endodontic Disease

Christine M. Sedgley, D.D.S., M.D.Sc., M.D.S.
This presentation is aimed at endodontists who would like to both review the relevant
literature and update their knowledge about endodontic microbiology.
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The major developments in endodontic microbiology and how they have influenced
the practice of endodontics.
Current concepts in endodontic microbiology and the significance of biofilm
communities in endodontic infections.
The effects of endodontic treatment procedures on the microflora and clinical
indications for antibiotics.
Disclosure: Dr. Sedgley has no past or present proprietary or relevant financial relationship
4:45 p.m. Break
5 p.m. ABE Boardwalk

Clara M. Spatafore, D.D.S., M.S.
The Boardwalk presentation is intended to provide valuable information regarding the
certification process. A detailed explanation of the examination sequence will be
provided. Helpful hints for preparation of the Written, Case History Portfolio and Oral
Examinations will be outlined. The current timeline for progression through the
certification process will be detailed along with current recertification guidelines. At the
conclusion of the presentation, questions will be fielded from the audience regarding
topics pertaining to endodontic Board certification.
Describe the different levels of candidate status for Board certification.
Describe the sequence and timelines for examinations required for endodontic Board
certification.
List the requirements for recertification.
6 8 p.m. Wine and Cheese Reception
DAY 2: Saturday, February 11, 2017
7 a.m. Breakfast
8 a.m. The Current Best Evidence for Endodontic Treatment Outcomes

Shimon Friedman, D.M.D.
The outcome of endodontic treatment modalities has been challenged because of
inconsistent reports on prognosis, especially for teeth requiring treatment of persistent
endodontic disease. This inconsistency is confusing to dentists and endodontists and it
may act to skew their treatment planning decisions. The definitive outcomes of treatment
need to be determined for specific endodontic treatment modalities (initial treatment,
retreatment, apical microsurgery, intentional replantation, autogenous transplantation,
vital pulp therapy, revascularization, apexification, etc.) and in relation to specific
outcome goals (healing, functional retention, survival). To do so, studies consistent with
the CURRENT BEST EVIDENCE should be identified as reference, and the definitive
outcomes effectively communicated to provide dentists better insight into endodontic
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prognosis. This lecture will define the outcomes of endodontic therapy in regards to
healing, functional retention and survival based on the current best evidence for the
major endodontic treatment modalities. Clinical factors will be highlighted that may
influence the outcomes.
Describe the methodological considerations for clinical research aimed at studying
prognosis.
Identify the current best evidence for different endodontic treatment modalities.
Summarize the prognosis, functional retention and survival after endodontic
treatment.
List the clinical factors that influence the prognosis after endodontic treatment.
Debate the impact of treatment techniques on prognosis after endodontic
treatment.
Disclosure: Dr. Friedman has received a past or present honorarium from DENTSPLY
Maillefer and DENTSPLY Sirona.
9:30 a.m. Break
9:45 a.m. Inflammation and Immunology

Ashraf Fouad, B.D.S., D.D.S., M.S.
Discuss the major systems that mediate the host response in pulpal and periapical
inflammation.
Identify the differences between innate and specific immune responses to endodontic
pathogens.
Describe the mechanism of bone resorption and deposition as it relates to
pathogenesis and healing of periapical lesions.
Disclosure: Dr. Fouad has no past or present proprietary or relevant financial relationship
11:15 a.m. Break
11:30 a.m. Diagnosis and Management of Cracked Teeth and Vertical Root Fractures and Restoration
of Endodontically Treated Teeth
Keith V. Krell, D.D.S., M.S., M.A.
The new definitions for crack and fractured teeth from 2015.
The diagnostic tests used for identifying cracks and fractures.
The known etiologies for cracks and fractures in teeth.
Recommended treatments for cracks and fractured teeth.
Possible outcomes after diagnosis and treatment.
What are the survival differences between vital versus endodontically treated teeth.
What makes endodontically treated teeth different from vital teeth.
When should dowel and cores be used in endodontically treated teeth.
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What are restorative options for endodontically teeth.
Current recommendations.
Disclosure: Dr. Krell has no past or present proprietary or relevant financial relationship or
receive gifts in kind (including soft intangible remuneration), consulting position or
1 p.m. Lunch
1:45 p.m. Regenerative Endodontics, Analgesics, Anesthetic Review on Regenerative Endodontics

and Stem Cells
Anibal Diogenes, D.D.S., M.S., Ph.D.
Clinicians are often faced with the challenge of treating underdeveloped, immature teeth
with pulpal necrosis. These cases have been traditionally treated with apexification
procedures. In the last decade, regenerative endodontic procedures have emerged as an
alternative for treating immature teeth. Although both procedures have the primary goal
of resolving the disease process, REPs aim to achieve additional goals related to the
restoration of a vital pulp-like tissue and the functional regeneration of normal
homeostatic functions. Therefore, these procedures share one goal but are fundamentally
different. In order to better understand and compare both procedures, clinicians must
understand patient-centered, clinician-centered and scientist-centered outcomes. This
three-level outcome assessment provides the framework for understanding the current
status of regenerative endodontic procedures, and in turn, provides the benchmark for
comparison with apexification procedures. This lecture focuses on discussing the current
evidence that supports both procedures, while providing the biological basis for clinical
decisionmaking. In addition, case selection, expected outcomes and technical pitfalls will
be presented and discussed.
Identify the different types of stem cells and the major oral stem cells likely involved
in regenerative endodontic procedures.
Understand the biologic foundation regenerative endodontic procedures.
Identify different levels of clinical outcomes.
How to overcome some technical pitfalls of currently employed regenerative
procedures.
Disclosure: Dr. Diogenes has no past or present proprietary or relevant financial
3:15 p.m. Break
3:30 p.m. Pain Management: Anesthetics and Analgesics

Anibal Diogenes, D.D.S., M.S., Ph.D.
The dental pulp is one of the most densely innervated tissues in the body. The pulpal
innervation is not only unique in quantity but there are several qualitative patterns that
make dental pain particularly challenging to treat. An astute clinician must understand the
peripheral and central neuronal changes that often follow inflammation. These plastic
changes in the neuronal system pose several challenges for intra- and post-operatory pain
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management. Local anesthesia is a prerequisite for adequate treatment. However,
inflammation modulates both the bioavailability and the efficacy of currently used local
anesthetics. Likewise, analgesics must be carefully selected to maximize therapeutic
efficacy while minimizing side effects. In this lecture the trigeminal nociceptive system and
its modulation will be reviewed. In addition, the pharmacology and therapeutics of local
anesthetics and most commonly used analgesics will be discussed.
Describe the major components of the trigeminal nociceptive pathway.
Understand the mechanism of action of local anesthetics and major reasons for
anesthesia failure.
Describe how NSAIDS work, their indication and contraindication.
Evaluate the therapeutic value of opioid in treating endodontic pain.
Disclosure: Dr. Diogenes has no past or present proprietary or relevant financial
5 6 p.m. Oral Board Exam: Strategies in Preparation and Execution

Donna J. Mattscheck, D.M.D.
Utilizing the Oral Examination developed by the ABE, this presentation will discuss some
strategies for preparation and propose potential techniques to aid Board Candidates.
Become aware of how daily involvement in the specialty of endodontics is already
helping you prepare for the Oral Exam.
Develop the ability to better understand questions posed during the exam.
Discover ways to answer questions that will best convey your clinical decisionmaking
and thought processes to the examiners.
Disclosure: Dr. Mattscheck has received past honorarium from DENTSPLY, and past and
present other financial or material support from the AAE, ABE and COD for travel.
DAY 3: Sunday, February 12, 2017
7 a.m. Breakfast
8 a.m. Periradicular Surgery and Repair

George Bruder, D.M.D.
In this lecture, review surgical endodontic literature and techniques with special focus on
diagnosing endodontically treated teeth that may be candidates for nonsurgical/surgical
retreatment or implant therapy will be reviewed.
Describe the metamorphoses that exist between classic and contemporary surgical
techniques.
Identify biologic aspects of surgical endodontics and spatial features.
Discuss the prognosis of surgical endodontics and future endodontic treatment
modalities.
Disclosure: Dr. Bruder has a past or present consulting position or affiliation with
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DENTSPLY Sirona.
9:30 a.m. Break
9:45 a.m. Traumatic Dental Injuries & Root ResorptionAn Endodontic Perspective
Garry Myers, D.D.S.
This presentation will provide an overview of traumatic dental injuries that may have an
impact on pulpal, dentinal and cemental tissues requiring the expertise of quality
endodontic care. Since there is a lack of prospective human studies on traumatic dental
injuries, many treatment principles have evolved from retrospective studies, animal
studies and case reports that have led to treatment guidelines that are continually being
modified. While some types of root resorption are a common sequelae to traumatic
injuries, over time several variations of root resorption have been identified and each
necessitate their own recommended treatment principles due to the nuances associated
with each type of resorption. These various types of root resorption will be discussed to
include clinical and radiographic presentations as well as strategies for treatment of these
conditions.
To provide a brief overview of a variety of traumatic dental injuries with
corresponding pulpal effects and treatment principles.
To develop an understanding of the similarities and differences between external,
internal and cervical root resorption.
To understand what needs to take place before root resorption can occur.
To develop concepts and strategies in managing the various types of root resorption
that an endodontist may encounter.
Disclosure: Dr. Myers has no past or present proprietary or relevant financial relationship
11:30 a.m. Closing Remarks
11:45 a.m. Program Conclusion
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Biographical Information
B. Ellen Byrne, DDS, PhD

(804) 828-9184
FAX: (804) 828-6072
EMAIL: bebyrne@vcu.edu
Dr. B. Ellen Byrnes academic background includes a BS in Pharmacy,

DDS, General Practice Residency, Certificate in Endodontics and a PhD in
Pharmacology and Toxicology all from Virginia Commonwealth University.
She is currently a professor of Endodontics and Senior Associate Dean of

the VCU School of Dentistry. Dr. Byrne has authored several chapters,
enjoyed national recognition as a speaker, a member of the Joint
Commission on National Dental Board Examinations and has won multiple
alumni awards. She is a fellow in the International College of Dentists,
American College of Dentists and Pierre Fauchard Academic. She is a
gifted and entertaining speaker on pharmacology.
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Top 20....
Top 20 questions about the Top 20

drugs you see.....

#20 fluticasone/salmeterol (Advir)
#19 warfarin (Coumadin)

#15 sertraline (Zoloft)
#14 atenolol (Tenormin)
#18 clopidogrel (Plavix) #13 zolpidem (Ambien)
#17 citalopram (Celexa) #12 furosemide (Lasix)
#16 montelukast (Singulair) #11 atorvastatin (Lipitor)
Top 20.... and the # 1 prescribed drug is...

hydrocodone + acetaminophen
#9 metformin (Glucophage) #5 amlodipine (Norvasc) 57.2M 131.2 million prescriptions/year
#8 amoxicillin #4 levothyroxine (Synthroid) 70.5M
#7 omeprazole (Prilosec) 53.4M #3 lisinopril (Zestril) 87.4M
#6 azithromycin (Z-pak) 53.8M #2 simvastatin (Zocor) 94.1M
#1.........
Drug Abuse Drug Abuse

Prescription drug abuse is the Nations fastest-growing drug From 1997 to 2007, the milligram per person use of prescription
problem. opioids in the US increased from 74 mg. to 369 mg. An increase of
402%.
While there has been a decrease in the use of some illegal drugs,
data from the National Survey on Drug Use and Health (NSDUH) Opiate overdoses, once almost always due to heroin use, are now
show that nearly one-third of people aged 12 and over who used increasingly due to abuse of prescription painkillers.
drugs for the first time in 2009 began by using prescription drugs Each day 44 people die in the US from overdose of prescription
non-medically. painkiller.
Seventy percent of people who abuse prescription drugs got them Each day, 7,000 people are treated in Emergency Rooms for
from friends or relatives and 5% got them from drug dealers. inappropriate use of prescription pain killers.
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Drug overdose death rates by state (2008)
Hydrocodone changed schedules.... tramadol (Ultram,Ultram ER, Ultracet)

MOA: mu-opioid agonist,
inhibits reuptake of
norepinephrine and serotonin
1/3 of analgesic activity from
October 6, 2014...changed from Schedule III to Schedule II mu activity
Must have new written Rx each time synthetic codeine analog used
for moderate pain
Can not call in (except for emergency supply)
No refills etc etc.....like Percocet regulations
Schedule IV-August 18, 2014;
before was Schedule VI
50 mg tablets: dose 50-100
mg q 4-6 h
tramadol (Ultram, Ultracet) tramadol (Ultram,Ultram ER, Ultracet)

FDA warnings
Do not prescribe ULTRAM for Immediate release
patients who are suicidal or
addiction-prone 50 mg tablets: dose 50-100 mg q
Prescribe ULTRAM tablets with 4-6 h with maximum of 400
caution for patients who are taking mg/day
tranquilizers or antidepressant
drugs and patients who use Extended release: 100 mg once
alcohol in excess and who suffer
daily.
from emotional disturbances or
depression
Ultracet: 37.5 mg tramadol + 325
Tramadol has mu-agonist activity. mg acetaminophen. Two tablets
ULTRAM can be abused and
every 4-6 hours.
may be subject to criminal
diversion
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Codeine
Mild to moderate pain, 12 fold less potent
than morphine
Enzyme CYP2D6 is involved in conversion of
codeine to morphine
10% of population does not have this
enzyme; therefore codeine not effective
Ultrarapid metabolizers carry multiple copies
of CYP2D6 gene
7% of whites, 3% of blacks and 1% of Asians
and Hispanics are ultrarapid metabolizers
Morphine poisoning in a breastfed neonate of a codeine-prescribed

mother
Koren et al. Lancet 2006;368:704
Tylenol
Tylenol with codeine No. 3: acetaminophen
Full-term healthy infant presented on day of life (DOL) 7 with lethargy
300 mg + codeine 30 mg
DOL 11: noted that infant had regained birth weight Tylenol with codeine No. 4: acetaminophen
DOL 12: noted grey skin and reduced milk intake 300 mg + codeine 60 mg
1-2 tablets every 4-6 hours to a maximum of
DOL 13: found dead
12 tablets/24 hours
Postmortem morphine concentration: 70 ng/mL (normal 0.2 2 ng/mL) maximum: 4000 mg/24 hours based on
Mother prescribed acetaminophen with codeine for post-delivery pain acetaminophen component
Schedule III when combined with
Maternal genotype consistent with UM
acetaminophen
Acetaminophen (N-acelyl-p-aminophenol or APAP) Dosage forms (OTC)

Actions Suppository: 120 mg, 125 mg, 325 mg, 650 mg
analgesic-as effective as Chewable tablets: 80 mg
antipyretic Junior tablets: 160 mg
NOT antiinflammatory Regular strength: 325 mg
2005, >28 billion doses of APAP- Extra strength: 500 mg
containing products purchased in
Liquid: 160 mg/teaspoonful
US alone
Drops: 100 mg/mL, 120 mg/2.5 mL
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Acetaminophen (N-acelyl-p-aminophenol or APAP) Acetaminophen (N-acelyl-p-aminophenol or APAP)

Safe
Lacks gi, renal and bleeding
Poorly labeled adverse effects seen with
APAP NSAIDs.
Risk
non-aspirin fever reduce or
pain reliever hepatotoxicity
Combine OTC ex. sleep aid which 1990-1998

has APAP: diphenhydramine with 56,000 ER visits
APAP 26,000 hospitalizations
458 deaths
Toxicity Acetaminophen (N-acelyl-p-aminophenol or APAP)

Narrow therapeutic Index
10 grams (30
Minimal Toxic Dose consume alcohol
tablets)
pre-existing liver disease
Minimal Lethal Dose 15 grams: adult (46 tablets) take drugs which induce enzymes
responsible for production of toxic
metabolite
Minimal Lethal Dose 4 grams: child (12 tablets)
ethanol, isoniazid, rifampin,
phenytoin, phenobarbital and
carbamazepine
Therapeutic Index Acetaminophen

FDA
Substance Safety Margin 3 years to decrease all combination
products to 325 mg, Jan. 2014
Alcohol 1:4-1:10 maximum adult dose 4 gm (4000 mg)
Rx
Aspirin 1:50
decreased maximum amount OTC
Caffeine 1:100 six 500 mg tablets or 3000 mg/day

vs 8 tablets
Marijuana 1:400-1:800 ten 325 mg tablets or 3250 mg
extended release six 650 mg or
3900 mg wont change
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Acetaminophen (APAP) Acetaminophen

Lortab (hydrocodone and APAP) is no longer made except in the Take one (1) to two (2) tablets
liquid for 10 mg/300 mg/15 ml every four (4) to six (6) hours as
needed for pain.
2.5/500
7.5/750 Do the math with 5/500
5/325
10/325 2 tablets every 6 hours
5/500
10/500 1000 mg q6h=4000 mg/24hrs
7.5/325
10/600 2 tablets every 4 hours
7.5/500
10/660 1000 mg q4h=6000 mg/24 hrs
7.5/660
Red Flags that might indicate substance

Toxicity abuse-hard to ID an abuser
stay within the recommended dose, NOT more than 4 grams per unusually sophisticated knowledge of drugs (i.e. requesting a specific narcotic by
day in an adult name)
stating an inability or unwillingness to take generic medications
enhanced with pre-existing liver disease
nothing else works
enhanced with greater that 3 drinks per day
refusing to participate in diagnostic workups or consultations
use correct measuring device for liquid dosage forms
appealing to physician or dentist, he or she is the ONLY person who can help
be aware of combination products with large amounts of APAP
lost or misplaced, stolen prescriptions
Red Flags that might indicate substance

abuse
National Drug Control Strategy
Education: raise awareness through education of parents, youth,
unusual behavior in waiting room patients and healthcare providers.
assertive personality, often demanding immediate action
PMPs: Enhance and increase utilization of prescription monitoring
unusual appearance...extremes of slovenliness or being over-dressed programs to help identify doctor shoppers, frequent flyers.
no regular doctor and often no insurance Drug disposal: Develop consumer-friendly and environmentally-
wants appointment at end of office hours responsible prescription drug disposal programs that help limit drug
diversion.
traveling long distances to prescribers office
low income, rural areas, Medicaid enrollees
The law: Provide law enforcement agencies support and tools to
shut down pill mills and stop doctor shopping.
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Some interesting facts Some dos and donts.....

Do
Use PMP
Most prescription painkillers are prescribed by primary care and
internal medicine doctors and dentists, not specialists. perform a through exam, diagnosis and document
in 2013 alone, 71.3% of prescription drug overdoses were from request picture ID and keep in patient record
opioids call previous practitioner or pharmacist
Roughly 20% of prescribers prescribe 80% of all prescription pain confirm address and telephone numbers at each visit
killers.
write for limited quanitities
Some dos and donts..... Patient information
Many types of pain medication and opioid medication is only one

Dont type.
Take the patients word for it when you are suspicious. Opiates/opioids can be safe and effective, but when used
inappropriately can be dangerous for the person and the
prescribe just to get rid of drug-seeking patients.
community.
prescribe out of scope of practice in the absence of a formal
Tell them the possibility of dependence with regular use.
practitioner-patient relationship.
Tell them the side effects.
Disposal of unused medications Statins

#2 simvastatin (Zocor) & #11 atorvastatin (Lipitor)
Medication take back programs antilipemic agents, HMG-CoA Reductase inhibitors
National Drug Take Back Day HMG-CoA reductase is the enzyme that catalyzes the rate-limiting
step in cholesterol biosynthesis
run by local/state/federal government
major side effect: 30% of patients report muscle aches and
Disposal in household trash weakness
mix medications with unpalatable substances such as kitty litter symmetrical and usually involves proximal muscles (thighs &
or used coffee grounds calves)
place in plastic bag and throw into household trash patients describe as: weakness, cramping, tenderness, soreness,
or heaviness
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Statins #3 lisinopril ( Prinivil, Zestril)

angiotensin-converting enzyme (ACE) inhibitor
used to treat hypertension
also anti-inflammatory, so is their action because of lipid major side effect
lowering abilities, or because anti-inflammatory????? TBD...
orthostatic hypotension
statins are metabolized by the enzymes CYP3A4, therefore do
not prescribe other drugs metabolized by this enzyme system, cough
such as erythromycin, clarithromycin, ketoconazole.....etc angioedema that involves head/neck (compromise
airway/intestine)
African Americans may be at higher risk
#3 lisinopril ( Prinivil, Zestril) Effects of Elevated BP

A 5-6 mm Hg long-term increase in blood
pressure could lead to a 25-30% increase in
cardiovascular events and 50-60% increase
NSAIDs can substantially reduce the antihypertensive response of in strokes.
ACE inhibitors. In most cases the effect is gradual, so short-term A 2 mm Hg reduction in diastolic blood
use in well-controlled hypertensive patient is unlikely to cause pressure results in about a 40% reduction in
problems. the rate of strokes and a 25% reduction in
cardiovascular events.
#4 levothyroxine (Synthroid) #5 amlodepine (Norvasc)
calcium channel blocker

used to treat hypertension, symptomatic chronic stable angina
replacement or supplement in hypothyroidism
major side effect
take on an empty stomach for best absorption
gingival hyperplasia, although less than with other CCB such
as nifedipine (Procardia), verapamil (Calan), diltiazem
(Cardizem)
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#6 azithromycin (Zithromax Z-pak) #6 azithromycin (Zithromax Z-pak)

Tennessee Medicaid cohort study in 347,795 prescriptions matched
macrolide antibiotic to patients who took no antibiotics, amoxicillin, ciprofloxacin or
FDA approved for levofloxacin
acute bacterial exacerbations of chronic pulmonary disease during 5 days of therapy, patients taking azithromycin, as compared
acute bacterial sinusitis with those who took no antibiotics, had an increased risk of
cardiovascular death
community acquired pneumonia
pharyngitis/tonsillitis estimated 47 additional cardiovascular deaths per 1 million courses
uncomplicated skin infections pronounced among patients with high baseline of cardiovascular
premedication in AHA/AAOS guidelines for patients allergic to PCN risk
Ray, WA, Murray KT, Arbogast PG, Stein, CM. N Engl J Med. 2012 May 17;336(20): 1881-90.
#6 azithromycin (Zithromax Z-pak) #7 omeprazole (Prilosec)

March 2013
Proton Pump Inhibitor (PPI)
FDA issued safety announcement warning the public that
Appropriate use, short term to treat
azithromycin can cause abnormal changes in electrical activity of
the heart. stress ulcer prophylaxis in hospitalized patients
gastrointestinal and duodenal ulcers
Patients at risk include those with:
mild gastroesophageal reflux disease (GERD) symptoms
existing QT interval prolongation, history of torsades de Helicobacter pylori (H. pylori) which can contribute to development of peptic ulcer
pointes disease, gastritis, and gastric cancer (treated with PPI, clarithromycin and
amoxicillin or PPI, tetracycline, metronidazole and bismuth)
patients on antiarrhythmic agents: quinidine, procainamide,
dofetilide, amiodarone, sotalol major side effect
dry mouth, altered taste, esophageal candidiasis and mucosal atrophy
(tongue)
PPI....whats the problem(s)? PPI....whats the problem(s)?

Drug Interactions
inhibit cytochrome P450 2C19 (CYP2C19) and drug interactions occur
with other medications that use this same enzyme pathway Drug Interactions
clopidogrel (Plavix) uses CYP2C19 to convert to the active FDA and US product labeling warns against using omeprazole
metabolite (Prilosec) and esomeprazole (Nexium) and clopidogrel
omeprazole (Prilosec) can decrease the antiplatelet activity by 20- (Plavix) together or within 12 hours of each other.
40%
creates potential to increase risk of cardiovascular events
Product information for Plavix. Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership. Bridgewater, NJ 08807, Feb. 2011 Product information for Plavix. Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership. Bridgewater, NJ 08807, Feb. 2011.
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PPI....whats the problem(s)?? PPI....whats the problem(s)???

pH: some medications require a specific pH for absorption
PPIs increase gastric pH, making it less acidic PPIs may decrease anti-fracture efficacy of bisphosphonates
anti-retroviral agents absorption not complete
hip fractures may significantly increase in patients over 70 who
atazanavir (Reyataz), delavirdine (Rescriptor), nelfinavir take a PPI with alendronate (Fosamax)(epidemiologic study)
(Viracept)
cause??? unknown...decrease calcium or Vit. B12 absorption
calcium, iron and Vitamin B12 may be decreased, but extent not
established inhibit proton pumps in osteoclasts???
calcium citrate absorption less affected by gastric acidity

Abrahamsen B, Eiken P, Eastell R. Proton pump inhibitor use and the antifracture efficacy of alendronate. Arch
Intern Med 2011 Feb 14.
PPI....whats the problem(s)?? PPI....whats the problem(s)??

PPIs may increase fracture risk in both men and women Infections
PPI use has been associated with a 25% increase in overall even short-term use (under one week) has been shown to increase the
fractures and a 47% increase in spinal fractures in postmenopausal incidence of infections.
women
PPIs increase pH which may allow more bacterial growth.
FDA requires this information be added to PPI prescription The change in GI and respiratory flora may increase the risk for
labeling infection.
not a problem for low dose and short periods of time Hospital-acquired and community acquired pneumonias appears to be
Abrahamsen B, Eiken P, Eastell R. Proton pump inhibitor use and the antifracture efficacy of alendronate. Arch increased with PPI therapy.
Intern Med 2011 Feb 14.
Gray, SL, LaCrois AX, Larson J, eta al. Proton pump inhibitor use, hip fracture, and change in bone mineral density in
Vakil N. Acid inhibition and infections outside the gastrointestinal tract. Am J Gastroenterol 2009; 104 (Suppl 12): S17-20
postmenopausal women: results from the Womens Health Initiative. Arch Intern Med 2010; 170: 765-71.
Clostridium difficile-associated
PPI....whats the problem(s)??
diarrhea (CDAD)
C. difficule: gram +, spore-forming, toxin producing, anaerobic
Infections bacillus
Increase in Clostridium difficile infections and associated most common cause of infectious diarrhea in hospitalized patients in
diarrhea N. America and Europe
For every 533 patients receiving a daily PPI in the hospital at increased alarmingly since 2000
least one will develop C. difficle
alcohol based hand sanitizers do not work against spores
FDA Drug Safety Communication dated Feb, 2012 warns of this
possibility http:www.fda.gov/Drugs/DrugSafety/ucm290510.htm symptoms range from asymptomatic carrier to mild, moderate
diarrhea to fulminant, possible fatal pseudomembranous colitis
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Clostridium difficile-associated #8 amoxicillin (Amoxil)

diarrhea (CDAD) beta-lactam antibiotic
watery stool, abdominal pain and fever
used to treat multiple types of infection including
community/assisted living, elderly
otitis media, sinusitis, infections caused by susceptible
broad spectrum antibiotics or antineoplastic agents within last 8 weeks
organisms in upper and lower respiratory tract, skin, and urinary
25% recover spontaneously tract; prophylaxis of infective endocarditis in patients undergoing
surgical/dental procedures; as part of multidrug regiment for H.
75% require treatment: vancomycin @ $1,300.00/10 days or
pylori eradication
fidaxomicin (Dificid) @ $2,800.00/10 days
do not use anti-motility drugs (Imodium)....toxic megacolon prolonged use may lead to development of oral candidiasis
What can be recommended for

Probiotics
antibiotic assoicated diarrhea?
Antibiotic associated diarrhea To help prevent diarrhea from antibiotics
self-limited, stop antibiotic, use probiotics Culturelle (lactobacillus GG) $26.29, Dan Active
(lactobacillus/strep thermophilus), or Florastor (saccharomyces
pseudomembranous colitis, needs treatment boulardii)
Agents use to prevent diarrhea caused by antibiotics: probiotics advise patients to take probiotics during antibiotic treatment and
live friendly gut microbes...bifidobacterium, lactobacillus, up to a week afterwards
saccharomyces, and others take 2 hours AFTER each antibiotic dose so probiotic more likely
idea is to recolonize the gut with good microbes and crowd out to survive
harmful ones
Candidiasis Treatment Candidiasis Treatment

miconazole buccal tablets: 50 mg (Oravig) approved April,
2010
clotriamazole 10 mg troches (lozenges)
apply rounded side to the upper gum region just above right of
$101.96/70 left incisor following brushing teeth in AM
use 5 times a day for 14 days apply daily for 14 days
allow to dissolve slowly over 15-30 minutes do not chew, crush or swallow
do not chew or swallow whole if the tablet falls off within 6 hours, reapply another one
miconazole oral gel (Daktarin) available OUTSIDE the US
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#9 metaformin (Gluophage) #10 alprazolam (Xanax)
antidiabetic agent benzodiazepine
used to treat: type 2 diabetes mellitus (non-insulin dependent) by used to treat: anxiety disorder, panic disorder, with or without
decreasing glucose production by the liver and increasing glucose agoraphobia, anxiety associate with depression
uptake in the muscle major side effect
major side effect sedation
decrease appetite, nausea and diarrhea dry mouth
taste disorder FDA pregnancy category....X (this went away, June 2015)
#12 furosemide (Lasix) #13 zolpidem (Ambien)
non benzodiazepine hypnotic

high-ceiling loop diuretic
used to treat: insomnia (short term)
used to treat: edema associated with heart failure and hepatic/renal
disease; acute pulmonary edema; treatment of hypertension major side effect
major side effect duration of action 6-8 hours
dry mouth may see increased sedation if you add anti-anxiety agent to
this for dental appointment
Selective Serotonin Reuptake

#14 atenolol (Tenormin)
Inhibitors (SSRI)
# 15 sertraline (Zoloft) & #17 citalopram (Celexa)
cardioselective beta blocker....good, do not need to limit
vasoconstrictor used to treat: depression, obsessive-compulsive disorder, panic
disorder, post-traumatic stress disorder, premenstrual dysphoric
used to treat: hypertension (alone or in combination with other
disorder, social anxiety disorder
agents); angina pectoris; secondary prevention postmyocardial
infarction major side effect
NSAIDs given over 3 or more weeks can reduce the drug mouth
hypotensive effect of beta-blockers. Short term....no problem.
impaired platelet aggregation
12
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Selective Serotonin Reuptake Selective Serotonin Reuptake

Inhibitors (SSRI) Inhibitors (SSRI)
Effect of Bleeding
Effect of Bleeding
platelet aggregation requires serotonin
reports range from relatively minor bruising to life threatening
platelets can not make serotonin, must take it up from the
hemorrhage
blood
increase risk with aspirin, NSAIDs, warfarin or other
by blocking uptake, inhibit aggregration
anticoagulants
SSRIs cause a threefold increase in risk of GI bleed
anticipate prolonged bleeding
absolute risk is still low (about 1 case for every 8000 Rxs)
Selective Serotonin Reuptake Selective Serotonin Reuptake

Inhibitors (SSRI) Inhibitors (SSRI)
Can the Selective Serotonin Re-uptake Inhibitors (SSRIs) Yes
contribute to or cause bruxism? Bruxism is multifactorial and has been attributed to
stress
anxiety
malocclusion
CNS dysfunction
#16 montelukast (Singulair)
leukotriene-receptor antagonist
used to treat: prophylaxis and chronic treatment of asthma, relief of
symptoms of seasonal allergic rhinitis and perennial allergic rhinitis;
prevention of exercise-induced asthma
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#18 clopidogrel (Plavix) #19 warfarin (Coumadin)
anticoagulant, Vitamin K antagonist

antiplatelet agent: irreversible inhibition used to treat: prophylaxis and treatment of thromboembolic
used to treat: reduces rate of atherothrombotic events, myocardial disorders (venous, pulmonary) and embolic complications arising
infarction, stroke, vascular deaths in patients with recent MI or from atrial fibrillation or cardiac valve replacement; adjunct to
stroke, vascular disease. reduce risk of systemic embolism after myocardial infarction
major side effect major side effect
bleeding bleeding
Dont give aspirin or NSAIDs
#19 warfarin (Coumadin) #20 fluticasone/salmeterol (Advir)
stopping may put patient at high risk for thrombotic event (DVT, long-acting corticosteroid combined with beta 2 agonist
stroke) used to treat: asthma and maintenance treatment of COPD
life threatening bleeding after dental surgery is rare major side effect
risk of thromboembolism off warfarin for as little as 2 days maybe as localized infection of Candida albicans or Aspergillus niger
high as 0.02%-1% have occurred frequently in the mouth and pharynx with
INR checked within 24 hours or 72 hours if INR has been stable repetitive use of oral inhaler of corticosteroids.
use hemostatic measures: gelatin sponge sutured into site, bite on treat with antifungals
gauze, observe hemostasis before patient leaves spacer
#20 fluticasone/salmeterol (Advir) #20 fluticasone/salmeterol (Advir)
Medication Delivery
Inhalers Child with nocturnal episodes best scheduled late morning
Spacers-holding chamber allows more time to inhale Always have rescue inhaler available
medications and decreases topical application of medication Medications have low pH and decrease salivary flow-rinse with
Neubulizer-3-5 year old, aerosol through mask connected to flow water after use
meter or compressor
Smith, AS, Sharp HK. Children with Asthma: What the treating Dentist Needs to Know 2007; 13:2 Smith, AS, Sharp HK. Children with Asthma: What the treating Dentist Needs to Know 2007; 13:2
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Osteonecrosis of the jaw (ONJ) Available Bisphosphonates (BPs)

alendronate (Fosamax)-oral
etidronate (Didrone)-IV/oral
BRONJ (bisphosphonate-related osteonecrosis of the jaw)
ibandronate (Boniva)-oral or IV q 3 mos
BRON (bisphosphonate-related osteonecrosis)
pamidronate (Aredia)-IV
BAONJ (bisphosphonate-associated osteonecrosis of the jaw)
risedronate (Actonel)-oral
ARAONJ (antiresorptive-associated osteonecrosis of the jaw)- risedronate (Atelvia) enteric coated + contains EDTA which binds stray cations (Ca,
accounts for necrosis associated with monoclonal antibody therapy Fe, etc) $135/mo
tiludronate (Skelid)-oral
zoledronic acid (Zometa, Reclast)-IV
Non-bisphosphonate antiresportive Bisphosphonates

agents
denosumab: RANK Ligand (RANKL) inhibitor, which inhibits osteoclast formation,
function and survival, thus helps prevent osteoclast from resorbing bone
2003 alone...the year ONJ emerged...
60 mg SQ every 6 months (Prolia)
indicated for prevention of osteoporosis

17 million prescriptions written for Fosamax
120 mg SQ every 28 days (Xgevia) indicated

for prevention of skeletal-related 6 million prescriptions written for Actonel
events in patients with bone metastases from solid tumors
As population ages, this number will continue to increase
5.4% of patients developed ONJ after median exposure of 20 doses
What is the problem with these

Therapeutic Uses of BPs
drugs...
Oral
bisphosphonate osteonecrosis of the jaw (BONJ)
treatment and prevention of osteoporosis
initially described by Marx and Stern-2002
affects 10-12 million people in US
in 2000 there were 9 million fractures world wide of which 1.6 million were hip fractures exposure of bone in the jaws persisting for more than 8 weeks in
IV
a patient who has or currently is taking a antiresportive agent
used for hypercalcemia of malignancy
2 types
including bisphosphonates, monoclonal antibodies or
the malignancy secretes parathyroid related protein (PTHrP) which increases bone resorption and renal antiangiogenic agents such as bevacizumab (Avastin) or with
retention of calcium. Bone metastases are minimal or absent. Any tumor can cause this, squamous cell
cancer of the head and neck, renal ovarian, etc.
no history of local radiation
osteolytic hypercalcemia from malignant cells with bone, usually associated with breast cancer, multiple
myeloma, and lymphoma
15
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Signs & Symptoms Pharmacology

N
exposed necrotic bone, grey to yellow with rough edges
bisphosphonates are similar to pyrophosphate which occurs
pain (or not) and exudate, irregular ulceration naturally in the body and inhibits bone resorption
sinus tracts, sequestrum formation also related to pyrophosphate used as anti-tarter agent in
toothpaste
swelling
bisphosphonates with nitrogen-containing R2 side-chain have
loose teeth, non healing extraction site increased potency and toxicity
radiographically: mottled appearance, widened PDL only nitrogen-containing bisphosphonates have been known to
produce osteonecrosis
Osteoclast/Osteoblast Interplay
Osteoclasts resorb bone

Osteoblasts lay down bone
Dependent upon each other for stimulatory and inhibitory feedback
Pharmacology Pharmacology
Mechanism of Action high affinity for sites of active bone turnover
inhibit bone resorption by causing cell death of the osteoclasts resistant to hydrolytic breakdown
results in inhibited bone turnover and renewal extremely long half-life (some>10 years)
reduces serum calcium cumulative build-up of BP in bone matrix contributes to the problem
increases bone density Biologic Catch-22
readily binds to mineral matrix BP can only be removed from mineral matrix by osteoclastic resorption
accumulates in bone matrix with repeated dosing resorption of BP laden bone is toxic to osteoclasts
anti-angiogenic
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Pharmacology Why the jaws?

Several theories
Bisphosphonate bone toxicity is both TIME and DOSE dependent. remodeling at alveolus is 10x the tibia
IV formulations accumulate very quickly in the bone and are much alveolar bone depends upon osteoclastic bone
more potent. resorption/remodeling more than any other bone in the adult
skeleton
Oral formulations have only 0.63% bioavailability
therapeutic dose to femur, hips and long bones constitutes toxic
takes up to 3 years to reach toxic levels dose to jaw...organ specific toxicity
Medical Comorbidities Dental Comorbidities

IV use of BP
multiple myeloma and use of other anti-angiogenic agents such as thalidomide and Precipitating events
glucocorticoids
2,408 cases of ONJ published since 2003, 89% were
oral steroid use
associated with malignancies
diabetes mellitus
tooth extraction preceded 67% of these cases
overall tumor burden and stage of disease
35% resolved (Filleul, 2010)
patients own health
degree of immunosuppression 88% associated with IV, primarily zoledronic acid and 12%
with alendronate
history of stem cell transplant
Why does this happen? The Perfect Storm

Dental Trauma
Antiangiogenic
increase need for repair and remodeling
while increasing its efficacy in the treatment of malignant bone
high levels of bisphosphonate in jaws
disease, this also decreases blood supply to bone
osteoclasts inhibited/decreased by BPs
Bone remodeling
hypovascularity from anti-angiogenic effect
physiologic function of normal bone
large bacterial load from oral cavity
remove microdamage and replaces damaged bone with new
elastic bone necrosis results
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Oral Bisphosphonates IV Bisphosphonates

prevention is key to reducing risk of developing BONJ
if condition permits, extract all non-restorable teeth and allow 14-
Risk exceedingly small, appears to increase when duration of 21 days for mucosalized/osseous healing
therapy is > 3 years
dental prophylaxis, caries control, restorative
Informed consent
full and partial dentures, examine areas for mucosal trauma
Need long-term prospective studies to establish efficacy of a drug
objectives of BONJ treatment: eliminate pain, control infection
holiday in reducing risk of BONJ
and minimize progression
Orthodontic Implications Orthodontic Implications

Igarashi et al
Kim et al
rats, 3 week, L and R molars moved with expansion spring
with bisphosphonate administered at the same time rats, pamidronate: studied relapse only
total movement was 40% control molars moved with elastics for 21 days
rats, 3 weeks, L and R molars moved then administered control, pamidronate one day before removal of elastics
bisphosphonate
measured relapse at days 5 and 10
total relapse was 50% of control
less relapse with pamidronate
Histological examinations: fewer osteoclasts
Relapse Antibiotics
Penicillins-Pen VK, amoxicillin
Day 0 Day 5 Day 10 Clindamycin (Cleocin)
Doxycycline
Erythromycin
Pamindronate 435 313 115
Metronidazole (Flagyl)
Quinolones-ciprofloxacin (Cipro), levofloxacin (Levaquin)
Control 435 198 57 Culture for actinomyces
ciprofloxacin 500 mg BID + metronidazole 500 mg TID
erythromycin ethylsuccinate 400 mg TID + metronidazole 500 mg TID
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CTX Side Effects

(C-terminal cross-linking telopeptide)
octapeptide fragment from type I collagen in bone cleaved by gastrointestinal upset, esophagitis
osteoclasts
ocular side-effects such as non specific conjunctivitis, scleritis
bone turnover marker which roughly correlates to systemic severe bone, joint pain
suppression of bone renewal caused by oral bispohsophonates
muscle pain
not a reliable tool for patients taking IV bispohsophonates-cancer
affects the values fever
very mixed results, PDL widening may be a more sensitive indicator renal toxicity
than CTX testing hypocalcemia
Fleisher KE et al. Predicting risk for bisphosphonate-related osteonecrosis of the jaws: CTX versus radiographic markers. 2010 110(4) 509-516Oral Surg, Oral Med, Oral Path, Oral Rad and Endo
spontaneous fracture of femur?
New???? New????
Cardwell CR, Abnet CC, Cantwell MM, Murray LJ. Exposure to oral bisphosphonates and risk of esophageal cancer. JAMA 2010;304:657-63.
Atypical fracture: 10-30% of all hip fractures

Bisphosphonates
subtrochanteric, low energy fracture take with a full glass of water and remain upright for 1 hour
prodromal thigh pain, worsening by weight bearing very irritating and cause injury, esophagitis
??? increase in esophageal cancer-observational data, weakest of data

hear or feel fracture occur during non-traumatic activities
not associated with IV
radiographically, see thickening of femoral cortex
even if true, means 1 additional care per 1000 in patients 60-70 taking BP for > 5 years
visible stress fracture on contralateral femur
Shane E, Burr D, Ebeling PR, et al. Atypical subtrochanteric and diaphyseal femoral fractures: report of a task force of the American Society for Bone and Mineral Research. J Bone Min Res
Report Events
FDA MEDWATCH program

1-800-FDA-1099
severe bone, joint pain
www.fda.gov/medwatch
19
M.S. in Oral and Maxillofacial Radiology, University of North Carolina at Chapel Hill, 2009
D.D.S., Bharati Vidyapeeth University, Pune, India, 2000
American Board of Oral and Maxillofacial Radiology
Dr. Rathore completed her specialty training in Oral and Maxillofacial Radiology from UNC School of Dentistry,
Chapel Hill, NC in 2009. She was also awarded a certificate for completion of clinical research scholars
program (a NIH training grant) in 2008. While a resident at Chapel Hill, she has won the Albert G. Richards
award for graduate student research in 2007 and the William H. Rollins awards in 2008, which are both very
prestigious awards from the American Academy of Oral and Maxillofacial Radiology. She joined VCU Dental
School in 2010 as an Assistant Professor in the department of Oral Diagnostic Sciences.
Dr. Rathore is board certified by the American Board of Oral and Maxillofacial Radiology. Board certification is
the highest recognition and academic hallmark of professionalism offered by a specialty. She has published in
several journals such as Dental clinics of North America and Dentomaxillofacial Radiology. She is also a
reviewer for journals such as Angle Orthodontist and Journal of Caries Research.
Applications of cone beam CT in dentistry
Dose considerations with advanced imaging

DENTAL RADIOGRAPHIC EXAMINATIONS: RECOMMENDATIONS FOR
PATIENT SELECTION AND LIMITING RADIATION EXPOSURE
REVISED: 2012
AMERICAN DENTAL ASSOCIATION

Council on Scientific Affairs
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service
Food and Drug Administration
TABLE OF CONTENTS
Background............................................................................................................................ 1
Introduction ............................................................................................................................ 1
Patient Selection Criteria ...................................................................................................... 2
Recommendations for Prescribing Dental Radiographs ......................................... 5
Explanation of Recommendations for Prescribing Dental Radiographs ................ 8
New Patient Being Evaluated for Oral Diseases............................................ 8
Recall Patient with Clinical Caries or Increased Risk for Caries ............... 11
Recall Patient (Edentulous Adult) ................................................................. 11
Recall Patient with No Clinical Caries and No Increased Risk for Caries . 11
Recall Patient with Periodontal Disease ...................................................... 12
Patient (New and Recall) for Monitoring Growth and Development .......... 13
Patients with Other Circumstances .............................................................. 14
Limiting Radiation Exposure .............................................................................................. 14
Receptor Selection ................................................................................................... 14
Receptor Holders ...................................................................................................... 15
Collimation ................................................................................................................ 15
Operating Potential and Exposure Time ................................................................. 16
Patient Shielding and Positioning ........................................................................... 16
Operator Protection .................................................................................................. 16
Hand-held X-ray Units .............................................................................................. 17
Film Exposure and Processing................................................................................ 17
Quality Assurance .................................................................................................... 17
Technique Charts/Protocols .................................................................................... 18
Radiation Risk Communication ............................................................................... 18
Training and Education ............................................................................................ 20
Conclusion ........................................................................................................................... 20
References ........................................................................................................................... 21
DENTAL RADIOGRAPHIC EXAMINATIONS: RECOMMENDATIONS FOR PATIENT
SELECTION AND LIMITING RADIATION EXPOSURE
BACKGROUND
The dental profession is committed to delivering the highest quality of care to each of its
individual patients and applying advancements in technology and science to continually
improve the oral health status of the U.S. population. These guidelines were developed
to serve as an adjunct to the dentists professional judgment of how to best use
diagnostic imaging for each patient. Radiographs can help the dental practitioner
evaluate and definitively diagnose many oral diseases and conditions. However, the
dentist must weigh the benefits of taking dental radiographs against the risk of exposing
a patient to x-rays, the effects of which accumulate from multiple sources over time.
The dentist, knowing the patients health history and vulnerability to oral disease, is in
the best position to make this judgment in the interest of each patient. For this reason,
the guidelines are intended to serve as a resource for the practitioner and are not
intended as standards of care, requirements or regulations.
The guidelines are not substitutes for clinical examinations and health histories. The
dentist is advised to conduct a clinical examination, consider the patients signs,
symptoms and oral and medical histories, as well as consider the patients vulnerability
to environmental factors that may affect oral health. This diagnostic and evaluative
information may determine the type of imaging to be used or the frequency of its use.
Dentists should only order radiographs when they expect that the additional diagnostic
information will affect patient care.
Based on this premise, the guidelines can be used by the dentist to optimize patient
care, minimize radiation exposure and responsibly allocate health care resources.
This document deals only with standard dental imaging techniques of intraoral and
common extraoral examinations, excluding cone-beam computed tomography (CBCT).
At this time the indications for CBCT examinations are not well developed. The ADA
Council on Scientific Affairs has developed a statement on use of CBCT. 1
INTRODUCTION
The guidelines titled, The Selection of Patients for X-Ray Examination were first
developed in 1987 by a panel of dental experts convened by the Center for Devices and
Radiological Health of the U.S. Food and Drug Administration (FDA). The development
of the guidelines at that time was spurred by concern about the U.S. populations total
exposure to radiation from all sources. Thus, the guidelines were developed to promote
the appropriate use of x-rays. In 2002, the American Dental Association, recognizing
that dental technology and science continually advance, recommended to the FDA that
1
the guidelines be reviewed for possible updating. The FDA welcomed organized
dentistrys interest in maintaining the guidelines, and so the American Dental
Association, in collaboration with a number of dental specialty organizations and the
FDA, published updated guidelines in 2004. This report updates the 2004 guidelines
and includes recommendations for limiting exposure to radiation.
PATIENT SELECTION CRITERIA
Radiographs and other imaging modalities are used to diagnose and monitor oral
diseases, as well as to monitor dentofacial development and the progress or prognosis
of therapy. Radiographic examinations can be performed using digital imaging or
conventional film. The available evidence suggests that either is a suitable diagnostic
method.2-4 Digital imaging may offer reduced radiation exposure and the advantage of
image analysis that may enhance sensitivity and reduce error introduced by subjective
analysis.5
A study of 490 patients found that basing selection criteria on clinical evaluations for
asymptomatic patients, combined with selected periapical radiographs for symptomatic
patients, can result in a 43 percent reduction in the number of radiographs taken without
a clinically consequential increase in the rate of undiagnosed disease.6,7 The
development and progress of many oral conditions are associated with a patients age,
stage of dental development, and vulnerability to known risk factors. Therefore, the
guidelines in Table 1 are presented within a matrix of common clinical and patient
factors, which may determine the type(s) of radiographs that is commonly needed. The
guidelines assume that diagnostically adequate radiographs can be obtained. If not,
appropriate management techniques should be used after consideration of the relative
risks and benefits for the patient.
Along the horizontal axis of the matrix, patient age categories are described, each with
its usual dental developmental stage: child with primary dentition (prior to eruption of the
first permanent tooth); child with transitional dentition (after eruption of the first
permanent tooth); adolescent with permanent dentition (prior to eruption of third
molars); adult who is dentate or partially edentulous; and adult who is edentulous.
Along the vertical axis, the type of encounter with the dental system is categorized (as
New Patient or Recall Patient) along with the clinical circumstances and oral
diseases that may be present during such an encounter. The New Patient category
refers to patients who are new to the dentist, and thus are being evaluated by the
dentist for oral disease and for the status of dental development. Typically, such a
patient receives a comprehensive evaluation or, in some cases, a limited evaluation for
a specific problem. The Recall Patient categories describe patients who have had a
recent comprehensive evaluation by the dentist and, typically, have returned as a
patient of record for a periodic evaluation or for treatment. However, a Recall Patient
may also return for a limited evaluation of a specific problem, a detailed and extensive
evaluation for a specific problem(s), or a comprehensive evaluation.
2
Both categories are marked with a single asterisk that corresponds to a footnote that
appears below the matrix; the footnote lists Positive Historical Findings and Positive
Clinical Signs/Symptoms for which radiographs may be indicated. The lists are not
intended to be all-inclusive, rather they offer the clinician further guidance on clarifying
his or her specific judgment on a case.
The clinical circumstances and oral diseases that are presented with the types of
encounters include: clinical caries or increased risk for caries; no clinical caries or no
increased risk for caries; periodontal disease or a history of periodontal treatment;
growth and development assessment; and other circumstances. A few examples of
Other Circumstances proposed are: existing implants, other dental and craniofacial
pathoses, endodontic/restorative needs and remineralization of dental caries. These
examples are not intended to be an exhaustive list of circumstances for which
radiographs or other imaging may be appropriate.
The categories, Clinical Caries or Increased Risk for Caries and No Clinical Caries
and No Increased Risk for Caries are marked with a double asterisk that corresponds
to a footnote that appears below the matrix; the footnote contains links to the ADA
Caries Risk Assessment Forms (0 6 years of age and over 6 years of age). It should
be noted that a patients risk status can change over time and should be periodically
reassessed.8
The panel also has made the following recommendations that are applicable to all
categories:
1. Intraoral radiography is useful for the evaluation of dentoalveolar trauma. If the
area of interest extends beyond the dentoalveolar complex, extraoral imaging
may be indicated.
2. Care should be taken to examine all radiographs for any evidence of caries, bone
loss from periodontal disease, developmental anomalies and occult disease.
3. Radiographic screening for the purpose of detecting disease before clinical
examination should not be performed. A thorough clinical examination,
consideration of the patient history, review of any prior radiographs, caries risk
assessment and consideration of both the dental and the general health needs of
the patient should precede radiographic examination.9-15
In the practice of dentistry, patients often seek care on a routine basis in part because
oral disease may develop in the absence of clinical symptoms. Since attempts to
identify specific criteria that will accurately predict a high probability of finding
interproximal carious lesions have not been successful for individuals, it was necessary
to recommend time-based schedules for making radiographs intended primarily for the
detection of dental caries. Each schedule provides a range of recommended intervals
that are derived from the results of research into the rates at which interproximal caries
progresses through tooth enamel. The recommendations also are modified by criteria
that place an individual at an increased risk for dental caries. Professional judgment
3
should be used to determine the optimum time for radiographic examination within the
suggested interval.
4
RECOMMENDATIONS FOR PRESCRIBING DENTAL RADIOGRAPHS
These recommendations are subject to clinical judgment and may not apply to every patient. They are to be used by dentists only after
reviewing the patients health history and completing a clinical examination. Even though radiation exposure from dental radiographs is
low, once a decision to obtain radiographs is made it is the dentist's responsibility to follow the ALARA Principle (As Low as
Reasonably Achievable) to minimize the patient's exposure.
Table 1.
PATIENT AGE AND DENTAL DEVELOPMENTAL STAGE
Child with Primary Child with Adolescent with Adult, Dentate or Adult, Edentulous
TYPE OF ENCOUNTER
Dentition (prior to Transitional Permanent Partially Edentulous
eruption of first Dentition (after Dentition (prior to
permanent tooth) eruption of first eruption of third
permanent tooth) molars)
New Patient* Individualized
being evaluated for oral radiographic exam
diseases consisting of selected
periapical/occlusal
views and/or Individualized Individualized radiographic exam consisting of
posterior bitewings if radiographic exam posterior bitewings with panoramic exam or
proximal surfaces consisting of posterior posterior bitewings and selected periapical Individualized
cannot be visualized bitewings with images. A full mouth intraoral radiographic radiographic exam,
or probed. Patients panoramic exam or exam is preferred when the patient has based on clinical
without evidence of posterior bitewings clinical evidence of generalized oral disease signs and symptoms.
disease and with and selected or a history of extensive dental treatment.
open proximal periapical images.
contacts may not
require a
radiographic exam at
this time.
Recall Patient* with Posterior bitewing exam at 6-12 month intervals if proximal surfaces Posterior bitewing
clinical caries or at cannot be examined visually or with a probe exam at 6-18 month Not applicable
increased risk for caries** intervals
Recall Patient* with no Posterior bitewing exam at 12-24 month
Posterior bitewing Posterior bitewing
clinical caries and not at intervals if proximal surfaces cannot be
exam at 18-36 month exam at 24-36 month Not applicable
increased risk for caries** examined visually or with a probe
intervals intervals
5
Child with Primary Child with Adolescent with Adult, Dentate and Adult, Edentulous
Dentition (prior to Transitional Permanent Partially Edentulous
TYPE OF ENCOUNTER
eruption of first Dentition (after Dentition (prior to
(continued)
permanent tooth) eruption of first eruption of third
permanent tooth) molars)
Recall Patient* with Clinical judgment as to the need for and type of radiographic images for the evaluation of
periodontal disease periodontal disease. Imaging may consist of, but is not limited to, selected bitewing and/or
Not applicable
periapical images of areas where periodontal disease (other than nonspecific gingivitis) can be
demonstrated clinically.
Patient (New and Recall) Clinical judgment as
for monitoring of to need for and type
dentofacial growth and of radiographic
development, and/or images for evaluation
assessment of Clinical judgment as to need for and type of and/or monitoring of
Usually not indicated for monitoring of growth
dental/skeletal radiographic images for evaluation and/or dentofacial growth
and development. Clinical judgment as to the
relationships monitoring of dentofacial growth and and development, or
need for and type of radiographic image for
development or assessment of dental and assessment of dental
evaluation of dental and skeletal relationships.
skeletal relationships and skeletal
relationships.
Panoramic or
periapical exam to
assess developing
third molars
Patient with other
circumstances including,
but not limited to,
proposed or existing
implants, other dental and Clinical judgment as to need for and type of radiographic images for evaluation and/or monitoring of these conditions
craniofacial pathoses,
restorative/endodontic
needs, treated periodontal
disease and caries
remineralization
*Clinical situations for which radiographs may be

indicated include, but are not limited to:
A. Positive Historical Findings

1. Previous periodontal or endodontic treatment
2. History of pain or trauma
3. Familial history of dental anomalies
6
4. Postoperative evaluation of healing
5. Remineralization monitoring
6. Presence of implants, previous implant-related pathosis or evaluation for implant placement
B. Positive Clinical Signs/Symptoms

1. Clinical evidence of periodontal disease
2. Large or deep restorations
3. Deep carious lesions
4. Malposed or clinically impacted teeth
5. Swelling
6. Evidence of dental/facial trauma
7. Mobility of teeth
8. Sinus tract (fistula)
9. Clinically suspected sinus pathosis
10. Growth abnormalities
11. Oral involvement in known or suspected systemic disease
12. Positive neurologic findings in the head and neck
13. Evidence of foreign objects
14. Pain and/or dysfunction of the temporomandibular joint
15. Facial asymmetry
16. Abutment teeth for fixed or removable partial prosthesis
17. Unexplained bleeding
18. Unexplained sensitivity of teeth
19. Unusual eruption, spacing or migration of teeth
20. Unusual tooth morphology, calcification or color
21. Unexplained absence of teeth
22. Clinical tooth erosion
23. Peri-implantitis
Factors increasing risk for caries may be assessed using the ADA Caries Risk Assessment forms (0 6 years of age and
over 6 years of age).
7
EXPLANATION OF RECOMMENDATIONS FOR PRESCRIBING DENTAL RADIOGRAPHS
The explanation below presents the rationale for each recommendation by type of encounter
and patient age and dental developmental stages.
New Patient Being Evaluated for Oral Diseases
Child (Primary Dentition)

Proximal carious lesions may develop after the interproximal spaces between posterior primary
teeth close. Open contacts in the primary dentition will allow a dentist to visually inspect the
proximal posterior surfaces. Closure of proximal contacts requires radiographic assessment. 16-
18
However, evidence suggests that many of these lesions will remain in the enamel for at
least 12 months or longer depending on fluoride exposure, allowing sufficient time for
implementation and evaluation of preventive interventions. 19-21 A periapical/anterior occlusal
examination may be indicated because of the need to evaluate dental development,
dentoalveolar trauma, or suspected pathoses. Periapical and bitewing radiographs may be
required to evaluate pulp pathosis in primary molars.
Therefore, an individualized radiographic examination consisting of selected

periapical/occlusal views and/or posterior bitewings if proximal surfaces cannot be examined
visually or with a probe is recommended. Patients without evidence of disease and with open
proximal contacts may not require radiographic examination at this time.
Child (Transitional Dentition)

Overall dental caries in the primary teeth of children from 2-11 years of age declined from the
early 1970s until the mid 1990s.22-24 From the mid 1990s until the 1999-2004 National Health
and Nutrition Examination Survey, there was a small but significant increase in primary decay.
This trend reversal was larger for younger children. Tooth decay affects more than one-fourth
of U.S. children aged 25 years and half of those aged 12-15 years; however, its prevalence is
not uniformly distributed. About half of all children and two-thirds of adolescents aged 1219
years from lower-income families have had decay.25
Children and adolescents of some racial and ethnic groups and those from lower-income
families have more untreated tooth decay. For example, 40 percent of Mexican American
children aged 68 years have untreated decay, compared with 25 percent of non-Hispanic
whites.25 It is, therefore, important to consider a childs risk factors for caries before taking
radiographs.
Although periodontal disease is uncommon in this age group,26 when clinical evidence exists
(except for nonspecific gingivitis), selected periapical and bitewing radiographs are indicated to
determine the extent of aggressive periodontitis, other forms of uncontrolled periodontal
disease and the extent of osseous destruction related to metabolic diseases. 27,28
A periapical or panoramic examination is useful for evaluating dental development. A

panoramic radiograph also is useful for the evaluation of craniofacial trauma. 15,29,30 Intraoral
radiographs are more accurate than panoramic radiographs for the evaluation of dentoalveolar
8
trauma, root shape, root resorption31,32 and pulp pathosis. However, panoramic examinations
may have the advantage of reduced radiation dose, cost and imaging of a larger area.
Occlusal radiographs may be used separately or in combination with panoramic radiographs in

the following situations: 1. unsatisfactory image in panoramic radiographs due to abnormal
incisor relationship, 2. localizations of tooth position, and 3. when clinical grounds provide a
reasonable expectation that pathosis exists.32-34
Therefore, an individualized radiographic examination consisting of posterior bitewings with

panoramic examination or posterior bitewings and selected periapical images is
recommended.
Adolescent (Permanent Dentition)

Caries in permanent teeth declined among adolescents, while the prevalence of dental
sealants increased significantly.35 However, increasing independence and socialization,
changing dietary patterns, and decreasing attention to daily oral hygiene can characterize this
age group. Each of these factors may result in an increased risk of dental caries. Another
consideration, although uncommon, is the increased incidence of periodontal disease found in
this age group compared to children.36
Panoramic radiography is effective in dental diagnosis and treatment planning. 30,37,38

Specifically, the status of dental development can be assessed using panoramic radiography. 39
Occlusal and/or periapical radiographs can be used to detect the position of an unerupted or
supernumerary tooth.40-42 Third molars also should be evaluated in this age group for their
presence, position, and stage of development.
Therefore, an individualized radiographic examination consisting of posterior bitewings with

panoramic examination or posterior bitewings and selected periapical images is
recommended. A full mouth intraoral radiographic examination is preferred when the patient
has clinical evidence of generalized oral disease or a history of extensive dental treatment.
Adult (Dentate or Partially Edentulous)

The overall dental caries experience of the adult population has declined from the early 1970s
until the most recent (1999-2004) National Health and Nutrition Examination Survey.43
However, risk for dental caries exists on a continuum and changes over time as risk factors
change.44 Therefore, it is important to evaluate proximal surfaces in the new adult patient for
carious lesions. In addition, it is important to examine patients for recurrent dental caries.
The incidence of root surface caries increases with age.45 Although bitewing radiographs can
assist in detecting root surface caries in proximal areas, the usual method of detecting root
surface caries is by clinical examination.46
The incidence of periodontal disease increases with age.47 Although new adult patients may
not have symptoms of active periodontal disease, it is important to evaluate previous
experience with periodontal disease and/or treatment. Therefore, a high percentage of adults
may require selected intraoral radiographs to determine the current status of the disease.
9
Taking posterior bitewing radiographs of new adult patients was found to reduce the number of
radiological findings and the diagnostic yield of panoramic radiography.48,49 In addition, the
following clinical indicators for panoramic radiography were identified as the best predictors for
useful diagnostic yield: suspicion of teeth with periapical pathologic conditions, presence of
partially erupted teeth, caries lesions, swelling, and suspected unerupted teeth.50
Therefore, an individualized radiographic examination, consisting of posterior bitewings with

selected periapical images or panoramic examination when indicated is recommended. A full
mouth intraoral radiographic examination is preferred when the patient has clinical evidence of
generalized oral disease or a history of extensive dental treatment.
Adult (Edentulous)
The clinical and radiographic examinations of edentulous patients generally occur during an
assessment of the need for prostheses. The most common pathological conditions detected
are impacted teeth and retained roots with and without associated disease. 51 Other less
common conditions also may be detected: bony spicules along the alveolar ridge, residual
cysts or infections, developmental abnormalities of the jaws, intraosseous tumors, and
systemic conditions affecting bone metabolism.
The original recommendations for this group called for a full-mouth intraoral radiographic
examination or a panoramic examination for the new, edentulous adult patient. Firstly, this
recommendation was made because examinations of edentulous patients generally occur
during an assessment of the need for prostheses. Secondly, the original recommendation
considered edentulous patients to be at increased risk for oral disease.
Studies have found that from 30 to 50 percent of edentulous patients exhibited abnormalities in
panoramic radiographs.51-55 In addition, the radiographic examination revealed anatomic
considerations that could influence prosthetic treatment, such as the location of the mandibular
canal, the position of the mental foramen and maxillary sinus, and relative thickness of the soft
tissue covering the edentulous ridge.51,53,55 However, in studies that considered treatment
outcomes, there was little evidence to support screening radiography for new edentulous
patients. For example, one study reported that less than 4 percent of such findings resulted in
treatment modification before denture fabrication, and another showed no difference in post-
denture delivery complaints in patients who did not receive screening pretreatment
radiographs.54,56
This panel concluded that prescription of radiographs is appropriate as part of the initial
assessment of edentulous areas for possible prosthetic treatment. A full mouth series of
periapical radiographs or a combination of panoramic, occlusal or other extraoral radiographs
may be used to achieve diagnostic and therapeutic goals. Particularly with the option of dental
implant therapy for edentulous patients,57 radiographs can be an important aid in diagnosis,
prognosis, and the determination of treatment complexity.
Therefore, an individualized radiographic examination, based on clinical signs, symptoms, and

treatment plan is recommended.
10
Recall Patient with Clinical Caries or Increased Risk for Caries
Child (Primary and Transitional Dentition) and Adolescent (Permanent Dentition)

Clinically detectable dental caries may suggest the presence of proximal carious lesions that
can only be detected with a radiographic examination. In addition, patients who are at
increased risk for developing dental caries because of such factors as poor oral hygiene, high
frequency of exposure to sucrose-containing foods, and deficient fluoride intake (see caries
risk assessment forms, 0 6 years of age and over 6 years of age) are more likely to have
proximal carious lesions.
The bitewing examination is the most efficient method for detecting proximal lesions. 16,18,58
The frequency of radiographic recall should be determined on the basis of caries risk
assessment.15,59,60 It should be noted that a patients caries risk status may change over time
and that an individuals radiographic recall interval may need to be changed accordingly. 61
Therefore, a posterior bitewing examination is recommended at 6 to 12 month intervals if

proximal surfaces cannot be examined visually or with a probe.
Adult (Dentate and Partially Edentulous)

Adults who exhibit clinical dental caries or who have other increased risk factors should be
monitored carefully for any new or recurrent lesions that are detectable only by radiographic
examination. The frequency of radiographic recall should be determined on the basis of caries
risk assessment.15,59,60 It should be noted that a patients risk status can change over time and
that an individuals radiographic recall interval may need to be changed accordingly. 61
Therefore, a posterior bitewing examination is recommended at 6 to 18 month intervals.
Recall Patient (Edentulous Adult)
A study that assessed radiographs of edentulous recall patients showed that previously
detected incidental findings did not progress and that no intervention was indicated.62 The data
suggest that patients who receive continuous dental care do not exhibit new findings that
require treatment.
An examination for occult disease in this group cannot be justified on the basis of prevalence,
morbidity, mortality, radiation dose, and cost.53-55
Therefore, no radiographic examination is recommended without evidence of disease.
Recall Patient with No Clinical Caries and No Increased Risk for Caries
Child (Primary and Transitional Dentition)

Despite the general decline in dental caries activity, recent data show that subgroups of
children have a higher caries experience than the overall population.63,64 The identification of
11
patients in these subgroups may be difficult on an individual basis. For children who present
for recall examination without evidence of clinical caries and who are not considered at
increased risk for the development of caries, it remains important to evaluate proximal surfaces
by radiographic examination. In primary teeth the caries process can take approximately one
year to progress through the outer half of the enamel and about another year through the inner
half.20,65-68 Considering this rate of progression of carious lesions through primary teeth, a time-
based interval of radiographic examinations from one to two years for this group appears
appropriate. The prevalence of carious lesions has been shown to increase during the stage of
transitional dentition.25,69 Children under routine professional care would be expected to be at a
lower risk for caries. Nevertheless, newly erupted teeth are at risk for the development of
dental caries.
Therefore, a radiographic examination consisting of posterior bitewings is recommended at

intervals of 12 to 24 months if proximal surfaces cannot be examined visually or with a probe.

Adolescents with permanent dentition, who are free of clinical dental caries and factors that
would place them at increased risk for developing dental caries, should be monitored carefully
for development of proximal carious lesions, which may only be detected by radiographic
examination. The caries process, on average, takes more than three years to progress
through the enamel.20,65-68 However, evidence suggests that the enamel of permanent teeth
undergoes posteruptive maturation and that young permanent teeth are susceptible to faster
progression of carious lesions.70-73

intervals of 18 to 36 months.
Adult (Dentate and Partially Edentulous)

Adult dentate patients, who receive regularly scheduled professional care and are free of signs
and symptoms of oral disease, are at a low risk for dental caries. Nevertheless, consideration
should be given to the fact that caries risk can vary over time as risk factors change.
Advancing age and changes in diet, medical history and periodontal status may increase the
risk for dental caries.

intervals of 24 to 36 months.
Recall Patient with Periodontal Disease
Child (Primary and Transitional Dentition), Adolescent (Permanent Dentition), and Adult
(Dentate and Partially Edentulous)
The decision to obtain radiographs for patients who have clinical evidence or a history of
periodontal disease/treatment should be determined on the basis of the anticipation that
important diagnostic and prognostic information will result. Structures or conditions to be
assessed should include the level of supporting alveolar bone, condition of the interproximal
bony crest, length and shape of roots, bone loss in furcations, and calculus deposits. The
12
frequency and type of radiographic examinations for these patients should be determined on
the basis of a clinical examination of the periodontium and documented signs and symptoms of
periodontal disease. The procedure for prescribing radiographs for the follow-up/recall
periodontal patient would be to use selected intraoral radiographs to verify clinical findings on a
patient-by-patient basis.28,74
Therefore, it is recommended that clinical judgment be used in determining the need for, and
type of radiographic images necessary for, evaluation of periodontal disease. Imaging may
consist of, but is not limited to, selected bitewing and/or periapical images of areas where
periodontal disease (other than nonspecific gingivitis) can be identified clinically.
Patient (New and Recall) for Monitoring of Dentofacial Growth and Development, and/or
Assessment of Dental/Skeletal Relationships
Child (Primary and Transitional Dentition)

For children with primary dentition, before the eruption of the first permanent tooth,
radiographic examination to assess growth and development in the absence of clinical signs or
symptoms is unlikely to yield productive information. Any abnormality of growth and
development suggested by clinical findings should be evaluated radiographically on an
individual basis. After eruption of the first permanent tooth, the child may have a radiographic
examination to assess growth and development. This examination need not be repeated
unless dictated by clinical signs or symptoms. Cephalometric radiographs may be useful for
assessing growth, and/or dental and skeletal relationships.
type of radiographic images necessary for, evaluation and/or monitoring of dentofacial growth
and development, or assessment of dental and skeletal relationships.

During adolescence there is often a need to assess the growth status and/or the dental and
skeletal relationships of patients in order to diagnose and treat their malocclusion. Appropriate
radiographic assessment of the malocclusion should be determined on an individual basis.
An additional concern relating to growth and development for patients in this age group is to
determine the presence, position and development of third molars. This determination can
best be made by the use of selected periapical images or a panoramic examination, once the
patient is in late adolescence (16 to 19 years of age).
type of radiographic images necessary for, evaluation and/or monitoring of dentofacial growth
and development, or assessment of dental and skeletal relationships. Panoramic or periapical
examination may be used to assess developing third molars.
Adult (Dentate, Partially Edentulous and Edentulous)

In the absence of any clinical signs or symptoms suggesting abnormalities of growth and
development in adults, no radiographic examinations are indicated for this purpose.
13
Therefore, in the absence of clinical signs and symptoms, no radiographic examination is
recommended.
Patients with Other Circumstances

(including, but not limited to, proposed or existing implants, other dental and craniofacial
pathoses, restorative/endodontic needs, treated periodontal disease and caries
remineralization)
All Patient Categories

The use of imaging, as a diagnostic and evaluative tool, has progressed beyond the
longstanding need to diagnose caries and evaluate the status of periodontal disease. The
expanded technology in imaging is now used to diagnose other orofacial clinical conditions and
evaluate treatment options. A few examples of other clinical circumstances are the use of
imaging for dental implant treatment planning, placement, or evaluation; the monitoring of
dental caries and remineralization; the assessment of restorative and endodontic needs; and
the diagnosis of soft and hard tissue pathoses.
Therefore it is recommended that clinical judgment be used in determining the need for, and
type of radiographic images necessary for, evaluation and/or monitoring in these
circumstances.
LIMITING RADIATION EXPOSURE
Dental radiographs account for approximately 2.5 percent of the effective dose received from
medical radiographs and fluoroscopies.75 Even though radiation exposure from dental
radiographs is low, once a decision to obtain radiographs is made it is the dentist's
responsibility to follow the ALARA Principle (As Low as Reasonably Achievable) to minimize
the patient's exposure. Examples of good radiologic practice include
use of the fastest image receptor compatible with the diagnostic task (F-speed film or
digital);
collimation of the beam to the size of the receptor whenever feasible;
proper film exposure and processing techniques;
use of protective aprons and thyroid collars, when appropriate; and
limiting the number of images obtained to the minimum necessary to obtain essential
diagnostic information.
RECEPTOR SELECTION
The American National Standards Institute and the International Organization for
Standardization have established standards for film speed.76,77 Film speeds available for dental
radiography are D-speed, E-speed and F-speed, with D-speed being the slowest and F-speed
the fastest. According to the U.S. Food and Drug Administration, switching from D to E speed
can produce a 30 to 40 percent reduction in radiation exposure. 78 The use of F-speed film can
reduce exposure 20 to 50 percent compared to use of E-speed film, without compromising
diagnostic quality.79-85
14
Exposure of extraoral films such as panoramic radiographs requires intensifying screens to
minimize radiation exposure to patients. The intensifying screen consists of layers of phosphor
crystals that fluoresce when exposed to radiation. In addition to the radiation incident on the
film, the film is exposed primarily to the light emitted from the intensifying screen. Previous
generations of intensifying screens were composed of phosphors such as calcium tungstate.
However, rare-earth intensifying screens are recommended because they reduce a patients
radiation exposure by 50 percent compared with calcium tungstate-intensifying screens.86-89
Rare-earth film systems, combined with a high-speed film of 400 or greater, can be used for
panoramic radiographs.86 Older panoramic equipment can be retrofitted to reduce the radiation
exposure to accommodate the use of rare-earth, high-speed systems.
Digital imaging provides an opportunity to further reduce the radiation dose by 40 to 60

percent.90-93 In digital radiography, there are three types of receptors that take the place of
conventional film: charge-coupled device (CCD), complementary-metal-oxide-semiconductor
(CMOS), and photo-stimulable phosphor (PSP) plates. Systems that use CCD and CMOS-
based, solid-state detectors are called direct. When these sensors receive energy from the x-
ray beam, the CCD or CMOS chip sends a signal to the computer and an image appears on
the monitor within seconds. Systems that use PSP plates are called indirect. When these
plates are irradiated, a latent image is stored on them. The plate is then scanned and the
scanner transmits the image to the computer.
RECEPTOR HOLDERS
Holders that align the receptor precisely with the collimated beam are recommended for
periapical and bitewing radiographs. Heat-sterilizable or disposable intraoral radiograph
receptor-holding devices are recommended for optimal infection control.94 Dental professionals
should not hold the receptor holder during exposure. 86 Under extraordinary circumstances in
which members of the patients family (or other caregiver) must provide restraint or hold a
receptor holder in place during exposure, such a person should wear appropriate shielding. 86
COLLIMATION
Collimation limits the amount of radiation, both primary and scattered, to which the patient is
exposed. An added benefit of rectangular collimation is an improvement in contrast as a result
of a reduction in fogging caused by secondary and scattered radiation. 89 The x-ray beam
should not exceed the minimum coverage necessary, and each dimension of the beam should
be collimated so that the beam does not exceed the receptor by more than 2 percent of the
source-to-image receptor distance.86 Since a rectangular collimator decreases the radiation
dose by up to fivefold as compared with a circular one, 86,95,96 radiographic equipment should
provide rectangular collimation for exposure of periapical and bitewing radiographs. 86 Use of a
receptor-holding device minimizes the risk of cone-cutting (non-exposure of part of the image
receptor due to malalignment of the x-ray beam). The position-indicating device should be
open ended and have a metallic lining to restrict the primary beam and reduce the tissue
volume exposed to radiation.86 Use of long source-to-skin distances of 40 cm, rather than short
distances of 20 cm, decreases exposure by 10 to 25 percent. 86,97 Distances between 20 cm
and 40 cm are appropriate, but the longer distances are optimal.86
15
OPERATING POTENTIAL AND EXPOSURE TIME
The operating potential of dental x-ray units affects the radiation dose and backscatter
radiation. Lower voltages produce higher-contrast images and higher entrance skin doses, and
lower deep-tissue doses and levels of backscatter radiation. However, higher voltages produce
lower contrast images that enable better separation of objects with differing densities. Thus,
the diagnostic purposes of the radiograph should be used to determine the selection of kilovolt
setting. A setting above 90 kV(p) will increase the patient dose and should not be used.89 The
optimal operating potential of dental x-ray units is between 60 and 70 kVp.86,89
Filmless technology is much more forgiving to overexposure often resulting in unnecessary

radiation exposure. Facilities should strive to set the x-ray unit exposure timer to the lowest
setting providing an image of diagnostic quality. If available, the operator should always
confirm that the dose delivered falls within the manufacturers exposure index. Imaging plates
should be evaluated at least monthly and cleaned as necessary.
PATIENT SHIELDING AND POSITIONING

The amount of scattered radiation striking the patients abdomen during a properly conducted
radiographic examination is negligible.98 The thyroid gland is more susceptible to radiation
exposure during dental radiographic exams given its anatomic position, particularly in
children.93,99,100 Protective thyroid collars and collimation substantially reduce radiation
exposure to the thyroid during dental radiographic procedures.101,102 Because every precaution
should be taken to minimize radiation exposure, protective thyroid collars should be used
whenever possible. If all the recommendations for limiting radiation exposure are put into
practice, the gonadal radiation dose will not be significantly affected by use of abdominal
shielding.86 Therefore, use of abdominal shielding may not be necessary.
Protective aprons and thyroid shields should be hung or laid flat and never folded, and
manufacturers instructions should be followed. All protective shields should be evaluated for
damage (e.g. tears, folds, and cracks) monthly using visual and manual inspection.
Proper education and training in patient positioning is necessary to ensure that panoramic
radiographs are of diagnostic quality.
OPERATOR PROTECTION
Although dental professionals receive less exposure to ionizing radiation than do other
occupationally exposed health care workers,75,86 operator protection measures are essential to
minimize exposure. Operator protection measures include education, the implementation of a
radiation protection program, occupational radiation exposure limits, recommendations for
personal dosimeters and the use of barrier shielding.103 The maximum permissible annual
dose of ionizing radiation for health care workers is 50 millisieverts (mSv) and the maximum
permissible lifetime dose is 10 mSv multiplied by a persons age in years.86 Personal
dosimeters should be used by workers who may receive an annual dose greater than 1 mSv to
monitor their exposure levels. Pregnant dental personnel operating x-ray equipment should
use personal dosimeters, regardless of anticipated exposure levels.86
16
Operators of radiographic equipment should use barrier protection when possible, and barriers
should ideally contain a leaded glass window to enable the operator to view the patient during
exposure.86 When shielding is not possible, the operator should stand at least two meters from
the tube head and out of the path of the primary beam.103 The National Council on Radiation
Protection & Measurements report Radiation Protection in Dentistry offers detailed
information on shielding and office design.86 State radiation control agencies can help assess
whether barriers meet minimum standards.
HAND-HELD X-RAY UNITS

Hand-held, battery-powered x-ray systems are available for intra-oral radiographic imaging.
The hand-held exposure device is activated by a trigger on the handle of the device. However,
dosimetry studies indicate that these hand-held devices present no greater radiation risk than
standard dental radiographic units to the patient or the operator. No additional radiation
protection precautions are needed when the device is used according to the manufacturers
instructions. These include: 1. holding the device at mid-torso height, 2. orienting the shielding
ring properly with respect to the operator, and 3. keeping the cone as close to the patients
face as practical. If the hand-held device is operated without the ring shield in place, it is
recommended that the operator wear a lead apron.
All operators of hand-held units should be instructed on their proper storage. Due to the
portable nature of these devices, they should be secured properly when not in use to prevent
accidental damage, theft, or operation by an unauthorized user. Hand-held units should be
stored in locked cabinets, locked storage rooms, or locked work areas when not under the
direct supervision of an individual authorized to use them. Units with user-removable batteries
should be stored with the batteries removed. Records listing the names of approved
individuals who are granted access and use privileges should be prepared and kept current.
FILM EXPOSURE AND PROCESSING

All film should be processed following the film and processer manufacturer
recommendations. Once this is achieved, the x-ray operator can adjust the tube current and
time and establish a technique that will provide consistent dental radiographs of diagnostic
quality. Poor processing technique, including sight-developing, most often results in
underdeveloped films, forcing the x-ray operator to increase the dose to compensate, resulting
in patient and personnel being exposed to unnecessary radiation.
A safelight does not provide completely safe exposure for an indefinite period of
time. Extraoral film is much more sensitive to fogging. The length of time for which a film can
be exposed to the safelight should be determined for the specific safelight/film combination in
use.
QUALITY ASSURANCE
Quality assurance protocols for the x-ray unit, imaging receptor, film processing, dark room,
and patient shielding should be developed and implemented for each dental health care
setting.86 All quality assurance procedures, including date, procedure, results, and corrective
action, should be logged for documentation purposes. A qualified expert should survey all x-
ray units on their placement and should resurvey the equipment every four years or after any
17
changes that may affect the radiation exposure of the operator and others.86 Surveys typically
are performed by state agencies, and individual state regulations should be consulted
regarding specific survey intervals. The film processor should be evaluated at its initial
installation and on a monthly basis afterward. The processing chemistry should be evaluated
daily, and each type of film should be evaluated monthly or when a new box or batch of film is
opened.86 Abdominal shielding and thyroid collars should be inspected visually for creases or
clumping that may indicate voids in their integrity on a monthly basis.86 Damaged abdominal
shielding and collars should be replaced. Table 2 lists specific methods of quality assurance
procedures, covering not only inspection of the x-ray unit itself but also of the film processor,
the image receptor devices, the darkroom and abdominal shielding and collars. 103,104
It is imperative that the operators manual for all imaging acquisition hardware is readily
available to the user, and that the equipment is operated and maintained following the
manufacturers instructions, including any appropriate adjustments for optimizing dose and
image quality.
TECHNIQUE CHARTS/PROTOCOLS
Size-based technique charts/protocols with suggested parameter settings are important for
ensuring that radiation exposure is optimized for all patients. Technique charts should be used
for all systems with adjustable settings, such as tube potential, tube current, and time or
pulses. The purpose of using the charts is to control the amount of radiation to the patient and
receptor. Technique charts are tables that indicate appropriate settings on the x-ray unit for a
specific anatomical area and will ensure the least amount of radiation exposure to produce a
consistently good-quality radiograph.
Technique charts for intraoral and extraoral radiography should list the type of exam, the
patient size (small, medium, large) for adults and a pediatric setting. The speed of film used, or
use of a digital receptor, should also be listed on the technique chart. The chart should be
posted near the control panel where the technique is adjusted for each x-ray unit. A technique
chart that is regularly updated should be developed for each x-ray unit. The charts will also
need to be updated when a different film or sensor, new unit, or new screens are used.
RADIATION RISK COMMUNICATION

Dentists should be prepared to discuss with their patients the benefits and risks of the x-ray
exam.105 To help answer patient and parent questions about dental radiology radiation safety,
the American Academy of Oral and Maxillofacial Radiology and the Alliance for Radiation
Safety in Pediatric Imaging partnered to create a brochure targeted at parents and patients. 106
18
Table 2.
Quality Assurance Procedures for Assessment of Radiographic Equipment
The following procedures for periodic assessment of the performance of radiographic equipment, film processing,
equipment, image receptor devices, dark room integrity, and abdominal and thyroid shielding are adapted from
86
the National Council for Radiation Protection and Measurements report, Radiation Protection in Dentistry.
Please refer to state guidelines for specific regulations.
Equipment Frequency Method
X-ray Machine On installation Inspection by qualified expert (as specified by

At regular intervals as government regulations and manufacturers
recommended by state recommendations).
regulations
Whenever there are any
changes in installation
workload or operating
conditions
Film Processor On installation Method 1: Sensitometry and Densitometry
Daily A sensitometer is used to expose a film,
followed by standard processing of the film.
The processed film will have a defined pattern
of optical densities.
The densities are measured with a
densitometer.
The densitometer measurements are
compared to the densities of films exposed and
processed under ideal conditions.
A change in densitometer values indicates a
problem with either the development time,
temperature or the developer solutions.
Advantages
Accuracy
Speed
Disadvantage
Expense of additional equipment
Method 2: Reference Film

A film exposed and processed under ideal
conditions is attached to the corner of a view
box as a reference film.
Subsequent films are compared with the
reference film.
Advantage
Cost effectiveness
Disadvantage
Less sensitive
Image Receptor Devices Monthly Method 1: Sensitometry and Densitometry
With each new batch of film (as described above)
Method 2: Reference Image (as described
above)
Visual inspection of cassette integrity

Intensifying Screen and Every six months Examination of intensifying screen for
19
Extraoral Cassettes scratches
Development of an unexposed film that has
been in the cassette exposed to normal lighting
for one hour or more
Darkroom Integrity On installation While in a darkroom with the safelight on, place
Monthly metal object (such as a coin) on unwrapped
After a change in the lighting film for a period that is equivalent to the time
filter or lamp required for a typical darkroom procedure
Develop film
Detection of the object indicates a problem with
the safelight or light leaks in the darkroom
Abdominal and Thyroid Monthly (visual and manual All protective shields should be evaluated for
Shielding inspection) damage (e.g., tears, folds, and cracks) monthly
using visual and manual inspection. If a defect
in the attenuating material is suspected,
radiographic or fluoroscopic inspection may be
performed as an alternative to immediately
removing the item from service. Consideration
should be given to minimizing the radiation
exposure of inspectors by minimizing
unnecessary fluoroscopy.
TRAINING AND EDUCATION

Where permitted by law, auxiliary dental personnel can perform intraoral and extraoral
imaging.103 Personnel certified to take dental radiographs should receive appropriate
education. Practitioners should remain informed about safety updates and the availability of
new equipment, supplies and techniques that could further improve the diagnostic quality of
radiographs and decrease radiation exposure. Free training materials are available for limiting
radiation exposure in dental imaging through the International Atomic Energy Agency.107
CONCLUSION
Dentists should conduct a clinical examination, consider the patients oral and medical
histories, as well as consider the patients vulnerability to environmental factors that may affect
oral health before conducting a radiographic examination. This information should guide the
dentist in the determination of the type of imaging to be used, the frequency of its use, and the
number of images to obtain. Radiographs should be taken only when there is an expectation
that the diagnostic yield will affect patient care.
Dentists should develop and implement a radiation protection program in their offices. In
addition, practitioners should remain informed on safety updates and the availability of new
equipment, supplies, and techniques that could further improve the diagnostic ability of
radiographs and decrease exposure.
20
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27
AAE and AAOMR Joint
Position Statement
The following statement was prepared by the Special Committee to Revise the Joint American Association of
Endodontists/American Academy of Oral and Maxillofacial Radiology Position on Cone Beam Computed
Tomography, and approved by the AAE Board of Directors and AAOMR Executive Council in May 2015.
AAE members may reprint this position statement for distribution to patients or referring dentists.
Use of Cone Beam Computed Tomography in Endodontics

2015 Update
INTRODUCTION
This updated joint position statement of the American Association of Endodontists and the American Academy of
Oral and Maxillofacial Radiology is intended to provide scientifically based guidance to clinicians regarding the
use of cone beam computed tomography in endodontic treatment and reflects new developments since the 2010
statement (1).The guidance in this statement is not intended to substitute for a clinicians independent judgment in
light of the conditions and needs of a specific patient.
Endodontic disease adversely affects quality of life and can produce significant morbidity in afflicted patients.
Radiography is essential for the successful diagnosis of odontogenic and nonodontogenic pathoses, treatment of the
root canal systems of a compromised tooth, biomechanical instrumentation, evaluation of final canal obturation and
assessment of healing.
Until recently, radiographic assessments in endodontic treatment were limited to intraoral and panoramic
radiography.These radiographic technologies provide two-dimensional representations of three-dimensional anatomic
structures. If any element of the geometric configuration is compromised, the image may demonstrate errors (2).
In more complex cases, radiographic projections with different beam angulations can allow parallax localization.
However, complex anatomy and surrounding structures can render interpretation of planar images difficult.
The advent of CBCT has made it possible to visualize the dentition, the maxillofacial skeleton, and the relationship
of anatomic structures in three dimensions (3). CBCT, as with any technology, has known limitations, including a
possible higher radiation dose to the patient. Other limitations include potential for artifact generation, high levels
of scatter and noise and variations in dose distribution within a volume of interest (4).
CBCT should be used only when the patients history and a clinical examination demonstrate that the benefits
to the patient outweigh the potential risks. CBCT should not be used routinely for endodontic diagnosis or for
screening purposes in the absence of clinical signs and symptoms. Clinicians should use CBCT only when the need
for imaging cannot be met by lower-dose two-dimensional radiography.
Volume Size(s)/Field of View

There are numerous CBCT equipment manufacturers, and several models are available. In general, CBCT is
categorized into large, medium and limited-volume units based on the size of their field of view. The size of the
FOV describes the scan volume of CBCT machines.That volume determines the extent of anatomy included. It is
dependent on the detector size and shape, beam projection geometry and the ability to collimate the beam.To the
extent practical, FOV should only slightly exceed the dimensions of the anatomy of interest.
Generally, the smaller the FOV, the lower the dose associated with the study. Beam collimation limits the radiation
exposure to the region of interest and helps ensure that an optimal FOV can be selected based on disease presentation.
2015, American Association of Endodontists/The American Academy of Oral and Maxillofacial Radiology
211 E. Chicago Ave., Suite 1100, Chicago, IL 60611 | Email: info@aae.org | Website: www.aae.org
Phone: 800-872-3636 (U.S., Canada, Mexico) or 312-266-7255 (International) | Fax: 866-451-9020 (U.S., Canada, Mexico) or 312-266-9867 (International)
Smaller scan volumes generally produce higher-resolution images. Because endodontics relies on detecting small
alterations such as disruptions in the periodontal ligament space, optimal resolution should be sought (5).
The principal limitations of large FOV CBCT imaging are the size of the field irradiated and the reduced resolution
compared to intraoral radiographs and limited-volume CBCT units with inherent small voxel sizes (5).The smaller
the voxel size, the higher the spatial resolution. Moreover, the overall scatter generated is reduced due to the
limited size of the FOV. Optimization of the exposure protocols keeps doses to a minimum without compromising
image quality. If a low-dose protocol can be used for a diagnostic task that requires lower resolution, it should be
employed, absent strong indications to the contrary.
In endodontics, the area of interest is limited and determined prior to imaging. For most endodontic applications,
limited FOV CBCT is preferred to medium or large FOV CBCT because there is less radiation dose to the patient,
higher spatial resolution and shorter volumes to be interpreted.
Dose Considerations
Selection of the most appropriate imaging protocol for the diagnostic task must be consistent with the ALARA
principles that every effort should be made to reduce the effective radiation dose to the patient as low as
reasonably achievable. Because radiation dose for a CBCT study is higher than that for an intraoral radiograph,
clinicians must consider overall radiation dose over time. For example, will acquiring a CBCT study now eliminate
the need for additional imaging procedures in the future? It is recommended to use the smallest possible FOV,
the smallest voxel size, the lowest mA setting (depending on the patients size) and the shortest exposure time in
conjunction with a pulsed exposure-mode of acquisition.
If extension of pathoses beyond the area surrounding the tooth apices or a multifocal lesion with possible
systemic etiology is suspected, and/or a nonendodontic cause for devitalization of the tooth is established clinically,
appropriate larger field of view protocols may be employed on a case-by-case basis.
There is a special concern with overexposure of children (up to and including 18 years of age) to radiation,
especially with the increased use of CT scans in medicine.The AAE and the AAOMR support the Image Gently
Campaign led by the Alliance for Radiation Safety in Pediatric Imaging.The goal of the campaign is to change
practice; to raise awareness of the opportunities to lower radiation dose in the imaging of children. Information on
use of CT is available at www.imagegently.org/Procedures/ComputedTomography.aspx.
Interpretation
If a clinician has a question regarding image interpretation, it should be referred to an oral and maxillofacial
radiologist (6).
RECOMMENDATIONS
The following recommendations are for limited FOV CBCT scans.
Diagnosis
Endodontic diagnosis is dependent upon thorough evaluation of the patients chief complaint, history and clinical
and radiographic examination. Preoperative radiographs are an essential part of the diagnostic phase of endodontic
therapy. Accurate diagnostic imaging supports the clinical diagnosis.
Recommendation 1: Intraoral radiographs should be considered the imaging modality of choice

in the evaluation of the endodontic patient.
Recommendation 2: Limited FOV CBCT should be considered the imaging modality of choice
for diagnosis in patients who present with contradictory or nonspecific clinical signs and
symptoms associated with untreated or previously endodontically treated teeth.
AAE and AAOMR Joint Position Statement 2

Rationale:
In some cases, the clinical and planar radiographic examinations are inconclusive. Inability to confidently
determine the etiology of endodontic pathosis may be attributed to limitations in both clinical vitality testing and
intraoral radiographs to detect odontogenic pathoses. CBCT imaging has the ability to detect periapical pathosis
before it is apparent on 2-D radiographs (7).
Preoperative factors such as the presence and true size of a periapical lesion play an important role in
endodontic treatment outcome. Success, when measured by radiographic criteria, is higher when teeth are
endodontically treated before radiographic signs of periapical disease are detected (8).
Previous findings have been validated in clinical studies in which primary endodontic disease detected with
intraoral radiographs and CBCT was 20% and 48%, respectively. Several clinical studies had similar findings,
although with slightly different percentages (9,10). Ex vivo experiments in which simulated periapical lesions
were created yielded similar results (11,12). Results of in vivo animal studies, using histologic assessments as the
gold standard, also showed similar results observed in human clinical and ex vivo studies (13).
Persistent intraoral pain following root canal therapy often presents a diagnostic challenge. An example is
persistent dentoalveolar pain also known as atypical odontalgia (14).The diagnostic yield of conventional
intraoral radiographs and CBCT scans was evaluated in the differentiation between patients presenting with
suspected atypical odontalgia versus symptomatic apical periodontitis, without radiographic evidence of
periapical bone destruction (15). CBCT imaging detected 17% more teeth with periapical bone loss than
conventional radiography.
Initial Treatment
Preoperative
Recommendation 3: Limited FOV CBCT should be considered the imaging modality of choice for
initial treatment of teeth with the potential for extra canals and suspected complex morphology,
such as mandibular anterior teeth, and maxillary and mandibular premolars and molars, and
dental anomalies.
Intraoperative
Recommendation 4: If a preoperative CBCT has not been taken, limited FOV CBCT should
be considered as the imaging modality of choice for intra-appointment identification and
localization of calcified canals.
Postoperative
Recommendation 5: Intraoral radiographs should be considered the imaging modality of choice
for immediate postoperative imaging.
Rationale:
Anatomical variations exist among different types of teeth.The success of nonsurgical root canal therapy
depends on identification of canals, cleaning, shaping and obturation of root canal systems, as well as quality of
the final restoration.
2-D imaging does not consistently reveal the actual number of roots and canals. In studies, data acquired by
CBCT showed a very strong correlation between sectioning and histologic examination (16,17).
In a 2013 study, CBCT showed higher mean values of specificity and sensitivity when compared to intraoral
radiographic assessments in the detection of the MB2 canal (18).
Nonsurgical Retreatment
Recommendation 6: Limited FOV CBCT should be considered the imaging modality of choice if
clinical examination and 2-D intraoral radiography are inconclusive in the detection of vertical
root fracture.

Rationale:
In nonsurgical retreatment, the presence of a vertical root fracture significantly decreases prognosis. In the
majority of cases, the indication of a vertical root fracture is more often due to the specific pattern of bone loss
and periodontal ligament space enlargement than direct visualization of the fracture. CBCT may be recommended
for the diagnosis of vertical root fracture in unrestored teeth when clinical signs and symptoms exist.
Higher sensitivity and specificity were observed in a clinical study where the definitive diagnosis of vertical root
fracture was confirmed at the time of surgery to validate CBCT findings, with sensitivity being 88% and specificity
75% (19). Several case series studies have concluded that CBCT is a useful tool for the diagnosis of vertical root
fractures. In vivo and laboratory studies (20, 21) evaluating CBCT in the detection of vertical root fractures
agreed that sensitivity, specificity, and accuracy of CBCT were generally higher and reproducible.The detection of
fractures was significantly higher for all CBCT systems when compared to intraoral radiographs. However, these
results should be interpreted with caution because detection of vertical root fracture is dependent on the size of
the fracture, presence of artifacts caused by obturation materials and posts and the spatial resolution of the CBCT.
Recommendation 7: Limited FOV CBCT should be the imaging modality of choice when
evaluating the nonhealing of previous endodontic treatment to help determine the need for
further treatment, such as nonsurgical, surgical or extraction.
Recommendation 8: Limited FOV CBCT should be the imaging modality of choice for nonsurgical
retreatment to assess endodontic treatment complications, such as overextended root canal
obturation material, separated endodontic instruments, and localization of perforations.
Rationale:
It is important to evaluate the factors that impact the outcome of root canal treatment.The outcome predictors
identified with periapical radiographs and CBCT were evaluated by Liang et al. (22) The results showed that
periapical radiographs detected periapical lesions in 18 roots (12%) as compared to 37 on CBCT scans (25%).
Eighty percent of apparently short root fillings based on intraoral radiographs images appeared flush on CBCT.
Treatment outcome, length and density of root fillings and outcome predictors determined by CBCT showed
different values when compared with intraoral radiographs.
Accurate treatment planning is an essential part of endodontic retreatment. Incorrect, delayed or inadequate
endodontic diagnosis and treatment planning places the patient at risk and may result in unnecessary
treatment.Treatment planning decisions using CBCT versus intraoral radiographs were compared to the gold
standard diagnosis (23). An accurate diagnosis was reached in 36%-40% of the cases with intraoral radiographs
compared to 76%-83% with CBCT. A high level of misdiagnosis was noted in invasive cervical resorption and
vertical root fracture. In this study, the examiners altered their treatment plan after reviewing the CBCT in 56%-
62.2% of the cases, thus indicating the significant influence of CBCT.
Surgical Retreatment
Recommendation 9: Limited FOV CBCT should be considered as the imaging modality of choice
for presurgical treatment planning to localize root apex/apices and to evaluate the proximity to
adjacent anatomical structures.
Rationale:
The use of CBCT has been recommended for treatment planning of endodontic surgery (24, 25). CBCT visualization
of the true extent of periapical lesions and their proximity to important vital structures and anatomical landmarks
is superior to that of periapical radiographs.
Special Conditions
Implant placement
Recommendation 10: Limited FOV CBCT should be considered as the imaging modality of choice
for surgical placement of implants (26).

Traumatic injuries
Recommendation 11: Limited FOV CBCT should be considered the imaging modality of choice
for diagnosis and management of limited dento-alveolar trauma, root fractures, luxation, and/or
displacement of teeth and localized alveolar fractures, in the absence of other maxillofacial or
soft tissue injury that may require other advanced imaging modalities (27).
Resorptive defects
Recommendation 12: Limited FOV CBCT is the imaging modality of choice in the localization
and differentiation of external and internal resorptive defects and the determination of
appropriate treatment and prognosis (28, 29).

REFERENCES
1. American Association of Endodontists; American Academy of Oral and Maxillofacial Radiology. Use of cone-beam
computed tomography in endodontics Joint Position Statement of the American Association of Endodontists
and the American Academy of Oral and Maxillofacial Radiology. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2011;111(2):234-7.
2. Grondahl HG, Huumonen S. Radiographic manifestations of periapical inflammatory lesions. Endodontic Topics.
2004;8:55-67.
3. Patel S, Durack C, Abella F, Shemesh H, Roig M, Lemberg K. Cone beam computed tomography in Endodontics
a review. Int Endod J 2015;48:3-15.
4. Suomalainen A, Pakbaznejad Esmaeili E, Robinson S. Dentomaxillofacial imaging with panoramic views and cone
beam CT. Insights imaging 2015;6:1-16.
5. Venskutonis T, Plotino G, Juodzbalys G, Mickevicien L.The importance of cone-beam computed tomography in
the management of endodontic problems: a review of the literature. J Endod 2014;40(12):1895-901.
6. Carter L, Farman AG, Geist J, Scarfe WC, Angelopoulos C, Nair MK, Hildebolt CF,Tyndall D, Shrout M.
American Academy of Oral and Maxillofacial Radiology executive opinion statement on performing and
interpreting diagnostic cone beam computed tomography. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2008;106(4):561-2.
7. De Paula-Silva FW, Wu MK, Leonardo MR, da Silva LA, Wesselink PR. Accuracy of periapical radiography and cone-
beam computed tomography scans in diagnosing apical periodontitis using histopathological findings as a gold
standard. J Endod 2009;35(7):1009-12.
8. Friedman S. Prognosis of initial endodontic therapy. Endodontic Topics 2002;2:59-98.
9. Patel S, Wilson R, Dawood A, Mannocci F.The Detection of periapical pathosis using periapical radiography and
cone beam computed tomography part 1: preoperative status. Int Endod J 2012;8:702-10.
10. Abella F, Patel S, Duran-Sindreu F, Mercad M, Bueno R, Roig M. (2012a) Evaluating the periapical status of teeth
with irreversible pulpitis by using cone-beam computed tomography scanning and periapical radiographs. J
Endod 2012;38(12):1588-91.
11. Cheung G, Wei L, MvGrath C. (2013) Agreement between periapical radiographs and cone-beam computed
tomography for assessment of periapical status of root filled molar teeth. Int Endod J 2013;46(10):889-95.
12. Sogur E, Grondahl H, Bakst G, Mert A. Does a combination of two radiographs increase accuracy in detecting
acid-induced periapical lesions and does it approach the accuracy of cone-beam computed tomography
scanning. J Endod 2012;38(2):131-6.
13. Patel S, Dawood A, Mannocci F, Wilson R, Pitt Ford T. (2009a) Detection of periapical bone defects in human jaws
using cone beam computed tomography and intraoral radiography. Int Endod J 2009;42(6):507-15.
14. Nixdorf D, Moana-Filho E, Persistent dento-alveolar pain disorder (PDAP): Working towards a better
understanding. Rev Pain. 2011;5(4):18-27.
15. Pigg M, List T, Petersson K, Lindh C, Petersson A. (2011) Diagnostic yield of conventional radiographic and cone-
beam computed tomographic images in patients with atypical odontalgia. Int Endod J 2011;44(12):1365-2591.
16. Blattner TC, Goerge N, Lee CC, Kumar V,Yelton CGJ. (2010) Efficacy of CBCT as a modality to accurately
identify the presence of second mesiobuccal canals in maxillary first and second molars: a pilot study. J Endod
2012;36(5):867-70.
17. Michetti J, Maret D, Mallet J-P, Diemer F. Validation of cone beam computed tomography as a tool to explore root
canal anatomy. J Endod 2010;36(7):1187-90.
18. Vizzotto MB, Silveira PF, Ars NA, Montagner F, Gomes BP, Da Silveira HE. (2013) CBCT for the assessment of
second mesiobuccal (MB2) canals in maxillary molar teeth: effect of voxel size and presence of root filling. Int
Endod J 2013;46(9):870-6.
19. Edlund M, Nair MK, Nair UP. Detection of vertical root fractures by using cone-beam computed tomography: a
clinical study. J Endod 2011;37(6):76872.
20. Metska ME, Aartman IH, Wesselink PR, zok AR. (2012) Detection of vertical root fracture in vivo in
endodontically treated teeth by cone-beam computed tomography scans. J Endod 2012;38(10):1344-7.
21. Brady E, Mannocci F, Wilson R, Brown J, Patel S. (2014) A comparison of CBCT and periapical radiography for the
detection of vertical root fractures in non-endodontically treated teeth. Int Endod J 2014;47(8):735-46.

22. Liang H, Li Gang, Wesselink P, WuM. Endodontic outcome predictors identified with periapical radiographs and
cone-beam computed tomography scans. J Endod 2011;37(3):326-31.
23. Ee J, Fayad I M, Johnson B. Comparison of endodontic diagnosis and treatment planning decisions using cone-
beam volumetric tomography versus periapical radiography. J Endod 2014;40(7):910-6.
24. Venskutonis T, Plotino G,Tocci L, Gambarini G, Maminskas J, Juodzbalys G. Periapical and Endodontic status scale
based on periapical bone lesions and endodontic treatment quality evaluation using cone-beam computed
tomography. J Endod 2015;41(2):190-6.
25. Low KM, Dula K, Brgin W, Arx T. Comparison of periapical radiography and limited cone-beam tomography in
posterior maxillary teeth referred for apical surgery. J Endod 2008;34(5):557-62.
26. Tyndall D, Price J,Tetradis S, Ganz S, Hildebolt C, Scarf W. Position statement of the American Academy of Oral
and Maxillofacial Radiology on selection criteria for the use of radiology in dental implantology with emphasis
on cone beam computed tomography. Oral Surg Oral Med Oral Pathol Oral Radiol 2012June;113(6):817-26.
27. May JJ, Cohenca N, Peters OA. Contemporary management of horizontal root fractures to the permanent
dentition: diagnosis, radiologic assessment to include cone-beam computed tomography. Pediatric Dentistry
2013;35:1204.
28. Estrela C, Bueno MR, De Alencar AH, Mattar R, Valladares Neto J, Azevedo BC, De Arajo Estrela CR. Method to
evaluate Inflammatory Root Resorption by using Cone Beam computed tomography. J Endod 2009;35(11):1491-7.
29. Durack C, Patel S, Davies J, Wilson R, Mannocci F. Diagnostic accuracy of small volume cone beam computed
tomography and intraoral periapical radiography for the detection of simulated external inflammatory root
resorption. Int Endod J.2011Feb;44(2):136-47.
Thank you to the Special Committee to Revise the Joint AAE/AAOMR Position Statement on Cone Beam-
Computed Tomography:
Mohamed I. Fayad, Co-Chair, AAE Madhu K. Nair, Co-Chair, AAOMR
Martin D. Levin, AAE Erika Benavides, AAOMR
Richard A. Rubinstein, AAE Sevin Barghan, AAOMR
Craig S. Hirschberg, AAE Board Liaison Axel Ruprecht, AAOMR

Biographical Information
John A. Svirsky, DDS, MEd

(804) 828-0547
FAX: (804) 828-6234
EMAIL: jasvirsk@vcu.edu
Dr. John Svirsky is a board certified oral and maxillofacial pathologist

at Virginia Commonwealth University (VCU) in Richmond, Virginia. He
received his dental degree in 1973 from VCU and went on to complete a
general practice residency at Long Island Jewish Medical Center/Queens
Hospital Center, as well as an oral pathology residency at the Catholic
Medical Center.
He is currently a professor of oral and maxillofacial pathology and

maintains a private practice in oral medicine and oral pathology. Dr.
Svirsky has developed a broad background in research, published numerous
articles in the dental literature, and earned a masters degree in adult
education. He is a sought after speaker with an international reputation as an
informative and entertaining lecturer.
Dr. Svirsky is an honorary member of the Thomas P. Hinman Dental

Society and has received a Presidential Citation from the American Dental
Association for significant contributions to the health of the public and the
profession of dentistry. In 2012 he received the William J. Gies Award from
the Greater New York Dental Meeting for contributions to oral health. The
MCV Alumni Association (MCVAA) of Virginia Commonwealth
University has chosen Dr. Svirsky to receive the 2013 MCVAA Outstanding
Alumnus Award. In 2015 Dr. Svirsky received the Distinguished Service
Award from the Dawson Academy for advancement of the Dental
Profession through Research, Publication and Education and awarded an
Honorary Membership in the American Academy of Oral Medicine.
Pathology and Endodontics
Radiographic Lesions
Endodontic Continuing Education
February 10, 2017
John A. Svirsky, DDS, MEd
804-828-0547
FAX: 804-828-6234
EMAIL: jasvirsk@vcu.edu
Common/Important Radiolucencies
I. Periapical Pathosis
A. Age, Sex, Race Adults.
B. Most Common Location Apex of permanent first molar, rare in primary teeth.
C. Clinical Findings Usually a history of pain often has a large restoration or history
of trauma. At least a portion or the entire tooth is nonvital.
D. Radiographic Features
1. Well-defined, circular.
2. Sclerotic border.
3. Usually at apex but can occur anywhere on root.
4. Slow growth.
E. Treatment Endodontics or extraction depending on the status of the tooth, along

with curettage of the lesion. No recurrence expected but surgery may lead to a
fibrous bony defect.
F. Synonyms Periapical cyst, apical periodontal cyst, periapical granuloma,

periapical abscess, fibrous bony defect.
II. Dentigerous Cyst
This is one of the most common developmental cysts of the jaws and accounts for
20% of the epithelial lined cysts of the jaws. It arises from separation of the follicle
from around the crown of an unerupted tooth.
1
A. Age, Sex, Race Young adults; if you dont have a dentigerous cyst by the age of
35 years, then you probably will not get one. Most cases between 10 and 30.
B. Most Common Location Mandibular third molars, maxillary canines,

mandibular premolars, and maxillary third molars. Roughly 2.5% of all patients
with unerupted teeth have a dentigerous cyst.
C. Clinical Findings Usually asymptomatic, often noticed during a routine

examination or because of the delayed eruption of a tooth. Rarely will cause
expansion.
1. Well-defined, around the crown of an impacted tooth.
2. >3.0 mm from crown to edge of radiolucency.
E. Treatment Curettage of cyst with extraction of impacted tooth. No recurrence

expected. Marsupialization of larger lesions.
1. May involve apex of adjacent tooth and cause resorption.
2. May give multilocular impression because of persistence of bone
trabeculae within radiolucency.
F. Synonyms Follicular cyst, paradental cyst.
G. Eruption Cyst - Soft tissue analogue of DC and results from separation of the
dental follicle from around crown of erupting tooth. This occurs in children less
than 20 in the mandibular molar region.
III. Residual Cyst
A. Age, Sex, Race Mean age = 52 years, males > females.
B. Most Common Location Maxilla > mandible.
C. Clinical Findings Usually asymptomatic but may cause expansion. In order to

make the diagnosis there has to be a history of a cyst (usually radicular or
dentigerous) that was incompletely removed.
1. Circular or elliptical
2. Sclerotic border.
E. Treatment Curettage, no recurrence expected.
IV. Odontogenic Keratocyst
2
A. Arises from rests of the dental lamina and accounts for 10-12% of odontogenic
developmental cysts. OKC grow in an anterior-posterior direction within
medullary bone without causing obvious bone expansion.
B. Age, Sex, Race Mean age = 38 years, 61.5% males, 87% Caucasian, 60%
between 10 and 30.
C. Most Common Location 70% mandible, 51% in molar region.
D. Clinical Findings 19% are symptomatic, most common complaints being

swelling
and pain. Four percent of cases are associated with the basal cell nevus syndrome.
E. Radiographic Features
1. Hazy Milky Way appearance to central portion of lesion.
2. Forty eight percent associated with impacted tooth.
3. Thin, well-defined borders.
F. Treatment Controversy as to treatment. Marsupialization is increasing in

popularity due to the difficulty in removing this lesion surgically. Some feel
aggressive curettage or resection is indicated because of the high recurrence rate
(42.6%) of the parakeratinized variant. I am against radical surgery. The treatment
is worse than the disease and this lesion is only a cyst. Multiple odontogenic
keratocysts strongly suggest the possibility of the autosomal dominant basal cell
nevus syndrome.
V. Traumatic Bone Cyst
A. Thought to be trauma to bone insufficient to cause fracture which results in an

intraosseous hematoma. If the hematoma does not organize, it may liquefy and
result in the empty bone cavity found on exploration.
B. Age, Sex, Race Rare before 5 or after 35; most cases between 10 and 20, mean
= 18 years; males = females; 75% Caucasian.
D. Most Common Location 98.5% mandible; 73% posterior.
E. Clinical Findings Teeth almost always vital, usually does not have a history of
Trauma; 25% will have expansion.
F. Radiographic Features
1. Well-defined margins may have sclerotic border.
2. Has a tendency to scallop between the roots of the teeth.
3. Above the mandibular canal.
4. Does not displace teeth or resorb roots.
3
G. Treatment Simple curettage of the bony wall is adequate. <5% recur. Untreated
lesions spontaneously resolve, which explains the rarity of traumatic bone cysts
in patients over the age of 40 years.
H. Synonyms simple bone cyst, solitary bone cyst, hemorrhagic bone cyst,
unicameral cyst, and idiopathic bone cavity.
VI. Lateral Periodontal Cyst
A. Age, Sex, Race Mean age = 50 years; 67% males.
B. Most Common Location 67% occur in mandibular premolar/canine region; 33%

in maxillary lateral incisor region.
C. Clinical Findings Occasionally causes expansion, teeth are vital. This is not
related to periodontal disease. This is the intraosseous counterpart to the soft tissue
gingival cyst.
1. Usually <1 cm in diameter.
2. Ovoid or elliptical shape.
3. The border is usually of variable thickness.
4. Rarely causes cortical perforation.
E. Treatment Curettage, very low recurrence rate.
VII. Nasopalatine Duct Cyst
A. Age, Sex, Race Mean age = 43 years, 54% males; 93% Caucasian.
B. Most Common Location Midline anterior maxilla.
C. Clinical Findings 52% have swelling 25% have drainage, and 20% have pain.
1. Minimum of 6 mm in diameter. Mean radiographic diameter = 17.1 mm.
There is no correlation between radiographic size and the presence of
symptoms.
2. Appears between the apices of the maxillary central incisors. Teeth are
vital.
3. Usually ovoid but may have the classical heart-shaped appearance when
viewed with an occlusal radiograph.
E. Treatment Curettage; 2% recurrence rate.
F. Synonyms Incisive canal cyst.
4
VIII. Central Giant Cell Granuloma
A. Age, Sex, Race Mean age = 26 years, females >> males
B. Most Common Location 96% anterior to the second molars 70% mandible.
C. Clinical Findings Expansion is a relatively common finding.
1. 18% are multilocular, but fine trabeculae are often seen.
2. Has a tendency to cross the midline.
3. Resorption of roots and displacement of teeth are common.
E. Treatment Curettage, low recurrence rate. The histologic findings are similar to
hyperparathyroidism so a serum calcium should be done to rule out this possibility if
there are multiple bony lesions present.
IX. Ameloblastoma
Most commonly clinically significant odontogenic tumor. Thought to arise from: 1.)
Cell rests of enamel organ; 2.) Developing enamel organ; 3.) Epithelial lining of
odontogenic cysts; 4.) Basal cells of oral mucosa.
A. Age, Sex, Race Mean age = 35 years.
B. Most Common Location 59% occur in posterior mandible, 85% in mandible. 80% of
the maxillary lesions are associated with the molars and/or antrum.
C. Clinical Findings 80% present with a painless expansion. 15-30% arise from a
dentigerous cyst but this is unlikely after the age of 40 years.
1. 53% are multilocular. The mean age for unilocular cases is about 10 years
younger than multilocular ones.
2. 80% show root resorption.
3. Many associated with impacted teeth.
4. Usually does not perforate the inferior border of the mandible.
5. Tends to infiltrate between intact cancellous bone trabeculae at periphery of
lesion before bone resorption becomes evident on s-ray. Therefore tumor islands
are approximately 1 cm further than they appear on radiographs.
E. Treatment Small unilocular lesions that have not perforated the cortex can be
successfully treated with aggressive curettage. However, multilocular ameloblastomas
or ones that have perforated the cortex should be treated by resection with an adequate
margin of uninvolved bone.
5
X. Lingual Mandibular Bone Defect
A. Age, Sex, Race Adult, 90% males.
B. Most Common Location Posterior mandible, but occasional cases are seen in the
anterior mandible.
C. Clinical Findings Found in 0.5% of adult panoramic radiographs. Asymptomatic.
1. Well-defined with sclerotic border.

2. Elliptical shape.
3. Below the mandibular canal.
4. Shows slow progressive growth but rarely exceed 2 cm in diameter.
E. Treatment No treatment indicated. However, if the lesion does not have all the
classical signs or if it occurs in the anterior mandible, sialography should be
considered.
F. Synonyms Stafnes bone cyst, static bone cavity, latent bone cyst, and developmental
lingual mandibular salivary gland depression.
XI Periapical Cemental Dysplasia
A. Age, Sex, Race Usually over 30 years, 93% in women, 71% in blacks.
B. Most Common Location Anterior mandible.
C. Clinical Findings Asymptomatic. Associated teeth are vital.
1. Multiple, well-defined lesions along the apices of the mandibular incisors.
2. Various radiographic stages are present: RL (29%), RL/RO (54%), RO (18%).
3. Amount of calcification increases with time but he separate lesions do not mature at
the same rate, therefore, there are various stages present at one time. Even the
mature RO lesions will have a thin RL rim around them.
E. Treatment None indicated, it would be prudent to check the vitality of the involved
teeth because it would be difficult to detect a true periapical pathosis within one of
these lesions.
F. Synonyms Cementoma.
6
XII. Florid Osseous Dysplasia
A. Age, Sex, Race Mean age = 50 years, 77-100% are women, 85% black.
B. Most Common Location Most cases involve the mandible, but all four quadrants are
involved in 59% of patients. Greater involvement is in the posterior mandible.
C. Clinical Findings Most are asymptomatic but some develop painful expansion and
mucosal ulceration. This is not related to periodontal disease.
1. Multiple, diffuse RL/RO lesions throughout the jaws. The lesions resemble
periapical cemental dysplasia except they are larger. With time, increased
calcification occurs.
2. The development of RL foci within a RO area should prompt you to consider the
possibility of a true osteomyelitis in the case.
3. Some people feel that this is a more severe variant of periapical cemental dysplasia.
E. Treatment No treatment indicated in the asymptomatic case. If symptomatic, need to

consider aggressive IV antibiotics, systemic steroids, or hyperbaric oxygen therapy. A
key factor to problems because of the compromised blood flow to the affected bone.
Synonyms Chronic diffuse sclerosing osteomyelitis, gigantiform cementoma, multiple

enostoses and sclerotic cemental masses.
XIII Metastatic Malignancies
A. Age, sex, race general > 40 years.
B. Most Common Location 5 mandible: 1 maxilla, soft tissues are infrequently

involved.
Premolar and molar regions are the most common. Most primary lesions arise from
either the breast, lung or kidney.
C. Clinical Findings Pain, swelling, paresthesia are common. Tooth mobility, tooth
displacement, and paresthesia are uncommon.
1. Usually RL but can have a RO component.
2. Ill-defined margins, cortical expansion.
3. Wide range of variability due to the primary tumor.
E. Treatment The prognosis for metastases to the jaw is poor, with death usually
occurring within one year.
7
Bradford R Johnson, DDS, MHPE
Dr. Johnson completed his undergraduate education at the University of Colorado,

received his DDS degree from Virginia Commonwealth University, and
endodontics specialty training at the University of Illinois at Chicago where he is
currently Department Head and Director of Postgraduate Endodontics.
Dr. Johnson has published over 50 clinical and research articles and abstracts in
peer-reviewed dental journals and is coauthor of five textbook chapters. In addition
to full time teaching, he maintains a part-time clinical practice limited to
endodontics.
RiskAssessmentand
ManagementoftheMedically
ComplexEndodonticPatient
8th Annual Board Review Course and Scientific Update
College of Diplomates of the ABE and

Virginia Commonwealth University School of Dentistry Johnson BR, Fischer DJ, Epstein JB. Management Considerations for the
Medically Complex Endodontic Patient. In: Ingle J, Bakland L, Baumgartner C,
February 10, 2017 editors, Endodontics, 6th edition, BC Decker Inc., 2008. pp767-797.
(and: Johnson and Epstein, Chapter 31 in 7th Edition, 2016? 2017? 2018?)
BradfordRJohnson,DDS,MHPE
UniversityofIllinoisatChicago
2016
Medical complexity and the ABE

exam process
info@icehealthsystems.com Written exam: part of the test matrix
Case portfolio: med comp case not
Electronic required after May 2013, but can be used
Medical Support in other category (the most significant
System aspect of this case must be management
of a medically compromised patient*)
Oral exam: 10 topics for each case, 1 is
medical history (ask for med hx and vitals
if not given in the case summary)
* requires modification of treatment procedures
1
ABE Case History Portfolio Submission
Guidelines Oral exam
(revised August 2013):
If medically compromised patient is used in Is it necessary to modify treatment? If so,
the other category:
how?
This requires modification of treatment Selection of anesthetic, analgesics and
procedures because of the patients medical antibiotics
condition. Recognition and/or documentation
of a medical problem does not meet this
criteria. Prescribing prophylactic antibiotic
coverage or treating patients with common
medical conditions does not satisfy the criteria
for this category. A one year recall is not
required for this case.
Overview of presentation Overview of presentation

Med history, vital signs, & consultation Med history, vital signs, & consultation
Risk assessment Risk assessment
Major systems review and possible Major systems review and possible
treatment modifications treatment modifications
Special cases Special cases
Potential drug interactions Potential drug interactions
Allergy to dental materials Allergy to dental materials
How were these topics selected? Medical History

Prevalence of condition Patients fail to see the connection between their
Risk (criticality) - potential consequences medical problems and the dental treatment.
of failure to identify condition and modify
treatment When asked: Are you in good health?
95% said yes,
Timeliness however, after further questioning, 32% had
medical conditions that were potentially relevant
to dental treatment
Smeets EC, et al. Detecting the Medically
Compromised Patient in Dentistry by Means
of the Medical Risk-Related History.
Preventive Medicine1998;27:530-535.
2
Medical History Medications
Study sample: 164 females and 158
Purpose/Methods: In a dental setting, 171 patients received
routine medical lab screening tests males, median age = 52 (range: 6 94)
64% taking Rx or OTC drugs (~ 2 per/pt)
Results: 83% of patients had one or more abnormal test
results and did not indicate a relevant (explanatory) Most common:
disease in medical hx Antihypertensives: 35%
Conclusions: Abnormal laboratory test results are Anticoagulants: 12%
detected frequently in the serum and urine of patients Psychiatric meds: 10%
arriving for dental treatment, which would indicate
undiagnosed disease and less than optimal management Hypoglycemic meds: 9%
Gastric ulcer meds: 8%
Miller and Westgate. JADA , Oct 2014 Fitzgerald J, et al. J Can Dent
Assoc. 2015
ASA Classification System Health Hx and Vital Signs

ASA 1: normal, healthy patient Positive responses to questions on
ASA 2: mild systemic disease, well- standard health hx forms do not clearly
controlled lead to specific determination of risk for
ASA 3: moderate to severe systemic dental tx
disease that limits activity, but is not List of medications should be consistent
incapacitating with health hx findings
ASA 4: incapacitating systemic disease Allergies, especially to latex, should be
that is a constant threat to life determined before clinical exam
BP, HR, resp (and weight and temp prn)
Physical status
ASA 1 ASA 2 ASA 3 ASA 4
Anxiety & Procedural Stress
4
9 10 11 12
Anxiety 3 8 9 10 11
1
2
7 8 9 10
11
12 4
When compared to NS-RCT, surgical RCT
6 7 8 9
9
10
11 3
induces more significant physiologic
6 7 8 9
4
9
10 Procedural
stress
changes, including increased HR and
higher SBP
2
8 10
5 6 7 8
Procedural 3 9
stress
7
8
9
1
Patients with above average dental
4 5 6 7
anxiety are also at greater risk for
2 8
7 4
1 3 4 5 6
6
2
3
Anxiety
significant physiologic changes (and
ASA 1 ASA 2 ASA 3 ASA 4
1
therefore increased risk of adverse cardio-
Physical status vascular event) Georgelin-Gurgel M, et al. Surgical and
Non-Surgical Endodontic Treatment-
Figure 20-2: Multi-Dimension Risk Assessment Model (MD-RAM)
induced Stress. J Endod 2009;35:19-22.
from Ingles Endodontics, Chapter 24, 6th Ed, 2008
3
Procedural stress scale Examples*
Denture adjustment; non-invasive
Dental anxiety scale Verbal descriptor
1 oral exam; radiographs
No anxiety
Procedures requiring local anesthesia; 1
2 prophylaxis with sub-gingival scaling;
simple restorative procedures; Mild anxiety
2
uncomplicated non-surgical root canal
treatment
Moderate anxiety
Patients with acute pain and/or
3
3 significant infection; extractions;
Severe anxiety
surgical root canal; periodontal 4
surgery
Bony impactions; trauma surgery
4
MD-RAM score Interpretation Cardiovascular Disease

No treatment modification usually
3-5
indicated Hypertension
6-7 Possible medical consultation and/or Ischemic heart disease
treatment modification Heart murmurs and valvular disease
Medical consultation often indicated Anticoagulant therapy & bleeding disorders
8-9
and probable treatment modification Arrhythmias and cardiac pacemakers
Medical consultation strongly advised; Congestive heart failure
10-12
may require treatment in a hospital or
specially equipped out-patient facility
Based on current standards for

defining hypertension,
approximately what percentage of
the U.S. adult population is
hypertensive?
398,079 patients aged 3 to 18 years with BP
A) 10% measured at three or more visits..3.3%
B) 20% met the criteria for hypertension and 10.1%
for prehypertension
C) 30%
CDC Morbidity and Mortality
D) 40% Weekly Report (MMWR).
September 7, 2012/61(35);703-
709 Pediatrics. Published online 11-22-2016
4
Case #1:
A 55 y/o male is referred for RCT #3. Case #1: Vital signs and med
His medical history is significant for hx review
HTN and atrial fibrillation. What
additional information do you need BP = 170/105; HR = 60
before treatment? Meds: lisinopril, 10mg qd; warfarin sodium
(Coumadin), 5mg qd patient reports INR
every month (most recent INR = 3.1)
Cardiac pacemaker implanted 12 months
ago
Treatment modifications?
Classification Systolic Blood Diastolic Blood

Pressure (SBP) Pressure (DBP)
Current 2014 Guidelines for
in mm Hg in mm Hg Management of Hypertension
Normal < 120 and < 80 (JNC 8 Dec 2013)
Prehypertension 120-139 or 80-89
Age BP Goal
Stage 1 140-159 or 90-99
Hypertension*
60 years old SBP < 150 mm Hg
Stage 2 160 or 100
Hypertension DBP < 90 mm Hg
* For patients with diabetes or renal disease, < 60 years old SBP < 140 mm Hg
the goal is to maintain blood pressure less than 130/80 mm Hg.
(or any age with DBP < 90 mm Hg
Figure 23-6: Blood pressure classification for adult patients
[adapted from Herman WW, et al. (36)] DM or CKD)
from Ingles Endodontics, Chapter 24, 6th Ed, 2008
SPRINT (Systolic Blood Hypertension

Pressure Intervention Trial)
SBP < 160 and DBP < 100:
NIH funded, multi-center study
should be OK for dental tx
Goal was to achieve target SBP < 120 with
SBP = 160 -180 and DBP = 100 - 110: probably
standard, commonly used meds OK (consider procedural stress and patient
~33% reduction in heart attack, heart failure, and anxiety)
stroke in study group compared to control group SBP > 180 and/or DBP > 110 : palliative tx prn;
(SBP < 140) in adults > 50 years old med consult prior to definitive treatment
Study stopped before target enrollment due to SBP > 210 and/or DBP > 120: refer for emergent
significant benefit found medical evaluation
Landmark NIH study shows intensive blood pressure management Little and Falaces Dental Management of the Medically Compromised Patient. Eighth Ed.
may save lives. Sept 11, 2015. NIH press release. 2013.
Patton LL and Glick M. The ADA Practical Guide to Patients with Medical Conditions.
Accessed online: 9-24-2015
Second Ed. 2016.
5
Anticoagulant therapy Drug interaction
Warfarin (Coumadin) Coumadin + metronidazole = significant
INR typical therapeutic range = 2.0 3.5 increase in plasma levels of Coumadin ,
Minimal bleeding risk for minor oral surgery therefore, increased PT/INR
procedures if within therapeutic range
(Jeske, 2003) (check INR day of surgery)
Aspirin (irreversible effect) and NSAIDs
(reversible within ~ 3 half-lives of drug)
Others: dipyridamole, ticlopidine,
clopidogrel, abciximab, integrelin, tyrafiban,
and lamifiban
Anticoagulant therapy -
Anticoagulant therapy - INR
revisited
~ 2% of patients in an urban dental school Balevi B. Should warfarin be discontinued
population had a history of warfarin use before a dental extraction? A decision-tree
43% of these patients had an INR that was analysis. OOOOE 2010;110:691-697
not within the therapeutic range (observed Decision should depend more on relative
INR values ranged from 0.2 to 7.0) risk of bleeding than on consequences of
a cardiovascular accident (decision tree
analysis slightly favors withholding
warfarin prior to extraction)
Kassab, MM, et al. JADA. Nov 2011
Drugs most commonly

2015 Update associated with emergency
Bajkin BV, et al. Risk factors for bleeding hospital admissions
after oral surgery in patients who
continued using oral anticoagulant Warfarin (coumadin) 33%
therapy. JADA 2015 (June)
Insulin (injection) 14%
Even in group of patients with INR
Aspirin, clopidrogrel and other anti-
between 3.5 4.2, no greater risk for
platelets meds 13%
bleeding following OS procedures than
group with INR between 2.0 3.5 Oral hypoglycemic agents 11%
New Engl J Med, 2011
6
Novel Oral Anticoagulant
NOAC Drugs
(NOAC) drugs
New alternatives to warfarin for most anti- apixaban (Eliquis)
coagulant indications (e.g., previous dabigratran (Pradaxa)
stroke, A. Fib., deep vein thrombosis) edoxaban (Lixiana)
EXCEPT mechanical heart valve
rivaroxaban (Xarelto)
Fewer interactions with foods, other drugs,
and no need for routine blood work
monitoring
Relative risk reduction for intracranial Reference for patient management: Peri-operative management
of patients who are receiving a new oral anticoagulant.
hemorrhage in A. Fib. patients ~ 50% Thrombosis Canada 2013 (accessed online 11-7-2014)
compared to warfarin**
NOAC Drugs NOAC Drugs: an example

Standard coagulation assays (e.g.: PT/INR;
aPTT; TT; and anti-factor Xa activity) are of Rivaroxaban (Xarelto)
limited value in measuring level of Inhibits factor X to Xa conversion
anticoagulation (1)
Prolongs PT, but PT test is not a reliable
Certain assays may give rough idea of measure of level of anticoagulation
anticoagulation, but different for each drug and
lack of standardization Half-life ~ 8-12 hours
Unlike coumadin, no reversal agent Recommend MD consult: should be OK for
NS-RCT but may want to d/c drug for 1 to 2
Breaking news - Reversal agent for days prior to surgical procedure
Pradaxa(2)
1: Noll A. Coagulation Assays and 2: FDA Approves Praxbind to Reverse
Return to normal coagulation levels within 1 to
the New Oral Anticoagulants. Anticoagulant Pradaxa. Medscape. Oct 2 days of discontinuing drug
American College of Cardiology. 16,2015
Jun 22, 2015
NOAP Drugs Bleeding disorders

Heavy EtOH consumption, liver disease,
inherited diseases
(e.g., thrombocytopenia, hemophilia, von
Johnston S.
JADA 2016 Willebrands disease)
Platelet count and function:
Examples: prasugrel (Effient) and ticagrelor
(Brilique); both are NOAPs that are often lab tests = PFA-100 and Ivy BT
prescribed in combination with aspirin Med consult usually advised
Replacement of deficient coagulation
Clinicians should treat carefully when managing the factors or platelet transfusion
care of dental patients taking NOAP drugs.
7
Arrhythmias
Lab tests
& cardiac pacemakers
Platelet count: normal = 150,000 to Abnormal impulse generation and/or
450,000/L (potential for clinically conduction
significant bleeding if < 50,000/L) Prevalence of serious arrhythmias:
Ivy bleeding time: normal = 1 to 6 min ~ 2-4% of population
(abnormal if > 6 min) Anxiety, dental procedural stress, oral
surgery procedures = increased risk
(especially if taking digoxin narrow
therapeutic range and potential drug
interactions)
Arrhythmias Azithromycin
& cardiac pacemakers (Zithromax Z-Pak)
Cardiac pacemakers and Risk for potentially fatal arrythmias
cardioverter/defibrillators (ICDs) risk for
electrical interference with EPT,EAL,and
Very low Patients at increased risk:
ultrasonic devices? (1,2,3,4,& 6) Prolonged QT interval
Antibiotic premed? (5) NO Low potassium or magnesium
1) Wilson BL, et al. J Endod 2006 (clinical study) Abnormally slow heart rate
2) Garofalo RR, et al. J Endod 2002 (in vitro study)
Taking drugs to treat arrhythmias
3) Beach CW, et al. J Endod 1996 (case report)
Elderly, especially those with CVD
4) Roedig JJ, et al. JADA, May 2010 (in vitro study)
5) Baddour LM, et al, JADA, Feb 2011 (review)
6) Idzahi K, et al, J Endod 2014 (in vitro study ICDs) New Engl J Med, May 2012
7) Elayi CS, et al, JADA, Feb 2015 (clinical study) FDA website: 3-12-2013
Clarithromycin (Biaxin) Clarithromycin (Biaxin)

Increased cardiac death risk When combined with certain statin drugs
37 excess deaths per 1,000,000 Rxs not metabolized by cytochrome P450 3A4
(CYP3A4) [e.g., Crestor], 65% increased
risk of acute kidney injury, 2X increased
risk of hyperkalemia, and 43% increased
risk of all mortality
Modest Increased Adverse-Event Risk with Clarithromycin

BMJ. Published online August 19, 2014 Plus Some Statins. Medscape. Dec 29, 2014
8
Case #1: Case #2: A 68 y/o female with
Treatment modifications? history of mitral valve prolapse
(with regurgitation) and MI
followed by CABG surgery 5 years
BP? ago is referred to you for RCT on
Anticoag? tooth #19. Her symptoms include
Pacemaker? increasing frequency and severity
of spontaneous pain and
sensitivity to cold liquids for past
4 days.
Case #2: Vital signs and med The maximum safe dose of
hx review epinephrine for patients with
BP = 140/95; HR = 70
CVD (except those with
Meds: propranolol (Inderal), 80mg, b.i.d.; severe CVD) is:
atorvastatin (Lipitor), 20mg qd; aspirin, A) 0.009 to 0.018mg
82mg, qd; nitroglycerin (Nitrostat), 0.4mg,
sub-lingual, prn
B) 0.018 to 0.027mg
Bypass surgery 5 years ago; patient C) 0.036 to 0.054mg
reports recent stress test and EKG WNL; D) 0.072 to 0.096mg
occasional angina on exertion
Treatment modifications?
Norepinephrine and levonordefrin should not be

used for patients with hypertension because of
their excessive alpha stimulation.
Ischemic heart disease
Little et al, Dental Management of the Medically
Compromised Patient, 7th ed, 2007 Natural progression of coronary
% activity on alpha % activity on beta atherosclerosis diminished O2 perfusion
receptors receptors
epinephrine 50 50
of the myocardium
norepinephrine 90 10
Angina chest pain when O2 demand
exceeds supply (physical activity and/or
levonordefrin 75 25
stress): treated with oral nitrates
Alpha1 = constriction of arterioles in skin and mucosa (increases
systolic and diastolic BP)
Unstable angina: progressive pain or pain
at rest ASA IV
Beta 1 = increases cardiac output and force, +/- HR
Beta 2 = dilation of arterioles in skeletal muscle (decreases diastolic BP)
9
Ischemic heart disease: Association between Apical
high risk patients Periodontitis and Coronary
Artery Disease?
Recent MI (< 1 month) or past MI with
significant residual damage An independent association between
Unstable angina periodontal disease and atherosclerotic
vascular disease has been demonstrated,
Decompensated CHF
but causation not proven (3)
Significant arrhythmias
Possible association with apical
Severe valvular disease periodontitis (1,2) 1) Caplan DJ, et al, J Dent Res,
2006
Multiple lower level risk factors increases 2) Rodrigues Costa TH, et al, J
overall perioperative risk Endod, 2014
3) Lockhardt PB, et al, Circulation,
2012
Heart murmurs &

valve disorders
Potential risk for infective endocarditis
J Endod 2015;41:353-357 related to procedure and type of valve
- Case control study
disorder
Risk for bleeding if on anticoagulant
- Premature birth and low birth weight therapy
were associated with radiographically
detected apical periodontitis
- Causality can not be determined from

this study design
Infective endocarditis:
Infective endocarditis
highest risk of adverse outcome
Antibiotic prophylaxis recommended
for all dental procedures that involve Prosthetic heart valve
manipulation of gingival tissue or the
periapical region of teeth or perforation Previous infective endocarditis
of the oral mucosa only for patients at Congenital heart disease (consult with MD
highest risk for an adverse outcome regarding repaired vs. unrepaired defects
and need for prophylaxis)
Cardiac transplant with valvulopathy
Wilson W, et al. Prevention of infective

endocarditis: guidelines..JADA 2007.
10
Infective endocarditis
Systemic conditions and possible
increased risk for infective endocarditis:
Lupus erythematosus
Dexfenfluramine and fenfluramine-
phentermine (fen-phen): weight reduction
drugs
Figure 1: Prescriptions of antibiotic prophylaxis by

prescriber type
Dayer M, et al. Incidence of Infective Endocarditis in England, 2000-13: a
secular trend, interrupted time-series analysis. Lancet 2014 (Nov).
Findings: This increase in the incidence of

infective endocarditis was significant for both
individuals at high risk of infective endocarditis
and those at lower risk.
Interpretation: Although our data do not

establish a causal association, prescriptions of
antibiotic prophylaxis have fallen substantially
and the incidence of infective endocarditis has
increased significantly in England since
introduction of the 2008 NICE guidelines.
Figure 5: Change point analysis for incidence of

infective endocarditis (Dayer et al, 2014)
Incidence and nature of adverse reactions Case #2: Treatment

to antibiotics used as endocarditis
prophylaxis. Thornhill MH, Dayer MJ, modifications?
Prendergast B, et al. J Antimicrob
Local anesthetic with epi?
Chemother 2015;70(8):2382-8
Antibiotic prophylaxis?
Amoxicillin pre-med: 0 fatal reactions Anticipated procedural stress, patient
reported for ~ 3 million Rxs and 23 non- health status, and patient anxiety level
fatal reactions/million Rxs
Clindamycin pre-med: 13 fatal and 149

non-fatal reactions/million Rxs
11
Differential Dx: odontogenic LA with epi Part II
vs cardiac pain
Intraosseous injection use with caution
in patients with CVD; 3% mepivicaine is
Kreiner M, et al. Craniofacial pain as the sole
symptom of cardiac ischemia: a prospective equally effective but may need more*
multicenter study. JADA 2007; 138(1):74-79. Epinephrine pellets for surgical
Jalali N, et al. The Tooth, The Whole Tooth, hemostasis should be OK**
and Nothing But the Tooth: Can Dental Pain
Ever be the Sole Presenting Symptom of a
Myocardial Infarction? A Systematic Review. *Replogle K, JADA, 1999
J Emerg Med 2014;46(6):865-872 **Vickers FJ, J Endod, 2002
**Vy CH, J Endod, 2002
Congestive heart failure Congestive heart failure

End stage of other CVDs such as coronary ~ 5.7 million in U.S. (most > 65 yrs old)
artery disease, hypertension, Poor prognosis after diagnosis
cardiomyopathy and valvular heart disease Dyspnea is a good predictor of extent of
Decreased ability of heart to pump blood disease and ability to handle stress
Diminished reserve capacity for handling Levels of disease: 1,2,3,4 or A,B,C,D
stress (including dental procedures)
If CHF is well managed, treat similar to
patients with ischemic heart disease
Herman WW, Ferguson HW.
JADA 2010
CVD general treatment

Congestive heart failure
modification considerations
Moderate to advanced CHF: may need to Medical consult as needed
use more upright chair position (pulmonary
Consider stress reduction protocol:
edema); limit vasoconstrictors
morning appointments, shorter
Advanced and/or uncompensated CHF: appointments, oral pre-med (e.g.:
medical consult; avoid vasoconstrictors; triazolam, 0.25mg prior to appt) or
may require tx in hospital-based clinic N2O/O2 sedation; limited use of LA with
vasoconstrictor; adequate pain
management
Pre-op AND post-op vitals signs
12
Statins and pulp chamber Diabetes
calcification?
Metabolic disorder characterized by
hyperglycemia
Systemic statins could be a contributing
factor for pulp chamber calcification Normal fasting blood glucose < 110mg/dL
(DM > 125mg/dL)
Glycated hemoglobin (HbA1c): normal
range = 4-6%; goal for DM patients < 7%
~ 7% of U.S. population (1/3 unaware of
condition)
Pettiette MT et al, J Endod, Polydipsia, polyuria, polyphagia, weight
2013. loss and weakness
Diabetes Diabetes management

considerations
Type 1 (insulin deficiency)
Normal diet and insulin schedule avoid
Autoimmune appointments that overlap with or would
5-10% of DM cases require patient to skip a regular meal
Absolute dependence on insulin Severe hypoglycemic episode can be a
Most commonly dxd in children & young adults medical emergency (signs: anxiety,
Type 2 (target tissue resistance) sweating, tachycardia, altered mental
Gradual onset state, seizures, and coma)
90-95% of DM cases Tx with oral carbohydrate: OJ, sugar,
LifeSavers, etc. or 1mg glucagon sub-cut
Age, obesity, family hx, physical inactivity, hx of
or IM
gestational DM
Diabetes clinical implications Pulmonary

Asthma
Well controlled DM = no increased risk for Chronic inflammatory disease
peri-operative complications although Attacks can be provoked by allergens, URT
prognosis for long-term healing??* infections, certain medications (possibly aspirin
Poorly controlled DM and NSAIDs), and stress
Consider prophylactic antibiotics due to Patient should bring inhaler (bronchodilator) to
altered neutrophil function and possibility of dental appointment
compromised microcirculation Avoid macrolide antibiotics for patients taking
Surgery may increase insulin resistance and theophylline
risk for hyperglycemia post-op N2O/O2 sedation OK for mild-moderate asthma,
but avoid if severe disease
* Fouad, AF, 2003; Britto RR, 2003
13
Pulmonary Pulmonary
COPD TB
Chronic, irreversible obstruction of airflow Bacilli containing airborne droplets
from lungs Tubercle is the classic TB lesion (granuloma
4th most common cause of death in U.S. formed by ingress of macrophages and
lymphocytes)
Semi-supine position Do not provide dental treatment to patient with
Low-flow O2 may be helpful but avoid N2O/O2 active TB until MD clearance
sedation in moderate to severe COPD* Rifampin and isoniazide are liver toxic avoid
May consider monitoring oxygen saturation acetominophen
(pulse oximetry) Streptomycin avoid aspirin
*direct irritation and gas can accumulate in
air spaces in lungs
CNS Renal disease & dialysis

CVA/stroke: thrombolic or hemorrhagic; Chronic renal failure slowly progressive
both result in oxygen and glucose to part and irreversible in glomerular filtration
of the brain rate leads to end-stage renal disease
Seizure disorders (ESRD)
Other neurological disorders Fatal without dialysis or kidney transplant
Renal disease Liver Disease

treatment modifications Viral hepatitis
Schedule dental tx on non-dialysis days >4 million chronic carriers is U.S.
(typically day after dialysis) HAV fecal/oral route, no carrier state,
Antibiotic premedication to decrease risk of serious complications are relatively rare
AV shunt infection may be indicated HBV - 1.25 million chronic carriers
HCV - 3.5 million chronic carriers
Adjust dosage schedule of drugs that are
metabolized primarily by kidneys to account HDV - co-infection with HBV
for longer half-life (e.g., some antibiotics) HEV - similar to HAV
Non-A-E everything else
Avoid NSAIDs in patients with renal
insufficiency (nephrotoxicity) but less of a Alcoholic liver disease
concern in ESRD Prevalence of alcohol abuse or dependence:
~ 7.5 to 10% (lifetime prevalence ~14 to 24%)
14
Acetaminophen (APAP) Treatment modification:
Problem: risk for toxicity and acute liver failure Dental drugs:
when dose > 4,000mg/day Local anesthetics (OK)
APAP is active ingredient in many OTC meds Analgesics caution
maximum dose can be exceeded when added to Aspirin and NSAIDs (+ bleeding)
Rx dose
Tylenol and narcotics (+ alcohol)
FDA requiring that Rx APAP be reduced to Sedatives caution
325mg/tab and warning label changes
Antibiotics most OK (EXCEPT
New J&J McNeil labeling for Tylenol: metronidazole and vanomycin)
maximum daily dose = 3,000mg
Treatment modification: Special cases

ARONJ*
Bleeding risk pre-surgical evaluation
Chemo and radiation therapy
Infection risk impaired function of Kupffer
Bone marrow and solid organ
cells (macrophages) and T-cell response
transplantation
Prosthetic joints
HIV
Sickle Cell anemia
Steroids and adrenal suppression
Rheumatoid arthritis *AntiResorptive agent-induced
OsteoNecrosis of the Jaw
Bisphosphonates MRONJ
BON or ONJ or BRONJ or ARONJ* or Risk for MRONJ with oral BPs ~ zero to
MRONJ?? 0.1%
(vs. USC study*, JADA, Jan 2009: ~ 4%)
30 million Rxs for oral bisphosphonates (e.g.: Fosamax [alendronate sodium])
(BPs) in the U.S. in 2006
Risk for MRONJ with IV BPs ~ 1.0 to 15%
BPs used in treatment of: osteopenia, (e.g.: Zometa [zoledronic acid] and Aredia
osteoporosis, Pagets disease of bone, [pamidronate])
multiple myeloma, and metastatic bone, Risk factors: > 65 years old, cancer,
breast and prostate cancer periodontitis,extraction,corticosteroids(?),
*ADA Council on Scientific Affairs, JADA,
Nov 2011 (Hellstein JW, et al); current
BP use > 2 years, smoking and diabetes
preferred term is MRONJ (8-11-2016) *Sedghizadeh PP, et al, JADA 2009
15
MRONJ prediction & prevention MRONJ
C-terminal cross-linking telopeptide of
(BP 1x yr dose regimen)?
Type I collagen (CTX) and urinary N- Grbic JT, et al. JADA, Nov 2010
telopetide of Type I collagen (NTX)? Incidence of ONJ (BON) of the jaw in
Drug holiday? Antibiotics?* patients receiving 5mg zoledronic acid
Should aggressively tx infection but avoid once yearly for osteopenia or osteoporosis
surgical intervention whenever possible was essentially same as placebo (1 case
(may do NS-RCT on non-restorable in 5903 patients = same as control group)
teeth and allow for passive exfoliation of
roots) S-CTX levels were lower in BP group
compared to control, but not associated
Endo surgery vs. extraction?
*ADA recommendations (2011): some limited evidence to support use of with increased risk of ONJ
antibiotics and CHX rinses to prevent BON; possible benefit in multiple
myeloma patients who have received BPs (Leuk Lymphoma 2008)
Cancer and MRONJ Possible treatment for MRONJ?

Prevalence ranges from 0.7 to 13.3% Teriparatide osteoanabolic drug
(difference is related to study design) approved by FDA for management of
osteoporosis
Stimulates osteoblast formation
Promising, but only case report level of
evidence at this time
Migliorati CA, et al. A systematic review of
Subramanian g, et al. A model for the pathogenesis of
bisphosphonate osteonecrosis (BON) in cancer.
bisphosphonate-associated osteonecrosis of the jaw
Support Care Cancer 2010;18(8):1099-1106
and teriparatides potential role in resolution. OOOOE
2011; 112(6):744-753
2014 OMFS position paper 2014 OMFS position paper

MRONJ (medication-related osteonecrosis Absent data, the committee considers the
of the jaw) risk for MRONJ after dental implant
Pathophysiology placement and endodontic or periodontal
Inhibition of osteoclastic bone resorption & procedures that require exposure and
remodeling manipulation of bone to be comparable to
Inflammation/infection the risk associated with tooth extraction
Inhibition of angiogenesis Discontinue BP 3 months before and 3
Overall estimated risk for MRONJ months after invasive dental treatment?
following tooth ext ~ 0.5%
(higher if IV dosing)
16
Retreat RCT or extract?
R. Lee and L. Heffez
Chemo and radiation therapy

Eliminate sources of inflammation and
infection 2 weeks prior to therapy
2-23-2011
Extract teeth with poor long-term prognosis
RCT to address apical periodontitis
Antibiotic premed for patients with indwelling
catheter?
Generally OK for dental tx if:
Neutrophil count > 2,000/L
Platelets > 50,000/L
3-11-2011 6-16-2011
Postradiation Osteonecrosis Bone marrow and solid organ

(PRON) transplantation
RCT preferred over extraction Similar considerations as chemo therapy
If extraction necessary, then use patients:
atraumatic technique Eliminate dental infections before tx
Local anesthetic without vasoconstrictor Consider prophylactic antibiotics for patients
with indwelling catheters and if neutropenic
Consider prophylactic antibiotics and
Consult with MD if dental treatment required
continue during healing within 1 year post-transplant (bone marrow)
Often long-term immunosuppressive drugs
17
Prosthetic joints Prevention of Orthopaedic
and dental treatment Implant Infection in Patients
Undergoing Dental Procedures
2003: AAOS/ADA/IDSA joint consensus
statement 1) The practitioner might consider
2009: AAOS information statement discontinuing the practice of routinely
2010: AAOM recommendations prescribing prophylactic antibiotics for
December 2012: AAOS/ADA clinical patients with hip and knee prosthetic joint
practice guidelines implants undergoing dental procedures
3 recommendations Grade of recommendation: Limited
January 2015: JADA (ADA Council on
Scientific Affairs report)
Pros joints (con.)

2) unable to recommend for or against
use of topical antimicrobials
Grade of recommendation: Inconclusive
3) maintain appropriate oral hygiene.

Grade of recommendation: Consensus
In general, for patients with prosthetic joint
implants, prophylactic antibiotics are not
recommended prior to dental procedures to
prevent prosthetic joint infection.
Sollecito TP et al. JADA, Jan 2015:146(1):11-16
Antibiotic pre-med
Skaar DD, et al. Antibiotic Prophylaxis: Dental
Cephalexin, cephradine, or Procedures and Subsequent Prosthetic Joint
amoxicillin, 2g, one hour before Infections: Findings From the Medicare
Current Beneficiary Survey. JADA 2011 (Dec);
dental appointment 142:1343-1351.
-Retrospective case control study
- no significant increase in risk of developing

PJI after dental visits.
18
HIV
Highly active anti-retroviral therapies
(HAART)
MD consult to determine CD4+ count and
liver and kidney function
Routine antibiotic prophylaxis not indicated
(unless..)
No significant difference in prognosis for
healing of necrotic teeth after NS-RCT
compared to non-HIV infected patients* 32 y.o. AA female; no history of trauma;
#9: necrotic with facial gingiva parulis (previous
* Suchina JA, et al, 2006 and Quesnell BT, et al, 2005
biopsy by OS = granuloma)
Etiology?
Sickle Cell Anemia Sickle Cell Anemia

Pulp necrosis in clinically intact permanent ~ 1 in 400 African-Americans
teeth was found to be 8.33X higher in SCA Potential for painful vasooclusive episodes
patients compared to non-SCA controls and infections
SCA is a potential risk factor for pulp Patients should be considered
necrosis immunocompromised, treat infections
aggressively (including antibiotics)
Infection can trigger sickle cell crisis
Costa CPS, et al. Association Risk for osteomyelitis
between Sickle Cell Anemia and
Pulp Necrosis. J Endod
Minimize use of vasoconstrictors
2013;39:177-181
Steroids and Adrenal

Rheumatoid Arthritis
Suppression
Adrenal insufficiency can result from Addisons Autoimmune, inflammatory disease
disease, hypothalmic or pituitary disease, or
exogenous corticosteroids ( 30mg/day Treatment often includes steroids,
hydrocortisone about 5mg prednisone) DMARDs (e.g., methotrexate), and
May consider supplemental steroids for surgical biologic agents (e.g., WBC modifiers
procedures (25 to 75mg hydrocortisone [Orencia]; and TNF inhibitors [Humira]
equivalent day of surgery and 1 day post-op)
Increased risk for serious infection due to
For lower dose steroid therapy, supplementation
should not be needed for minor oral surgery with immune system depression
local anesthesia
Miller CS, et al, JADA, 2001
19
Potential drug interactions -
NSAIDs
Lithium: increased lithium levels = toxicity
Anticoagulants: increased risk of GI bleeding
ACE inhibitors, Beta-blockers, & diuretics:
decreased antihypertensive effect
Methotrexate: can result in toxic levels of
methotrexate if on high dose
Increased risk of adverse event in CVD
patients (naproxen vs ibuprofen?)
NSAIDs and CV risk Potential drug interactions -

new FDA mandated labeling aspirin
for OTC NSAIDs
Heart attack or stroke risk can increase
as early as the first weeks of NSAID use, Anticoagulants: increased risk of GI bleeding
and the risk may increase with longer use. Oral hypoglycemics (Type 2 DM): increased
The risk appears to be greater at higher hypoglycemic effect
doses.
Risk is greater in patients with existing
CVD, but also increased risk for CV events
even in patients without CVD
FDA Strengthens NSAID Warning for Heart,
Stroke Risks. Medscape. Jul 09, 2015
Potential drug interactions - Potential drug interactions -

antibiotics vasoconstrictors
Interaction between bacteriocidal and Non-selective blockers hypertension
bacteriostatic antibiotics and bradycardia
Tetracyclines: insulin, antacids, and digoxin MAO inhibitors
Metronidazole: lithium, ethanol, and warfarin Tricyclic antidepressants
E-mycin & clarithromycin: digoxin, warfarin, Epinephrine preferred over norepinephrine
theophyline, prednisone, statins, H1 blocker, and levonordefrin due to relatively less
cimetidine, cyclosporine, carbamazepine, alpha1 stimulation
benzodiazepines
Oral contraceptives?
20
Pregnancy and dental
medications
J Endod 2015;41:588-593
Acetaminophen = OK
Codeine = use with caution
Aspirin = avoid Recent review article questions
Ibuprofen = avoid, especially in third assumption of acetaminophen safety
trimester for use during pregnancy (and also
raises other safety issues)
Pregnancy and dental Risk for Clostridium difficile

medications infection
Highest risk: 3rd generation cephalosporins
Category B antibiotics: amoxicillin, and clindamycin
azithromycin, cephalexin, topical
Lower risk: penicillins
chlorhexidine, clindamycin, & penicillin
Category B local anesthetics: lidocaine
(with or without epi) and prilocaine
Slimings and Riley, J Antimicrob

Donaldson M, Goodchild JH. JADA, August 2012
Chemother, 2013
General drug interaction

advice
Use an electronic Rx database to cross-
check for potential drug interactions
(e.g., Epocrates or Medscape mobile app
can download version to chairside
computer and most handheld devices
iPhone, Droid, etc)
JAMA Internal Medicine

September 2016
21
Allergy to materials used in
endodontic therapy
Most common medication

Research shows that although 10% of
allergy is antibiotics inpatients claim to have a penicillin allergy,
(penicillin = 11%; only about 10% of those show an intolerance
on testing, and even fewer are actually
sulfa = 5%) allergic.
Medscape Medical News, November 16, 2016: reporting on

American College of Allergy, Asthma & Immunology (ACAAI)
Fitzgerald J, et al. J Can Dent Assoc. Annual Scientific Meeting. Abstract O054 (Nov 14, 2016)
2015
Why is this important?

Predicting flare-ups & post-op
pain Conflicting
Are patients with multiple LOE 4
There is no risk for cross-sensitivity allergies more prone to post-op evidence
between antimicrobial sulfonamides flare up and pain?
and sulfur-containing compounds, Delayed or incomplete healing Case reports

Does delayed hypersensitivity rxn only
such as sulfites. = delayed healing?
Prevention of a medical
Brackett CC, et al. 2004 emergency
Hemstreet BA, et al. 2006
22
Interview questions for
patients with reported allergy Very basic immunology
to a dental material Type I Immediate, systemic, IgE
mediated
Nature of adverse event?
Previous dental care, including Type II
exposure to the material?
Personal and family hx of atopy, Type III
multiple allergies, hypersensitivity?
Origin of the suggestion that patient Type IV Delayed, localized, cell-
might be allergic to the material? mediated (T-lymphocytes)
Adapted from: Rood JP, BDJ, 2000.
Mast cells
Type I Type IV
Irritant contact dermatitis Overview

Non-immune
Gradual onset (days) Local anesthetics
Hand washing, contact with antiseptics Barriers
and chemicals (including gloves) Irrigating solutions
Redness, cracks, fissures, scaling Intracanal medications, cements, &
filling materials
23
Amide local anesthetics:
The most common adverse Evidence for Type I allergic rxn?
reaction to local anesthetic is: Case reports: + allergy to LA (LOE 5 - or less!)
A.) psychogenic Prospective clinical study1 (LOE 3)
5,018 dental patients
B.) systemic toxicity 25 (0.5%) adverse reactions, 2 possibly allergic
C.) sensitivity to preservative 0 true allergy based on provocative challenge
D.) allergy to epinephrine Cohort study2 (LOE 3)
236 patients that experienced adverse reaction
All negative to intradermal injection of LA
What about other ingredients?
1: Baluga JC et al, 2002.
2: Berkun Y et al, 2003.
2% lidocaine with 1:100k epi Allergy testing

3% mepivicaine without vaso
4% articaine with 1:100k epi Give patient a cartridge of LA to bring
to allergist
Selection of local anesthetic based on: Potential for false negative and false
positive reactions
Pregnancy category B Lidocaine
Even if negative for LA allergy, a
Reported sensitivity to sufiltes Mepivicaine
thorough evaluation may identify
Potential risk for patients with Type I another problem
allergic reaction to latex All of the above, if
latex diaphragm or
stopper (LOE 5)
Alternatives for patients with

true LA allergy Over the past 10 years, the
Consider testing with different LA
prevalence of Type I allergy to
Sedation or general anesthesia latex (NRL) in dentists has:
Electronic anesthesia A.) decreased 25%
1% diphenhydramine with 1:100 epi B.) remained the same
(maximum dose = 50mg) C.) increased 25%
D.) increased 50%
24
Sources of natural rubber latex
(NRL) in an Endodontic office Latex allergy is more likely in
Gloves*
patients who report a history
Rubber dam* of allergic reaction to:
Tubing & suction tips A.) aspirin
Bite block B.) shellfish
Rubber stoppers on files
Blood pressure cuff
C.) bananas
Local anesthetic?? D.) dust mites
Gutta percha???
dipped* vs molded NRL
Treatment modifications Non-latex alternatives

Medical consultation prn Vinyl (polyvinyl chloride)
Non-latex gloves, rubber dam, etc. Nitrile (acrylonitrile and butadiene)
Schedule as first patient of the day Polychlororene (Neoprene)
Premedicate with corticosteroid or
antihistamine?
Alternative filling materials?
Be prepared to manage an acute
allergic reaction
Allergic potential: irrigating

Irrigating solutions
solutions
Iodine potassium iodide ++

Sodium hypochlorite +
Chlorhexidine +
Hydrogen peroxide
EDTA
Citric acid
MTAD ?
++ = definite; + = reported; - = minor or none
(from Zehnder, J Endod, 2006)
25
Which of the following
Intracanal
occupations could predispose to
medications,
allergy to sodium hypochlorite
cements,
irrigating solution?
& filling materials
A.) Health care professional
B.) Maintenance engineer
C.) Airline pilot
D.) Carpenter
Allergic potential: intracanal Allergic potential: sealers and

medications filling materials
Phenols, aldehydes, and iodine ZnO and ZnOE materials (various
containing pastes = YES sealers and temporary filling materials)
= YES
Calcium hydroxide = NO
Epoxy resins = YES
Glass ionomers = NO
MTA = NO
Composite resins = ?
Resilon = ?
Gutta percha
ZnO, GP sap, waxes & resins, coloring
agents, & heavy metals
+ + =
26
Treatment modifications for
patients with demonstrated Which of the following materials
allergy to any component of GP has the highest allergenic
filling material potential?
A.) Silver
First, establish nature of allergy B.) Nickel
Is there a risk that filling material may C.) Gold
contact periapical tissues?
D.) Zinc
Consider alternative materials:
Resilon, CPoint, or MTA
Questions?
Allergic to nickel?
Should you worry about using
Nickel-titanium instruments?
A) Yes
B) No Thank You!
C) Maybe bjohnson@uic.edu
D) I fell asleep an hour ago could
you repeat the question?
27
Christine Sedgley is Professor and Chair of the Department of Endodontology. She received her BDS,
MDS, MDSc (Endodontics), FRACDS, and MRACDS(ENDO) in Australia, her PhD in oral microbiology at
the University of Hong Kong, and her Certicate in Endodontics from the University of Michigan. After
arriving in the US in 2000 she was an Assistant Professor at the University of Michigan. She joined the
Department of Endodontology at the Oregon Health & Science University as Associate Professor and
Department Chair in 2010. She has participated in more than 120 research and continuing education
presentations, and published more than 60 papers and chapters. Dr. Sedgley is a Diplomate of the
American Board of Endodontics and an Associate Editor of the Journal of Endodontics.
Sedgley COD 2017
2017 Endodontic Board Review and Scientific Update of the College

of Diplomates of the ABE at Virginia Commonwealth University! Overview"
!
! Part 1 "Basic microbiology update " ""
"
!
Part 2 "Methods used for evaluating endodontic microflora""
Endodontic microbiology " " " " " ""
Part 3 "Microorganisms in primary endodontic infections ""

""
Part 4 "Microorganisms and unsuccessful endodontic treatment"
Christine Sedgley ! !
MDS, MDSc(Endo), FRACDS, MRACDS(ENDO), PhD ! Part 5 "Microorganisms in periapical lesions"
February 2017" !
Part 6 !Antimicrobial efficacy of endodontic treatment and antibiotics """
"
" "!
!
Classification - cell wall!

Basic microbiology"
Gram positive and Gram negative"
Gram-positive
Prokaryotes" Eukaryotes "

bacteria" fungi, animals"
No nucleus!
! Chromosomes
" in nucleus! Gram-negative
EPS - Extracellular Polymeric Substance!

What are biofilms?"
- a matrix of polysaccharides, DNA and proteins "
Aggregates of microbial cells enclosed in a Multi-functional"
self-produced matrix adherent to a surface"
Biofilm Composition!
Bacterial cells! 20% by volume!
EPS/glycocalyx, 80% by volume!

biofilm matrix !
Flemming 2008!
1
Sedgley COD 2017
EPS - Extracellular Polymeric Substance! How is activity in the EPS regulated?"

Whats happening in the EPS?" Quorum sensing = how bacteria talk"
Means of regulating gene expression and diverse
physiological activities within community"
Regulation is dynamic:" Spatial wisdom of crowds:"

Stressors" Texts, tweets, snapchat etc"
Population density" "
Flemming 2016!
Biofilms and antimicrobial resistance" Intracanal biofilms"

First observed by Nair using
Microbes in biofilms can more easily microscopy in 1987"
interact with each other and exchange
genes encoding:" Described as clusters of self-
Virulence factors" aggregating colonies of one
Antibiotic resistance" distinct type or
coaggregating communities
of several types "
Biofilm microorganisms are more
resistant to antimicrobial agents than
Described as biofilms by
planktonic bacteria " Svensater & Bergenholt (2005)" LM, TEM: Nair 1990!
"
"
Root canal biofilms are complex,

polymicrobial and heterogenous"
Biofilm morphology varies between and within cases" Proposed that apical periodontitis be included
" in the set of biofilm-induced diseases"
Entombed biofilms in the root canal system"
Nair et al. 2005 Ricucci and Siqueira 2010!
2
Sedgley COD 2017
What is virulence?" Potential virulence factors associated with a

bacterial cell"
The degree of pathogenicity or disease-

producing ability of a microorganism"
The pathogenicity of an organism is

determined by its virulence factors "
Sedgley 2016!
Microbial virulence ! Microbial virulence !

Specific virulence factors and endodontics" Gram negative cell wall - Endotoxin "
Endotoxin (LPS)"
"
Others?"
Hemolysin (Sedgley et al. 2005)!
Lipoteichoic acid (Baik et al. 2008)!
Peptidoglycan (Hahn and Liewehr 2007)!
Gelatinase (Sedgley 2007, Sato et al. 2009)!
Short chain fatty acids (Ho and Chang 2007, Provenzano et al. 2015)!
Fimbriae (Figdor and Davies 1997, Ras and Siqueira 2010)!
Proteases (Ogawa et al. 2006, Nandakumar et al. 2009)! Endotoxin is an established pathogenic factor in
! endodontic infections!
!
!
!
Microbial virulence ! Microbial virulence !

Endotoxin and endodontics" What about host factors?"
"Endotoxin is positively associated with: "

"
"
Pulpal pain and periapical inflammation" Periapical pathology is multifactorial"
Schein and Schilder 1975, Horiba et al. 1991,
Yamasaki et al. 1992, Khabbaz et al. 2001, !
Jacinto et al. 2005 and others!
Bone destruction " The host determines the response
Dahln et al. 1981, Dwyer and Torabinejad 1981,
Pitts et al. 1982, Mattison et al. 1987! to microorganisms . "
Gomes et al. 2012 and others!
"
3
Sedgley COD 2017
Periapical pathology is multifactorial" Overview 2"

Part 1 Basic microbiology update"
Pulpal infection! "
Part 2 Methods used for evaluating endodontic microflora""
!
Immune response!
Cytokines!
Systemic factors!
Bone resorption!
Adapted from Stashenko!
Methods used for evaluating endodontic Evaluating endodontic infections !

microflora" 1. Histology"
Limited to observing morphology, and "
" more recently, viability!
1. Histology" Light microscopy (LM) (Ricucci and Bergenholtz 2003, Ricucci et al. 2015)"
Transmission electron microscopy (TEM) (Nair 2005)"
Scanning electron microscopy (SEM) (Leonardo et al. 2002)!
2. Culturing and biochemical tests" Environmental SEM (Bergmans et al. 2005)!
Confocal laser SEM (Parmar et al. 2011)!
3. Microbial bioinformatics" Combination LM, TEM, SEM (Richardson et al. 2009)!
!
"
DEAD! LIVE!
Evaluating endodontic infections ! Evaluating endodontic infections now and the future !
2. Culturing" 3. Microbial bioinformatics"
Genome( Transcriptome( Proteome( Metabolome(
Gene$
sample! Expression$
transfer!
analyses!
DNA( Rela%onal(Databases(
Sequence( Compare,(Cluster(&(Integrate(
anaerobic culturing! Databases(
identification! Correla%on(of(Genes(&(Gene(Products(
Standardized sampling method" Iden%ca%on(of(Gene(Func%ons(
Use of clinical sterility controls" Gene(Annota%on(
Pre-reduced transport media" Iden%ca%on(of(Pathways(
Anaerobic culturing"
Biological(Knowledge,(
Pure culture and identification "
Gene%c(&(Metabolic(Engineering(
Adapted from Libault et al. 2010"
4
Sedgley COD 2017
Evaluating endodontic infections !

Genomics DNA based identification"
"
Polymerase chain reaction (PCR)"
Nested PCR"
Multiplex-PCR"
Real-time PCR"
DNA-DNA hybridization"
Pyrosequencing"
Siqueira and Ras 2005 !
Genomics DNA based identification! Bottom line !

Pyrosequencing" Advantages of genomic approaches"
Enables more comprehensive analysis than "
!
traditional (Sanger) sequencing" More sensitive than culturing

" " ""
!
Many microbes that are not easily cultured,
600-fold difference" or are unculturable, have been identified"
Multiple studies have clarified and confirmed

that flora is diverse and not limited to a
single species"
Li et al. 2010!
Disadvantages of using genomic methods to Evaluating endodontic infections !

study endodontic infections" 3. Microbial bioinformatics"
!"#$%" & & &&&&&&&&&'()#*+(,-.$%"& & &/($."$%" & &&0".)1$2$%"&
Strong binding affinity between DNA and dentin <"'"(
>I/0",,7&'(
may compromise root canal sampling (Brundin et al.
2014, Figdor et al. 2016)"
Methods are very technique sensitive"
)FC( !"#$%&'$#()$*$+$,",(
Preparation methods destroy microorganisms so G"H2"'8"( -&./$0"1(-#2,*"0(3(4'*"50$*"(
)$*$+$,",(
cannot do further phenotypic analyses" -&00"#$%&'(&?(<"'",(3(<"'"(@0&;28*,(
4;"'%A8$%&'(&?(<"'"(B2'8%&',(
Most methods used dont address cell viability" <"'"(C''&*$%&'(
4;"'%A8$%&'(&?(@$*D:$E,(
Many nucleic acid sequences are unidentifiable"
67&#&578$#(9'&:#";5"1(
<"'"%8(3(="*$+&#78(>'57'""07'5(
Adapted from Libault et al. 2010"
5
Sedgley COD 2017
Evaluating endodontic infections !

Overview 3"
Proteomics"
Part 1 "Basic microbiology update " ""
Microbial proteins in 7 samples:" "
Part 2 "Methods used for evaluating endodontic microflora"
adhesins, autolysins, proteases, virulence factors, !
and antibiotic-resistance proteins" Part 3 "Microorganisms in primary endodontic infections "
""
" " " " "" Nandakumar et al. 2009! "
!
Microbial and human proteins in 24 cases:"
Microbial proteins: metabolism and housekeeping,
adhesion, biofilm formation, antibiotic resistance,
stress proteins, exotoxins, invasins, proteases "
Human proteins: cellular processes and
metabolism, immune defense "
Provenzano et al. 2013, 2016!
Are microorganisms the cause of apical Microbial etiology"

periodontitis?" Classic papers - Rats"
YES" Used germ-free rats to prove that bacteria in

Animal studies have proven that bacteria in the pulp are essential to the development
the pulp are essential to the development of periapical disease"
of periapical disease"
Kakehashi et al. 1965, Mller et al. 1981, ! ! !! !Kakehashi, Stanley and Fitzgerald 1965"
Fabricius et al. 1982a, 1982b"
Microbial etiology" Primary endodontic infections"

Classic papers - Monkeys" Classic CULTURE studies - bottom line"
Mller, Fabricius, Dahln et al. 1981, 1982 Mixed flora dominated by"
Gram negative anaerobes"
1. Relative number of obligate anaerobes increases "
with time "
Polymicrobial"
"
2. Proportionally more anaerobes apically with time" Mller 1966!
Bergenholtz 1974!
3. Mixed infections show greatest capacity for Sundqvist 1976!
inducing apical periodontitis " Cvek et al. 1976!
Kantz and Henry 1974!
and others!
"
6
Sedgley COD 2017
Specific microorganisms and symptoms" Geographic location"
Are specific symptoms associated with specific

microorganisms?" Microflora of infected root canals may vary
according to geographic location!
Yes! !
Griffee et al. 1980, Haapasalo 1986, Yoshida et al. 1987, !
Hashioka et al. 1992, Hahn et al. 1993, Gomes et al. 1996, !
Chavez 2002, Jacinto et al. 2003 and many others !! !
!
!
No ! !
Baumgartner et al. 1999, Jung et al. 2000, Ras et al. !
2001, Fouad et al. 2002, Chu et al. 2005 and many others" !
!
!
!
Siqueira et al. 2005, Ras et al. 2006"
Summary - Primary endodontic infections" Summary - Primary endodontic infections"

Histology and culture-based studies" Molecular-based studies"
_____________________________________________________________ Li et al. 2010!
Facultative anaerobes
Gram positive cocci
Anaerobes
Multiple species (highly diverse) "
Biofilms" Streptococcus
Enterococcus
Micromonas
Peptostreptococcus
Gram negative cocci

Peptococcus
Significantly more species detected The Rest"
Neisseria Veillonella
Polymicrobial" Gram positive rods

Lactobacillus Actinomyces
than in culture-based studies"
Eubacterium
Gram negative rods

Propionibacterium
Many species as yet unidentified and
Enterobacter Porphyromonas
Predominantly Pseudomonas
Eikonella
Prevotella
Fusobacterium
unculturable"
Capnocytophaga Bacteroides family
anaerobic Gram Dialister
Filifactor "
Spirochetes Pyrosequencing studies:!
negative rods! Treponema
_______________________________________________________________________ Li et al. 2010, Siqueira et al. 2011, Saber et al.
Fungi Candida
Viruses HIV, Epstein-Barr virus, human cytomegalovirus, Herpes simplex virus-1
2012, Hong et al. 2013, Tzanetakis et al. 2015 !
How well can root canal systems be

Overview 4"
cleaned in a single visit .. or ever?"
" Microorganisms remain after debridement in
Part 2
!
"Methods used for evaluating endodontic microflora" isthmuses"
Part 3 "Microorganisms in primary endodontic infections""
!
Part 4 Microorganisms and unsuccessful endodontic treatment"
"
"!
!
Nair et al. 2005
7
Sedgley COD 2017
Microflora in primary and secondary Secondary endodontic infections !

endodontic infections differs" Enterococci"
Primary endodontic infections!
Biofilms"
Polymicrobial"
Enterococci predominate in culture-positive
Predominantly Gram negative anaerobic rods" root-filled teeth with chronic apical
Many species as yet unidentified and unculturable" periodontitis"
Molander et al. 1998, Sundqvist et al. 1998, Hancock et al. 2001,
Peciuliene et al. 2001, Pinheiro et al. 2003 and many others!
Previously root filled canals!
Biofilms" Enterococci are associated with persistence
Polymicrobial, reduced microbial load" of infection during endodontic treatment "
Frequently recovered in culture-based studies - Siren et al. 1997!
Gram positive facultatively anaerobic cocci:
Enterococcus faecalis"
Many species as yet unidentified and unculturable"
Reasons E. faecalis could resist root canal E. faecalis can survive for extended periods in
treatment procedures and survive" obturated root canals ex vivo"
Ability to invade dentinal tubules and adhere to

collagen in the presence of human serum "
" " " " " " Love et al. 2001" 48 hours Viable E. faecalis were
A proton pump which allows E. faecalis to survive recovered from teeth
CaOH2 treatment "
" " " " " " Evans et al. 2002! for 2 years after
Expression of virulence factors "" obturation!
12 months
" " "Sedgley et al. 2005, Mathew et al. 2010, Wang et al. 2011"
An efflux pump that may render E. faecalis biofilms
more susceptible to antimicrobials"
" " " "Upadya et al. 2011" 2 years
!
Sedgley et al. 2005, Sedgley and Jacinto 2014!
E. faecalis in secondary endodontic infections!

Bottom line "
They survive "
obturation for at least 12 months"
and have the potential to be virulent"
Is there proof that residual E. faecalis cause

endodontic treatment failure? "
"" "No"
Are they harmless hitchhikers?"
Are they persisters in biofilms?" Firmicutes phylum e.g. Enterococcus, Lactobacillus, Eubacterium"
"" "" Tzanetakis et al. 2015!
8
Sedgley COD 2017
Summary Secondary endodontic infections" Summary - Secondary endodontic infections"

Culture-based studies" Molecular-based studies"
________________________________________________________________
Multiple species (highly diverse) "

Facultative anaerobes Anaerobes
____________________________________________________________
Fewer species and Gram positive cocci
Enterococcus Micromonas (formerly Peptostreptococcus)
reduced microbial load

Streptococcus
Gram negative cocci

Staphylococcus
Less predominance of E. faecalis
Veillonella Anaeroglobus
compared with Gram positive rods

than in culture studies"
primary infection"
Bacillus Propionibacterium (formerly Arachnia)
Many species as yet unidentified

Pseudoramibacter Eubacterium
Polymicrobial"
Gram negative rods
Escherichia Porphyromonas
and unculturable"
Pseudomonas Prevotella
Proteus Fusobacterium
E. faecalis frequently Klebsiella Bacteroides family
Chugal et al. 2011!

Enterobacter Wolinella
Tannerella
recovered, but not ________________________________________________________________

Fungi
Candida
Anderson et al. 2012!
exclusively" ________________________________________________________________ Tzanetakis et al. 2015!
Siqueira et al. 2016!
and others" Siqueira et al. 2016!
"
Overview 5"
"
!
Part 3 "Microorganisms in primary endodontic infections" ""
"
Part 4 "Microorganisms and unsuccessful endodontic treatment " "
""
Part 5 "Microorganisms in periapical lesions "!
!
Ricucci et al. 2015!
Periapical lesions! Microorganisms in periapical lesions!

Histology study - humans" Sampling"
Microbiological sampling of periapical tissue
Not detected in granulomas " presents difficulties"
Submarginal incision better than marginal

Bacteria only detected in incision to avoid contamination of surgery site "
Sunde et al. 2000, Gatti et al. 2000!
abscesses or cysts" "
" However.."
Disinfection procedures do not destroy the
DNA "
"
Ricucci et al. 2006!
9
Sedgley COD 2017
Microorganisms in asymptomatic periapical lesions!

Tronstad et al. 1987"
Anaerobic bacteria are able to survive Evaluated 39 PA lesions (root-filled teeth
with asymptomatic apical periodontitis)"
and maintain an infectious disease
process in periapical tissues " Used CLSM for 3D observations, and
FISH to detect specific microorganisms"
" " "" Observed microcolonies throughout "
Detected P. gingivalis, P. intermedia,T.

forsythia, Streptococcus spp. and
unidentified morphotypes "
Sunde et al. 2003!
Summary Periapical lesion infections"

Culture-based studies"
Examined 34 apicoectomy samples for bacterial _______________________________________________________
Facultative anaerobes Anaerobes
DNA in root end and soft tissue (including one
control sample which was neg for DNA)" Sampling challenges" Gram positive cocci
Streptococcus
Enterococcus
Micromonas (formerly Peptostreptococcus)
Gemella
Staphylococcus
Persistent PA lesions 1/3 symptomatic" Gram negative cocci
Polymicrobial"
Veillonella
All except one root end and six periradicular tissue Gram positive rods
samples showed bacterial DNA" Bacillus Eubacterium
Propionibacterium (formerly Arachnia)
" Predominantly Gram Gram negative rods

Enterobacter Porphyromonas
Pseudomonas Prevotella
positive and Gram Vibrio

Capnocytophaga
Tannerella
Fusobacterium
Bacteroides family
negative anaerobes" Fungi

Aspergillus
Candida?
Subramanian and Mickel 2009!
Summary Periapical lesion infections"

Overview 6"
Molecular-based studies"
"
Sampling challenges" !
Part 3 !Microorganisms in primary endodontic infections" ""
Multiple species (polymicrobial) " "
Part 4 "Microorganisms and unsuccessful endodontic treatment"
Many species as yet unidentified " ?
Part 5 "Microorganisms and periapical lesions"
and unculturable"
!
Part 6 "Antimicrobial efficacy of endodontic treatment"

Viruses" " "and antibiotics " ""
Sunde et al. 2003!

"
10
Sedgley COD 2017
Biofilms grow on root canals

Clinical management of infected root canals"
walls and in dentinal tubules"
Aiming to remove:"
Microorganisms "
in biofilm and planktonic state "
dead and alive"
whole cells and parts of cells "
Debris from instrumentation, smear layer "
Pulpal remnants - cellular, fibrous"
Metabolic by-products"
Previous root filling material " Siqueira and Ras 2011!
Pathways of the Pulp!
Microbe tactics and strategies !

Why its hard to get rid of biofilms"
Microbe tactics and strategies"
Winners" Losers!
Howard Hughes Medical Institute! Virulence factors" Accessible?!
Biofilm interactions" Disruptible!
Resistance"
Antimicrobials!
!
!
Clinician tactics and strategies !

Clinical management of infected root canals" Mechanical disruption"
! Conventional irrigation"
Mechanical!
Antimicrobials!
disruption!
! Activation of irrigant"
Different file systems"

!
Mechanical!
removal!
!
11
Sedgley COD 2017
!
!
Clinician tactics and strategies
Apical pressure varies according to needle type!
Conventional irrigation of root canals"
"
"
Do irrigants reach apical part of the canal?!
There is little fluid exchange and displacement

of particles beyond the tip of the needle !
"
Chow 1983"
Needle tip
positioned 3mm
short of WL"
Boutsioukis et al. 2010!
! Mechanical disruption"
What influences irrigant flow?" Sonic activation"
"
Increased canal taper and apical size improves Lower frequency than ultrasonic "
irrigant replacement and wall shear stress and " "EndoActivatorTM "
reduces irrigant extrusion" " " " Sonicare CanalBrushTM"
Albrecht et al. 2004, Falk and Sedgley 2005, Boutsioukis et al. 2010!
" " " " ""
Needle depth placement influences irrigation
efficacy" " " " VibringeTM"
Sedgley et al. 2005, Boutsioukis et al. 2010! " " " " " GentleWaveTM"
Irrigation significantly less effective in curved ll remove debris/smear layer in vitro "
A
compared to straight canals ! Need independent data on antimicrobial activity
Nguy and Sedgley 2005" and biofilm removal in clinical situations"
" Salman et al. 2010, Kanter et al. 2011, Rodig et al. 2011, Molina et al. 2015!
Photon-Initiated Photoacoustic Photon-Initiated Photoacoustic

Streaming (PIPSTM)" Streaming (PIPSTM)"
Uses pulsed erbium:YAG laser to create In vitro E. faecalis study - culture"
photon-initiated photoacoustic streaming" Extracted premolars prepared to apical #25.06"
In vitro study culture of samples infected with PIPSTM with NaOCl/EDTA generated more
oral flora" negative bacterial samples than NaOCl/EDTA
Extracted premolars prepared to apical #20.07" conventional irrigation"
PIPSTM generated more negative bacterial
samples than conventional and ultrasonic PIPS "
(10/10, 10/10)"
activation" Max-I-Probe 25g "
(6/10, 0/10)"
Peters et al. 2011! Olivi et al. 2014!
12
Sedgley COD 2017
Photodynamic therapy (PDT) reduced

Photodynamic therapy"
biofilms in root canals"
Uses photosensitizer solutions (e.g. methylene Grew multispecies biofilms (4 species) in root canals"
blue, tolonium chloride) and low-power laser light"
Photodynamic therapy : up to 80% reduction of CFU"
"Rationale "
Solution binds to microbial cell"
Laser light applied (via plastic B.Viable biofilms (arrows)"
flexible fiber) activates dye" "
Free radicals produced destroy
C. After PDT : destruction of
cell" biofilms, with some foci of live
bacteria (arrow)"
Soukos et al. 2006! Fimple et al. 2008!
3 clinical studies reviewed"

52 extracted teeth
with pulpal necrosis
All showed PDT had a positive effect in
& PARL" private office clinical setting"
PDT significantly Review authors conclusions: "
reduced residual
bacteria within the Limited clinical information available on the use of
root canal system " PDT in root canal disinfection "
" If supported by future clinical research, PDT may
Diamonds 6% NaOCl" have efficacy for additional root canal disinfection,
Circles PDT"
especially in the presence of multidrug-resistant
Open initial"
Closed post Rx" bacteria"
Ng et al. 2011! Chrepa et al. 2014!
In vitro studies comparing different file Clinical studies comparing different file
systems to reduce microbial load" systems to reduce microbial load"
No difference between:"
No difference between:"
SAF, Twisted File and Reciproc"
Siqueira et al. 2013! Hand NiTi using alternated rotation motion
WaveOne and One Shape" or BioRace"
Nabeshima et al. 2014! Ras and Siqueira 2013!
Hand (K-file) and ProTaper" Self-Adjusting File and Twisted File Adaptive
Nakamura et al. 2013"
for retreatment cases "
Single Reciproc file and BioRaCe series" Rodrigues et al. 2015!
Alves et al. 2012!
WaveOne and ProTaper"
Single Reciproc file and BioRaCe series"
Pinheiro et al. 2016! Neves et al. 2016!
" Studies used real-time qPCR" "
13
Sedgley COD 2017
Clinician challenges! Clinician tactics and strategies !

Uninstrumented niches for biofilms" Antimicrobials"
Sodium hypochlorite"
Chlorhexidine"
EDTA"
Calcium hydroxide"
Antibiotics"
Peters 2004!
Sodium hypochlorite !
Sodium hypochlorite (NaOCl)" Classic clinical studies using culture-based techniques"
"
Is sodium hypochlorite an effective 0.5% NaOCl better than saline " "
antimicrobial agent?" ! ! ! ! ! !Bystrm and Sundqvist 1983"
YES" No sig difference between 0.5% & 5% NaOCl "

" " Cvek et al. 1976, Bystrm and Sundqvist 1985"
5% NaOCl effects enhanced by EDTA"

! ! ! ! Bystrm and Sundqvist 1985!
NaOCl inactivates the lipid moiety of lipotechoic acid
through deacylation of the lipid moiety"
Hong et al. 2016!
NaOCl + H2O NaOH + HOCl Na+ + OH- + H+ + OCl-"
Chlorhexidine!
Chlorhexidine"
Antimicrobial spectrum"
Is CHX an effective antimicrobial agent?"
Bacteriostatic or bacteriocidal (depending on
Yes, but not as effective as NaOCl"
concentration used) for a wide range of Gram
Does not have tissue solvent capacity" positive and Gram negative bacteria. Disrupts
cell membrane"
CHX has limited activity against non-enveloped

viruses and some bacterial and fungal spores"
"
14
Sedgley COD 2017
Chlorhexidine! NaOCl versus CHX !

Effect on biofilms" Effect on biofilms"
In vitro multispecies"
Bacteria in mature biofilms and nutrient-limited
biofilms are more resistant to CHX killing than
bacteria in young biofilms " 6% NaOCl rendered bacteria nonviable and
physically removed polymicrobial biofilms from
root segments (EDTA, MTAD, CHX did not)"
Clegg et al. 2006!
!
2% NaOCl was more effective against
multispecies biofilms in dentin than 2% CHX"
2 days " " " "2 weeks " "12 weeks" Yang et al. 2016!
Shen et al. 2011!
NaOCl versus CHX !

Chlorhexidine + NaOCl precipitates"
Antimicrobial activity" 1. Standard
In vitro studies !
2. OR15
3. OR17
4. OR37
5. OR31
Clinical studies using molecular methods"

6. OR47
7. OR62
8. OR64
CHX and NaOCl precipitates when combined "

9. OR68
10. OR92
11. ER3
12. ER5
"
13. JG2
14. OG1
15. JH2-2
Canals with necrotic pulp - 2.5% NaOCl killed more

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Basrani et al. 2007!
MOs than 2% CHX gel and removed more cells "" !
Vianna et al. 2006! !
!
Teeth with AsAP - no difference between 0.12% CHX !
and 2.5% NaOCl" CHX and NaOCl precipitate blocks dentinal tubules "
"Ras and Siqueira 2011!
! Bui et al. 2008!
CONSORT trial - Retreatment cases: no difference
between 2% CHX and 1% NaOCl"
"Zandi et al. 2016!
Neg control" 6% NaOCl + 2% CHX"
Other chlorhexidine interactions" EDTA"

! ""
CHX and EDTA precipitates when combined " Introduced to endo as a chelating agent"
Rasimick et al. 2008! Nygaard-Ostby 1957!
CHX and Ca(OH)2 results in immediate degradation In vitro: EDTA can act as an antibiofilm acid
of CHX " for limiting S. aureus biofilm attachment by
Barbin et al. 2008! decreasing iron availability"
Al-Azemi et al. 2011!
Destabilizes biofilms by sequestering
calcium, magnesium, zinc, and iron "
Finnegan and Percival 2015!
15
Sedgley COD 2017
Alternate irrigation with EDTA and NaOCl" Calcium hydroxide"

Biofilm removal enhanced by alternate
irrigation with NaOCl and EDTA rather Can calcium hydroxide kill
than using EDTA all at once as a final rinse endodontic microflora?"
after NaOCl"
YES .. but not always"
Soares et al. 2010!
Calcium hydroxide! Calcium hydroxide!

Effect on biofilms in dentinal tubules" Antimicrobial effectiveness"
Canals infected with E. faecalis" Clinical study - culture"
Tooth slices (1mm) obtained" 7 day intracanal application effective in
eliminating bacteria"
DEAD! LIVE! 10 minute application ineffective "
Intracanal Ca(OH)2 for at least 1 wk rendered
Top. Treated with CaOH2: 92.5% of canals bacteria-free"
Survival 29%-50%" Sjgren et al. 1991, Shuping et al. 2000!
!
DEAD! LIVE! "
Intracanal medication for 4 weeks with Ca(OH)2
Bottom. Untreated controls: limited but did not prevent regrowth of
Survival 83%-96%" endodontic bacteria"
Peters et al. 2002"
Parmar et al. 2011!
Calcium hydroxide versus CHX medicament! Calcium hydroxide versus CHX medicament!
Antimicrobial effectiveness" Healing outcome"
Prospective randomized clinical trial" Clinical study (case series, retrospective)!
69 single rooted adult teeth" "
Used real-time qPCR and viable counts to 2-4 yr follow-up on previous study of 22 teeth with
compare antimicrobial effectiveness of apical periodontitis medicated with CHX "
intracanal 2% CHX gel and Ca(OH)2 paste"
14 day dressing with Ca(OH)2 paste was
significantly more effective, particularly in cases No sig difference in healing outcome between 2%
with apical periodontitis" CHX liquid (94%) and Ca(OH)2 (90%)(historical
control)"
!
!
Teles et al. 2014 Tervit et al. 2009
16
Sedgley COD 2017
Some other recent antimicrobial approaches." Antibiotics"
Etidronic acid: Arias-Moliz et al. 2016!

D-Enantiomeric peptide: Zhang et al. 2016! Intracanal applications brief (See Regendo)"
Strong Acid Electrolyzed water: Cheng et al. 2016"
Peracetic acid: Arias-Moliz et al. 2015!
Indications and dosage "
Ferula gummosa plant essential oil: Abbaszadegan et al. 2015" Prophylaxis ADA/AHA/AAOS/AAE guidelines"
Photosentitizer-functionalized bioactive nanoparticles: Shrestha
and Kishen 2014" Endodontic treatment - AAE guidelines"
Cold plasma: Pan et al. 2013! In vitro Antibiotic resistance in endodontic infections"
Phage therapy: Phee et al. 2013!
N-acetylcysteine: Quah et al. 2012! studies! Antibiotic Stewardship CDC guidelines"
Vanadium chloroperoxidase: Persoon et al. 2012!
and others!
!
!
!
"
Regenerative endodontics!
Intracanal antibiotics" Survival of SCAP cells exposed to medicaments"
Early penicillin and polyantibiotic paste used
until allergy/resistance issues raised "
Grossman 1945, 1946, 1951 !
Local application of antibiotics more effective than
systemic to treat intracanal infections? !
Review. Mohammadi and Abbott 2009!
Triple antibiotic paste.."
Sato et al. 1992!
!
Metronidazole
TAP: triple antibiotic paste (metronidazole, minocycline, ciprofloxacin) "
DAP: double antibiotic paste (metronidazole, ciprofloxacin)"
Minocycline!
Jung et al. 2008!
Althumairy et al. 2014!
Regenerative endodontics!
Removal of intracanal medicaments" Antibiotics"
Triple Antibiotic Paste" Ca(OH)2"
Intracanal applications see Regendo lecture"
Prophylaxis ADA/AHA/AAOS/AAE guidelines"
PP positive pressure side vented needle"

PUI passive ultrasonic irrigation"
EA EndoActivator"
EV EndoVac" Berkhoff et al. 2014!
17
Sedgley COD 2017
ADA regimens for Antibiotic Prophylaxis 2008"
Originally published in JADA 2008 !

Reprinted in AAE Antibiotic Prophylaxis Quick Reference Guide 2008 AAE Colleagues for Excellence 2012
AHA Guidelines on Antibiotic Prophylaxis ! AHA Guidelines on Antibiotic Prophylaxis !

Antibiotic Prophylaxis prior to a dental procedure Antibiotic Prophylaxis prior to a dental procedure
RECOMMENDED" NOT recommended"
Artificial heart valves "
Infective endocarditis history" Mitral valve prolapse "
Certain specific, serious congenital (present from Rheumatic heart disease "
birth) heart conditions, including: " Bicuspid valve disease "
Unrepaired or incompletely repaired cyanotic congenital heart
disease, as well as those with palliative shunts and conduits " Calcified aortic stenosis "
Completely repaired congenital heart defect with prosthetic Congenital heart conditions, such as ventricular
material or device, whether placed by surgery or by catheter
intervention, during the first six months after the procedure "
septal defect, atrial septal defect and hypertrophic
Any repaired congenital heart defect with residual defect at site cardiomyopathy"
or adjacent to site of a prosthetic patch or a prosthetic device "
Cardiac transplant that develops a problem in a
heart valve"
AAE Quick Reference Guide 2008 AAE Quick Reference Guide 2008
AAE Colleagues for Excellence 2012 ! AAE Colleagues for Excellence 2012 !
Antibiotic Prophylaxis ! Antibiotic Prophylaxis !
Special Circumstances" Patients with Joint Replacement"
Patients already receiving antibiotics"
If taking antibiotic normally used for endocarditis prophylaxis, select a
drug from a different class"
If possible, delay Rx until at least 10 days after completion of antibiotic to
2003"
allow re-establishment of usual oral flora"
If receiving long-term parenteral antibiotic for IE, time Rx to occur 30 to
60 min after the parenteral antibiotic delivered"
Inadvertent failure to administer pretreatment antibiotic" American Academy of Orthopedic Surgeons recommends that
Dosage may be administered up to 2 hours after procedure " clinicians consider antibiotic prophylaxis for all total joint
replacement patients prior to any invasive procedure that may
"
cause bacteremia. (2009)"
Individuals with permanent kidney dialysis shunts "
Use same protocol as for IE"
AAE Colleagues for Excellence 2012 AAE Colleagues for Excellence 2012
18
Sedgley COD 2017
AAOS, ADA Release Clinical Practice Guidelines

for Prophylactic Antibiotics (2012)" Antibiotics"

Prophylaxis AHA/AAOS/AAE guidelines"
Endodontic treatment - AAE guidelines"
Indications?"
Which antibiotic?"
http://www.aaos.org/AAOSNow/2013/Jan/cover/cover1/?ssopc=1
Systemic antibiotics do NOT prevent

post-operative pain and flare-ups"
Localized acute apical abscess (Fouad et al. 1996)"
Symptomatic necrotic teeth (Henry et al. 2001)"
Indicated " NOT indicated"
Irreversible pulpitis (Nagle et al. 2000)"
Asymptomatic necrotic teeth (Pickenpaugh et al. 2001)"
Asymptomatic apical periodontitis (Walton & Chiappinelli 1993)"
Periapical endodontic surgery (Lindeboom et al. 2005)"
AAE Colleagues for Excellence 2006
Aminoshariae
and Kulild 2016
Preoperative administration to prevent post-op pain?

Ineffective" Letter to the Editor JADA 2016"
Asymptomatic necrotic teeth (Pickenpaugh et al. 2001)"
Post-operative administration to prevent pain or flare-ups?

Ineffective"
Localized acute apical abscess (Fouad et al. 1996)"
Symptomatic necrotic teeth (Henry et al. 2001)"
Asymptomatic apical periodontitis (Walton & Chiappinelli 1993)"
Aminoshariae and Kulild 2016
19
Sedgley COD 2017
Localized acute apical abscess (Fouad et al. 1996)" Localized acute apical abscess (Fouad et al. 1996)"
Symptomatic necrotic teeth (Henry et al. 2001)" Symptomatic necrotic teeth (Henry et al. 2001)"
.. there was insufficient evidence to determine the
effects of the administration of systemic antibiotics to This was a study with a small number of participants
adults with symptomatic apical periodontitis or acute and the quality of the evidence for the different
apical abscess" outcomes was rated as low. There is currently
insufficient evidence to be able to decide if antibiotics
help for this condition"
Cope et al. 2014 Agnihotry et al. 2014
Antibiotics"
Not allergic to penicillins"
Penicillin VK: antibiotic of choice, effective against target microflora,
narrow spectrum, low toxicity, low cost"
Intracanal applications see Regendo lecture" "1g loading dose then 500mg every 4-6 hrs for 5-7 days"
Amoxicillin: rapid absorption and longer half-life than PenVK BUT
Prophylaxis AHA/AAOS/AAE guidelines" extended spectrum may select for additional resistant "
Endodontic treatment - AAE guidelines" strains of bacteria. Restrict use to prophylaxis. "
Indications?" "1g loading dose then 500mg every 8 hrs for 5-7 days"
Which antibiotic?"
Amoxicillin with clavulanate (Augmentin): reserve for "
"unresolved infections and immunocompromised patients "
"1mg loading dose then 500/125mg every 8 hrs for 5-7 days"
AAE Colleagues for Excellence 2006
Metronidazole: only effective against anaerobes"

Clindamycin: antibiotic of choice for patients allergic to penicillin"
Use in combination with penicillin or clindamycin if "
Effective against gram-positive facultatives and anaerobes"
symptoms worsen 48-72 hrs after initial treatment "
Reaches concentration in bone that approximates plasma"
and continue with penicillin or clindamycin"
"600mg loading dose then 300mg every 6 hrs for 5-7 days"
1,000mg loading dose then 500mg every 6 hrs for 5-7 days"
"
Macrolides:"
Not recommended: "
Clarithromycin: spectrum of activity includes endo anaerobes"
Erythromycin - GIT upset "
"500mg loading dose then 250mg every 12 hrs for 5-7 days"
Tetracyclines - widespread resistance "
"
Ciprofloxacin and 1st gen cephalosporins - limited spectrum
Azithromycin: spectrum of activity includes endo anaerobes"
of activity against endo microflora "
"500mg loading dose then 250mg once a day for 5-7 days"
2nd gen cephalosporins - cross-allergenicity with penicillin"
" AAE Colleagues for Excellence 2006 AAE Colleagues for Excellence 2006
20
Sedgley COD 2017
Antibiotic resistance in endodontic microflora!

Antibiotics" (Classic studies basis for AAE Colleagues 2006 guidelines)"
Resistance phenotype (culture, MICs) to:"
Metronidazole (54%), Pen V (15%) in Oregon study"
Intracanal applications see Regendo lecture" Baumgartner and Xia 2003"
Indications and dosage " "
Endo abscesses. Oregon"
Antibiotic resistance in endodontic infections" Acute endo infections. Thailand"
Khemaleelakul et al. 2002!
Antibiotic resistance in endodontic microflora! Antibiotic resistance in endodontic microflora!

Molecular studies Genes (PCR products)" Molecular studies Proteins (Metaproteome)"
Tetracycline, erythromycin, beta-lactams"
TetR, beta-lactamase, MarR regulator, efflux pump, "
No vancomycin
resistance found"
Jungermann et al. 2011"
Pretreatment samples from 2 of 12 RCT cases

had proteins related to beta-lactam and
tetracycline resistance"
Ras and Siqueira 2013"
Provenzano et al. 2013
Bottom line: Is antibiotic resistance in

endodontic microflora a clinical problem?"
Analyzed 10 root apexes and matched inflammatory
lesions from RCT treated teeth with apical periodontitis" Resistance phenotype (Culture, MICs) to:"
7 cases exhibited proteins related to antibiotic resistance" Metronidazole, beta-lactams "
Khemaleelakul et al. 2002, Baumgartner and Xia 2003"
TetR was found in both root apex and lesion in one case"
"
Genes (PCR) associated with resistance to:"
Tetracycline, erythromycin, beta-lactams"
Jungermann et al. 2011, Ras and Siqueira 2013!
"
Proteins (enzymes) related to resistance:"
TetR, beta-lactamase, MarR regulator, efflux pump "
Provenzano et al. 2016
"
21
Sedgley COD 2017
Antibiotics"

Antibiotic resistance in endodontic infections"
Antibiotic Stewardship"
2013
65.6% were prescribed in situations with no

evidence of spreading infection"
70.6% were used without provision of an operative

intervention"
"
Patients placed on antibiotic therapy for an orofacial infection should
be clinically evaluated on a daily basis.When there is sufficient clinical Only 19.0% were prescribed in situations where their
evidence that the patients host defenses have regained control of the use was indicated by clinical guidelines"
infection and that the infection is resolving or resolved, the antibiotic
therapy should be terminated"
AAE Colleagues for Excellence 2012 Cope et al. 2016
Analyses of BC PharmaNet database from 1996-2013"

Physician prescribing declined 18.2%, but dental
prescribing increased 62.2%"
Rate of prescribing increased the most for dental
patients 60 years or older "
Use of narrow spectrum Pen VK, has decreased significantly"

Broad spectrum amoxicillin and amoxicillin with enzyme
inhibitors has increased"
Of concern as Pen VK is recommended as first-line agent for
dental indications & retains suitable coverage across oral flora"
Marra et al. 2016 Marra et al. 2016
22
Sedgley COD 2017
2013
CDA webinair with dentists in Canada & USA identified the

following explanatory themes:"
Unnecessary prescriptions for periapical abscess and
irreversible pulpitis"
Dental implants and their complications"
Slow adoption of guidelines for less antibiotic coverage for
patients with valvular heart disease and prosthetic joints"
Emphasis on cosmetic practices reducing the surgical skill set
of average dentists "
Underinsurance practices driving antibiotics to be substitute
for surgery"
Aging population "
Marra et al. 2016
Sample question.! Bottom line.the present !

How do you control microbes in endo Rx?" "
Aseptic technique"
Effective debridement"
Local antimicrobials" Rochas et al. 2008"
Systemic antibiotics only if "

" indicated"
Ross Mitchell"
Apical and coronal seal"
The Future!
Bioinformatics"
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<"'"(
>I/0",,7&'(
)FC( !"#$%&'$#()$*$+$,",(
G"H2"'8"( -&./$0"1(-#2,*"0(3(4'*"50$*"(
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<"'"%8(3(="*$+&#78(>'57'""07'5(
Adapted from Libault et al. 2010!
23
Colleagues for Excellence
PUBLISHED FOR THE DENTAL PROFESSIONAL COMMUNITY BY THE AMERICAN ASSOCIATION OF ENDODONTISTS Summer 2006
Welcome to ENDODONTICS: Colleagues for Excellencethe newsletter covering the latest in endodontic treatment,
research and technology. We hope you enjoy our coverage on the full scope of options available for patients through endodontic
treatment and that you find this information valuable in your practice. All issues of this ENDODONTICS newsletter are available on
the AAE Web site at www.aae.org, and cover a range of topics on the art and science in endodontic treatment.
E ndodontic infections range from being asymptomatic to

life threatening. This issue of ENDODONTICS: Colleagues for
Figure 1: Patient with cellulitis caused
by premolar root canal infection.
Excellence reviews the objectives of endodontic treatment in

managing infected root canal systems, specifically addressing
antibiotics and their impact on patients. Guidelines for the
prescription of specific antibiotics are provided for use as an
adjunct to clinical treatment of the patient.
The Nature of Endodontic Infections
Root canal infections are polymicrobial infections
characterized by mostly anaerobic bacteria and some
facultative bacteria (1). A tooth with an infected necrotic While normal flora may prevent pathogenic organisms from
pulp becomes a reservoir of infection isolated from the invading the tissues and causing disease, they may become
patients immune response. Eventually, bacteria and bacterial opportunistic pathogens if they gain access to tissues not
by-products will produce a periradicular inflammatory previously colonized. Such is the case when normal oral
response. With microbial invasion of periradicular flora gain access to the pulp cavity and periradicular tissues.
tissues, an abscess and cellulitis may develop. The Microbes associated with endodontic disease include bacteria,
inflammatory response may give rise to both protective fungi and viruses (1).
and immunopathogenic effects; it may also be destructive Clinical signs and symptoms of an infection are the result
to surrounding tissue and contribute to adverse signs and of damage to the tissues caused by the microbe and the
symptoms. Severe infections may develop depending on inflammatory response produced by the host. Patient
the pathogenicity of the microorganisms involved and the evaluation and the appropriate diagnosis/treatment of
resistance of the host (Figure 1). the source of an infection are of utmost importance.
The spread of infection and the inflammatory response will
continue until the source of the irritation is removed.
Clinical Treatment of Endodontic Infections and pulpal debris from the infected root canal
Soft tissue swelling of endodontic origin should be system. This establishes a favorable condition
incised for drainage (Figure 2). for periradicular inflammation to resolve.
When a patient has signs and symptoms associated
with a severe endodontic infection (Table 1), the root
canal system should be filled with calcium hydroxide,
and the access opening sealed to prevent coronal
leakage of bacteria from the oral cavity. If there is
continuous drainage, the canal may be left open
until the next day. Drainage allows the accumulated
irritants and inflammatory mediators to decrease to
a level where a healthy patient can initiate healing.
However, leaving the tooth open for drainage for
Figure 2: Intraoral drainage of purulent exudate. a longer time allows gross contamination with no
benefit to the patient.
In most cases, a drain placed in the incision for 24-48
Table 1. Indications for Adjunctive Antibiotics
hours will allow for adequate drainage (Figure 3).
Figure 3: Intraoral Fever > 100 F
drain sutured into
incision for drainage. Malaise
Lymphadenopathy
Trismus
Increased Swelling
Cellulitis
Osteomyelitis
Persistent Infection
However, effective treatment of endodontic infections
also includes removal of the reservoir of infection
A regimen of antibiotics is not indicated in an otherwise
by either endodontic treatment or tooth extraction.
healthy patient for a small localized swelling without
Successful management of the infected root canal
systemic signs and symptoms of infection or spread of
system requires chemomechanical debridement of the
infection (2-6) (Tables 1, 2). Swellings increasing
root canal system. Three to 12 species of bacteria can
usually be cultured from infected root canals in size or associated with cellulitis should be
incised for drainage and adjunctive antibiotics
Figure 4: Cultivation administered.
of polymicrobial
endodontic infection.
Table 2. Conditions Not Requiring Adjunctive Antibiotics
1. Pain without signs and symptoms of infection

a. Symptomatic irreversible pulpitis
b. Acute periradicular periodontitis
2. Teeth with necrotic pulps and a radiolucency
3. Teeth with a sinus tract (chronic
periradicular abscess)
(Figure 4); it is important that debridement of the root 4. Localized fluctuant swellings
canal be accomplished aseptically using rubber dam
isolation to prevent further microbial contamination.
The objectives for endodontic treatment are
removal of the microbes, their by-products
2 ENDODONTICS: Colleagues for Excellence

Magic Bullets Versus Resistant Bacteria additional resistant organisms. Empirical selection
The term antibiotic is used for chemicals that of an antibiotic without susceptibility tests is based
are produced either by bacteria and/or synthetic on knowledge of the organisms usually involved in
antimicrobials produced in a laboratory that kill endodontic infections. Antibiotics are indicated when
or inhibit the growth of bacteria. The discovery of there is systemic involvement or evidence of spread of
penicillin by Fleming in 1928 revolutionized health infection. Signs and symptoms include: fever above 100
care for the treatment of bacterial infections such degrees Fahrenheit, malaise, cellulitis, unexplained
as tuberculosis, pneumonia and syphilis. Because trismus, lymphadenopathy and swelling beyond a
antibiotics are relatively harmless to the host, they simple localized mucosal enlargement.
can be used to treat infections including those of
Systemic administration of the appropriate antibiotic
endodontic origin. However, antibiotics may have
dosage is usually for five to seven days. Clinical signs
adverse effects by altering the normal flora and by
and symptoms will usually diminish in two to four days
producing allergic reactions. The interaction of
after diagnosis and removal of the cause of the infection.
antibiotics with other drugs may also produce harmful
Patients should continue to take the antibiotic for an
side effects or render them ineffective.
additional two to three days to prevent rebound of the
Antibiotics have been called magic bullets because infections. Noncompliance by a patient not taking the
they target the organisms producing disease. prescribed antibiotic regimen may allow a rebound of the
Unfortunately, the wide use of antibiotics has fostered infection. A seven-day prescription is usually adequate.
the selection of resistant bacteria. Antibiotics alter
Incision for drainage is important to remove purulent
the natural balance of normal flora by selecting for
material consisting of bacteria, bacterial by-products,
organisms that are resistant. Resistant genes are
disintegrated inflammatory cells, enzymes (spreading
transferred vertically to all daughter cells. In addition,
factors) and other inflammatory mediators.
resistant genes can be transferred horizontally to other
Drainage improves circulation to the infected tissues
strains of bacteria by transduction, transformation and
and improves delivery of a minimum inhibitory
conjugation. Thus, strains of bacteria never exposed
concentration of the antibiotic to the area. Because
to the antibiotic may acquire resistance without ever
endodontic infections are polymicrobial, no single
coming in contact with the antibiotic.
antibiotic is likely to be effective against all the strains
The selection of resistant organisms is enabled when of infecting bacteria. However, it is likely that if an
a low dose of an antibiotic is administered, when antibiotic is effective against several of the strains of
antibiotics are taken for long periods of time or bacteria, it will disrupt the microbial ecosystem.
through noncompliance by patients. Another source
One of the more common side effects of antibiotic
of resistant organisms is from the use of low doses of
therapy is diarrhea, which results from the antibiotic
antibiotics in agricultural feed and fertilizers. A prime
disrupting the normal balance of intestinal flora.
example of acquired resistance is Staphylococcus Antibiotic-associated colitis/pseudomembranous
aureus, which now has resistance to multiple colitis has been associated with the use of many
antibiotics including vancomycin. In addition, antibiotics, but only rarely associated with dental
the development of resistance by bacteria therapy (7). Patients requiring extraoral drainage or
because of inappropriate prescriptions hospitalization should be referred to an oral surgeon
raises questions and concerns for health care (Figure 5).
workers.
Responsible Use of Antibiotics in

Endodontic Treatment
Antibiotics are used in addition to appropriate
treatment to aid the host defenses in the elimination
of remaining bacteria. Narrow-spectrum antibiotics
should be the first choice to be prescribed because
broad-spectrum antibiotics produce more alterations
in the normal gastrointestinal tract and select for Figure 5: Extraoral drain sutured into incision for
drainage.
ENDODONTICS: Colleagues for Excellence 3

Some patients, especially immunocompromised higher and more sustained serum levels than penicillin
patients, are at high risk for infections, and a culture VK. Because of these traits, amoxicillin is often used
of the infecting organisms with susceptibility testing for antibiotic prophylaxis of patients that are medically
may be indicated. Identification of the bacteria and compromised (11, 12). Amoxicillin may be used for
results of susceptibility tests may take several days serious odontogenic infections, however, its extended
to a couple of weeks, depending on the microbes spectrum may select for additional resistant strains of
involved in the infection. Good communication with bacteria. The usual oral dosage for amoxicillin is 1,000
a laboratory will ensure that the sample is properly mg loading dose followed by 500 mg every eight hours
collected, transported, cultured and identified. If for five to seven days.
there is any question about the patient being
The combination of amoxicillin with clavulanate
medically compromised, or if the patients
(Augmentin ) was the most effective antibiotic
TM
condition deteriorates, referral should be combination in recent susceptibility tests (8, 9).
considered. Clavulanate is a competitive inhibitor of the beta-
Types of Antibiotics and lactamase enzyme produced by bacteria to inactivate
Recommended Dosages penicillin. The usual oral dosage for amoxicillin with
Based on recent antibiotic susceptibility tests, clavulanate is 1,000 mg loading dose followed by 500
penicillin VK is the drug of choice for periradicular mg every eight hours for five to seven days.
abscesses (8, 9) (Figure 6). Clindamycin is effective against gram-positive
facultative microorganisms and anaerobes. Clindamycin
is a good choice if a patient is allergic to penicillin
Efficacy of Antibiotics
or a change in antibiotic is indicated. Penicillin and
100%
90% 100
96
clindamycin have been shown to produce good results
80%
85
91
89 in treating odontogenic infections (13). Clindamycin
70%
60%
is well distributed throughout most body tissues and
Percentage 50% reaches a concentration in bone approximating that of
40%
45 plasma. The oral adult dosage for serious endodontic
30%
20%
infections is a 600 mg loading dose followed by 300 mg
10% every six hours for five to seven days.
0%
Penicillin VK Amoxicillin Amoxicillin- Clindamycin Clarithromycin Metronidazole
clavulanate
Metronidazole may be used in combination with
Figure 6: Antibiotic susceptibility for bacteria from endodontic penicillin or clindamycin. If a patients symptoms
infections.
worsen 48-72 hours after initial treatment and the
prescription of either penicillin or clindamycin,
metronidazole may be added to the original
It is effective against facultative and anaerobic
antibiotic. It is of utmost importance to review
microorganisms associated with endodontic infections.
the diagnosis and treatment to confirm
Penicillin VK remains the antibiotic of choice because
that the management of the infection has
of its effectiveness, low toxicity and low cost. However,
about 10 percent of the population will give a history been appropriate. Metronidazole is a synthetic
of allergic reactions to penicillin. To achieve a antimicrobial agent that is bactericidal and has activity
steady serum level with penicillin VK, it should be against anaerobes, but lacks activity against aerobes
administered every four to six hours (10). A loading and facultative anaerobes. Susceptibility tests have
dose of 1,000 mg of penicillin VK should be orally shown significant numbers of bacteria resistant to
administered, followed by 500 mg every four to six metronidazole (8, 9). It is important that the patient
hours for five to seven days. Following debridement of continue to take penicillin or clindamycin, which are
the root canal system and drainage of facial swellings, effective against the facultative bacteria and those
significant improvement of the infection should be seen resistant to metronidazole. The usual oral dosage for
within 48-72 hours. metronidazole is a 1,000 mg loading dose followed by
500 mg every six hours for five to seven days. When
Amoxicillin is an analogue of penicillin that is rapidly patients fail to respond to treatment, consultation with a
absorbed and has a longer half-life. This is reflected in specialist is recommended.
4 ENDODONTICS: Colleagues for Excellence

Erythromycin is a macrolide that has traditionally The AAE Public and Professional Affairs Committee
been prescribed for patients allergic to penicillin; and the Board of Directors developed this issue
however, it is not effective against anaerobic bacteria. with special thanks to the author, Dr. J. Craig
Erythromycin is no longer recommended for treatment Baumgartner, and reviewers, Drs. James A. Abbott,
of endodontic infections because of this poor spectrum Gerald C. Dietz Jr., David C. Hansen and Louis E.
of activity and significant gastrointestinal upset. Rossman.
Clarithromycin and azithromycin are macrolides
that have a spectrum of activity that includes some
anaerobes involved in endodontic infection and offer
improved pharmacokinetics. Food slows down but
does not affect the bioavailability of clarithromycin. The information in this newsletter is
Food and heavy metals may inhibit the absorption designed to aid dentists. Practitioners
of azithromycin. The oral dosage for clarithromycin must use their best professional
is a 500 mg loading dose followed by 250 mg every
12 hours for five to seven days. The oral dosage for judgment, taking into account the needs
azithromycin is a 500 mg loading dose followed by 250 of each individual patient when making
mg once a day for five to seven days. diagnoses/treatment plans. The AAE
Cephalosporins are usually not indicated for the neither expressly nor implicitly warrants
treatment of endodontic infections. First-generation any positive results, nor expressly nor
cephalosporins do not have activity against the
anaerobes usually involved in endodontic infections. implicitly warrants against any negative
Second-generation cephalosporins have some efficacy results, associated with the application
for anaerobes, however, there is a possibility of cross- of this information. If you would like
allergenicity of cephalosporins with penicillin.
more information, call your endodontic
Doxycycline occasionally may be indicated when colleague or contact the AAE by e-mail at
the above antibiotics are contraindicated. However,
many strains of bacteria have become resistant to the info@aae.org.
tetracyclines.
Ciprofloxacin is a quinilone antibiotic that is not
effective against anaerobic bacteria usually found in
endodontic infections. With a persistent infection it may
be indicated if culture and sensitivity tests demonstrate
the presence of susceptible organisms.
Conclusion
The use of improved culturing and molecular methods
now detect the presence of many more organisms in
endodontic infections than previously determined. It
is important that clinicians understand the nature of
polymicrobial endodontic infections and realize the
importance of removing the reservoir of infection
by endodontic treatment or tooth extraction. The
prescription of antibiotics should be considered
adjunctive to the clinical treatment of the patient;
antibiotics should not be substituted for root
canal debridement and drainage of purulence
from a periradicular swelling.
ENDODONTICS: Colleagues for Excellence 5

ENDODONTICS: Colleagues for Excellence
References
1. Baumgartner JC, Hutter JW, Siqueira JF. Endodontic Microbiology and Treatment of Infections. In: Cohen S, Hargreaves KM, editors.
Pathways of the Pulp. Ninth ed. St. Louis: Mosby; 2006.
2. Fouad AF, Rivera EM, Walton RE. Penicillin as a supplement in resolving the localized acute apical abscess. Oral Surg 1996;81(5):590-
595.
3. Henry M, Reader A, Beck M. Effect of penicillin on postoperative endodontic pain and swelling in symptomatic necrotic teeth. J
Endodon 2001;27(2):117-123.
4. Nagle D, Reader A, Beck M, Weaver J. Effect of systemic penicillin on pain in untreated irreversible pulpitis. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 2000;90:636-40.
5. Pickenpaugh L, Reader A, Beck M, Meyers WJ, Peterson LJ. Effect of Prophylactic amoxicillin on endodontic flare-up in asymptomatic,
necrotic teeth. J Endodon 2001;27(1):53-56.
6. Walton RE, Chiappinelli J. Prophylactic penicillin: effect on posttreatment symptoms following root canal treatment of asymptomatic
periapical pathosis. J Endodon 1993;19(9):466-470.
7. Jaimes EC. Lincocinamides and the incidence of antibiotic-associated colitis. Clin Therapeu 1991;13(2):270-280.
8. Baumgartner JC, Xia T. Antibiotic susceptibility of bacteria associated with endodontic abscesses. J Endodon 2003;29(1):44-47.
9. Khemaleelakul S, Baumgartner JC, Pruksakorn S. Identification of bacteria in acute endodontic infections and their antimicrobial
susceptibility. Oral Surg Oral Med Oral Pathol 2002;94(6):746-55.
10. Pallasch TJ. Pharmacokinetic principles of antimicrobial therapy. Periodontol 2000 1996;10:5-111.
11. ADA. Antibiotic prophylaxis for dental patients with total joint replacements. JADA 2003;134(July):895-899.
12. Dajani AS, et al. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. JAMA
1997;277(22):1794-1801.
13. Gilmore WC, Jacobus NV, Gorbach SL, Doku HC. A prospective double-blind evaluation of penicillin versus clindamycin in the
treatment of odontogenic infections. J Oral Maxillofac Surg 1988;46:1065-1070.
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ENDODONTICS
Colleagues for
Excellence
Winter 2012
Use and Abuse of Antibiotics
Published for the Dental Professional Community by the

www.aae.org/colleagues
Cover artwork: Rusty Jones, MediVisuals, Inc.

F or the past 80 years, antibiotic therapy has played a major role in the treatment of bacterial infectious diseases. Since the
discovery of penicillin in 1928 by Fleming and sulfanilamide in 1934 by Domagk, the entire world has benefited from one
of the greatest medical advancements in history. The discovery of safe, systemic antibiotics has been a major factor in the
control of infectious diseases and, as such, has increased life expectancy and the quality of life for millions of people. Ac-
cording to the Centers for Disease Control and Prevention, life expectancy of individuals in the United States born in 1900
was 47 years, while those born in 2005 is projected to be 78 years.1 At the beginning of the 20th century, the infant (< 1 year)
mortality rate in the United States was 100/1,000 live births compared to 6.7/1,000 in 2006.2 The major reason for these
phenomenal achievements has been the ability to control infectious diseases.3
Development of Antibacterial Drug Resistance

Along with the dramatic benefits of systemic antibiotics, there has also been an explosion in the number of bacteria that
have become resistant to a variety of these drugs. The problem is not the antibiotics themselves. They remain one of medi-
cines most potent weapons against diseases. Instead, the problem is in the way the drugs are used. The inappropriate
overuse of antibiotics has resulted in a crisis situation due to bacterial mutations developing resistant strains.
Many worldwide strains of Staphylococcus aureus exhibit resistance to all medically important antibacterial drugs, includ-
ing vancomycin, and methicillin-resistant S. aureus has become one of the most frequent nosocomial, or hospital-acquired,
pathogens. The rate at which bacteria develop resistance to antibacterial drugs is alarming, demonstrating resistance soon
after new drugs have been introduced. This rapid development of resistance has contributed significantly to the morbidity
and mortality of infectious diseases, especially nosocomial infections.4
A nosocomial infection is a hospital-acquired infection that develops in a patient after admission. It is usually defined as
an infection that is identified at least 48 to 72 hours following admission, so infections incubating, but not clinically appar-
ent at admission are excluded. Nosocomial infections are costly, resulting in increased morbidity, requiring longer periods
of hospitalization and limiting access of other patients to hospital resources. The direct costs of hospital-acquired infections
in the United States are estimated to be $4.5 billion per year. Nosocomial infections also contribute to the emergence and
dissemination of antimicrobial-resistant organisms. Antimicrobial use for treatment or prevention of infections facilitates
the emergence of more resistant organisms. Patients with infections caused by antimicrobial-resistant organisms are then
a source of infection for hospital staff and other hospitalized patients. These drug-resistant infections may subsequently
spread to the community.5
The British Society for Antimicrobial Chemotherapy published a review in the Journal of Antimicrobial Chemotherapy.
This review examined the contributions antibiotic prescribing by general dentists in the United Kingdom has made to the
selection of antibiotic resistance in bacteria of the oral flora.6 The review concluded that inappropriate antibacterial drug
prescribing by dental practitioners is a significant contributing factor in the selection of drug-resistant bacterial strains.
The American Dental Association reported the results of a survey of antibiotic use in dentistry in the November 2000
Journal of the American Dental Association.7 The authors surveyed all licensed dentists practicing in Canada and found
that confusion about prescribing antibiotics and inappropriate prescribing practices was evident, and that inappropriate
antibiotic use, such as improper dosing, duration of therapy and prophylaxis are all factors that may affect development of
antibiotic resistant microorganisms.
There is a Glimmer of Hope

A report from Aker University in Oslo, Norway, strongly suggests that bacterial resistance to antibacterial agents can be
reversed.8 While dangerous and contagious staph infections kill thousands of patients in the most sophisticated hospitals in
Europe, North America and Asia, there is virtually no sign of this killer superbug in Norway. The reason? Norway stopped
taking so many antibiotics.
We dont throw antibiotics at every person with a fever. We tell them to hang on, wait and see, and we give them a Tyle-
nol to feel better, said Dr. John Haug, infectious disease specialist at Aker University Hospital.8
In Norways simple solution, there is a glimmer of hope.
The Proper Clinical Use of Antibacterial Drugs

In 1997, the ADA Council on Scientific Affairs issued a position statement on Antibiotic Use in Dentistry.9 The Council
stated: Microbial resistance to antibiotics is increasing at an alarming rate. The major cause of this public health problem
2
is the use of antibiotics in an inappropriate manner, leading to the selection of dominance of resistant microorganisms
and/or the increased transfer of resistance genes from antibiotic-resistant to antibiotic-susceptible microorganisms.9
The Councils position statement further identified that Antibiotics are properly employed only for the manage-
ment of active infectious disease or the prevention of metastatic infection, such as infective endocarditis, in medically
high-risk patients.9
One method of education is to teach from errors rather than principles. Psychologists from the University of Exeter
have identified an early warning signal in the brain that helps us avoid repeating previous mistakes. Published in the
Journal of Cognitive Neuroscience,10 their research identifies for the first time, a mechanism in the brain that reacts, in
just 0.1 of a second, to things that have resulted in us making errors in the past. Evaluating the following eight miscon-
ceptions or myths may help to establish general guidelines to aid us in making clinical decisions regarding the use of
antibiotic therapy, thereby leading to optimum use and therapeutic success.11
Myth #1: Antibiotics cure patients. Except in patients with a compromised immune system, antibiotics are not curative,
but instead function to assist in the re-establishment of the proper balance between the hosts defenses (immune and
inflammatory) and the invasive agent(s). Antibiotics do not cure patients; patients cure themselves.
Myth #2: Antibiotics are substitutes for surgical intervention. Very seldom are antibiotics an appropriate substitute for
removal of the source of the infection (extraction, endodontic treatment, incision and drainage, periodontal scaling
and root planing). Occasionally, when the infection is too diffuse or disseminated to identify a nidus for incision, or the
clinical situation does not allow for immediate curative treatment, the prudent dentist will choose to place the patient
on appropriate antibacterial therapy until such time as curative treatment can be implemented. It is imperative to re-
move the cause of the infection prior to, or concomitant with, antibiotic therapy, when the cause is readily identifiable.
Whenever antibiotic therapy is used the risk of bacterial selection for antibiotic resistance is present.
Myth #3: The most important decision is which antibiotic to use. To avoid the deleterious effects of needless antibiotics on
patients and the environment, the most important initial decision is not which antibiotic to prescribe but whether to use
one at all. It has been estimated that up to 60% of human infections resolve by host defenses alone following removal
of the cause of the infection without antibiotic intervention.
Endodontic disease is infectious. Microorganisms cause virtually all pathoses of the pulp and periapical tissues. There
is ample evidence to support that opportunistic normal oral microbiata colonize in a symbiotic relationship with the
host, resulting in endodontic infections.12 The majority of endodontic infections do not require systemic antibiotic ther-
apy when the cause of the infection has been properly managed (complete debridement of the pulp space and proper
obturation and sealing of the pulp space from the oral environment).
Apical periodontitis lesions of pulpal origin are generated by the immune system and are the
result of intraradicular infections (Figure 1). In most situations, this inflammatory process success-
fully eliminates the bacteria emerging from the apical foramen and prevents their spread to the
periapical tissues. This process is primarily facilitated by the polymorphonuclear leukocytes that
eventually phagocytize and kill the bacteria.13 Asymptomatic apical periodontitis of pulpal origin
does not routinely require systemic antibiotic therapy for satisfactory resolution and healing. End-
odontic therapy alone is usually sufficient.
When the intraradicular infection is able to overwhelm the hosts immune response, viable bac-
Fig. 1. Asymptomatic apical teria are able to gain access to the periapical tissues and colonize forming an active infection.
periodontitis.
This results in the formation of an apical abscess. A chronic apical abscess usually presents with
gradual onset, no to mild symptoms and the presence of a sinus tract or parulis (Figure 2). The
majority of chronic apical abscesses of endodontic origin
do not require systemic antibiotic therapy for satisfactory
resolution and healing.
An acute apical abscess usually presents with rapid
onset, spontaneous pain and swelling, both localized and
intraoral, sometimes with exudate present, or with diffuse
facial cellulitis. When the abscess is intraoral and localized
(Figure 3), debridement of the pulp space and placement
of calcium hydroxide and surgical incision for drain- Fig. 3. Acute apical abscess with intraoral
localized swelling.
Fig. 2. Chronic apical abscess. age is usually sufficient to resolve the problem. Systemic
3 Continued on p. 4
antibiotic therapy is not routinely indicated, depending on the patients general medical sta-
tus. However, when the patient presents with diffuse facial swelling (cellulitis) resulting from
an acute apical abscess or an infection with systemic involvement (fever or malaise) (Figure
4), debridement of the pulp space with placement of calcium hydroxide, surgical incision for
drainage, when possible, and an appropriate regimen of systemic antibiotics (oral or IV) are
the treatments of choice.
Understanding the enemy is an important factor in winning any battle. The rational
Fig. 4. Acute apical abscess with choice and use of antimicrobial agents begins with the knowledge of the microorganisms
extraoral diffuse facial cellulitis.
most likely responsible for common dental infections of pulpal origin. The bacterial flora
found in endodontic infections is indigenous, mixed (Gram-positive and Gram-negative) and
predominately anaerobic. Several species have been implicated with acute apical abscesses. These species include dark-
pigmented bacteria (Prevotella and Porphyromonas), eubacteria, fusobacteria and Actinomyces.12
Baumgartner and Xia published a report of the susceptibility of bacteria recovered from acute apical abscesses to five
commonly used antibiotics in dentistry. Antibiotic susceptibility data from 98 species of bacteria recovered from 12 acute
apical abscesses led to the following conclusions:
1. Pen-V-K is the antibiotic of choice for endodontic infections due to its effectiveness in polymicrobial infections, its
relative narrow spectrum of activity against bacteria most commonly found in endodontic infections, its low toxicity
and low cost.
2. Clindamycin is the antibiotic of choice for patients allergic to penicillins.
3. While amoxicillin and augmentin (amoxicillin plus clavulanate) demonstrated a higher antibacterial effectiveness
than Pen-V-K, due to the broader antibacterial spectrum of amoxicillin and the increased cost of augmentin, the
authors recommended that amoxicillin/augmentin be reserved for unresolved infections and patients who are
immunocompromised.
4. Metronidazol demonstrated the greatest amount of bacterial resistance and is only effective against anaerobes.
Therefore, it should not be used alone for the treatment of endodontic infections.14
Myth #4: Antibiotics increase the hosts defense to infection. The increased prevalence in organ and tissue transplants, resulting
in patients with compromised immune systems, has heightened the interest in the potential effects of antimicrobial drugs on
the hosts resistance to infection.15 In vivo and in vitro studies are highly variable and sometimes contradictory. However,
the following considerations appear valid: 1) Antibiotics that can penetrate into the mammalian cell (erythromycin, tetracy-
cline, clindamycin and metronidazole) are more likely to affect the host defenses than those that cannot (beta-lactams); 2)
Tetracyclines may suppress white cell chemotaxis; 3) Most antibiotics (except tetracycline) do not depress phagocytosis; and
4) T- and B-lymphocyte transformation may be depressed by tetracyclines. The greatest potential harm to the host defenses
may result from antibiotics that easily penetrate into the mammalian cell and the least harm is observed with bactericidal,
nonpenetrating agents (penicillins and cephalosporins).
Myth #5: Multiple antibiotics are superior to a single antibiotic. It is often assumed that a combination of antibiotics is superior
to a single carefully chosen antibacterial agent. When the purported benefits of antibiotic combinations are weighed against
the possible consequences to the host as well as to the bacterial environment, this assumption is not always reality. The
usual sequela to combined antibiotic therapy results in a greater selective pressure on the microbial population to develop
drug resistance. The greater the antibacterial spectrum of the antimicrobials used, the greater the number of drug-resistant
microorganisms that develop, and the more difficult it is to treat a resulting superinfection. The primary clinical indication
for combined antimicrobial therapy is a severe infection in which the offending organism(s) is unknown and major con-
sequences may ensue if antibiotic therapy is not instituted immediately before culture and sensitivity tests are available.3
Myth #6: Bactericidal agents are always superior to bacteriostatic agents. Bactericidal agents are required for patients with im-
paired host defenses.3 However, bacteriostatic agents are usually satisfactory when the hosts defenses against infections are
unimpaired. Postantibiotic effects (PAEspersistent suppression of bacterial growth after previous exposure to antibiotics)
are more persistent and reliable with bacteriostatic agents (erythromycin, clindamycin) than with bactericidal agents (beta-
lacatamase) because the clinical effects of bacteriostatic agents are less dose-dependent.
Myth #7: Antibiotic dosages, dosing intervals and duration of therapy are established for most infections. After more than 80 years
of antibiotic usage, the proper dosages, dosing intervals and duration of therapy are essentially unknown for most specific
4
infections.3 Infectious diseases are associated with a high number of variables that affect treatment outcome (microbial
characteristics and drug sensitivity, diverse resistance mechanisms, tissue barriers to antibiotic diffusion, and the integ-
rity and activity of the hosts defense mechanisms). However, basic principles are available to guide the dental health
care provider in establishing proper dosages, dosing intervals and duration of therapy once the microbial pathogen(s)
is suspected or identified and a rational choice of antimicrobial agent is made.
The following principles of antibiotic dosing are adapted from Dr. Thomas J. Pallasch3:
1. The current recommendation is to employ an antimicrobial on an intensive basis with vigorous dosage for as short
a period of time as the clinical situation permits. The major factor in the clinical success of most antimicrobial
agents is the height of the serum concentration of the drug and the resulting amount in the infected tissue(s). Also
important is to expose the host to the antimicrobial agent for as short a duration of therapy as possible. The shorter
the duration of therapy the lower the risk to the patient for the development of antibiotic-induced toxicity and/or
allergy, and a reduced risk of developing resistant microorganisms.
2. The goal of antibiotic dosing is to achieve drug levels in the infected tissue equal to or exceeding the minimal
inhibitory concentration of the target organism. Serum levels of antibiotics do not necessarily reflect those in
tissues. Blood concentrations of the antibiotic should exceed the MIC by a factor of two to eight times in order to
offset the tissue barriers that restrict access of the drug to the infected site.
3. It is advisable to initiate antibiotic therapy with a loading dose (an initial dose higher than the maintenance
dose). An antibiotic loading dose should be used whenever the half-life of the drug is longer than three hours or
whenever a delay of 12 hours or longer to achieve a therapeutic blood level is expected. Most antibiotics used in
the treatment of orofacial infections have a half-life shorter than three hours but, due to their acute nature, most
orofacial infections require therapeutic drug blood levels sooner than 12 hours. Steady-state blood levels of any
drug are usually achieved in a time equal to three to five times the drugs half-life. Amoxicillin has a half-life of
one to one-and-a-half hours. A steady-state blood level would then be achieved in three to seven-and-a-half hours
thereby leading to a substantial delay in achieving therapeutic antibiotic blood levels. A loading dose of two times
the maintenance dose is recommended for acute orofacial infections, which better achieves the goal of rapid, high
blood levels rather than initiating therapy with the maintenance dose.
4. An oral antibiotic should ideally be administered at dosing intervals of three to four times its serum half-life,
particularly if steady-state blood levels are desired (as may be indicated with beta-lactam agents). For example,
the serum half-life of Pen-V-K is 0.75 hours. Higher continuous blood levels of this antibiotic are more likely to be
obtained with four-hour rather than six-hour dosing intervals. The shorter the serum half-life of the drug, the shorter
the dosing interval will need to be in order to maintain continuous therapeutic blood levels of the drug. When
determining the appropriate dosing interval, it is also important to consider the following: 1) The postantibiotic
effects of the drug; and 2) the relative merits of continuous or pulse dosing. PAEs are more persistent (two to seven
hours) with antibiotics that act intracellularly within the microbial cytoplasm (erythromycin, clindamycin and
tetracycline) or by suppression of nucleic acid synthesis (metronidazole, quinolones). As a result, these antibiotics
are more effective with pulse dosing (high antibiotic dosing at widely spaced intervals). The beta-lactam antibiotics
however, have a slow, time-dependent killing activity and demonstrate very little PAE. Beta-lactam microbial
killing requires microbes in the process of cell division (interference with cell wall development); hence, they must
be continuously present (steady-state blood levels) because bacteria divide at different rates or times.
Myth #8: Bacterial infections require a complete course of antibiotic therapy. There is no such thing as a complete course
of antibiotic therapy.3 The only guide for determining the effectiveness of antibiotic therapy, and hence, the duration of
treatment, is the clinical improvement of the patient.16 A common misconception asserts that prolonged (after clinical
remission of the disease) antibiotic therapy is necessary to prevent rebound infections from occurring. Orofacial in-
fections do not rebound if the source of the infection is properly eradicated. Most orofacial infections persist for two
to seven days, and often less. Patients placed on antibiotic therapy for an orofacial infection should be clinically evalu-
ated on a daily basis. When there is sufficient clinical evidence that the patients host defenses have regained control of
the infection and that the infection is resolving or resolved, the antibiotic therapy should be terminated.
Continued on p. 6
5
Antibiotic Prophylaxis for Medically At-Risk Patients

Antibiotic prophylaxis is the administration of antibiotics to patients without evidence of infection to prevent bacterial
colonization and reduce subsequent postoperative or post-treatment complications. The only established use of antibiotic
prophylaxis in dentistry is in the attempt to reduce the potential consequences of bacteremias induced by dental treatment
in certain medically at-risk patients. The principle indication for antibiotic prophylaxis for dental patients is the preven-
tion of infective endocarditis in patients with specific medical conditions that are receiving specified dental treatments.
Controversial indications include dental patients with orthopedic prosthetic devices, indwelling catheters and impaired
(immunosuppressed) host defenses.
Dental patients presenting for treatment with impaired host defenses (chemotherapy, organ transplant or tissue graft
recipient, insulin-dependent diabetes, alcoholics) or patients with indwelling catheters (hemodialysis) may benefit from
antibiotic prophylaxis if their white cell count is below 2,500 (normal = 4,000-11,000). It is not currently recommended that
patients with AIDS receive routine antibiotic prophylaxis prior to dental treatment. The opportunistic pathogens common
to this disorder are not susceptible to routine prophylactic antibiotics and such a practice may result in the development of
antibiotic-resistant microorganisms, thereby resulting in a serious superinfection.3
Antibiotic Prophylaxis for Prevention of Infective Endocarditis

The American Heart Association has published guidelines for the prevention of IE in medically at-risk patients for more than
50 years. The most recent guidelines, published in April 2007, represent a significant change from the previous guidelines.17
One of the stated reasons for the development of the current revised guidelines was that the risk of antibiotic-associated
adverse events exceeds the benefit, if any, from prophylactic therapy (Table 1). It is well accepted that the risk for develop-
ing bacterial resistant strains to the antibiotic drug used is considered an antibiotic-associated adverse event.
The majority of published studies regarding IE being caused by oral bacteria have focused on dental procedures. Al-
though the infective dose required to cause IE in humans is unknown, the number of microorganisms present in the blood
following a dental procedure is low. It has long been assumed that dental procedures may cause IE in patients with un-
derlying cardiac risk factors and that antibiotic prophylaxis is effective. However, scientific proof is lacking to support this
assumption. Cases of IE caused by oral bacteria probably result more from exposures to low inocula of bacteria in the
bloodstream that result from routine daily activities (brushing and flossing) and not from a dental procedure.17
The 2007 AHA report regarding prevention of IE concludes: If prophylaxis is effective, such therapy should be re-
stricted to those patients with the highest risk of adverse outcomes from IE and who would derive the greatest benefit from
prevention. In patients with underlying cardiac conditions associated with the highest risk of adverse outcomes from IE,
prophylaxis for some dental procedures is reasonable, even though we acknowledge that its effectiveness is unknown.17
Therefore, the 2007 AHA guidelines suggest that antibiotic prophylaxis should be considered for patients presenting for
treatment with the cardiac conditions identi-
fied in Table 2, and who are undergoing any
Anitbiotic Prophylaxis Recommendations (see newsletter insert)
dental procedure that involves the gingival
Table 1: Primary Reasons for Revision of Infective Endocarditis Guidelines
tissues or periapical region of a tooth and for
those procedures that perforate the oral mu- Table 2: Medical Conditions for Which Endocarditis Prophylaxis is Recommended
cosa. This would include procedures such as Table 3: Dental Procedures for Which Antibiotic Prophylaxis is Reasonable
biopsies, suture removal, placement of orth-
Table 4: Patients at Potential Risk of Experiencing Hematogenous Total Joint Infection
odontic bands, and intraligamentary and
intraosseous local anesthetic injections, but it Table 5: Suggested Patient Type, Drug and Regimen for Antibiotic Prophylaxis for
Total Prosthetic Joint Infection
does not include routine local anesthetic injec-
tions through noninfected tissue (Table 3).
Antibiotic Prophylaxis for Prevention of Delayed Prosthetic Joint Infection

In 1997, the ADA and the American Academy of Orthopaedic Surgeons convened an expert panel of dentists, orthopaedic
surgeons and infectious disease specialists and published its first Advisory Statement on Antibiotic Prophylaxis for dental
patients with prosthetic joints.18 The 2003 advisory statement included some modifications of the classification of patients at
potential risk and the stratification of bacteremic dental procedures (Table 4), but no changes in terms of suggested antibiot-
ics or antibiotic regimens.19 Antibiotic prophylaxis is not indicated for most dental patients with total joint replacements or
6
for patients with pins, plates or screws. However, it is advised to consider antibiotic premedication in a small number of
patients who may be at potential increased risk of experiencing hematogenous total joint infection (Table 5).
While bacteremias can cause hematogenous seeding of total joint implants, it is likely that more oral bacteremias are
spontaneously induced by routine daily events than are dental treatment-induced. Patients who have undergone total joint
arthroplasty should be encouraged to perform effective daily oral hygiene procedures in order to maintain good oral health.
The risk of bacteremia is much higher in a mouth with chronic inflammation than one that is healthy and well maintained.
Occasionally, a patient with a total joint prosthesis may present for dental treatment with a recommendation from
his or her physician that is inconsistent with the current guidelines. In this case, the dentist is encouraged to consult with
the patients physician to discuss the nature of the needed dental treatment, to review the current guidelines regarding
antibiotic prophylaxis and to determine if there are any special considerations that might affect the physicians decision
regarding antibiotic prophylaxis for the patient. After this consultation, the dentist may decide to follow the physicians
recommendation or, if in his or her professional judgment antibiotic prophylaxis is not indicated, decide to proceed with
the needed dental treatment without antibiotic prophylaxis. The dentist is ultimately responsible for making treatment
decisions for his or her patient based on the dentists professional judgment.
In February 2009, the AAOS published an information statement in which the organization, recommends that clini-
cians consider antibiotic prophylaxis for all total joint replacement patients prior to any invasive procedure that may
cause bacteremia.20 In response to this statement, the American Academy of Oral Medicine published a position paper
in the June 2010 edition of the Journal of the American Dental Association.21
The authors of the AAOM position paper stated that they reviewed the available literature on the subject as it re-
lates to the AAOS 2009 information statement and concluded: The risk of patients experiencing drug reactions or
drug-resistant bacterial infections and the cost of antibiotic medications alone do not justify the practice of using anti-
biotic prophylaxis in (all) patients with prosthetic joints. The authors called for a future multidisciplinary, systematic
review of the literature relating to antibiotic prophylaxis use in patients with prosthetic joints. In the meantime, they
concluded that the new AAOS 2009 information statement20 should not replace the 2003 joint consensus statement.19
Summary
Since their discovery eight decades ago, safe systemic antibiotics have revolutionized the treatment of infections,
transforming once deadly diseases into manageable health problems. However, the growing phenomenon of bacterial
resistance, caused by the use and abuse of antibiotics and the simultaneous decline in research and development of
new antimicrobial drugs, is now threatening to take us back to the pre-antibiotic era. Without effective treatment and
prevention of bacterial infections, we also risk rolling back important achievements of modern medicine such as major
surgery, organ transplantation and cancer chemotherapy.22
A fundamentally changed view of antibiotics is needed. They must be looked on as a common good, where indi-
viduals must be aware that their choice to use an antibiotic will affect the possibility of effectively treating bacterial
infections in other people. All antibiotic use, appropriate or not, uses up some of the effectiveness of that antibiotic,
diminishing our ability to use it in the future. For current and future generations to have access to effective prevention
and treatment of bacterial infections as part of their right to health, all of us need to act now. The window of opportunity
is rapidly closing.22
References
1. Health, United States, 2009: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health
Statistics, 2009.
2. Health, United States, 2010: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health
Statistics, April 2010.
3. Pallasch TJ. Pharmacology of Anxiety, Pain and Infection. In: Endodontics. 4th ed. Williams and Wilkins, Malvern, PA, 1994.
4. ADA Council on Scientific Affairs. Combating antibiotic resistance. J Am Dent Assoc 2004;135:484.
5. Nicolle L. Nosocomial Infections. Gale Encyclopedia of Public Health. Macmillan Reference USA, Farmington Hills, MI, 2002.
6. Sweeney LC, Jayshree D, Chambers PA, Heritage J. Antibiotic resistance in general dental practicea cause for concern. J Antimicrobial Chemotherapy
2004;53:567.
7
7. Epstein JB, Chong S, Le ND. A survey of antibiotic use in dentistry. J Am Dent Assoc 2000;131:1600.
8. Associated Press. Killer superbug solution discovered in Norway. www.msnbc.com, December 2009.
9. ADA Council on Scientific Affairs. Antibiotic use in dentistry. J Am Dent Assoc 1997;128:648.
10. Wills A. Why we learn from our mistakes. J Cognitive Neuroscience 2007;19:1163.
11. Pallasch TJ. Antibiotic myths and reality. J Cali Dent Assoc 1986;14:65.
12. Baumgartner JC. Microbiology of Endodontic Disease. In: Endodontics. 6th ed. B.C. Decker Inc. Hamilton, Ontario, Canada, 2008.
13. Baumgartner JC, et al. Experimentally induced infection by oral anaerobic microorganisms in a mouse model. Oral Microbiol Immunol 1992;7:253-6.
14. Baumgartner JC, Xia T. Antibiotic susceptibility of bacteria associated with endodontic abscesses. J Endodon 2003;29:44-7.
15. Korzeniowski OM. Effects of antibiotics on the mammalian immune system. Infect Dis Clin NA 1989;3:469.
16. Hessen MT, Kaye D. Principles of selection and use of antimicrobial agents. Infect Dis Clin NA 1989;3:479.
17. Wilson W, Taubert K, et al. Prevention of Infective Endocarditis: Guidelines From the American Heart Association, J Amer Heart Assoc 2007;116:1736-54.
18. American Dental Association, American Academy of Orthopaedic Surgeons. Advisory statement: Antibiotic prophylaxis for dental patients with total joint
replacements. J Amer Dent Assoc 1997;128;1004-8.
19. American Dental Association, American Academy of Orthopaedic Surgeons. Advisory statement: Antibiotic prophylaxis for dental patients with total joint
replacements. J Amer Dent Assoc 2003;134:895-8.
20. American Academy of Orthopaedic Surgeons. Information statement: Antibiotic prophylaxis for bacteremia in patients with joint replacements.
www.aaos.org. 2010.
21. Little JW, et al. The dental treatment of patients with joint replacements: A position paper from the American Academy of Oral Medicine. J Amer Dent
Assoc 2010;141:667-71.
22. Cars, O. Meeting the challenge of antibiotic resistance, BMJ 2008;337:726-8.
The AAE wishes to thank Dr. Steven G. Morrow for authoring this issue of the newsletter, as well as the following article
reviewers: Drs. James A. Abbott, Reid S. El-Attrache, Gary R. Hartwell, William T. Johnson and James F. Wolcott.
AAE Colleagues Online

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r1SFWFOUJPOPG*OGFDUJWF&OEPDBSEJUJT(VJEFMJOFT'SPNUIF"NFSJDBO)FBSU"TTPDJBUJPO
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Dental Association and American Academy of Orthopaedic Surgeons, 2003.
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The information in this newsletter is designed to aid dentists. Practitioners must use their best professional judgment, taking into
account the needs of each individual patient when making diagnosis/treatment plans. The AAE neither expressly nor implicitly
warrants against any negative results associated with the application of this information. If you would like more information,
consult your endodontic colleague or contact the AAE.

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Anitbiotic Prophylaxis Recommendations
Table 1
Primary Reasons for Revision of Infective Endocarditis Guidelines

1. IE is much more likely to result from frequent exposure to random bacteremias associated with daily activities than from bacteremias caused
by a dental, GI tract or GU tract procedure.
2. Prophylaxis may prevent an exceedingly small number of cases of IE, if any, in individuals who undergo a dental, GI tract or GU tract
procedure.
3. The risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophylactic antibiotic therapy.
4. Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and is more important than
prophylactic antibiotics for a dental procedure to reduce the risk of IE.
Table 2
Medical Conditions for Which Endocarditis Prophylaxis is Recommended:

Premedication is recommended ONLY for patients with the following conditions associated with the highest risk of adverse outcomes
from endocarditis:
1. Prosthetic cardiac/heart valve.
2. History of IE.
3. Cardiac transplant recipients who develop valve pathology.
4. One of the following congenital heart diseases:
t6OSFQBJSFEDZBOPUJD$)% JODMVEJOHQBMMJBUJWFTIVOUTBOEDPOEVJUT
t$PNQMFUFMZSFQBJSFEDPOHFOJUBMIFBSUEFGFDUTXJUIQSPTUIFUJDNBUFSJBMPSEFWJDF XIFUIFSQMBDFECZTVSHFSZPSCZDBUIFUFSJOUFSWFOUJPO
during the first six months after placement of the material or device (because endothelialization of prosthetic material occurs
within six months after the procedure).
t3FQBJSFE$)%XJUISFTJEVBMEFGFDUTBU PSBEKBDFOUUP UIFTJUFPGBQSPTUIFUJDQBUDIPSQSPTUIFUJDEFWJDF XIJDIJOIJCJUTFOEPUIFMJBMJ[BUJPO

5. Special situations and circumstances:
tPatients already receiving antibioticsOccasionally, a patient may be taking an antibiotic when coming for a dental appointment. If
the patient is taking an antibiotic normally used for endocarditis prophylaxis, it is prudent to select a drug from a different class rather
that increase the dose of the current antibiotic. If possible, you should delay the dental procedure until at least 10 days after completion of
the antibiotic. This will allow for the usual oral flora to be re-established. If an individual receiving long-term parenteral antibiotic therapy
for IE requires dental treatment, the treatment should be timed to occur 30 to 60 minutes after the parenteral antibiotic therapy has been
delivered.
tFailure to administer pretreatment antibiotic doseIf the dosage of an antibiotic is inadvertently not administered before the
procedure, the dosage may be administered up to two hours after the procedure.
However, administration of the dosage after the procedure should be considered only when the patient did not receive the preprocedure
dose.
tIndividuals with kidney dialysis shuntsIndividuals with permanent kidney dialysis shunts should be placed on prophylactic
antibiotics using the same protocol as for IE.
Use and Abuse of Antibiotics: Winter 2012

Table 3
Dental Procedures for Which Antibiotic Prophylaxis is Reasonable

t%FOUBMFYUSBDUJPOT
t1FSJPEPOUBMQSPDFEVSFT JODMVEJOHTVSHFSZ TVCHJOHJWBMQMBDFNFOUPGBOUJCJPUJDCFST
strips, scaling and root planing, proving, recall maintenance
t%FOUBMJNQMBOUQMBDFNFOU
t3FQMBOUBUJPOPGBWVMTFEUFFUI
t&OEPEPOUJD SPPUDBOBM
JOTUSVNFOUBUJPOPOMZJGCFZPOEUIFSPPUBQFYBOEFOEPEPOUJD
surgery
t*OJUJBMQMBDFNFOUPGPSUIPEPOUJDCBOET OPUCSBDLFUT
t*OUSBMJHBNFOUBSZBOEJOUSBPTTFPVTMPDBMBOFTUIFUJDJOKFDUJPOT
t1PTUPQFSBUJWFTVUVSFSFNPWBM JOTFMFDUFEDJSDVNTUBODFTUIBUNBZDSFBUFTJHOJDBOU
CMFFEJOH
t1SPQIZMBDUJDDMFBOJOHPGUFFUIPSJNQMBOUTXIFSFCMFFEJOHJTBOUJDJQBUFE
Table 4
Patients at Potential Risk of Experiencing Hematogenous Total Joint Infection19

Patient Type Condition Placing Patient at Risk
"MMQBUJFOUTEVSJOHGJSTUUXPZFBSTGPMMPXJOHKPJOUSFQMBDFNFOU N/A
Inflammatory arthropathies such as rheumatoid

Immunocompromised/immunosuppressed patients arthritis, systemic lupus erythematosus
%SVHPSSBEJBUJPOJOEVDFEJNNVOPTVQQSFTTJPO
Malnourishment
Patients with comorbidities Hemophilia
(Conditions listed for patients in this category are examples only; HIV infection
there may be additional conditions that place such patients at
risk of experiencing hematogenous total joint infection) *OTVMJOEFQFOEFOU UZQF
EJBCFUFT
Malignancy
Table 5
Suggested Patient Type, Drug and Regimen for Antibiotic Prophylaxis for Total Prosthetic Joint Infection
Patient Type Drug Regimen*
Patients not allergic to penicillin Cephalexin, cephradine or amoxicillin 2g orally 1 hour prior to dental procedure
Patients not allergic to penicillin and unable to $FGB[PMJOHPSBNQJDJMMJOH*.PS*7IPVSQSJPSUP

$FGB[PMJOPSBNQJDJMMJO
take oral medication dental procedure
Patients allergic to penicillin Clindamycin 600mg orally 1 hour prior to dental procedure
Patients allergic to penicillin and unable to take

Clindamycin 600mg IV 1 hour prior to dental procedure
oral medication
*Note: No second doses are recommended for any of these dosing regimens.
Use and Abuse of Antibiotics: Winter 2012

AAE Quick Reference Guide
The following was reviewed by the AAE Clinical Practice Committee. AAE members may copy this quick
reference guide for distribution to patients or referring dentists.
ANTIBIOTIC PROPHYLAXIS
The American Heart Association recently revised its guidelines on antibiotic prophylaxis. The current practice
of giving patients antibiotics prior to a dental procedure is no longer recommended EXCEPT for patients with
the highest risk of adverse outcomes resulting from bacterial endocarditis. In response, the American Association
of Endodontists has prepared a reference guide for applying the revisions to dental/endodontic procedures and
patient care.
The new AHA guidelines for antibiotic prophylaxis are based on a comprehensive review of published studies that
suggests infective endocarditis is more likely to occur as a result of daily activities such as brushing and flossing
than from a dental procedure. For patients at risk of bacterial endocarditis, the AHA emphasizes the importance of
good oral health and regular dental visits.
The new recommendations apply to many dental procedures, including teeth cleaning and extractions. Patients
with congenital heart disease can have complicated circumstances. If there is any question at all as to the category
that best fits their needs, these patients should check with their cardiologists before treatment.
BACTERIAL ENDOCARDITIS
Endocarditis Prophylaxis Recommended
Preventive antibiotics prior to a dental procedure are advised for patients with:
Artificial heart valves
Infective endocarditis history
Certain specific, serious congenital (present from birth) heart conditions, including:
Unrepaired or incompletely repaired cyanotic congenital heart disease, as well as those with palliative shunts
and conduits
Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or
by catheter intervention, during the first six months after the procedure
Any repaired congenital heart defect with residual defect at the site or adjacent to the site of a prosthetic
patch or a prosthetic device
Cardiac transplant that develops a problem in a heart valve
Endocarditis Prophylaxis Not Recommended

Patients who have taken prophylactic antibiotics routinely in the past but no longer need them include
people with:
Mitral valve prolapse
Rheumatic heart disease
Bicuspid valve disease
Calcified aortic stenosis
Congenital heart conditions, such as ventricular septal defect, atrial septal defect and hypertrophic
cardiomyopathy
2008, American Association of Endodontists, 211 E. Chicago Ave., Suite 1100, Chicago, IL 60611
Phone: 800/872-3636 (North America) or 312/266-7255 (International); Fax: 866/451-9020 (North America) or 312/266-9867 (International)
E-mail: info@aae.org; Web site: www.aae.org
Regimens for a Dental Procedure1
Regimen: Single Dose 30 to 60 min
Before Procedure
SITUATION AGENT ADULTS CHILDREN
Oral Amoxicillin 2g 50 mg/kg
Unable to take oral Ampicillin 2 g IM* or IV+ 50 mg/kg IM or IV

medication OR
Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV
Allergic to penicillins or Cephalexin 2g 50 mg/kg

ampicillinoral OR
Clindamycin 600 mg 20 mg/kg
OR
Azithromycin or clarithromycin 500 mg 15 mg/kg
Allergic to penicillins or Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV
ampicillin and unable to OR
take oral medication Clindamycin 600 mg IM or IV 20 mg/kg IM or IV
* IM: Intramuscular
+ IV: Intravenous
Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.
Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or
urticaria with penicillins or ampicillin.
1
American Dental Association Division of Legal Affairs. An Updated Legal Perspective of Antibiotic Prophylaxis.The Journal of the
American Dental Association. 2008; 139:10-21S.
Patients With Joint Replacement

There have been no changes to the American Academy of Orthopaedic Surgeons recommendations. Please
visit www.aaos.org for more information.
Copyright 2007 American Dental Association. All rights reserved. Reprinted by permission.
Name: Shimon Friedman, D.M.D.
Address: 514 Melrose Ave., Toronto, Ontario M5M 2A2, Canada
Phone: 416/787-0164; Fax: 416/785-8808; E-mail: shimon.friedman@dentistry.utoronto.ca
BIO-SKETCH
Prof. Shimon Friedman is Professor at the Faculty of Dentistry, University of Toronto.
He received the D.M.D. degree (1975) and certificate in endodontics (1983) from the Hebrew University in
Jerusalem, where he had taught for 17 years. Dr. Friedman is board-certified in endodontics in Israel and had
served as Chairman of the Israel Endodontic Society from 1985 to 1988.
Prof. Friedman was appointed Head of Endodontics in Toronto in 1992, a position he had held for 20 years. In
1993 he established the first graduate program in Endodontics, and had served as Program Director for 22 years
until stepping down in 2015. Under his leadership, the M.Sc. Endodontics Program at the University of Toronto
has gained international recognition for its excellence.
Prof. Friedman has published over 140 articles in peer-reviewed scientific journals, 11 textbook chapters and
many research abstracts, has presented over 300 national and international lectures, and has served on the
editorial boards of all major endodontic journals.
In recognition of his research and education contributions, Prof. Friedman in 2003 received the Medal of Merit
from the City of Paris and in 2006 the French Endodontic Society's Grossman Award. In 2008, he was awarded
the prestigious Louis I. Grossman Award by the American Association of Endodontists, for cumulative
publication of significant research studies that have made an extraordinary contribution to endodontology. In
2013, the Association of Canadian Faculties of Dentistry presented Prof. Friedman with the W.W. Wood Award
for excellence in dental education. In 2014, he received the Award of Distinction from the Faculty of Dentistry,
University of Toronto.
Prof. Friedman also maintains a private practice limited to Endodontics in Toronto.
No lesion (%)
0
100
20
40
60
80
De Moor et al. 2000
Kirkevang 2000
Tronstad et al. 2000
Kirkevang 2001
Dugas et al. 2002
Hommez et al. 2002
Lupi-Pegurier et al. 2002
Boucher et al. 2002
Boltacz-Rzepkowska 2003
Pinzon 2004
Segura 2004
Barthel et al. 2004
Tsuneishi et al. 2004
Kabak & Abbott 2005
Georgopoulou 05
Loftus et al. 2005
Siqueira et al. 2005
Peciuliene et al. 2006
Dr. Shimon Friedman
Stassen et al. 2006

Skudutyte-Rysstad 2006
Kirkevang et al. 2006
Sunay et al. 2007
Eckerbom et al. 2007
Chen et al. 2007
Gulsahi et al. 2008
Frisk et al. 2008
Tavares et al. 2009
Moura et al. 2009
Da Silva et al. 2009
apical surgery
Kim et al. 2011
Outline
zbas et al. 2011
Peters et al. 2011
General population
Kambieri et al. 2011
Root-filled teeth
Al-Omar. 2011
n = 48 (29 countries)
Matijevic et al. 2011
Marotta et al. 2012
Moreno et al. 2013
Appraisal of evidence
Outcomes, predictors:
Jersa & Kundzina 2013
Song et al. 2014
Current best evidence

Lemagner et al. 2015 CBCT
Oginni et al. 2015
General Population
Alrahabi, Younes 2016
Karabucak et al. 2016 CBCT
Cross-sectional studies (2000-2017)

non-surgical treatment
Dawson et al. 2016
Pedro et al. 2016
Van der Veken et al. 2016 CBCT
Prognosis diverse reports

Department of Clinical Sciences
University of Toronto
Faculty of Dentistry
Page 1
No lesion (%)
0
100
20
40
60
80
Hansen & Johansen 1976
Hugoson & Koch 1979
Hugoson et al. 1986
Allard & Palmqvist 1986
100
0
20
40
60
80
Petersson et al. 1986
Bergstrm et al. 1987
Eriksen et al. 1988
Petersson et al. 1989
Petersson 1989
Odesjo et al. 1990
Eriksen & Bjertness 1991
Imfeld 1991

De Cleen et al. 1993
Petersson 1993
Root-filled teeth
Root-filled teeth
Ray & Trope 1995

n = 25 (10 countries)
Buckley & Spangberg 1995

Eriksen et al. 1995
Soikkonen 1995
Saunders 1997
Up to 71% of teeth appear to have

General Population
General Population
Weiger 1997
Post-treatment Apical Periodontitis

Marques et al. 1998
(likely to compromise the outcome)

Sidaravicius et al. 1999
33-87% of root fillings appear sub-optimal
suboptimal fillings
Success rate (%) Success rate (%) Success rate (%)
0
20
40
60
80
100
0
20
40
60
80
100
0
20
40
60
80
100
Strindberg 1956 Weiger et al. 2000
Lipski 2000 Strindberg 1956
Grahnen & Hansson 1961 Ricucci et al. 2000
Engstrm et al. 1964 Pettiete et al. 2001 Grahnen & Hansson 1961
Chugal et al. 2001
Selden 1974 Heling et al. 2001 Seltzer et al. 1963
Bergenholtz 1979 Peak et al. 2001
Waltimo et al. 2001 Zeldow & Ingle 1963
Pekruhn 1986 Benenati & Khajotia 2002
Peters & Wesselink 2002 Bender et al. 1964
Molven & Halse 1988 Friedman et al. 2003 (Toronto Study)
Allen et al. 1989 Hoskinson et al. 2002 Engstrm et al. 1964
Huumonen et al. 2003
n = 27
Sjgren et al. 1990 Fouad & Burleson 2003 Grossman et al. 1964
Tani-Ishii & Teranaka 2003
v. Nieuwenhuysen et al. 1994 Travassos et al. 2003 Engstrm & Lundberg 1965
Friedman et al. 1995 Field et al. 2004
Farzaneh et al. 2004 (Toronto Study) Ingle et al. 1994
Danin 1996 Gagliani et al. 2004
Piowska 1997 Peters et al. 2004 Oliet & Sorin 1969
Calsikan 2004
Sundqvist 1998 Kabak 2004 Storms 1969
still poor
Marending et al. 2005
Kvist & Reit 1999 Spili et al. 2005 Harty et al. 1970
Abbott 2000 Moshonov 2005
Chu et al. 2005 Heling & Tamshe 1970
n = 49
n = 24
Chugall et al. 2001 Quesnell et al. 2005

Marquis et al. 2006 (Toronto Study)
Farzaneh et al. 2004 (TS) Gesi et al. 2006 Cvek 1972
Gorni & Gagliani 2004 Aqrabawi 2006
Suchina et al. 2006 Tamse & Heling 1973
Imura 2007 Molander et al. 2007
Conner et al. 2007 Lambjerg-Hansen 1974
Ercan 2007 Imura et al. 2007
Initial Treatment
Initial Treatment
de Chevigny et al. 2008 (TS) Zhong et al. 2008 Selden 1974

Genc et al. 2008
Ng et al. 2011 Penesis et al. 2008 Adenubi & Rule 1976
Ricucci et al. 2011 de Chevigny et al. 2008 (Toronto Study)
Cotton et al. 2008 Heling & Shapira 1978
Orthograde Retreatment
Touboul et al. 2014 Siqueira et al. 2008
Metzger et al. 09* Jokinen 1978
Pirani et al. 2014 Fonzar et al. 2009
Ozer & Aktener 2009 Soltanoff 1978
Follow-up studies (1956-2017)

Azim et al. 2015
Cheung & Liu 2009
Nekovi et al. 2016 Tehrany 2009 Ashkenaz 1979
Selected Population
Selected Population
Selected Population
Tervit et al. 2009

Davies et al. 2016 CBCT
Mente et al. 2009 Bergenholtz 1979
He et al. 2017 Hsiao et al. 2009
Suter et al. 2009 Kerekes & Tronstad 1979
28
98
Discrepancy of 70%!
Page 2
Success rate (%) Success rate (%)
0
20
40
60
80
100
0
20
40
60
80
100
Zmener & Pameijer 2007/10/12 Barbakow et al. 1980

Gilbert et al. 2010
Hession 1981
Xiao et al. 2010
Liang et al. 2011
Barbakow et al. 1981
Setzer et al. 2011 Rudner & Oliet 1981
Koralet 2011 Cvek et al. 1982
Ng et al. 2011
Nelson 1982
Ricucci et al. 2011
n = 35
Lee 2012
Klevant 1983
Periodontitis
Patel et al. 2012 Morse et al. 1983
Liang et al. 2012 Oliet 1983
Paredes-Vieyra & Enriquez 2012
a longer term
Swartz et al. 1983
Saini et al. 2012
Berenstein et al. 2012 Pekruhn 1986
teeth may have

Martins et al. 2012 Bystrm et al. 1987
Souza et al. 2012 Matsumoto et al. 1987
Hale et al. 2012
rstavik et al. 1987
van der Borden 2013
Halse & Molven 1987
n = 28
0 to 72% of treated
Cheung et al. 2013
Post-treatment Apical
Liang et al. 13 Safavi et al. 1987
after 6 months or in
Castelot-Enkel et al. 2013 Eriksen et al. 1988
Fernndez et al. 2013
kerblom & Hasselgran 1988
Goldfein et al. 2013
Mente et al. 2013
Molven & Halse 1988
Initial Treatment
Initial Treatment
Prognosis
Pirani et al. 2014 Sjgren et al. 1990
Touboul et al. 2014
poor* supported by evidence
Murphy 1991
Jordan et al. 2014
Cvek 1992
Martins et al. 2014
Smith et al. 1993
Craveiro et al. 2015
Zhang et al. 2015 Friedman et al. 1995
Wong et al. 2015 Caliskan & Sen 1996

Azim et al. 2016
Selected Population
Selected Population
rstavik 1996
Demirci & Caliskan 2016
Ricucci et al. 2016
Sjgren et al. 1997
Sigurdsson et al. 2016 Trope et al. 1999
29
Discrepancy of 71%!
100
Diverse Reports Methodology
Characteristics of population
Methodology Characteristics of treatment
Elimination of bias
A systematic error that enters
a clinical trial and distorts the
data obtained.
Spilker 1991
Navigate Diverse Reports Evidence-based Care
The conscientious, explicit

Evidence-based and judicious use of current
best evidence in making
Healthcare decisions about the care of
individual patients.
Sackett 1991
Level of Evidence Methodology Parameters
Research question Cohort (population)

Effectiveness of therapy, prognosis? at inception, end-point
Study design
Exposure (intervention)
relevant, qualified providers
Randomized controlled trial, cohort Assessment
Methodology (to avoid bias) unbiased, sufficiently long
Rigorous, compromised Analysis
multivariate, evaluated unit
Page 3
0
20
40
60
80
100
0
20
40
60
80
100
Zmener & Pameijer 2007/10/12 Zmener & Pameijer 2007/10/12
Gilbert et al. 2010 Gilbert et al. 2010
Xiao et al. 2010 Xiao et al. 2010

Liang et al. 2011 Liang et al. 2011
0
Setzer et al. 2011 Setzer et al. 2011
4
Koralet 2011 Koralet 2011
Ng et al. 2011 Ng et al. 2011
5
Ricucci et al. 2011 Ricucci et al. 2011
Lee 2012 Lee 2012
>4
1
Patel et al. 2012 Patel et al. 2012
Paredes-Vieyra & Enriquez 2012 Paredes-Vieyra & Enriquez 2012

1
Saini et al. 2012 Saini et al. 2012

Berenstein et al. 2012 Berenstein et al. 2012
3-5
Martins et al. 2012 Martins et al. 2012
0.5
Souza et al. 2012 Souza et al. 2012

Hale et al. 2012 Hale et al. 2012

van der Borden 2013 van der Borden 2013

Cheung et al. 2013 Cheung et al. 2013
4-9
Cohort
Exposure
<1.5
1
Castelot-Enkel et al. 2013 Castelot-Enkel et al. 2013
5
0
Fernndez et al. 2013 Fernndez et al. 2013
Assessment
0
Goldfein et al. 2013 Goldfein et al. 2013

Mente et al. 2013 Mente et al. 2013
Pirani et al. 2014 Pirani et al. 2014
Touboul et al. 2014 Touboul et al. 2014
10-19
0
Jordan et al. 2014 Jordan et al. 2014
1
Martins et al. 2014 Martins et al. 2014

Follow-up (years)
Craveiro et al. 2015 Craveiro et al. 2015
Zhang et al. 2015 Zhang et al. 2015

Wong et al. 2015 Wong et al. 2015
Proportion of AP (%)
Azim et al. 2016 Azim et al. 2016

Demirci & Caliskan 2016 Demirci & Caliskan 2016
Relevant Procedures
4
1
Sigurdsson et al. 2016 Sigurdsson et al. 2016
100
Morse et al. 1983
Page 4
Friedman et al. 1995
No signs, symptoms
Cohort
6 months
Assessment
Assessment
Success ?
Case Selection
Follow-up Period
2 years
1.5 years
PARL still present- not categorized as healed

Success ? Epidemiologic Data
Combined normalcy Outcome measure de Chevigny 08 Ng 11
no radiolucency
no symptoms Radiogr. normalcy 87% 85%
Strindberg 1956
Clinical normalcy 95% 91%
Clinical normalcy
Combined success 86% 83%
no symptoms
Seltzer et al. 1963 Difference 9% 8%
strict vs loose criteria
Success Outcome Definition

Assessment
Attainment of a specific goal: Success - Failure

Healed
Prevention, healing of Healing
Apical Periodontitis Disease AP
Retention of function Function
without symptoms 2 years
Evaluated Unit Bivariate Analysis

Analysis
Teeth Roots Teeth with overfilling poorer

outcome ?
100 200 Teeth with AP poorer outcome
Overfilling occurred mainly in
50% 75% teeth with AP
healed healed
1.5 years Halse, Molven 1987
Page 5
0
20
40
60
80
100
0
20
40
60
80
100
Strindberg 1956
Grahnen & Hansson 1961
No
Engstrm et al. 1964
Selden 1974
n-
Bergenholtz 1979
cu
Pekruhn 1986
r
Molven & Halse 1988
re
Allen et al. 1989
nt
Cohort
Sjgren et al. 1990
v. Nieuwenhuysen et al. 1994
Analysis
Danin 1996
Piowska 1997
Sundqvist 1998
Kvist & Reit 1999
Abbott 2000
n = 84
Chugall et al. 2001
n = 8+22
Farzaneh et al. 2004 (TS)
Gorni & Gagliani 2004
Imura 2007
Ercan 2007
de Chevigny et al. 2008 (TS)
Definitive Outcome
Ng et al. 2011
NOT a systematic review!

Ricucci et al. 2011
Intervention 1990
Touboul et al. 2014

Pirani et al. 2014
Initial Treatment
Assessment 2 years
% healed

Azim et al. 2015
50 teeth
Nekovi et al. 2016

Davies et al. 2016 CBCT
Current Best Evidence
multivariate
He et al. 2017
cohort, exposure, assessment, analysis
Follow-up studies (1956-1989; 1990-2017)

Methodology (3 parameters):
Orthograde Retreatment
Page 6
Healed (%) Healed (%) Success rate (%)
0
20
40
60
80
100
0
20
40
60
80
0
20
40
60
80
100
100
Sjgren et al. 1990

Sjgren et al. 1990
rstavik 1996
Sjgren et al. 1997

Sundqvist 1998
No n-
Weiger et al. 2000

c
Toronto Study 2008 Peters et al. 2004
n = 5 / 27
urren
n = 43+9
Marending et al. 2005

t
n = 9 / 136
Ng et al. 2011
de Chevigny et al. 2008 (TS)
Retreatment

Initial Treatment
Initial Treatment
Ng et al. 2011
Ricucci et al. 2011
Ricucci et al. 2011

Follow-up studies (1956-1989; 1990-1999)
Healed (%)
0
20
40
60
80
100
Sjgren et al. 1990
Initial
Initial
rstavik 1996
Hoskinson et al. 2002
treatment
treatment
Peters etal. 2004
Toronto Study 2008
Ng et al. 2011
Initial treatment
Ricucci et al. 2011
Sjgren et al. 1990 outlier

Therapy of AP
Toronto Study 2008
Prevention of AP
Pre-operative AP
Ng et al. 2011
Orthograde
Orthograde
retreatment
retreatment
Ricucci et al. 2011
Retreatment
Page 7
Healed; Functional (%) Healed (%)
0
20
40
60
80
100
0
20
40
60
80
100
Sjgren et al. 1990
Sjgren et al. 1990
rstavik 1996
rstavik 1996
Sjgren et al. 1997
Weiger et al. 2000
Peters etal. 2004
Gesi et al. 2006
Peters et al. 2004
Initial treatment
Toronto Study 2008

75%86%; 90%95%
Toronto Study 2008

92% to 98%
Initial treatment
Ng et al. 2011 Ng et al. 2011
healed (front)- AF (back)
75% to 85%
Sjgren et al. 1990 outlier
Sjgren et al. 1990
Intra-operative (RCTs)
Therapy of AP
Sundqvist 1998
Outcome predictors
Toronto Study 2008
Prevention of AP
Toronto Study 2008
Ng et al. 2011
Ng et al. 2011
Retreatment
Ricucci et al. 2011
Can we project the particular

90% to 98%
Retreatment
Ricucci et al. 2011
Pre-operative (Cohort studies)

Projection of Prognosis
prognosis for a specific case?

74%84%; 90%93%
Prognosis Pre-operative Predictors
Non-surgical Treatment (without AP)
The prospect of recovery from a No significant

disease: predictors
Anticipated from the usual identified
course of the disease
Indicated by special features of
the case
Medline Medical Dictionary
Majority of studies
Pre-operative Predictors Perforation

Retreatment (with AP)
Perforation
poorer outcome
50% 84%
Toronto Study 2008

Ng 2011 ?
MTA 1.5 years
Perforation Repair Perforation Repair

MTA MTA
Meta-analysis of 5 studies yielded

Study Teeth Years Healed
a pooled success rate of 81%
Main 2004 16 1 100%
Ghoddusi 2007 28 1 93% (range 57100%) for MTA repairs.
Pace 2008 10 5 90% Preoperative radiolucency at the
Ree, Schwartz 12 3 4.5-13 100%
Krupp 2013 90 1-10 73% site impaired the outcome.
Pontius 2013 50 0.5-10 90%
Mente 2010, 2014 64 1-9 86%* Siew et al. 2015
Gorni 2016 110 1-8 92-75%
Page 8
Intra-operative Predictors Intra-operative Predictors
Retreatment (with AP) Retreatment (with AP)
Apical patency 82% Added irrigation 87%

regained with EDTA
better outcome better outcome
Weak evidence! Weak evidence!
Ng 2011 70% Ng 2011 78%

Retreatment (with AP) Initial Treatment (with AP)
Treatment in one Added irrigation

session with CHX
better outcome poorer outcome
Weak evidence! Weak evidence!
66% 83%
de Chevigny 2008 77% 100% Ng 2011

Non-surgical Treatment (with AP) Non-surgical Treatment (with AP)
Extruded filling 67% Defective / no

poorer outcome restoration
poorer outcome
Sjgren 1990
Ng 2011 (+Rtx) 50% 80%
Ricucci 2011 (+Rtx)
Not: Weiger 2000 Ng 2011
de Chevigny 08 (+Rtx) 86% Not: Ricucci 2011
Page 9
Equivocal Variables Equivocal Variables
Pre-op. Initial Treatment (with AP)
?
Patients systemic health * Impaired immune
Single/multiple roots, tooth type system, diabetes
Pulp status w/o AP, lesion size *
Swelling, sinus tract poorer outcome
Previous root filling quality
Flare-up
Root filling technique
Short root filling * Marending 2005 ?
Mid-treatment complications * Not: Ng 2011 78% 83%
p value is .05, but CI drops below one and

above one;
thus when you cross the one, it is no longer
a sig finding

Pre-op. Initial Treatment (with AP) Pre-op. Initial Treatment (with AP)
Single root 90%

better outcome
Fouad 2003 de Chevigny 2008

Marending 2005 ? Not: Ng 2011
Ricucci 2011 79%

Pre-op. Initial Treatment Pre-op. Initial Treatment (without AP)
Premolars 94% Vital pulp 91%

better outcome better outcome
than molars
Ricucci 2011
Not: Ng 2011 Ng 2011
de Chevigny 2008 85% Not: de Chevigny 2008 81%
Page 10
Equivocal Variables Very large lesion!
Pre-op. Non-surgical Treatment (with AP)
Small lesion 86%

better outcome
Weiger 2000
Ng 2011 (+Rtx)
Not: Sjgren 1990/97
de Chevigny 2008 (+Rtx)
Ricucci 2011 (+Rtx) 67% 1.5 years 3 years
Large Lesions Equivocal Variables

Pre-op. Non-surgical Treatment (with AP)
Long-term (2-10 years) follow-up Swelling, sinus

of 42 large lesions (7-18 mm) with tract poorer
cholesterol crystals: outcome
74% healed 67% 85%
Ng 2011 (+Rtx)
10% reduced Not: Sjgren 1990
Weiger 2000
alikan 2004 de Chevigny 08 (+Rtx)
Ricucci 2011

Pre-op. Retreatment (with AP) Intra-operative (with AP)
Inadequate 86% Mid-treatment flare up

previous root poorer outcome
filling
62% 83%
better outcome
Ng 2011
de Chevigny 2008 Not: Sjgren 1990
Not: Ng 2011 50% de Chevigny 2008
Page 11
Intra-op. Initial Treatment (with AP) Intra-op. Initial Treatment (with AP)
Vertical comp. 87% Short root filling 74%

better outcome poorer outcome
than lateral comp.
Sjgren 1990
Weak evidence! rstavik 1993
Ricucci 2011
de Chevigny 2008 Not: Weiger 2000
Not: Peters 2004 Peters 2004
Ng 2011 77% de Chevigny 2008 86%
Retained instrument; short root filling? Equivocal Variables

Intra-op. Initial Treatment (with AP)
Mid-treatment
complications
poorer outcome
4 years Sjgren 1990 50% 80%

de Chevigny 2008
if we believe separated instruments are sign.
Excessive dentin removed! Retained Instrument

roots filled with files- 94% healed Fox 1972
No effect on outcome Ng 2011
Prognosis not affected Spili 2005
Prognosis not sig. lower Panitvisai 10
Outcome not sig. different Fu 2011
1 year Insufficient evidence Murad, Murray 11
Page 12
Retained Instrument
Retained fractured instrument !
Reduces prognosis in presence of AP

Attempting removal is recommended,
but not supported in absence of AP
Stage of treatment at which fracture
occurs not associated with outcome
McGuinan et al. 2013
8 years
Perforation Non-predictive Variables

MTA 3 years
Non-surgical Treatment (with AP)
?
Age, gender
Jaw, anatomy
Periodontal defect, symptoms
Time since initial treatment
Cleaning-shaping parameters
Treatment sessions
Perforation no effect Ng 2011 Restoration type, post
Cleaning and Shaping Treatment Sessions

Initial Treatment (with AP)
Healed / sessions
Type of instruments no effect Study Years 1 2
Peters 2004 Marending 2005 Ng 2011
Friedman 1995 1.5 55% 64%
Degree of taper no effect Trope 1999 1 64% 74%
Hoskinson 2002 Ng 2011 Weiger 2000 1-5 83% 71%
Peters 2002 1-4 81% 71%
Enlargement no, little effect Molander 2007 5 65% 75%
Kerekes 1979 n-c Peters 2002 sample Ng 2011 Toronto S. 2008 4-6 77% 83%
rstavik 87/ 04 Peters 2004 Saini 2012 Penesis 2008 1 63% 68%
Hoskinson 2002 Toronto S. 2008 Liang 2012 2 80% 65%
Paredes-Vieyra 12 2 97% 89%
sample size- too small.
Page 13
Contradictions Bacterial Elimination
?
Article(s)
Extensive apical enlargement
107
promotes disinfection
rstavik 1991 Card 2002 106
105
Medication required to eliminate 104
infection 103
Bystrm 1983, 1985, 1985 Shuping 2000
102
Elimination of infection in one 101
session is less predictable
Sjgren 1997 Vera 2012 1st session 2nd session
Methodology- measures; CFU (initial vs finish)
and culture
Bacterial Elimination
Bacterial Elimination
Colony forming units Syto 9/Propidium iodide DAPI/Dihydroethidium Therapeutic measure No growth (%n)
Therapeutic measure No bacteria (%n) Files, inactive irrigation 20-40
Bystrm 1981/3/5 Kvist 2004 Schirrmeister 07 Rtx Files, 5% NaOCl, IKI, CHX 40-90
rstavik 1991 Waltimo 2005 Wang 2008
Sjgren 1991 McGurkin-Smith 05 Huffaker 2010
Sjgren 1997 Zerela 2005Rtx Pawar 2012 Bystrm 1985 Peciuliene 2001Rtx Zerela 2005Rtx
Dalton 1998 Chu 2006 Ras 2013 rstavik 1991 Peters 2002 Vianna 2006
Shuping 2000 Vianna 2006 Xavier 2013 Sjgren 1991 Card 2002 Manzur 2007
Peciuliene 2001 Rtx
Manzur 2007 Paiva 2012/13 Sjgren 1997 Kvist 2004 Paquette 2007
Peters 2002 Paquette 2007 Siqueira 2013 Dalton 1998 Waltimo 2005 Malkhassian 2007
Card 2002 Malkhassian 2007 Shuping 2000 McGurkin 2005 Wang 2008
Many margins of error with methodology
regarding culture
Bacterial Elimination Bacterial Elimination

Bystrm et al. 1981/3/5
Bystrm et al. 1981/3/5 Shuping et al. 2000
McGurkin-Smith et al. 2005
107 107
106
no dressing (2d) 106
Ca(OH)2 (1-4w)
105 105
104 104
103 103
102 102
101 101
1st session 2nd session 1st session 2nd session
Page 14
Bacterial Elimination Bacterial Elimination
Therapeutic measure No growth (%n) Therapeutic measure No growth (%n)
Files, inactive irrigation 20-40 Files, inactive irrigation 20-40
Files, antibacterial irrigation 40-90 Files, antibacterial irrigation 40-90
Files, NaOCl, Ca(OH)2 80-97 Files, NaOCl, Ca(OH)2 60-80
Bystrm 1985 Peciuliene 2001Rtx Zerela 2005Rtx Bystrm 1985 Peciuliene 2001Rtx Zerela 2005Rtx
rstavik 1991 Peters 2002 Chu 2006 rstavik 1991 Peters 2002 Chu 2006
Sjgren 1991 Card 2002 Vianna 2006 Sjgren 1991 Card 2002 Vianna 2006
Sjgren 1997 Kvist 2004 Manzur 2007 Sjgren 1997 Kvist 2004 Manzur 2007
Dalton 1998 Waltimo 2005 Schirrmeister 2007Rtx Dalton 1998 Waltimo 2005 Paquette 2007
Shuping 2000 McGurkin 2005 Wang 2008 Shuping 2000 McGurkin 2005 Huffaker 2010
Bacterial Elimination Treatment Sessions

rstavik et al. 1991 Manzur et al. 2007
Peters et al. 2002 Xavier et al. 2013
107
Biological benefit of multiple visits
106
Ca(OH)2 (1-4w) not supported by clinical evidence
105 Sathorn 2005
104
103 No difference in outcome between
102
101 single and multiple visits
Naito 2007 Figini 2008 Su 2011
1st session 2nd session
bacterial counts
Best Prognosis (with AP)

Healed ~ 85%; Functional ~ 95%
No previous perforation
Use of EDTA (Rtx)
?
No CHX initial
Patency regained (Rtx)
Adequate filling length
One-session treatment (Rtx)
Adequate restoration
Page 15
Shallow Cavity, Bevel Internal Seal
Carr 1990 ultrasonic tips
Shallow interface
3 mm
Achilles heel
Beveled surface is
9 mm
permeable 6 mm
3 mm
Internal Seal External Seal

Rud et al. 1989 Retroplast
1 year
External Seal Retrograde Retreatment

Nygaard-stby 1973
Courtesy Dr. V. Rud 9 years
Page 16
0
20
40
60
80
100
0
20
40
60
80
100
Toronto Study 2010 Dorn & Gartner 1990
von Arx et al. 2010 Grung et al. 1990
Taschieri et al. 2010 (AS without Rtx)
Friedman 1991
Song et al. 2011
Wlivaara et al. 2011 Rapp et al. 1991
Song et al. 2011 Lasaridis et al. 1991
OMFS
OMFS
Taschieri et al. 2011 Waikakul & Punwutikorn 1991
Taschieri et al. 2011 (GTR)
Zetterqvist et al. 1991
von Arx et al. 2012
Song & Kim 2012 Rud et al. 1991
Song et al. 2012 Frank et al. 1992
Villa-Machado et al. 2013
Cheung et al. 1993
Asgary & Ehsani 2013
Tascheir et al. 2013 Pantschev et al. 1994
Song et al. 2013 Jesslen et al. 1995
Li et al. 2014
n = 29
n = 23
Rud et al. 1996
Song et al. 2014
August 1996
Kurt et al. 2014
Lui et al. 2014 Sumi et al. 1996
von Arx et al. 2014 Danin et al. 1996
Tawil et al. 2015
Rud et al. 1997
Shinbori et al. 2015
Jansson 97
Dhiman et al. 2015
Apical Surgery
Apical Surgery
von Arx et al. 2015 Bader & Lejeune 1998
alikan et al. 2016 Testori et al. 1999

Kim et al. 2016
Kvist & Reit 1999
Kruse et al. 2016 (MTA group)
ENDO
ENDO
Kim et al. 2016 Rubinstein & Kim 1999 7 years
Kim et al. 2016 von Arx & Kurt 1999
Discrepancy of 60%!
Retro-retreatment
37
97
irrigate with CHX, sealer and thermoplastisized GP
Page 17
0
20
40
60
80
100
0
20
40
60
80
100
Zuolo et al. 2000 Persson 1966

Rahbaran 2001
Mattila & Altonen 1968
Rud et al. 2001
von Arx et al. 2001 Nord 1970
Jensen et al. 2002 Nordenram 1970
Rubinstein & Kim 2002
Nordenram 1970
Maddalone et al. 2003
OMFS
OMFS
Chong et al. 2003 Harty et al. 1970

Schwartz-Arad 2003 Lehtinen & Aitasalo 1972
Wesson & Gale 2003
Wang et al. 2004 (Toronto Study) Rud et al. 1972
Gagliani et al. 2005 Ericson et al. 1974
Lindeboom et al. 2005
Persson et al. 1974
Taschieri et al. 2005
Tsesis et al. 2006 ( modern technique ) Altonen & Mattila 1976
Taschieri et al. 2006 Finne et al. 1977
Marin-Botero et al. 2006
Hirsch et al. 1979
n = 31
n = 23
Filippi et al. 2006

Penarrocha et al. 2007 Malmstrom et al. 1982
von Arx et al. 2007 Persson 1982
Wlivaara et al. 2007
Mikkonen 1983
Yazdi et al. 2007
Taschieri et al. 2007 Ioannides & Borstlap 1983
Skoglund et al. 1985
Garcia et al. 2008
Apical Surgery
Apical Surgery
Saunders 2008 Reit & Hirsch 1986

Kim et al. 2008 Forsell et al. 1988
Jonasson et al. 2008

Amagasa et al. 1989
Ortega-Sanchez et al. 2009
Crosher et al. 1989
ENDO
ENDO
Christiansen et al. 2009 (root-end filled)
Methodology
Wlivaara et al. 2009 Allen et al. 1989
Navigate Diverse Reports

short F/U: underestimation in initial but
in surgery its the oposite
Follow-up (years) Definitive Outcome

Assessment Assessment
100 1 4
Regression of 5% to 25%
1 4 6-10 1-2 2
1-2 4 4-8 1 4 1
1 4 4 1 5 1 6
Success rate (%)
80 4-8 5 1
1-2 2-6 1 Rubinstein 2002 Song 2012 Tawil 2015
Taschieri et al. 2010 (AS without Rtx)
Wesson 2003 von Arx 12,14 Kruse 2016

60 Yazdi 2007 Song 2014
Kim et al. 2016 (MTA group)

Taschieri et al. 2011 (GTR)
Villa-Machado et al. 2013
1
Years Success (weighted)
Asgary & Ehsani 2013
40
Wlivaara et al. 2011
alikan et al. 2016

Tascheir et al. 2013
Toronto Study 2010
Shinbori et al. 2015

Dhiman et al. 2015
von Arx et al. 2015
von Arx et al. 2014
von Arx et al. 2010
von Arx et al. 2012

Song & Kim 2012
Kruse et al. 2016

Song et al. 2014
Song et al. 2012
Song et al. 2013

Song et al. 2011
Song et al. 2011
Tawil et al. 2015

<2 95%
Kurt et al. 2014
Kim et al. 2016
Kim et al. 2016

Lui et al. 2014
Li et al. 2014
20
2-4 90%
0
>4 82%
Kang et al. 2015 SR
Regression Definitive Outcome

Assessment
Retrograde Retreatment GP
Study Years Healed Regress
Rubinstein 99,00 15-7 9792% 8%
Kim 08, Song 12 <56-10 9293% ? 7%
von Arx 07, 12 15 8476% 10%
Song 2014 14-8 9188% 9%
von Arx 10, 14 15 8685% 6%
Tawil 2015 13 6769% 9%
Song 12, Kim 16 14 9489% 5%
6 months 2.5 years Christiansen 09, Kruse 16* 16 7984% 20%
* MTA group
5-20%, causes the long term outcomes to drop
Outcome Classification Dichotomized Outcome

Favorable Unfavorable
Complete healing Uncertain healing Healed:
Complete healing
Unsatisfactory healing
Incomplete healing
Incomplete healing
Uncertain healing
Rud 1972
Molven 1987, 1990 Taschieri et al. 2013
lumped into the healed category..so overestimate
Page 18
Fibrous Scars Incomplete Healing
Develop in a small Clear reduction of radiolucency Gagliani 2005

proportion of cases
Altonen 1976 Grung 1990 Reduced radiolucency at periphery
Ortega-Snchez 2009
Remain stable Molven 1996 Reduced radiolucency clinical normalcy

Taschieri 2013
Obviously reduced large lesions Li 2014
Incomplete healing = success
Rud 1972 Molven 1990
Some reduction of radiolucency Zhou 2016
lump them into success category bc they are
scars so success is not classified well. Over
estimated SR
Scar ? Fibrous Scar

Courtesy Dr. R. Rubinstein, Michigan
Assessment
Healing
Study Complete Incomplete
Grung 1990 65% 7%
Yazdi 2007 77% 5%
von Arx 2012 71% 6%
von Arx 2014 79% 6%
alikan 2016 74% 6%
Kim 2016 86% 3%
1 year 5 years Kruse 2016 67% 3%
Does this look like a scar? It was

classified as one and was used as an
example. it was misclassified
Fibrous Scar Systematic Reviews

Assessment
Healing
Study Complete Incomplete Study Years Outcome
Chong 2003 63% 27% Torabinejad 2009 4-6 72%
Lindeboom 2005 57% 32%
?
Tsesis 2009 >1 92%
Taschieri 05,06,07,08,10,11 91-93% Del Fabbro 2010 1-4 > 90%
Marin-Botero 2006 50% 37% von Arx 2010 1-8 80%
Song, Kim 2012 74% 20% Setzer 2010/11 > 0.5 94%
Li 2014 60% 33% Tsesis 2013 >1 89%
Kang 2015 1-5 92%
Page 19
Systematic Reviews Current Best Evidence
Definitive Outcome
Study Years Success Methodology (3 parameters):

Rubinstein, Kim 1999 1 97%
Taschieri 05,06,07,08,09 1-2 > 91% Cohort 50 teeth
Maddalone 2003
von Arx 03,07,10
3
1
92%
> 90%
no, little Retx
Lindeboom 2005 1 91% Exposure microsurgery
Filippi 2006 1 93%
Chong 2003 2 90% Assessment 3 years
Kim 2008
Christiansen 2009
1-5
1
95%
100%
% healed
Wlivaara 09,11 1 88% Analysis multivariate
SR did not appraise the recall rates.
Apical Surgery Apical Surgery

n = 23+23 n = 60
100 100
Success rate (%)
Success rate (%)
80 80
60 60
t
40 40
n- curren
No
20 20
0 0
Follow-up studies (1966-1989; 1990-1999) Follow-up studies (2000-2017)
61 studies
Prognosis Projection of Prognosis

n 4/107
n = 4/106 Healed 74% to 89%; Functional 94%
100
74% to 89%
Healed; Functional (%)
80
Can we project the particular
60
prognosis for a specific case?
Barone et al. 2010 (TS)
von Arx et al. 2012
von Arx et al. 2014
40
Kim et al. 2016
20
Preoperative outcome
0 predictors
Page 20
Pre-operative Predictors Intra-operative Predictors
Proximal bone 78% Crypt diameter of 80%

level >3 mm from >10 mm poorer
CEJ poorer outcome
outcome
von Arx 2012 53% Barone 2010 53%

MTA better outcome MTA MTA similar

than S-EBA, Retroplast 86-93% outcome to S-EBA MTA
(at 5 years) (at 6 years) 92%
Weak evidence! Retroplast Adequate evidence!

77-79%
cohort studies S-EBA
von Arx 2012 S-EBA 90%
67%
von Arx 2014 Kim 2016
RCTrials
Intra-operative Predictors Equivocal Variables

Apical Surgery
?
common sense
Skillful operator Age

better outcome Previous root filling length
79% 50% not consistent

Nord 1970
Altonen 1976
Lustmann 1991
Page 21
Pre-op. Apical Surgery Pre-op. Apical Surgery
Older patients Short/long root

(>45 years) filling better
better outcome outcome
84% 68%
Barone 2010 Barone 2010 84% 68%
Not: von Arx 2012 Not: von Arx 2012
Emerging Variables Emerging Variables

Intra-operative Intra-operative
Dentinal defects Isthmus cavity

observed prepared 87%
poorer outcome poorer outcome
32% 97%
62%
Tawil 2015 Kim 2016
may adversely affect the outcome
Non-predictive Variables Adjunctive Use of GTR
?
Gender, tooth location For through-and-through lesions,
Symptoms, lesion size GTR achieved better results than
Post-retreatment, repat surgery controls. For lesions with four
Root filling material, density walls, GTR had no significant
Restoration type, post advantage.
Laser, bone grafting, barriers
Complications, antibiotics SR Tsesis et al. 2011
Page 22
Best Prognosis
Healed 85%; Functional ~ 95%
Thank You
Proximal bone 3 mm from CEJ
?
Effective root-end seal:
Retrograde retreatment
Deep cavity, MTA, S-EBA shimon.friedman@dentistry.utoronto.ca
Skillful operator
Page 23
Dr. Fouad obtained his DDS, Certificate of Endodontics and MS at the University of
Iowa. He served as Assistant then Associate Professor of Endodontology at the
University of Connecticut Health Center from 1992 2004, and as Chair of the
Department of Endodontics, Prosthodontics and Operative Dentistry at the University of
Maryland, from 2005 2015. He assumes the position of Professor and Chair of
Endodontics at the University of North Carolina in January 2016.
Dr. Fouad has published over 75 manuscripts and textbook chapters, over 110
abstracts, and edited and co-authored the textbooks: Endodontic Microbiology and the
fifth edition of Endodontics: Principles and Practice. He is a Diplomate and Past
President of the American Board of Endodontics, and an Associate Editor of the Journal
of Endodontics. He has lectured widely in the U.S. and internationally, and his research
interests include: endodontic molecular microbiology, effectiveness of antibiotic therapy,
dental pulp regeneration, endodontic treatment outcomes and the pathogenesis and
healing of periapical lesions in the host with normal and compromised systemic health.
Board Review and Scientific Update LearningObjectives
College of Diplomates of the ABE
Discussthemajorsystemsthatmediatethe
February 11, 2017
hostresponseinpulpalandperiapical
inflammation
Inflammation and Identifythedifferencesbetweeninnateand
specificimmuneresponsestoendodontic
Immunoregulation pathogens
Describethemechanismofboneresorption
Ashraf F. Fouad, D.D.S., M.S. anddepositionasitrelatestopathogenesis
University of North Carolina andhealingofperiapicallesions
ProgressionofPulpalandPeriapical Sourcesofbacterialirritationtothepulp
PathosisduetoBacterialIrritation
DentalCaries
TraumaticInjuries
Cracks&fractures
Abrasion,Attrition&Erosion
PeriodontalDisease
CongenitalAnomalies
Externalinvasiveresorption
Microleakageofrestorations
Persistentdiseasefollowingtreatment
SeverityofPulpitisdependsondegreeofirritation
PulpalInflammationwithincipientCaries
Fissure Caries
1 2
Experimental cavities in monkey
teeth, treated with
Inflammation
1) gutta percha temporary
dressing (mild reaction)
2) left open to oral environment
Pulp (moderate reaction) or
3) filled with soft carious dentin
(severe inflammation)
From Ingle, Stanley, Langeland, Chapter 6, in Ingle and Bakland, Endodontics, 4th ed. 3 Mjor and Tronstad, Oral Surg 1972
1
Pulpabscessdespiteunexposedpulp CariousPulpExposure
Calcio-traumatic line
Pulp abscess
Reactionary Dentin
Simon J et al., Pulpal Pathosis in Ingle JI, Bakland

LK. Endodontics. Fourth Ed Courtesy of Dr. Larz Spangberg
PulpExposureandInitialNecrosis Vasodialation
Site of pulp
exposure
Pulp
Necrosis
Pulp
Necrosis
Inflammatory infiltrate
(mostly PMNs)
Pulpitis
High Magnification of previous specimen
PulpNecrosis Periapical Lesion Expansion in

Normal and scid mice
Correlation Coefficient for Pulp Status and Periapical Area
r= 0.65
Spearman Rank Correlation p<0.0001
Observed Frequencies for Pulp Status by Strain
Control scid No B cells

Vital 2 1
Bacterial stain showing Necrotic/Vital 6 5
bacteria within tubules.
Necrotic 15 9
pulp necrosis
throughout the canal Chi Square p=0.88 Fouad, J Dent Res 1996
2
Radiographic Induction of Periradicular
CBCTofteethwithIrreversiblePulpitis
Lesions in Ferrets
100
80
LesionPresent
60
LesionAbsent
40
20
15% vs 3%
0
Periapical CBCT
The prevalence of AP lesions detected with CBCT

was significantly higher in the symptomatic group
compared with the asymptomatic group (P < .05)
Abella et al., J Endod 2012 Fouad et al., Endod Dent Traumatol 1992
ProgressionofEndodonticPathosis Tooth #10 Asymptomatic AP

(casenottreatedinatimelymanner) virulence vs host response
Sept 2007 April 2008 February2011 February2012
PeriapicalLesion Periapical
Granuloma
PMN
Macrophages
Lymphocytes
innate Plasma Cells
Fibroblasts
Mouse mandibular molar, distal root Heavy inflammatory infiltrate, mostly
PMNs, macrophages and lymphocytes.
3
Percentage ofCystsvs.Granulomas
PeriradicularCyst
SampleCystsGranulomas
Priebe etal.1954 101 54 46
Sommer etal.1956 170 7 84
Pattersonetal.1964 510 14 20
Bhaskar 1966 2308 42 48
Lalonde&Luebke1968 800 44 45
Mortensenetal.1970 396 41 59
Blocketal.1976 230 7 93
Winstock 1980 9804 8 83
Radicular Inflammatory cyst: Epithelial Proliferation Stockdale1988 1108 17 77
Epithelium is from the cell rests of Mallassez Spataforeetal.1990 1659 42 52
Nairetal.1996 256 15 50
Koivisto etal.2012 9723 33 40
KOT-
Periapical Abscess
Areaoftissuenecrosis/liquifaction /pus
Surroundedbyheavyinfiltrationof
inflammatorycells,mainlypolymorphonuclear
leukocytes(PMNs)
Surroundedbyareaofsparseinflammatory
cellsmainlymacrophagesandlymphocytes
Koivisto etal.,JOE2012
LongtermEndodonticInfections
CC: Numbness and tingling lower lip after root canal treatment
fragments of bone no osteocytes. Osteomyelitis
4
Innate (Non- Specific (Adaptive) CellsinPulpandPeriradicularInflammation
Specific) Immunity Immunity INFLAMATORY CELLS NON-
- Lymphocytes: INFLAMMATORY
- Skin, epithelium T-cells: CD4+ Th-1 CELLS
- To common microbial - Microbial and Th-2
non-microbial antigens Th17
structures (e.g. LPS) - Odontoblasts
- Very large diversity CD8+
- Limited diversity - Fibroblasts
Treg
- Memory - Vascular Endothelium
- No memory B-cells, plasma cells
- Antibodies cells
- Antimicrobial chemicals - Activated Lymphocytes - Osteoblasts
NK cells
- Osteoclasts
- Non-specific - Macrophages (M1 and M2)
- Epithelial cells
inflammatory cells - Dendritic cells
- PMNs
- Mast cells
PMNs - Neutrophils
5462%ofblood
leukocytes
Lysosomal
enzymes
Cytokines
Phagocytosis
Oxygenderived
freeradicals
Apical foramen, apical periodontitis
Short half-life: 1011 produced daily, circulate for 6h,

if not recruited to inflammation site, undergo apoptosis
Dendritic Cells in the Dental Pulp
- Fc receptor negative
- Lacks long-term
adherence
Jontell, J Dent Res 1989
Pulpal Dendritic Cells can migrate to

regional lymph nodes
Bhingare et al., J Dent Res 2014

activates lymphocytes-b cell immunity
5
Macrophage Macrophage
Peptidoglycan Lipopolysaccharide
Lipopolysaccharide
Lipoteichoic acid
TLR2 TLR4 MyD88: Signal TLR4
Trasduction protein
Nuclear Factor
kappa B:
Trascription factor
MAPKs:
Mitogen-activated
protein kinases
mediators
Macrophage
Lipopolysaccharide
TLR4
Pro-inflammatory
Cytokines IL-1
IL-6
TNF-
IL-10
translation
6
Fouad & Acosta, Int Endod J, 2001
GWAS- study Pattern

TLR2 Recognition
Receptors
(PathogenAssociated
TLR2knockoutmicedeveloped MolecularPatterns
significantlylargerperiapicallesions PAMP)
andmoreosteoclaststhancontrols
Da Silva et al. J Endod 2012

Abbas, Litchman & Pillai
Basic Immunology 2014
TLR Profiles in Dental Pulp Stem Cells

TLR1,2,4,
Bacteria 5,6,9 Normal Medium TLR 1-10
Inflammatory Medium: IL-1, IFN-, IFN-, TNF-:

Viruses TLR3,7,8 TLR-2, 3, 4, 5 & 8
TLR-1, 7, 9 & 10
Some Abolished TLR-6
TLR2
fungi
Fawzy El-Sayed et al., JOE 2016
7
Phagocytosis Genetic Predisposition to
Phagocytic cell
opsonization Persistent Apical Periodontitis
Fc Opsonins: Patientsweretypedforthefollowinggenes
Antibodies (alleles):FcRIIA(R131orH131),FcRIIIB(NA1
Fab Complement orNA2),IL1A(1or2),andIL1B(1or2).
Lectins
Non-opsonic: N= 44 Patients with Healed Apical status
LPS And 18 patients with Persistent Disease
Peptidoglycan Two genetic conditions associated with persistent disease:
Lipopeptides
Bacterial cell Nonspecific 1. Allele H131 of the FcRIIA gene (P = .04)
Fibrinogen 2. A combination of this allele with allele NA2 of the
Lysosomes
C-reactive protein FcRIIIB gene (P < .01).
Formation of Phagosome Siqueira et. al, J Endod 2009
Genetic Predisposition to
Persistent Apical Periodontitis iNOS
Patientsweretypedforthefollowinggenes M1 NO Th1 IFN-
(alleles):FcRIIIA(3genes&2alleles) M
N= 43 Patients with Healed Apical status

And 26 patients with Persistent Disease
All patients with preoperative disease
Arginase
There were no significant associations with persistent M2 Ornithine Th2 IL-4
disease
Siqueira et. al, J Endod 2011 Mills, Crit Rev Immunol 2012
DensityofInflammatoryCellsin ODONTOBLASTIC RESPONSE

PrimaryandPersistentLesions No Exposure: Reactionary Dentin
Exposure: Reparative Dentin
- Stem cell involvement
- Faster Rate of formation
- Permeability
- Protective function
Physiologic barrier
Cytokines: IL-1 and IL-8
Toll-like Receptors 4 and 2
Esterela et al., JOE 2016
8
Non-Specific Immune Mediators
Horst et al., BMC
Complement
Immunol 2011 Neuropeptides
Clotting and fibrinolytic pathways
?
Kallikrein system
Cytokines & Chemokines
Adhesion molecules
Matrix metalloproteinases
Defensins
Heat shock proteins
Heat Shock Proteins Heat Shock Proteins

Heat Shock Proteins are significantly increased in
Induced by stress signals such as:
periapical granulomas compared to normal
periodontal ligament Elevated temperature
Goodman et al., JOE 2014 Reduced oxygen

Infectious agents in area of inflammation
In 400 patients with deep caries, those who had Role in the synthesis, transport & folding of proteins
periapical lesions (compared with those with vital Trigger innate immune response by activating M
pulp) had significantly more Single Nucleotide Increase cellular response to LPS to produce
Polymorphisms in 2 Heat Shock Protein genes. proinflammatory cytokines
SNIPS Maheshwari et al., JOE 2016

Maheshwari et al., JOE 2016
Genetic variability to response to caries
Vasodilation & Increase in Vascular Pain Mediators in Pulp and Periapex

Permeability:
- Histamine Prostaglandins
- Prostaglandins Leukotrienes ??
- Nitric Oxide - Increase blood flow
}{
- Leukotrienes Bradykinin
Vasoactive - Plasma extravasation
- Bradykinin Serotonin - Leukocyte migration
Mediators - Substance P
Histamine - Proliferation of sensory
- CGRP
- Platelet activating factor (low doses) Neuropeptides nerve fibers
- SP - Reduced pain threshold
Vasoconstriction:
- Serotonin (5-HT)
- CGRP
- Thromboxane - VIP
- PAF (regular doses) - NKA
Neurogenic Inflammation - NPY
9
INNATE Adhesion to Endothelial Cells
Venuoles
Integrins
P-/E- Selectins
ICAMs/VCAMs/PECAMs
Fouad, Chapter 11,

The Dental Pulp 2012
Fouad, Chapter 11,

C3a & C5a:

Lectin Chemotaxis /MC
degranulation
C3b: Opsonization
Fouad, Chapter 11,
10
Matrix Metalloproteinases
Zinc-dependant endopeptidases: Protease Inhibitors
- Collagenases (MMP-1, 8, 13, and 18),
- Gelatinases (MMP-2 and 9),
- Stromelysins (MMP-3, 10, and 11), TissueInhibitorsofMetalloproteinases(TIMP)
- Membrane-Type MMPs (MT-MMPs) (MMP-14, 15, 16, 17, 24,
and 25)
- Minimal domain MMPs (MMP-7 and 26)
Linetal.JOralPathol Med1997
- Others (MMP-12, 19-23, 27, and 28)
alpha1antitrypsinandalpha2macroglobulin
- Upregulated by cytokines (inhibitPMNelastaseandotherproteases)
- Responsible for remodeling of tissues by degrading extracellular
matrix components, e.g. during inflammation.
McClanahanetal.1991
Tjaderhane etal.JDR1998 Rauschenberger etal.1994
Wahlgren etal.IEJ2002
Palosaari etal.Eu JOralSci 2003
PulpLevelsofMMP9andTIMP1 Nitric Oxide

inteethwithpulpexposures ProducedbyNOsynthase(NOS)
MMP9
NeuronalNOS
1- Asymptomatic
2- Reversible Pulpitis EndothelialNOS
3- Irreversible Pulpitis w/ NSAIDS InducibleNOS(iNOS)
4- Irreversible Pulpitis w/o NSAIDS
TIMP1 Actions:
Relaxessmoothmuscle,causingvasodilation
can we distinguish level differences between groups Reducesadhesiontoendothelialwalls
Differences were
statistically significant Actiondependsondose;bothpro andanti
inflammatoryfunctionshavebeendescribed
- iNOS and NADPH co-factor in inflamed pulp
Mente et al., JOE 2016 Law et al., JDR 1999
Oxygen-Derived Free Radicals

Superoxideanion(O2),
Hydrogenperoxide(H2O2)
Hydroxylradical(OH) Specific Immunity
CancombinewithNOtoformperoxynitrite andother
toxicnitrogenintermediates
ODFRsareknownasreactiveoxygenintermediates
Upregulate theproductionofIL8
Theenzymesuperoxidedismutase(SOD)isthemain
intracellularscavengerofODFRs,particularlyO2
Baumgardner et al., O4E 1999
11
NK cells are non-specific in their action
Quantified level of caries; as you get deeper, increase in T and B

IL2
HumanCariouslesions T-helper/inducer
Immunohistochemistryfor
various
Inflammatorycells
T-suppressor
Izumi et al. Arch Oral Biol 1995
HumanCariouslesions B-cells HumanCariouslesions Macrophages

Immunohistochemistryfor Immunohistochemistryfor
various various
Inflammatorycells Inflammatorycells
Plasma Cells Neutrophils
Izumi et al. Arch Oral Biol 1995 Izumi et al. Arch Oral Biol 1995
12
Specific immunity in Periapical Lesions RoleofTreg Cells
- Lymphocytes are a significant, and

predominant cell population in
periradicualr lesions
- T-cells are more prevalent than B-cells
- T-helper cells are more predominant in the

early expansion phase whereas T-suppressor
cells prevailed in the later chronic phase
Wang & Stashenko Francisconi et al., J Endod 2016
Wild Type: suppresed T reg cells; PARL grew 21 days
Pro-inflammatory
Type 1 Cytokines
Mediatorsofperiapical inflammation IL-1, TNF-, IL-6, IL-12, IFN
IL-2, IFN , IL-12 Produced mainly by monocytes/macrophages, but may
also be produced by PMNs, fibroblasts and endothelial
cells, particularly in response to LPS , Peptidoglycans
IL-4, IL-5, IL-6, IL-10, IL-13
and lipoteichoic acid
TGF- , IL-17 Have several systemic effects such as fever, production
of acute phase proteins, prostaglandins, platelet
IgG, IgM, IgA, IgE activation factor, or NO
Activate T-cells and stimulates them to produce IL-2
IL-1 , IL-1 , TNF
Activate endothelial cells and induce the expression of
adhesion molecules on their membranes, thereby aiding
IL-1, TNF , IL-6, others
in the recruitment of inflammatory cells to the site of
Chemokines: IL-8, MCP-1, Rantes inflammation
Genetic Predisposition to IL-17

Persistent Apical Periodontitis Produced by Th17 cells, T cells,
IL-1 Allele2 neutrophils, and macrophages
Adequately performed RCT, 1 year post-operative
CASES(Lesions) CONTROLS
Potent bone resorption in periapical
(Healed) lesions
Oseko et al. Microb Immunol 2009
N 34 61
%withAllele2 71% 25% IL-17 receptor antagonist was protective

against periapical bone resorption
P<.001 AlShawaimi et al., J Immunol 2013
Morsani et. al, J Endod 2011
13
Bone-Modulating Cytokines in
TH1 vs. TH2 cytokines in the Pulp Periradicular lesions
Type 1 Type 2
Interleukin-1
Interleukin-1 Interleukin-4
Tumor Necrosis Factor- Interleukin-10
Tumor Necrosis Factor- Interleukin-6?
Interleukin-11? Interleukin-13
Interferon- ?
Interleukin 17
Hahn et al. Inf &Imm 2000 (Prostaglandins (PGE2)
attract cells to local site of inflammation
Chemokines
*IL8
Huangetal.,OOOOE1999
(odontoblasts)Levinetal.,Eu JOralSci 1999
*MCP14
Rahimi etal.,Endocrinol,1995
*MCP1,MIP1a&b,IP10
CCR3,CCR5&CXCR3
Kabashima etal.Cytokine2001
*RANTES
Marton etal.,OralMicroImmunol,2000
Regulation of osteoclast formation and Interactionsbetweenosteoblastsandosteoclast

differentiation. precursorsduringboneremodeling
B.F. Boyce J Dent Res 2013 Fouad, Dent Clin North Am, 2017
14
Activevs.InactiveLesions
basedonRANKL/OPGratio
Receptor Activator of NF-kB Ligand
(RANK-L) in Periradicular Lesions
(5foldorgreater)
ActiveLesions InactiveLesions
Present in 21 periradicular lesion TNF(cytokine) SERPINE1(remodelingenzyme)
CXCL11(chemokine) TIMP1(remodelingenzyme)
biopsies, but not in 3 periodontal
COL1A1(ECMComponent)
ligament specimens from normal teeth
TGFB1(Growthfactor)
ITGA4(Cellularadhesion)
Sabeti et al. JOE 2005
N= 83 granulomas and 24 control pdl specimens
N= 84 wound healing genes PCR array
Garlet et al., J Endod 2012
chairside tool: OPG ratio
Drug Modulation of
Activevs.InactiveLesions
Periapical Lesions
basedonDiagnosis
Bisphosphonates
MMP-2, -3, -7, -9, -14, -16, and -25; TIMP-1; and TIMP-2 Xiong et al., Int Endod J 2010
Kang et al., J Bone Min Res 2013
ChronicApicalAbscess AsymptomaticApical
(n=15) Periodontitis(n=18) Statins (simvastatin)
MMP2 TIMP1 Lin et al., J Endod 2013
MMP7
MMP9 Metformin
Liu et al., J Endod 2012
Letra et al., J Endod 2013
Antagonist for Receptor

Activator of NF-kB Ligand
(RANK-L) caused Osteonecrosis
in an animal model
Aghaloo et al. J Min Bone Res 2014
estrogen is protective
15
No B cells, swell
Pulp Necrosis and PA Lesion Effect of T or B cell deficiency on

Progression in normal and scid mice Pathogenesis of Periapical Lesions
Area/ 105 sq. m
3.50
Deficiency Result
MeanandS.D.ofPeriapicalLesionArea
3.00
Wallstrom et al. 1993 T No difference
2.50
* Tani Ishii et al. 1995 T No difference
SCID
2.00 BALB/c Fouad 1997 T&B No difference
1.50
1.00
Teles et al. 1997 T&B Swelling
(with bacterial inoculations)
0.50
0
Control 1W 2W 3W 4W Hou et al. 2000 T&B, T, B B: swelling
* = Statistically significant (p < 0.05)
Fouad, J Dent Res 1996 (with bacterial inoculations)
affect of AB
Immunologic Memory
Immunoglobulins in dentinal tubules
Staining for Secretory

Staining for Ig G
component of Ig A
From: Ackermans et al., Arch Oral Biol 1981; 26:883
IGs- PARL had higher systemic IGs than controls
16
GrowthFactorsinPeriapicalLesions
TGFandTGF
Lietal.,MolPathol,1997
Tyleretal.,JEndod,1999
EpidermalGF
Linetal.,IntEndodJ,1996
VEGF
Bletsa etal.JEndod2012
Virtej etal.,JEndod2013
BMP2
Matsumotoetal.JEndod2014
Are in
PARL-
thompson IEJ 2017- large reservoir of GF in dentin
17
Biography for Dr. Keith V. Krell DDS, MS, MA
Dr. Krell has been in full-time private practice with Endodontics PC in
West Des Moines, Iowa for 27 years. He is an adjunct clinical
Professor in the department of Endodontics at the University of Iowa
College of Dentistry where he also served as graduate program
director until 1989 for three years. In 1993, he retired from the United
States Army National Guard as a lieutenant colonel after 22 years of
service.
He received his D.D.S. and M.S. degrees from the University of Iowa in
1981 and 1983, respectively. He earned his BA in Sociology from
Washington University in St. Louis, and his M.A. degree in sociology-
anthropology in 1975, from the United States International University
in San Diego, Calif while serving in the USN.
Dr. Krell is a Diplomate of the American Board of Endodontics, as well

as a past president of the American Board of Endodontics (2007) and
Past president of the American Association of Endodontists
Foundation(2014). He is the past secretary of the American
Association of Endodontists. He currently is an examiner for the
American Board of Endodontics.
Dr. Krell was a counselor for the College of Diplomates of the ABE for 9
years and provided reviews for taking the Oral exam for 7 years.
Dr. Krell is a member of the Scientific Advisory Board of the Journal of

Endodontics and is a reviewer for both the JOE and JADA.
Cracked teeth and Vertical Root Dr. Rob Roda,
Fractures: Past AAE President
What do we know now? Cracked teeth seem to be a
result of repetitive stress
injury, and so the longer
teeth are in use, the more
likely they will become
February 11th, 2017 cracked. This is a modern
Richmond, Virginia epidemic and something we
have never before as a
Keith V. Krell D.D.S., M.S.,M.A. profession had to deal
Diplomate, American Board of Endodontics with.
What does the literature show? How I will proceed!

Bader et.al 1995 JADA estimate 1 in 20 people
fracture a tooth a yr. New definitions from 2015!
Diagnostic tests
Krell and Rivera 2007 JOE 796 of 8175 cases (9.7%)
cracked teeth Etiologies
mandibular 2nd molars (30%) > mandibular 1st Treatments
molars (29%) > maxillary 1st molars (21%)
Outcomes
Tsesis, et al. 2010 JOE unable to do a systematic Prevention??
review for VRF!
What is a cracked tooth versus a

REPORT TO THE BOARD OF DIRECTORS
root fracture?
Annual Meeting May 4-5, 2015
SPECIAL COMMITTEE ON CRACKED TOOTH
INITIATIVE

Louis H. Berman, Chair
Scott L. Doyle
Gary G. Goodell
Keith V. Krell
H Mark A. Odom, Board Liaison
Helen Jameson, Staff Liaison
1
Cracked tooth definitions:
AAE Glossary: A phenomenon involving posterior teeth in

which fractures usually involve the marginal ridges;
primarily in minimally restored mandibular first and second
molars; symptoms may vary but pain to chewing and
thermal sensitivity are common.
Issues: There are a number of problems with the
definition. First, a cracked tooth is not a phenomenon.
The 2008 Colleagues for Excellence article states that,
cracks present in teeth are findings only; they are not to be
considered a pulpal or periapical diagnosis. Second, the
definition does not differentiate a crack from a fracture.
Third, describing where they occur on a tooth and on what
type of teeth they occur is too specific and limiting.
New Definitions from 2015! New Definitions from 2015!

Cracked tooth A thin surface disruption of Root fracture A fracture that exists or extends
enamel and dentin, and possibly cementum, of into the root, to include dentin, cementum, and
unknown depth or extension. possibly pulpal space, which may progress to or
from the enamel.
Longitudinal fracture A root fracture
extending in the axial plane within the tooth.
New Definitions from 2015! New Definitions from 2015!

Longitudinal fracture A root fracture extending in Longitudinal fracture A root fracture extending in
the axial plane within the tooth. the axial plane within the tooth.
split root A continuation of a crack or vertical vertical root fracture A fracture in the root
whereby the fractured segments are
root fracture whereby the fractured segments are
incompletely separated; it may occur buccal-
completely separated longitudinally; it may occur lingually or mesial-distally; it may cause an
buccal-lingually or mesial-distally; it may cause an isolated periodontal defect(s) or sinus tract; it
isolated periodontal defect(s) or sinus tract; it may be radiographically evident.
may be radiographically evident.
2
CTS Cracked Tooth Syndrome
CTS This term is a misnomer
Since syndrome is defined as A number of
symptoms occurring together and characterizing a
specific disease
A crack is NOT a disease nor is it a pathological entity
But cracks may become portals for bacteria and
subsequent diseases:
o Pulpitis reversible or irreversible
o Pulp necrosis and infection the root canals
o Periodontitis lateral and/or apical
What are predisposing features

What is really the resulting in a cracked tooth?
difference?
The difference between cracks and
fractures are a matter of degrees of severity.
However, the etiology may be very different.
REPORT TO THE BOARD OF DIRECTORS Survey AAE Members Perceptions

Annual Meeting, April 4-5, 2016 on RC/F
941 of 5204 members responded
THE SPECIAL COMMITTEE ON METHODOLOGY
OF CRACKED TOOTH STUDIES Half the participants (49%) perceived that
occurrence of RC/F in the past decade increased
Dr. Shimon Friedman, Chair compared to previous years
Dr. Amir Azarpazhooh Majority of participants (72%) agreed that
Dr. George Bruder occurrence of RC/F in root-filled teeth was a
Dr. Keith V. Krell, Dr. Isabel Mello major concern in endodontics
Dr. Donald Nixdorf 58% agreed it should be a priority to revise
Dr. Robert S. Roda, Board Liaison endodontic treatment protocols so as to mitigate
Helen Jameson, Staff Liaison the risk of RC/F
3
How do we diagnose a cracked tooth Diagnostic Tests
or vertical root fracture? Cracked Teeth!
Start with the dental
history!
A good dental history can be important ,
especially, if a recentbiting event has occurred
and they felt something pop!
Patient comments of pain when chewing,
pain upon release, or pain when I hit the tooth
a certain way all suggest a crack.
Fillings that keep falling out
Diagnostic Tests Diagnostic Tests

Cracked Teeth! Cracked Teeth!
The Tooth Slooth for a directed bite test Transillumination-

Cracked Teeth! Cracked Teeth!
Magnification-
Restoration Removal Dyes Probing
4
Diagnostic Tests Clinical Criteria for
Diagnostic Tests High Confidence of fractured roots
Root Fractures THE SPECIAL COMMITTEE ON METHODOLOGY OF CRACKED TOOTH
Location: Roots STUDIES
Direction: Facial-Lingual, mesial-distal Triggered biting pain
Orientation: Root, extending coronal and apical
Symptoms: Usually none, may present as a Swelling
periodontal problem One or more sinus tracts
Signs: Variable Percussion sensitive Mobility
Radiograph: Bone loss pattern
CBCT: Study dependent and load dependent Root crack associated with probing is visible with or without
Probing: A sudden increase in probing magnification
depth can suggest VRF when all other probings Probing greater than 6 mm
are normal
ID: Visualization, flap reflection Conventional radiographs
Treatment: Removal of the fractured root Visible fracture or separation of root
Prognosis: Hopeless, but not all the time! J shape radiolucency
Small FoV CBCT imaging with visible fracture or separation of root

Root Fractures Root Fractures
Radiograph: Bone loss pattern with 2-D
radiographs Radiograph: Bone loss pattern with CBCT
Halo lesion, perilateral radiolucency, and
angular resorption of the crestal More accurate than 2D (Bernardes, R. 2009.
boneindicated a high probability of vertical OOORE)
root fractures in maxillary premolars.
Tamse et al. 1999 Oral Surg. Accuracy is Machine dependent (Metska, M.E.
et al., 2012 JOE)
Technique dependent- Double Scan TQ

(Bruno Azevedo, 2015)
A Tridimensional
Journey
Bruno Azevedo DDS MS

Board Certified OMFR
5
Baseline Wax
Double Scan Technique
6
No Wax Wax
Diagnostic Tests
No Wax Wax Root Fractures
Better visualization due
to fracture separation Probing: A sudden increase in probing
depth can suggest VRF when all other
probings are normal
Diagnostic Tests
Root Fractures
Visualization, flap reflection Etiliogies for Enamel cracks
Thermal Cycling
Pin Placement
Cementation of Inlays
Masticatory Forces
Age!
7
Etiologies-
Etiology
Cracked teeth
Enamel Crazings- From the definitions it is obvious there is a
Most likely Naturally occurring through normal mastication-
(Rivera and Walton 2015, Endo Topics)
difference of degrees of the extension of the
crack. This is determined by:
or
Thermocycling (Brown,72 JDR) -Magnitude of Stress experienced by the tooth
-Mechanical properties of remaining tissue for
resisting fracture
Arola,D et. al Microstructure and mechanical
behavior of radicular and coronal dentin
Endodontic Topics, 2012 pp30-51
Fatigue Crack Growth Fracture Toughness

Propagation life of a material or tooth is The ability to resist fracture caused by
comprised of the number of loading cycles extension of an existing crack.
required to propagate an existing crack to a Radicular dentin has greater fracture
critical length that facilitates bulk fracture. toughness than coronal dentin
Coronal fracture is related to orientation of
tubules to the force.
Arola,D et. al Microstructure and mechanical behavior
of radicular and coronal dentin Endodontic Topics, Arola,D et. al Microstructure and mechanical
behavior of radicular and coronal dentin Endodontic
2012 pp30-51 Topics, 2012 pp30-51
Etiologies-
Age of dentin! Cracked teeth
Age alone has been shown to be a significant Hydration of dentin
factor in dentin fracture. Kishen, A. and S. Vedantam (2007). "Hydromechanics in dentine: Role of dentinal tubules and
hydrostatic pressure on mechanical stress-strain distribution." Dent Mater.
Dentin from patients < 35 vs >55 shows a 50% External compressive loads were conteracted by the
reduction in strength of >55 residual stresses and strains loads.
Dentin from patients < 35 vs >55 shows 75% Hydrated specimens showed greater toughness vs
reduction in energy require to FX >55 partially dehydrated specimens. The stress at
fracture was significantly higher in Dehydrated
>55 has greater mineral content and avg rate specimens than in partially dehydrated specimens
of crack growth 100 X that of <35.
Arola,D et. al Microstructure and mechanical behavior Strain at fracture was significantly higher in hydrated
of radicular and coronal dentin Endodontic Topics, dentine specimens (p=0.037).
2012 pp30-51
8
Etiologies-
Etiologies
Cracked teeth
Cracked teeth
Hydration of dentin
IATROGENIC CONSIDERATIONS
Kishen, A. and S. Vedantam (2007). "Hydromechanics in dentine: Role of dentinal tubules and
hydrostatic pressure on mechanical stress-strain distribution." Dent Mater. Orofacial piercings, Chadwick, et al. 2005. Prim. Dent. Care
SIGNIFICANCE: These experiments highlighted the distinct role

of free water in the dentinal tubules and hydrostatic pressure
on the stress-strain distribution within the bulk dentine.
Etiologies Etiologies
Cracked teeth Fractured roots
Stress from occlusal forces
IATROGENIC CONSIDERATIONS
Pin Placement (Standlee et al.,1970, JPD)
Canal preparation
Cavity preps (Reeh, et al., 1989. JOE,) Physical
Endodontic procedures have only a small effect on the tooth, Chemical
reducing the relative stiffness by 5%. This was less than that of an
occlusal cavity preparation (20%). The largest losses in stiffness Lateral condensation of gutta percha
were related to the loss of marginal ridge integrity. MOD cavity Expansion of root fillings
preparation resulted in an average of a 63% loss in relative cuspal
stiffness. Cementation of posts
Fractured roots Fractured roots
Stress from occlusal forces Stress from occlusal forces
Yang S.F., Rivera, E.M., Walton, R.E. 1995. Chan C.P., et al. 1998. JOE.
Vertical root fracture in nonendodontically
treated teeth. JOE.
9
Etiologies
Etiologies-Fractured roots
Fractured roots
Canal preparation technique Canal preparation: length-control
Adorno, C.G. et al. 2009. Int Endod. J
yes: Bier et al. 2009. JOE.
Length-control is critical
yes: Liu et al. 2013. JOE.
Fractured roots Fractured roots
Canal preparation technique Canal preparation technique
Tang, Wu, Smales. 2010. JOE.
Irrigants
Conclude: CaltS ,SerperA.Smear layer removal by EDTA. 2000 JOE
Irrigated with 5.25% NaOCl,2.5% NaOCl ,3% H2O2,
Overinstrumentation of root canals + noncircular 17%EDTA, All irrigants were found to reduced dentine
canals and thin canal walls= Increased risk for root surface hardness.
fracture.
Effect from various Ni-Ti rotary files is somewhat

controversial, but hand files have fewer FX
Etiologies
Etiologies-Fractured roots
Fractured roots
Canal preparation technique Lateral condensation of gutta percha
Saw, L.H., Messer, H.H. 1995. JOE.
Calcium Hydroxide,MTA NaOCl
WhiteJD,et al..The effect of three commonly used Obtura >Lateral condensation > Thermafil
endodontic materials on the strength and hardness of condensation
root dentin. 2002 JOE. Thermal expansion large part. Obtura and Thermafil
After 5 weeks 32% mean decrease in strength after groups was found to be thermal strain.
calcium hydroxide treatment,
33% decrease in strength after mineral trioxide
The mean load required to cause vertical root fracture
aggregate treatment, was five to six times higher than the load used in
59% decrease in strength after sodium hypochlorite obturation.
treatment
10
Etiologies-Fractured roots Etiologies-Fractured roots
Expansion of root fillings
Lateral condensation of gutta percha
Wilcox, L.R. et al. 1995. JOE. The Properties of Endocal10 and Its Potential
Impact on the Structural Integrity of the Root
Using a fine finger spreader and standard loads during
lateral compaction resulted in craze lines in all 34 maxillary Goldberg, R. et al., 2004. JOE.
incisor tooth specimens and root fractures when the root
canal diameter were enlarged to 40%50% of the total
root widths
No FX at 20-30% of total root widths
Etiologies-Fractured roots Etiologies-Fractured roots

Cementation of posts
Obermayr G. et al.1991. JPD.
Morando G. et al. 1995. JPD.
Treatments-
Treatments-
Cracked Crown/Root
Treatment depends on the severity of the Remember!! A crack is now a thin disruption of
crack or fracture. Split teeth/fractured roots enamel and dentin, and possibly cementum, of
unknown depth or extension.
are considered hopeless by most.
Ricucci D, et al. JOE 2015 concluded cracks are
Treatment planning for cracked teeth and always colonized with bacterial biofilms. The pulp
cracked roots becomes dependent on the tissue response varies according to the location,
clinical findings at the time of the discovery. direction, and extent of the crack.
Treatment planning for cracked crowns and
cracked roots becomes dependent on the clinical
findings at the time of the discovery.
11
Treatments-Cracked Crown/Root
Reversible pulpitis- no periodontal pockets
associated with the crack-
Crown it!
Krell and Rivera, 2007. JOE.
Around 20% will eventually need Rctx within
a yr.
Treatments-
Cracked Crown/Root
Reversible pulpitis- no periodontal pockets
associated with the crack
Sedative Lining and interim restoration
Abbott and Leow. 2009. Aust. Dent. J.
20 % eventually needed Rctx within 5yrs
Treatments- Treatments-
Cracked Crown/Root Cracked Crown/Root
Reversible pulpitis- no periodontal pockets Irreversible pulpitis- no periodontal pockets
associated with the crack- associated with the crack-
Bonded restoration N= 72 of 476 crowned were Dx cracked
Opdam, et al. 2008. JOE. (45/60) had IP symptoms=> root canal
7 % eventually needed Rctx within 5yrs treatment
Kim, et al. 2013.
75 % eventually needed Rctx within 5yrs
12
Treatments- Treatments-
Cracked Crown/Root Cracked Crown/Root
Irreversible pulpitis/necrosis- no periodontal Necrosis- no or minimal restoration and
periodontal pockets associated with the crack-
pockets associated with the crack- (fracture necrosis)
Resin filling, inlays or prov. crown Extraction!
Krell
Kang, Kim and, Kim. 2016. JOE. Berman and Kuttler 2010 JOE
--Retention!
50 % eventually needed Rctx within 5yrs Kang et. al. 2016 JOE
Berman
Multivariate analysis revealed a weak correlation

between multiple crack directions and pulp necrosis at
initial examination
Cracked Tooth
Reversible Irreversible
Pulpitis Pulpitis Necrotic
Remove Restoration Remove Restoration

Evaluate Crack Root Involved Evaluate Crack
Extract
Initiate Root
Canal Treatment
Pulp Exposure
Temporary Restoration By Crack/Caries Crack Extends Crack
(SS band/temp crown) On Root or Floor Eliminated
Temporary Restoration
(SS band/temp crown)
Re-evaluation/Testing Re-evaluation/Testing
2-3 weeks 2-3 weeks
Symptoms Symptoms Symptoms Symptoms

Resolve Continue Continue Resolve
Re-evaluation Complete
Normal Necrotic Add 2-3 weeks Root Canal
Restoration Extraction Restoration

Onlay or Crown Recall Onlay or Crown
Evaluations
Treatment Treatments-
Blast from the past! Root Fracture
Remember!! Now, A fracture that exists or extends into the root, to
include dentin, cementum, and possibly pulpal space, which may
progress to or from the enamel.
JDR 2016 Vol 95, 5-6.
Hemisection
Teeth even compromised because of Root amputation
periodontal disease or endodontic problems
may have a longevity that surpasses by far that Extraction- last resort!!
of the
average implant (Carnevale et al. 1998; Hardt
et al. 2002; Lang and Zitzmann 2012; Salvi et
al. 2014; Klinge et al. 2015).
Giannobile and Lang, 2016
13
Treatments- Treatments
Root Fracture Root Fracture
Hemisection Root amputation
Herodontics in the 80s Herodontics in the 80s
Herodontics in the 80s Herodontics in the 80s
14
Treatments
Outcomes - changes in thinking!
Root Fracture (excerpts from Dr. Hargreaves Jan, 2016)
split tooth= Extraction
survival (a patient-centered outcomes) and
radiographic success (a clinician-centered
outcome)
levels of evidence may be only one way to measure
clinical relevance of research. An entirely alternative
approach is comparative effectiveness research (also
called pragmatic clinical trials)
Outcomes Outcomes
Reversible pulpitis+ restoration Irreversible pulpitis?- no periodontal pockets
80% survival without rctx associated with the crack
Krell and Rivera, 2007 JOE Ortho band + vitality tests=>200 Rctx + Cr
Abbott and Leow, 2009 Aust Dent J Sim, et al., 2016 JOE
The 5-year survival estimate in the absence
and presence of crack extension onto the
pulpal floor was 99% and 88%, respectively
Outcomes-Cracked crown/root with Outcomes-rctx-fractured root + root

root canal treatment resection=
50 teeth had a 85% survival rate (2 yrs) 92% survival over 12 yrs
Tan, Chen, Poon and Wong 2006 IEJ Basten CH. Ammons WF Jr. Persson R. 1996
88 teeth had a 90% survival rate (5 yrs) International Journal of Periodontics &
Kang, Kim and, Kim 2016 JOE Restorative Dentistry
(>6mm probings decreased survival)
15
Outcomes-Rctx+fractured root +
Prevention???
hemisection=
79% success over 1-7 yrs Physical anthropologists estimate tooth longevity
without modern care to be 30-40 yrs based on
Erpenstein H. A 3-year study of enamel wear patterns.
hemisectioned molars. 1983 Journal of Simon Hillson-Dental Anthropology 1996
Clinical Periodontology Average Life Expectancy USA Circa 1900
Men= 46.3 yrs
Women= 48.3 yrs.
Average Life Expectancy USA Circa 2016
Men=76.6 yrs
Women= 81.5 yrs
Summary Summary
The truth is we are all potentially outliving the structural Endodontics never abandoned the need to preserve the
limits of our natural teeth! natural dentition and we can reassert our leadership role
Endodontics is the specialty for definitively diagnosing as the only specialty devoted to preserving the natural
cracks and fractures! dentition!
Periodontists are re-examining their decades old shift to
implants and are again realizing the need to preserve the
natural dentition.
Summary
Are all fractured teeth Hopeless?
Maybe split teeth, but multi-rooted teeth
can survive, in part, if we want to put forth
the effort. Let us all respond to Dr.
Giannobles request to save the natural
dentition again!
Lets Make Endodontics Great Again!
16
Restoration of Endodontically
Treated Teeth
February 11th, 2017 Some Lectures are fun, some lectures are
Richmond, Virginia cruel,youll remember this one, because it is SO
Keith V. Krell D.D.S., M.S.,M.A.
Diplomate, American Board of Endodontics
cool!--Anonymous
How I will proceed!
What are the survival differences between Clinical Studies on Survival - Crowns:
vital vs RCT? Crowned, RCT teeth have similar survival
What makes Rctx teeth different from vital rates as crowned teeth with a vital pulp.
Valderhaug et al., 1997
teeth?
No significant differences were found between
Dowel and Cores in Rctx teeth. restorations on post and cores vs. restorations
on vital teeth.
Restorations for Rctx teeth.
De Backer et al., 2006
Summary and conclusions
Fate of vital pulps beneath a metal-ceramic crown or a

Clinical Studies on Survival - FPD bridge retainer.
Abutments: GS Cheung, S C Lai, RP Ng
Int Endod J 2005;38(8): 521-530.
Non-vital abutment teeth have decreased The survival of the vital pulp in teeth restored with a single-unit CMC was
survival rates. significantly higher (103/122=85%) than those serving as an abutment of a fixed-
fixed bridge (52/77=68%). Maxillary anterior teeth used as bridge abutments had a
Anterior abutments. higher rate of pulpal necrosis than any other tooth types.
Fernandes et al., The survival rates for pulp vitality were 84.4% (CMC) and 70.8% (BR) after 10 years,
Distal Abutments. 2001 and 81.2% (SC) and 66.2% (BR) after 15 years. The difference between the two
groups was significant.
RPD Abutments. Hochman et al., (Incidence of teeth requiring endodontics following single crown or fixed bridge
Cantilever FPD abutments. 2003 abutment is similar to need for endodontics following restoration of cracked teeth
with original diagnosis of reversible pulpitis.
Walton, 2003
DeBacker et al.,
2006
1
Are Endodontically Treated Teeth Are Endodontically Treated Teeth
Different? Different?
Primary factor in the decreased Loss of Tooth Structure:
fracture resistance of RCT teeth is the Reeh et al., 1989
Endodontic procedures reduce stiffness by 5% whereas MOD
loss of tooth structure: cavity preparation reduced stiffness by 60% in premolars.
Panitvisai & Messer, 1995
Architectural changes. Endodontic access led to significant 2 and 3 fold increases in
cuspal flexure as compared to MOD cavity preparations in
Loss of structural integrity. molars.
Gutmann, 1992
Schwartz et al.,
2004
Restoration of Endodontically Restoration of Endodontically

Treated Teeth Treated Teeth
Goal in restoring RCT teeth is to replace When the retention and resistance form is derived
missing tooth structure and restore the primarily from the core material, the retention and
structural integrity of the tooth. strength of the foundation restoration directly
This usually involves the placement of a core influence crown survival.
restoration or foundation to provide adequate Core retention and resistance form can be
retention and resistance form for teeth requiring provided by the remaining tooth structure or
extra coronal restorations. augmented by the use of a dowel (post).
Morgano and Brackett 1999

In RCT molars there is usually Anterior teeth and premolars: with
sufficient depth and width of the Molars: substantial coronal destruction
pulp chamber to provide adequate generally require a dowel (post).
retention and resistance of the core
foundation without a post. Their pulp chambers are too small to
Nayyar et al., 1980; Kane etOnlay,
al., or complete crown provide adequate R&R form for the
1990; Hunter et al., 1988; Goodacre core foundation material.
et al., 1994; Schwartz et al., 2004 Hunter et al., 1988; Schwartz et al.,
Amalgam core
2004
Gutta percha
2
Treated Teeth
Dowel and Core Foundations
Significantly less resistance to

Dowel Length:
Retention and Resistance:
shearing forces in premolars Equal to the clinical crown.
restored with coronal radicular Longer than the clinical crown.
amalgam foundations vs. teeth Equal to 1 1/3 the clinical crown.
restored with posts. Terminate way between the crestal bone
Christian et al., 1981; Kern et al., and the root apex.
1984 Goodacre and Spolnik 1995
Dowel and Core Foundations Dowel and Core Foundations
Dowel Length: Dowel Length:

Retention and Resistance: Posts that were greater or equal
1/2 of the root length. to the root length had 20-30%
2/3 of the root length. increase in retention vs. posts
4/5 of the root length.
that were the root or equal to
As long as possible without disrupting the
apical seal.
the length of the clinical crown.
Goodacre and Spolnik 1995 Johnson and Sakumura 1978

Post length >/= the crown length Minimum post length should be
provides better stress distribution in 9mm.
the root and increased resistance to
fracture. frac
ture
Fernandes and Dessai 2001 Turner 1982
Insufficient
post length
3

A marked increase in success In-vivo studies have suggested
rate was found when the post that clinical success of posts is
was equal to or greater than the directly proportional to post
length of the clinical crown. length.
Sorenson and Martinoff 1984 Morgano and Brackett 1999
Dowel Length - Summary: Dowel Diameter:

Apex of the post should be beyond the Maintain as much sound tooth
alveolar crest. structure as possible.
Post should be as long as possible
without violating the apical seal or Post should be no wider than 1/3 of
cause root perforation. root width.
Posts that are the root length give There should be at least 1mm of
greater rigidly. sound dentin remaining
Minimum post length ~ 9mm. circumferentially around the post
preparation.
Fernandes and Dessai 2001 Hunter and Flood 1989
Dowel Diameter: Dowel Diameter:

Post diameter should be controlled to Coronal and radicular dentin should be
preserve tooth structure at decrease the conserved.
risk of perforations and fracture. Post preparation should require
Tip should be < 1mm in diameter. minimal removal of radicular dentin
beyond the requirements of root-canal
treatment.
Goodacre and Spolnik 1995
Schwartz and Robins 2004
4
Dowel Configuration: Dowel Configuration -

Parallel sided posts more retentive than Summary:
tapered, but may be more likely to lead to Parallel, serrated, vented, and passive
root perforation. post produce the least stress and show a
Tapered posts may have the potential for lower frequency of root fracture.
increased root fracture via wedging action. Tapered posts show greater stress
concentration at the coronal shoulder and
Threaded posts are most retentive but less stress at the apex.
least desirable due to root fracture. Tapered posts without a positive vertical
Hunter and Flood 1989 stop on the core may cause a wedging
effect.
Fernandes and Dessai 2001
Dowel Configuration - Dowel Configuration Clinical

Studies:
Summary: No difference in failure rates between
Parallel sided posts more uniformly parallel sided and tapered post designs.
distribute stresses along their length
except at the apex where stress
concentration occurs. Assif et al.,
1993
Active (threaded) posts have Robins et al.,
increased retention but exhibit 1993
unfavorable stress patterns on Walton, 2003
placement and during function.
Dowel Configuration Clinical Dowel Materials:

Studies: Metals, carbon fiber, ceramic, woven
No difference in tapered custom cast post and
core foundations and parallel sided preformed fiber composites.
cast post and cores in teeth restored with a Post should have the same modulus of
2mm ferrule. elasticity as the root dentin.
Overall success rate of 98% over 8 years.
Rigid posts are capable of resisting
greater forces without distortion.
Ellner et al., 2003
5
Dowel Materials: Dowel Materials - Fiber Posts:

Literature provides conflicting results More flexible than metal with
regarding post materials. approximately the same modulus of
However metal posts have superior elasticity as dentin.
mechanical properties and are time May allow forces to be more evenly
tested. distributed through the root.
Fernandes and Dessai 2001 Schwartz and Robins 2004
Dowel Materials Fiber Dowel Materials - Ceramic

(flexible) posts: (Zirconia) Posts:
May allow micro-movement of the core.
Used for increased esthetics
Problems with composite core retention
Resulting in increased microleakage and combination was not considered
under the crown and failure. clinically acceptable.
Morgano and Brackett 1999 Retrieval is very difficult and should be
Schwartz and Robins 2004 avoided.
Butz et al., 2001
Dowel Materials - Ceramic Posts: Dowel Materials In-vitro

Influence of post and cores on light
transmission through different all ceramic
studies:
crowns. Studies using continuous loading to
Spectrophotometric difference in chroma and catastrophic failure are mixed but slightly
luminance with the all ceramic posts and cores more favorable toward metal posts.
in the cervical to middle thirds. Studies using cyclic loading are also mixed
No significant differences were detected with metal posts performing slightly better as
among the different crown post and core well.
combinations under clinical observation. When looking at failure modes, fiber posts
result in more restorable types of failure.
Carossa et al 2001 Schwartz and Robins 2004
6
Dowel Materials In-vitro studies: Dowel Materials In-vivo studies:

Naumann et al., 2005:
Fracture resistance and failure mode of
6.7% annual failure rate with of fiber
premolars restored with crowns, with a limited reinforced post restorations observed for 5
ferrule, was independent from the post-and- - 56 months.
core systems (cast post-and-cores, 45% of the failures were due to post
prefabricated metal posts, prefabricated glass fracture.
fiber posts, and custom-made glass fiber 29% of the failures were loss of retention.
posts). Incisors and canines had 3 fold higher
failure rates than premolars and molars.
Wietske et al., 2006
Dowel Materials In-vivo studies: Dowel Materials In-vivo

King et al., 2003 (prospective clinical
trial):
studies:
CFRC posts did not perform as well Segerstrom et al 2006 (retrospective
as conventional wrought noble alloy clinical trial):
posts.
25% failure rate for CFRC Teeth restored with carbon fiber posts
endodontic posts. had shorter survival times than those
9% failure rate for conventional gold of cast posts after a mean
alloy cast post and cores. observation time of 6.7 years.
Dowel Materials In-vivo studies: Dowel Materials Meta-

Bolla et al., 2007 (Cochrane analysis Cohort studies:
Systematic Review) The pooled survival rate was 90% (95%
Evaluated the clinical effectiveness of carbon confidenceinterval, 85.593.3) for metal-based posts and
fiber posts vs. cast post and cores.
83.9% (95% confidence interval, 67.692.8) for fiber-
Of the 52 studies identified, only 1 study of
200 people fit their inclusion criteria (Ferrari et reinforced posts. The overal incidence rate of root
al., 2000). fractures (catastrophic failures) was similar between
Concluded that there is weak, unreliable metal and fiber posts. Prefabricated metal posts and
evidence that carbon fiber posts have fewer carbon fiber posts had a 2-fold increase in the incidence
failures after 4 years than metal-cast posts. rate of root fractures compared with cast metal posts and
glass fiber posts, respectively.
Figueiredo et.al.JOE 2015
7
Direct Core Materials: Direct Core Materials:

Amalgam, Composite, Glass-ionomer, Ceramic.
Amalgam: Adequate strength; good sealing Amalgam
capacity; delayed preparation.
Material of choice in high stress
Composite: Adequate strength; rapid set;
immediate preparation; poorer sealing areas and with minimal remaining
capacity. tooth structure (<1mm) due to:
Glass ionomer: Inadequate strength.
Decreased microleakage.
Hunter and Flood 1989
Increased compressive strength and
rigidity.
Tjan and Chiu 1989;
Direct Core Materials: Direct Core Materials: Composite

Most popular material.
Amalgam Acceptable core material when substantial
Problems: coronal tooth structure remains.
Esthetics, delayed crown preparation, lack High tensile strength, can be bonded and
of bonding to remaining tooth structure. prepared immediately.
Good esthetics.
Schwartz and Robins 2004 Morgano and Brackett 1999; Schwartz and
Robins 2004
Direct Core Materials: Direct Core Materials: Glass Ionomer

Composite Not acceptable for a core foundation.
Lacks adequate strength and fracture toughness.
Problems: Highest rate of defects.
Polymerization shrinkage, hydrophilic Morgano and Brackett 1999
nature; poor adhesion to pulpal dentin; Bonilla et al., 2000
requires strict isolation. Fernandez and Dessai 2001
Less desirable when there is limited Schwartz and Robins 2004
supporting dentin.
8
Dowel and Core Foundations
Treated Teeth
Direct Core Materials:
Teeth restored with amalgam cores and
Ferrule Effect
prefabricated posts had significantly lower The design and fabrication of the final
failure rate (33%) than teeth restored with restoration that surrounds the tooth
composite (83%) or reinforced glass ionomer
(100%) and prefabricated posts. protectively.
Reinforced glass ionomer did not have An essential important part of the
adequate strength to withstand simulated crown preparation for endodontically
occlusal forces. treated teeth.
Kovarik et al. 1992 Eissman and Radke 1987

Ferrule Height: Ferrule Effect

1-2 mm Hoag and Dwyer 1982 Post design did not influence
1 mm Sorenson and resistance to fracture if the core was
Engelman 1990 covered with a complete cast crown
> 1.5 mm Libman and Nicholls that extended 2 mm apical to the finish
1995 line of the core.
Assif et al. 1993

Ferrule Effect Ferrule Effect

Remaining dentin height" had a significant
No difference in tapered custom cast effect on the survival of post-and-core
post and cores and parallel sided restorations.
preformed cast post and cores in teeth The type of post and core was not relevant
with respect to survival.
restored with a 2mm ferrule. The remaining dentin height after
preparation most influenced the longevity of
a post-and-core restoration.
Ellner et al. 2003
Ferrule:
> 1.5 mm vertical
Creugers et al., 2005
tooth structure
9
Definitive restoration: Posterior Definitive restoration: Posterior

teeth teeth
There is convincing evidence that RCT teeth that were not crowned
cuspal coverage increases the survival following endodontic treatment were
of posterior RCT teeth. lost at a rate 6.0 times greater than
Sorenson and Martinoff 1984 teeth that were crowned controlling for
Hunter and Flood 1988 tooth type and caries at access.
Fernandes and Dessai 2001 Aquilino and Caplan 2002
Heydecke and Peters 2002

Definitive restoration: Posterior Definitive restoration: Anterior

teeth teeth
Not all anterior teeth require posts cores
The placement of a crown therefore and/or crowns.
appears more important that the type Teeth with minimal destruction (i.e., access
of foundation for the survival of RCT opening only or small class III cavity
teeth. preparations) can be restored with
composite resin materials.
Aquilino and Caplan 2002 Hunter and Flood 1988
Sorensen and Martinoff 1984

Definitive restoration: Anterior Clinical studies and systematic

teeth reviews:
Teeth with substantial coronal Overall success rate of 90.6% to
destruction generally require a post 98.5% for RCT teeth restored with
and core foundation to provide the tapered custom cast post and cores
necessary retention and resistance and complete-coverage crowns.
form for a crown. Bergman et al., 1989
Weine et al., 1991
Hunter and Flood 1989
10
Causes of Failure: Clinical studies and systematic

Primary Cause - Loss of retention reviews:
~5%. Post placement had no significant effect on
Secondary Cause - Root fracture ~3%. the success rate for either anterior or
posterior RCT teeth.
Mentink et al., 1993 Crown placement had no significant effect
Torbjorner et al., 1995 on the success of anterior teeth but
Goodacre et al., 2003 significantly improved the clinical success
rates of posterior teeth.
Sorenson and Martinoff 1984,1985

Clinical studies and systematic Clinical studies and systematic

reviews: reviews:
3-year prospective study on RCT teeth
restored with crowns. Anterior teeth restored with cast post-
Overall 5.5% failure rate. and-core foundations and a crown had
No difference between resin composite cores a higher risk of failure that similarly
with screw-type posts; parallel-sided restored posterior teeth.
cemented posts; or cast posts and cores.
Mentink et al., 1993

Hatzikyriakos et al., 1992


reviews:
Overall success rate 87.7%. reviews:
8% cumulative failure rate for parallel-sided Loss of retention was the most frequent type
Para-Posts. of failure.
15% cumulative failure rate for tapered Maxillary anterior teeth had a higher failure
custom cast post and cores.
rate.
Parallel-sided posts were significantly more
successful regarding failure rates and the RPD abutments and distal cantilever FPD
severity of failure. abutments had a higher failure rate.
Torbjorner et al., 1995 Torbjorner et al., 1995
11

reviews: reviews:
6 studies identified. 8-year prospective study on four P&C
Cumulative survival at 72 months (6 years) combinations.
ranged form ~86% to ~92%.
Overall success rate of 98%
The lack of consistency of the clinical data
makes it impossible to deem either cast or No difference in tapered custom cast post
direct post and core restorations superior. and core foundations and parallel sided
Heydecke and Peters 2002 preformed cast post and cores in teeth
restored with a 2mm ferrule.
Ellner et al., 2003


reviews: reviews:
15-year longitudinal study. Clinical evaluation of a carbon fiber reinforced
Evaluated 515 FPDs involving 1209 carbon endodontic posts.
abutments.
CFRC material and a composite resin luting
No difference in failure rates between parallel
agent do not perform as well as conventional
sided preformed stainless steel serrated
posts and cast-gold alloy posts. wrought precious alloy posts.
King et al., 2003
Walton 2003


reviews: reviews:
5-year prospective clinical trial.
Overall survival was 96%. The type of post and core was not relevant
No difference was found between the with respect to survival.
survivals of the different types of restorations. The amount of remaining dentin height after
Remaining dentin height had a significant preparation influenced the longevity of a post-
effect on the survival of post-and-core and-core restoration.
restorations.
Creugers et al., 2005 Creugers et al., 2005
12

reviews: reviews:
Comparison of composite post and cast gold Cochrane Systematic Review.
post-and-core foundations. There is weak evidence from one clinical trial
8.5 year observation period. of 200 people that carbon fiber posts have
No statistically significant differences could fewer failures after 4 years than metal-cast
be found regarding survival and complication posts, but the evidence is unreliable.
rates.
Bolla et al., 2007
Jung et al., 2007

Summary of key findings: Summary of key findings:

RCT teeth have a higher risk of failure. Primary difference in RCT treated teeth vs.
Maxillary anterior teeth had a higher failure rate. vital teeth is due to the loss of tooth
RPD abutments and distal cantilever FPD structure.
abutments had a higher failure rate. Resulting in architectural changes and a loss of
structural integrity.


Posts primary function is to provide retention Post length should extend beyond the
and resistance for the core. alveolar crest and be as long as possible
Posts do not reinforce RCT tooth roots. without violating the apical seal (~5 mm).
Post diameter should be sufficient to resist
bending and preserve as much dentin as
possible.
13

Posterior RCT teeth have significantly higher The amount of remaining dentin height after
survival rates with coronal coverage. preparation influences the longevity of a
Anterior RCT teeth may or may not require post-and-core restoration.
coronal coverage depending on amount of
remaining tooth structure.
Pratt et.al. JOE, 2016

Aquilino and Caplan, 2002
Restoration of Endodontically Questions?

Treated Teeth
Summary of key findings:

A 2 mm ferrule significantly improves
survival of RCT teeth.
In RCT teeth with a 2 mm ferrule and coronal
coverage the type of post and core is not
relevant with respect to survival.
14
Dr. Anibal Diogenes received his D.D.S. from the Federal University of Pernambuco
in Brazil, his M.S. in Molecular Biology from the University of Nebraska, and his Ph.D.
in Pharmacology and Certiicate in Endodontics from the University of Texas Health
Science Center at San Antonio. Dr. Diogenes is an associate professor and the
director of the endodontic residency program at the University of Texas Health
Science Center at San Antonio. His areas of research include pain, neuroscience and
regenerative endodontics. He is also an Associate Editor for the Journal of
Endodontics, past-President of the Pulp Biology of Regeneration Group of the
International Association of Dental Research and a Diplomate of the American
Board of Endodontics.
REVIEW ON
REGENERATIVE ENDODONTICS
AND STEM CELLS
Anibal R Diogenes, DDS, MS, PhD

diogenes@uthscsa.edu
REGENERATIVE
ENDODONTICS
Biologically-based
procedures designed to
replace damaged
structures, including
dentin and root
structures, as well as
cells of the pulp-dentin
complex
PIONEER STUDY
In general pathology and in surgery the significance of
the Male
29yo bloodwithclot has
pulpal Fibrous C.T.
been recognized.Therefore
necrosis, it seems
bleeding
strange established
that in endodontic treatment bleeding is more or
less looked upon as a complication to be feared.
Pre-op 14 months
2mm
The present investigation may be said to introduce a
Cementum
biologic view of the treatment problems: the utilization of
the growth potentials of the body.
The organization of the blood clot in the apical

periodontium and in the root canal may be directly
Open
compared Just before
with wound healing.
Apex extraction
Collagen Bundles
Nygaard-Ostby in main canal
Acta Odont Scan 19:323, 1961
THE BLOOD CLOT AND
WOUND HEALING
Haemophilia
pages 11-16, 4 JUL 2012 DOI: 10.1111/j.1365-2516.2012.02889.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2516.2012.02889.x/full#f1
Continued Development of
Re-implanted incisors
Revascularization of Re-Implanted Human Incisors
% Pulpal Healing
Pulpal Healing
= + EPT/Ice
Narrowing or obliterat
RC space
N = 66
Andreasen et al., EDT 11:59, 1995
Continued Development of
Re-implanted incisors
Revascularization of Re-Implanted Human Incisors
% continued development
without disease
Revascularization
= continued development
of root and pulp lumen
without PARL
N = 159
Kling et al., EDT 2:83, 1986
Mature teeth can revascularize
after autotransplantation
Remove pulp
Apicoectomy
Re-implant the tooth
No difference in
revascularization between
mature apicoectomized and
immature teeth
Emphasizes the importance of
an open apex
Revascularization
within 18 days
Laureys et al. Am J Orthod Dentofacial Orthop 119:346, 2001.
IN THE 2000S
Used Double Antibiotic

(Ciprofloxacin and
Metronidazole)
Pre-op 5mo 30mo

Iwaya et al., 2001
Used Triple Antibiotic
(Ciprofloxacin,
Minocycline and
Metronidazole)
Pre-op 18mo
Banchs and Trope 2004
IN THE 2000S
Used Double Antibiotic

(Ciprofloxacin and
Metronidazole)
More than 300 published

Pre-op cases in30mo
5mo the
literature nowadays
Iwaya et al., 2001
Used Triple Antibiotic
(Ciprofloxacin,
Minocycline and
Metronidazole)
Pre-op 18mo
Banchs and Trope 2004
HEALTHY YOUNG PULP HAS
REMARKABLE REGENERATIVE POTENTIAL
10yo boy 2 years later
Dx Necrotic pulp; Dx : normal pulp

symptomatic apical Periodontitis normal periradicular tissues
STAGES OF ROOT
DEVELOPMENT
% of 95% 85% 73% 46%

participants
Diogenes and Ruparel , 2016. Dent Clin North Am (in press)
ROOT FORMATION
ARE REPS STEM CELL-BASED
THERAPIES?
ARE REPS STEM CELL-BASED
THERAPIES?
ARE STEM CELLS DELIVERED INTO
THE RC SYSTEM?
Local
Stem
Cell
Delivery
Lovelace et al., JOE 2011

ARE STEM CELLS DELIVERED INTO
THE RC SYSTEM?
Lovelace et al., JOE 2011

ADD VAMPIRE 2!
BLEEDING IN REPS
No Bleeding Bleeding
23%
77%
Kontakiotis EG. et al., 2014. J Endodon
STEM CELLS
Cells with the ability to divide for indefinite periods in culture and to
give rise to specialized cells (NIH)
1- Self Renewal
2-Differentiate into
more specialized cells
SCAP
DIFFERENT POTENCIES
OF STEM CELLS
Totipotent can make all cells in a body plus the

extraembryonic cells that are required for maintenance of
life, such as the plascenta
Example: Embryonic cells up to 2 cell divisions after fertilization
Pluripotent-can make all cells in a body (all three germ
layers).
Example : Embryonic cells and induced pluripotent cells (iPSCs)
Multipotent can develop into more that a cell type (from a
single germ layer) but not all cells in a body
Example : Adult stem cell (including all oral stem cells ) and
cord blood stem cells
2008 Science Breakthrough of the Year
Reprogramming
adult cells into
stem cells by switching
2012 Nobel Prize in the activity of four genes
Medicine
MESENCHYMAL STEM CELLS
Oh and Nor , 2015. Front Physiol

A 56 yo german male underwent
semi-total madibulectomy
Disfigured and unable to have a

solid meal for 9 years, he demanded
reconstruction
36th week after transplantation
Warnke et al. Lancet 2004; 364: 76670

Warnke et al. Biomaterials 27 (2006) 31637
Stem cells gave rise to newly formed dentin,
periodontal ligaments and bone. A porcelain
crown could be retained for 3 months under
normal functional loading cemented to a
bioengineered root.
Sonoyama et al. PLoS one. 2006. 1:e79

First clinical trial to evaluate the use of dental stem cells in regenerating bone.
60.71% greater bone regeneration was detected in the test site as compared
to its contralateral control by blinded observers. Histological evaluation of punch
biopsies revealed a more organized and dense regenerated bone than control samples
3rd molars extracted

DPSC isolated and sorted
Collagen gel only in C sites
Collagen + Stem Cells in T sites
N=7
Regeneration Control
STEM CELLS LIKELY INVOLVED
IN REPS
BMSCs: Bennet et al., 1991 ( J Cell Sci)
DPSCS : Gronthos et al., 2000(PNAS)
PDLSCs: Gronthos et al., 2000 (PNAS)
SCAP: Sonoyama et al., 2006 ( PLoS One)
DPSCs IPAPCs: Liao et al., 2011 ( J Endodon)
SCAP
BMSCs
PDLSCs
iPAPCs
Diogenes et al., Endodontic Topics 2013

SCAP: Stem Cells from Apical Papilla
SCAP Expresses STRO-1
Continued Root Development After NSRCT
Differences
This case supports periapical source of

Stem cells since RC system was obturated
Pre-Op Post-Op 3m 7m
Sonoyama et al., JOE 34:166, 2008

Huang et al., JOE 34:645, 2008
Apical Papilla
Apical Papilla Survival and Apical
Periodontitis
J Endodon, 2014
Surviving Apical Papilla Substantial

Inflammatory
90 days after pulpal exposure Infiltrate within the
apical papilla
Complete Liquefaction Necrosis

of the pulp
How can the apical papilla survive
infection and apical periodontitis?
Apical Papilla
Dental Pulp
6
***
5
Relative Density
4 **
3
0
Innervation Blood Vessels
Diogenes et al., 2013. Endodontic Topics

DOES THE APICAL PAPILLA
Mechanical Disruption of Apical Tissues
SURVIVE THE INFECTION?
Chrepa, Pitcher and Diogenes, 2017 ; J Endodon (in press)

A DELICATE BALANCE
Healing/Repair Persistent Pathosis
o b i al
M ic r d
n s a n
e
antig onic
chr tion
m m a
in fl a
c ti o n
i n fe
Dis C e ll
Stem ival,
Sur v iation
r e n t
Diffe
Diogenes, Chrepa and Ruparel. In Waddington and Sloan, 2016 (in press)
A COMPLEX INTERACTION
Smith et al., 2016. J Endodon

HOW IMPORTANT IS
DISINFECTION IN TREATING
IMMATURE TEETH?
2009
No AP AP
100
100 N=78
75
78
% Success
50
25
0
Apexification
2015
PERSISTENT BIOFILMS ASSOCIATED
WITH LACK OF REGENERATION/REPAIR
Verma et al (Fouad) , 2016-JDR

THE IMMATURE TOOTH
Challenges
Mechanical Instrumentation is contra-indicated

due to already thin fragile dentinal walls.
Large canals harbor large concentration of
microorganisms
Young immature teeth are more susceptible to
bacterial colonization
Advantages
Root canal anatomy is less complex

Larger volume improves fluid dynamics of
solutions and greater medication reservoir
Young healthy individuals
Greater vascularity and angiogenic potential
Is the microbial flora different ?

2014
N=15; Traumatized teeth
Actinomyces naeslundii
Porphyromonas endodontalis
Parvimonas micra
Fusobacterium nucleatum
Porphyromonas gingivalis
Prevotella intermedia
Tannerella forsythia
Filifactor alocis
Treponema denticola
0 17.5 35 52.5 70
% incidence
BACTERIAL INVASION
N=28 extracted teeth/
group
Young=18-25 yo
Old=>60 yo
Young Old
Kakoli et al (Fouad), 2009 J Endodon

DENTIN, A RESERVOIR OF GROWTH
FACTORS
TGF1 Expression (% Increase)
Dentin Matrix Extract (ug/ml)
Graham et al.,
Biomaterials 27:2865, 2007
Smith J Dent Ed 67:678, 2003
SHED in a PLL scaffold
DENTIN CONDITIONING
MATTERS
5%NaOCl:
resulted in lack of odontoblast-like
cells and presence of clastic cells
17% EDTA:
resulted in well-organized tissue with
odontoblast-like cells lining the
dentinal wall
Galler et al., 2011, J Endodon

2015
2016
NaOCl+EDTA
EDTA
2016
Disinfectants
Medicamen Bioactive
Irrigants
ts Molecules
STEM
DENTIN
CELLS
MOST COMMONLY USED
IRRIGANTS
CHX
Diogenes et al., 2013. Endodontic Topics

Trevino et al., 2011
WHAT CONCENTRATION OF
HYPOCHLORITE SHOULD BE USED?
Martin et al., J Endodon 2014

DENTIN CONDITIONING WITH NAOCL
DECREASES ODONTOBLASTIC DIFFERENTIATION
Martin et al., J Endodon 2014

Stem Cell Survival (% max)
50
100
1.5
3
Hypochlorite Concentration %
6
OVERALL EFFECT
50
100
Odontoblastic Differentiation (% max)

SODIUM HYPOCHLORITE VS
STEM CELLS
5 or 6 % NaOCl
Prevents SCAP survival and differentiation in an organotype root

canal model (Trevino et al., 2011 and Martin et al 2014)
Prevents odontoblastic differentiation and co-determines MSC fate in

vivo (Casagrande et al., 2010; Galler et al., 2011)
Deleterious effects are partially reversed by EDTA
Denatures growth factors in dentin (Zhao et al, 2000)

GROWTH FACTORS
RELEASED BY DISINFECTANTS
Transforming growth factor beta (TGF-
b)
Basic fibroblast growth factor (bFGF)
Vascular endothelial growth factor

(VEGF)
Bone morphogenetic proteins (BMPs)
Insulin-like growth factor (IGF-1 and -2)
Platelet-derived growth factor (PDGF)
Placenta growth factor (PIGF)

Roberts-Clark DJ., et al 2000
Smith AJ. et al., 2012
Hepatocyte growth factor (HGF) Ferracane JL. et al., 2013
Epidermal growth factor (EGF) Galler et a., 2015
Disinfectants
Medicamen Bioactive
Irrigants
ts Molecules
STEM
DENTIN
CELLS
INTRACANAL MEDICAMENTS
Ciprooxacin, minocycline and Ciprooxacin and metronidazole
metronidazole (Double An7bio7c Paste; DAP)
(Triple An7bio7c Paste; TAP)
Ca(OH)2
Diogenes et al., Endo Topics 2013
USE OF ANTIBIOTIC PASTE
Not a new concept in Endodontics, several

formulations have been used for decades in root
canal therapy.
The combination of metronidazole, ciprofloxacin

and minocycline (Triple Antibiotic Paste, TAP) was
introduced by Dr. Hoshino in 1990s.
1.5mg total of drug mixture was placed in
extracted teeth inoculated with E. coli
directly on plates (25mg/ml) and it was
found to sterilize canals
The medication penetrated 1mm and
killed bacteria into tubules
Teeth were deemed sterile after 48hrs
Exposed to a dynamic
concentration medicaments for
3 days
Characterized SCAP cell line

Live cell counting
(Ruparel et al 2013-J Endodon)
DIRECT EFFECT OF INTRACANAL
MEDICAMENTS ON SCAP SURVIVAL
Ruparel , Teixeira, Ferraz and Diogenes. 2012 J Endodon

CALCIUM HYDROXIDE IS
CONDUCIVE TO STEM CELL SURVIVAL
Ruparel , Teixeira, Ferraz and Diogenes. 2012 J Endodon

ARE LOWER CONCENTRATIONS
OF ABS ANTIMICROBIAL?
MBC for TAP =0.3mg/ml

MBC for DAP= 0.14mg/ml
Clinically used concentrations as a paste slurry are ~3,000 to 10,000

times greater than concentrations found effective against bacteria
Reyhani et al., 2015; JODDD
1 wk 2 wk 3 wk 4 wk
300
225
Bacterial CFU
150
75
0
1,000 100 10 1 0.1 0.01 saline
Concentration of TAP
Is the Diluted Antibiotic Paste still effective ?
1mg/ml has minimal cytotoxicity agains stem cells and excellent

effectiveness agains bacteria =more selective concentration
Indirect Effect of Medicaments on SCAP
survival
SCAP in GFR
Matrigel Cell Counting
+
Add cover o
7 days culture
Standardized dentin slices

Pre-treated (conditioned)
with medicaments
(7 or 30 days)
Followed by irrigation with 1.5%
NaOCl and 17% EDTA
Indirect Effect of Medicaments on SCAP
survival
SCAP in GFR
Matrigel
Dentin slices
Pre-treated
(conditioned)
with medicaments
(7 days)
7 days culture
Cell Counting
Althumairy RI, Teixeira FB, Diogenes A ., 2014 J Endodontics

EDTA
Ca(OH)2
10mg/ml demonstrated the best results in killing E. faecalis
(panel B)
How well do we remove TAP from root canal
systems?
ADD COVER OF JULIEs PAPER
Berkhoff et al., (Diogenes Lab )2014 J Endodon

How well do we remove TAP from root canal
systems?
Incorporate I125 into TAP
100
80
% of labeled-TAP removed
28 days 60
40 n.s
Irrigate groups
(NaOCL, EDTA) 20
0
Measure radioactivity Maxiprobe Activator EndoVac PUI
Irrigant collection vs.
Remaining radioactivity
How well do we remove Ca(OH)2 from root
canal systems?
Incorporate Ca40 into TAP
28 days
Irrigate groups
(NaOCL, EDTA)
Measure radioactivity
Irrigant collection vs.
Remaining radioactivity
OTHER STUDIES THAT HAVE
INVESTIGATED THE REMOVAL OF TAP
Impossible to remove TAP from canal. Passive ultrasonic irrigation

was better than other treatments (Arslan et al., 2014. J Endodon)
Not possible to remove TAP from canals. Ultrasonic activation of

NaOCl works better thank use of CHX Ok et al., 2015 Scanning
Canal brush and sonic activation provide better removal but do

not remove TAP, particularly from the apical third (Thakur et al.,
2015. Cont Clin Dent)
Antibiotic Paste Studies
! These medicaments should not be used as as thick

slurry. Instead, concentrations of 1 to 10mg/ml should
be used, if required.
! So far, Ca(OH)2 appears to be the most compatible

antibacterial intracanal medicament for stem-cell
based therapies.
DISINFECTION ADJUVANTS
Use of Negative Pressure (Da Silva et al., 2010; OOOOE)
Use of Passive Ultrasonic Irrigation (Galler et al., 2016;Clin

Oral Invest )
Photodynamic disinfection (Johns et al., 2015- J Con Dent)
Chitosan Nanoparticles (Shresta et al., 2016; J Endodon)

Overview of Current Procedures
EVALUATION OF OUTCOMES
CLINICAL VS SCIENTIFIC
AAE CLINICAL GUIDELINES FOR
REGENERATIVE PROCEDURES
Clinician-Based Outcomes
TRI-LEVEL OUTCOME PYRAMID
Scientist-based Histologic
Evidence
of complete
regeneration
Clinician-based Radiographic healing

Radiographic Root Development
Positive Vitality Responses
Resolution of Disease
(absence of swelling, drainage and pain)
Patient-based Tooth Survival and Function
Tooth Esthetics
Diogenes, Ruparel, Yoav, Hargreaves. 2016 JADA

CASE REPORTS
More than 300 case have been published so far
Although they provide insight into what is possible and is done in

actual , the report is unilateral.
Results are often reported in a subjective fashion
Nonetheless, results from case series can be used to identify

potentially important parameters that can guide the design of
future prospective clinical trials
STANDARDIZING AND
QUANTIFYING
2009 2009
2014
2014
2009
2009
18 months for 30% root width gain

36 months for 30% root length gain
Resolu.on of Apical Periodon..s %
90
80
70 77% recall rate
N=18-22
60 No stat di between Regendo and MTA plugs
% Incidence
But signicant to ApexicaMon with Ca(OH)2

50
40
Regendo Group : MTA Group :
30 60% Dens Evaginates 21% Dens Evaginates
20 35% Trauma 58% Trauma
5% caries 21% caries
10
0
Regendo MTA plug Ca(OH)2
Healed 80 68.4 77.3
Healing 20 26.3 0
Failed 0 5.2 22.7
Jeeruphan et al. 2012. J Endodon
N.S
100
100 95
75
77
% Survival
50
25
0
Regendo MTA apex Ca(OH)2 apex
% gain Width
0
22.5
15
30
7.5
Re
ge
n
25
do
M
TA
0
ap
ex
Ca
(O
H
)2
1.5
ap
ex
% gain Length
12
16
0
4
8
Re
ge
n
15
do
M
TA
1.5
ap
ex
Ca
(O
H
)2
0.5
ap
ex
100
100
92
N=12
75 83
Prospective,
% of Healed
Randomized clinical trial

Blind observations
Standardized radiographs 50
Used RRA
25
0
MTA apex Regen Regen (Sca+Gro)
MTA
Root Width Gain Regen Root Length Gain
Regen(Sca+Gro)
0.4 1.4
0.3 1.05
Root gain in mm
Root gain in mm
0.2 0.7
0.1 0.35
0 0
3 6 12 18 3 6 12 18
months after Tx months after Tx
2014
100
90.3
16 cases treated with
standardized protocol 75
Most were traumatized
% Incidence
(62.5%) 67
Quantitative assessment of
62.5
50
root development was made
TAP and MTA were used
25
0
Healed Apical Narrowing Anasthetic Results
2014
2014
10 cases were quantified

Heterogeneity of responses
Small n no predictors identified
highlighted that quantification can be challenging
2016
N=10/group 9-13yo 14-18yo

0.7
Standardized Treatment
Increased in Thickness (mm)

and radiographic eval
groups : 0.525
9-13yo (n; <1mm apex)
9-13yo(w;>1mm apex) 0.35
14-18yo (n;<1mm apex)
14-18(w;<1mm apex)
0.175
Overall Healing of 94%

0
Narrow Wide
2016
9-13yo 14-18yo 9-13yo 14-18yo

1.3 0.7
Increased in Thickness (mm)

Increased in Length (mm)
0.975 0.525
0.65 0.35
0.325 0.175
0 0
Narrow Wide Narrow Wide
2014
1. Traumatized
cases seem to
have less
predictable root
development
Other reasons :
1. short follow up
2. varied protocols
3. case selection
bias
# of cases: 20
Recall: 12 months
Etiology: Trauma
2014
Revasc Apexification
100
95 100 100
n.s
Retrospective study n=12-19/group 75
Severe trauma as etiology= 78
% of Incidence
Revasc (32%); Apexification (8%)
50
42
25
11
0
Survival Healing Adverse events
Patient-Based Outcomes:
SUMMARY
Resolution OF HEALING
of Disease
93.9% average
Cehrelli et al
100% 2011
Chen et al 2012
Kahler et al
75% 2014
Nagata et al
2014
Jeeruphan et al
50% 2012
Nagy et al 2014
Saoud et al
25% 2014
Alobaid et al
2014
0%
Diogenes et al., 2016 .JADA
Regendo
SUMMARY
Clinician-Based Outcomes:
Continued Root Development
Studies that measured RRA
Apex
45
% Change in Root Width
40 Regen
35
30
25
20
15
10
5
0
-5
09
4
14
12
14
01
20
20
20
20
,2
.,
.,
.,
.,
l.
al
al
al
al
a
et
et
et
et
et
se
er
d
ag
ha
hl
uo
Bo
Ka
N
up
Sa
er
Je
PATIENT CENTERED OUTCOME-
ESTHETICS
Discoloration in Regenerative Endodontic Procedures:

Use of antibiotic pastes
Use of MTA (white and grey)*
Bleeding in esthetic zones
Discoloration can be avoided by:

Use of calcium hydroxide instead of antibiotic pastes
Use of non-staining pro-mineralizing materials (eg. Biodentine)
Bonding the coronal dentinal tubules in the chamber with a dental
adhesive
Discolored teeth can be bleached with walking bleaching techniques
Reynolds et al. 2009, IEJ,

Petrino et al.,2010, J Endodon
2016
medicaments Coronal Barrier

Discoloration Other
4%
Other
13%
Ca(OH)2
45% yes 19%

ProRoot MTA
MTA 36%
55% no TAP Angelous
68% 60%
Lenherr et al., 2012 IEJ
RESTORATIVE MATERIAL
STAINING
Staining with white MTA is worse with contact with blood (Felman and
Parashos, 2013; J Endodon)
MTA but not biodentine changes color in contact with dentin treated
with hypochlorite (Marciano et al., 2015; Clin Oral Investig)
MTA from different brands lead to coronal discoloration (Ioannidis et

al., 2012; IEJ)
MTA staining is worsened with curing light application (Valles et al.,

2013; Clin Oral Invest )
No Staining with Biodentine in human teeth (Valles et al., 2015; J

Endodon), but detected in bovine teeth (Beatty and Svec 2015; J
Endodon)
TRI-LEVEL OUTCOME PYRAMID
Scientist-based Histologic
Evidence
of complete
regeneration
?
Clinician-based Radiographic healing
Radiographic Root Development
Positive Vitality Responses
Resolution of Disease
(absence of swelling, drainage and pain)
Patient-based Tooth Survival and Function
Tooth Esthetics
Diogenes, Ruparel, Yoav, Hargreaves. 2016 JADA

HISTOLOGIC EVIDENCE
Scientist-Based Outcomes
OF
PULP REGENERATION
Re
ge
ne
R
No epa ratio
thi ir ? n ?
ng
??
?
SUMMARY OF HISTOLOGIC
Summary of Histological Findings
FINDINGS
Shimizu E., et al., 2013 Un-inammed CT, cementum- and bone-like
Necrosis; Chronic Apical Abscess Issue
Lin LM. et al., 2014 ResorpIon lacunae covered by cementum,

Previously iniIated; Acute Apical Abscess bone, bacterial biolm
Nosrat A., 2013 Empty canal

Necrosis; Acute Apical Abscess
MarIn G. et al., 2013 Un-inammed CT; cementoid- and osteoid-

like Issue
Necrosis; SymptomaIc Apical PeriodonIIs
Fibrous CT, acellular cementum, denIn

Becerra P. et al., 2014 spicules, bacterial cells
Necrosis; SymptomaIc Apical PeriodonIIs
Lei L. et al., 2016 Bone-like, cementum-like Issue, nerve cells

Necrosis; Acute Apical Abscess
Nosrat A., 2015 CT, bone, cementum

Normal; Normal
REGENERATION OR REPAIR
Guided-Endodontic Repair (GER) -Diogenes et al., 2016 JADA
AL PULP ?
FUNCTION VS HISTOLOGY
Arola et al., Int J Fatigue 2010

CLINICAL FUTURE FOR REPS
FUTURE EVALUATIONS
FUTURE EVALUATIONS
Other Advanced Imaging
Thank you for the
Attention!
Pain Management
Analgesics and Anesthetics
Anibal R Diogenes, DDS, MS, PhD
diogenes@uthscsa.edu
An unpleasant sensory
and emotional
experience associated
with actual or
potential tissue
damage, or described
in terms of such
damage. (IASP, APS)
Pain
and Achilles tendon rupture

CIP patient with multiple fractures
Shea and Showalter, 2003. J Bone Joint Surg; 85:1816-8

Orofacial Pain
Odontalgia Oral Lesions TMJ
Face/Cheek Burning Mouth 22% of the U.S population
3% suffers from some kind of
5%
orofacial pain
19%
44%
30% Lipton et al., JADA 124:115, 1993.

Anatomy & Physiology of Pain
Detection Processing Perception
A Fiber
C Fiber
Periphery N. Caudalis Cerebral

et al., Cortex
Trigeminal Nociceptive Pathway
Diogenes & Henry in: Seltzer and Benders Dental Pulp, 2012
Pain Perception
Brain Imaging Following Thermal Stimulation of Forearm with Innocuous and Noxious Temperatures
Thalamus
Pre-Frontal
Cortex
Coghill et al., 1999. J Neurophys
Dental Pulp Innervation
A B
MSN
PO
PI
C PC
Pain Detection
Dental Pulp Innervation
Fiber Function Size(um) Cond. Veloc (m/sec). % of total

innervation
A Pain, Temp. 2-5 12-30 25-50%
C Pain, sympathetic 0.5-1 0.5 2 50-75%
A Touch/Pain 5-10 35-70 ?
Most Sensory Neurons in Dental Pulp are
Myelinated, but Lose Their Sheath Coronally
All Fibers That are Stained with a Myelinated Marker (N52 in red) should
Also have staining for myelin (MBP in green). Uniquely, in the dental pulp this is an exception
Henry, Luo and Levinson. BMC Neuroscience 2012

Most Sensory Neurons in Dental Pulp are
Myelinated, but Lose Their Sheath Coronally
Uniquely in the dental pulp, unmyelinated fibers

have accumulation sodium channels (NaCh) in
nodes of Ranvier (seen as green staining for Casper)
Henry, Luo and Levinson. BMC Neuroscience 2012

Detection
(Polymodal Nociceptors)
Inflammatory Pain
Hyperalgesia
Allodynia
Hyperalgesia-Increased response to noxious stimulus (eg. Cold test and Symptomatic IP)
Alodynia-Painful response to a non-noxious stimulus (eg. Percussion test in Symptomatic AP)
Inflammatory Pain
Peripheral Amplification
Inflammatory pain
An inflammatory cocktail of
inflammatory mediators are present
in the dental pulp and periradicular
tissues.
These mediators (eg. TNF-, IL-1
and PGE2) sensitize the nociceptors
causing nociceptive firing to stimuli
not previously painful (Allodynia)
and/or exaggerated nociceptive
firing to noxious stimulus
(hyperalgesia)
Pain Processing
3-sites of possible intervention
In Hargreves & Conhens Pathways of the Pulp

Copyright 2001 Sinauer Associates, Inc.
Management of Intraoperative
Endodontic Pain
Effect of Root Canal Therapy on
Pain
Systematic review, n=421
Pak JG and White S . J Endod. 2011 Apr;37(4):429-38

Before TreatmentSuccessful
Anesthesia is needed
Dental Pulp
Anesthetic Challenges
Dental pain
N52affect approximately 12-14% of the
CGRP
populationTLR4
in the U.S
One of the most innervated tissues in the human

body
All innervation of the dental pulp when stimulated

elicit pain
Tissue is confined in a mineralized casing which is

non-compliant but succeptible to bacterial infections
Local Anesthesia
} Definition
A reversible sensory loss in a defined area
of the body associated with the transient
inhibition of peripheral nerve conduction
Desirable characteristics:
Profound, reversible local anesthesia with
rapid onset of action
Satisfactory duration of action
Minimal adverse local and systemic effects
Local Anesthetics Mechanism of
Action
Voltage Gated Sodium Channels

Family of Voltage
Gated Sodium Channels
Theile and Cummins. Front. Pharmacol. 2011

Voltage-gated Sodium channels
Cycle through 3 states
Local anesthetics gain access to the pore of a
Inactivated
Inactivated
sodium channel and "stabilizes"
dOpen
Close
the channel in its inactive state.
Thus voltage-gated sodium channels become

unavailable to be reactivated,
resulting in an increase in the refractory period
Fig 16-6. Pharmacology and Therapeutics for Dentistry. 5th edition

Yagiela JA.
Use-Dependent Block
Vehicle
% Channels Active
100
80
60
40 Lidocaine
20
0
1 2 3 4 5 6 7 8 9 10
Stimulation #
Grant et al Circ Res 1989

Primitive Local Anesthetics
late 1800s 1905 (Novacaine)
1940s
1990s
Articaine
DIFFUSION DEPENDS ON
DISSOCIATION:
Both Ionized and Base Forms
pH PkA = log(Base/Acid)
vanat.cvm.umn.edu/neurHistAtls/pages/pns1.html
RN + H+
Cell
Membrane
RNH+ RN + H+
Reasons for Increased Anesthetic Failures ?
pH of the inflamed tissue
Pt apprehension
Technique
Changes in
Neuronal plasticity nociceptive
pathways due to
Neuronal modulation
inflammation and
Genetics chronic pain
Effect of pH on availability of LA
H+
Hargreaves and Keiser. Endodontic Topics 2002, 1, 2639

ION TRAPPING
100%
75%
% LA Ion Trapped
Lidocaine
50% Mepivacine
Bupivacaine
25%
0%
7.40
7.30
7.20
7.00
6.66
6.30
6.00
5.66
5.30
Tissue pH
Hargreaves and Keiser Endo Topics 2002

pH of Local Anesthetics
Obs: Local anesthetics are packaged in acid solution to improve water-solubility

and shelf-life
Goodchild and Donaldson. 2016 Compend Cont Educ
How about buffering the LA?
N=30
Anesthesia of un-inflammed
max canines
Anesthesia=2x 80 readings
(EPT)
www.onpharma.com
Hobeich et al, 2013. J Endodon
How about Buffering the LA?
Control (pH 5) Buffered (pH 7.3)
N=20 80
IAN block, normal (uniflammed teeth)
% successful anesthesia
Anesthesia = no cold, no EPT responses
Teeth tested within 2 min of injections 60
40
Authors also report the 20

injections to be less painful
So, faster and more 0
comfortable
Malamed et al., 2013 Comped Contin Educ

Another Study
N=40,
Normal teeth, (-) EPT
Whitcomb et al., 2010 Anesth Prog

Buffered LA in Endodontic Study
N.S (p=0.381)
N=40/group
70
Man Molar with SIP
% of no pain on access and C&S

IAN BLOCK (2 cart of 2%lido/
epi) 52.5
success=no pain on access and

cleaning and shaping 35
Procedures started 15min post
injection
17.5
0
Control Buffered
Saatchi et al., 2015. J Endodon

Buffered LA in Endodontic Study
N.S (p=0.381)
N=40/group
70
Man Molar with SIP
% of no pain on access and C&S

IAN BLOCK (2 cart of 2%lido/
epi) 52.5
success=no pain on access and

cleaning and shaping 35
Procedures started 15min post
injection
17.5
0
Control Buffered
Saatchi et al., 2015. J Endodon

Does Buffering Provide Faster
Anesthesia ?
Yes No
Malamed et al. 2013 Hobeich et al., 2013 (JOE)
(Compedium)
Whitcomb et al. 2010 (Anesth
Kashyap et al., 2011 (Br J Prog)
OMS)
Ridenour et al., 2011 (Anest
Welch et al, 2012 Prog)
(Ophthalmology)
How about when injecting
directly where tissue pH is lower?
control Buffered
90 N=40/group, Patients with buccal
swelling (Acute apical abscess) with
% of patients experiencing
moderate to severe pain
need of I &D
67.5
Randomized trial
45 no difference in pain upon
injection
Patients reported lower scores for
22.5 Moderate to severe pain but the
difference was not SS
0 approx. 60% still hurt so success
Incision Drainage Dissection was less than 40% no matter the
solution
Balasco, Drum, Reader, Nusstein, Beck. 2013. J Endodon

Clinical Rationale for Buffering
Due to significant reduction of shelf-life (~4 weeks if kept

at 4C protected from light) , sodium bicarbonate must be
added immediately before use increasing the chances for
contamination and procedural errors.
Does the faster onset (?) and less painful injections justify
this approach?
Effect of Apprehension
IAN block
100 (2% Lido-epi)
% Successful anesthesia
90
80
70
60
50 n.s.
40
30 57%
43%
20
10
0 Placebo triazolam
1
(Halcion)
Lindeman M, Reader A, Nusstein J, Drum , Beck M. J Endod. 2008 Oct;34(10):1167-70
Nitrous Oxide and LA Success
100 N=50/group
Mand Molars with Symp. I. Pulpitis
% Successful Anesthesia
75 Success=
no pain on access/instrumentation
50
The increase in anesthesia is
believed to be due activation
25
of endogenous opioid system
and the modulation of
spinal NMDA channels
Placebo Nitrous
Stanley, Drum, Nusstein, Reader, Beck et al., 2012. J Endodon

Effect of Technique
on Local Anesthesia
ASYMPTOMTIC TEETH
100
90 NO DIFFERENCE WITH TECHNIQUE

80 Dx: normal pulp
70 Normal
60 periradicular
N=40
50
40
30 53%
20 38%
27%
10
0 Vazirani-
IAN Gow-
1
Gates Akinosi
Goldberg et al. J Endodon 2008. 34:1306-1311.
Effect of Technique
on Local Anesthesia
100GG slightly better than IAN or VA,
90
but80 still unpredictable when dealing with
70 irreversible pulpitis
60
50
40 Dx=I.P.
30 52% N=25/group
20 36%
27%
10
0 Gow- Vazirani-
1
IAN Gates Akinosi
Aggarwal et al . 4OE. 2010109 (2):303-8

Intraosseous Anesthesia
Stabident
X-tip
100
Addtl 1xI.O 98%

90 (3%Mepi)
80
70
88%
60 1xI.O 1x I.O 80%
50 (2%Lido) (3%mepi)
40
30
20
IAN 25%
10 IAN 19%
0 Nusstein et al. 1998 Reisman et al.1997
1
JOE OOOe
Considerations for Intraosseous Anesthesia
Avoid Important Anatomical Structures
-Mental Nerve, IAN, Sinuses, Roots
Use proper technique perforating the cortical plate as overheating

may cause osteonecrosis (Woodmansey et al., 2010)
-Do not use it in patients taking bisphosphonates

Considerations for Intraosseous
Anesthesia
Immediate onset but lasts only 30min when used as the primary
LA route (Jensen et al 2008 JOE).
Intraosseous with epinephrine-containing LA increases the

duration of anesthesia but temporarily raises the heart rate in 21-28
beats/min for 2 min but it can be reduced to 10-12 beats/min if
given as a slow (45sec) injection(Susi et al. 2008 .Anesth. Prog)
How about Supplemental Intraligamentary
PDL injections?
First PDL injection increase success up to 63%, re-

injection increases success to 92% (Walton and
Abbot, JADA 1981).
However, in inflamed mandibular molars is only 56%

successful (Nusstein et al., 2005 J Endodon).
86% of patients experience post injection discomfort

and 36% feel like the tooth is extruded (White,
Reader, Beck and Meyers. 1988J Endodon).
PDL injections are basically systemic injections of

low volume (approx. 0.2ml) Walton. J 1986Endodon.
Walton. 1986 J Endodon

Intrapulpal Anesthesia
100
75
50
25
0
Saline Lidocaine
Birchfield and Rosenberg. J Endodon 1975(1):26-7

Length of the Exposed Nerve
Percent Nerve Activity Matters
Raymond et al Anesth Analg 1989

Besides the pH and Technique
Why is it so hard to get numb?
I gave a block distal to the

Inflamed tooth. All adjacent
teeth are anesthetized
But the inflamed tooth is still
hot.
WHAT IS GOING ON??

Beware of the numb lip
Differential Anesthesia
Touch fibers (A-beta) and
Fast conduction low
threshold A-delta fibers are
more susceptible to local
anesthetics
Clinical Significance:
Lip numbness and cold
hyperalgesia are not true
indicators that c-fibers
located deep in the dental
pulp are blocked
Hargreaves and Keiser. Endodontic Topics 2002, 1, 2639

TTX-RESISTANT NA+ CHANNELS
Nav 1.8
Nav 1.9
Are relatively resistant to LAs
Require Four-Fold increase in lidocaine concentration

for effective blockade
Roy and Narahashi J. Neuroscience 1992.

Lidocaine is Less Effective in Blocking
TTX-Resistant Sodium Channels
1.0
TTX
0.8 TTX Resistant
Sensitive Channels
Sodium Current
Channels
0.6 (Kd = 200M)
(Kd = 50M)
Lidocaine
0.4 has 1/4
Consider Addnl potency
LA Dose for Severe for TTX-R
Pain patients Channels
0.2
INTRAOSSEOUS
0
-7 -6 -5 -4 -3 -2 -1
Lidocaine Concentration [log (M)]
Roy M. J. Neuroscience 12:2104, 1992.
TTX-R Channels Increase During Irreversible
Pulpitis
NaV 1.8 NaV 1.9
Warren et al. 2008; JOE Wells et al. 2007; JOE

Quantitative and Qualitative
Increase in Sodium Channels
Normal Painful
Luo, Perry, Levinson and Henry.2008 Mol Pain

Effect of experimental inflammation on
blockade of sodium channels
100
90
80
70
60
50 100%
40
30
20
10 10%
0 Normal Inflamed
1
Modaresi et al 2008. JOE.

Effects of PGE2 on TTX-Resistant
Sodium Channel Activity
0.5 After
1M PGE2 Peak current
Consider Fast Acting by 225%
Sodium Current
NSAIDs for Severe Pain
Also note
0.25 threshold
Before
PGE2
Capsaicin-
Sensitive neurons
0
-40 -20 0 +20
Voltage (mV)
Gold M. Proc Natl Acad Sci USA 93:1108, 1996.
Since peripheral inflammation has an effect
on dental pulp neurons
Can NSAIDS improve the success rate of LA?

Preemptive Analgesics and Anesthesia Success
% successful anesthesia (pulp access)

100
80
(IAN) 1.8 ml of
2% Lido with 60
78%
1:80,000 epi
40
n=50/group
20
32%
0
Placebo Ibu 600mg
1
1hr pre-Tx
Parirokh et al . Journal of Endodontics 2010;36(9):1450-4.
Preemptive Analgesics and Anesthesia
Success
(IAN) 3.6 ml of 2% Lido with
80 1:100,000 epi
n=13/group
60 No pain upon access=
Successful anesthesia
Irreversible pulpitis teeth
40
20
0
Placebo APAP 500mg APA 1g/Ibu 600mg
Ianiro et al . Journal of Endodontics 2007;33(1):11-4.

Preemptive Analgesics
and Anesthesia Success
P=0.001
Medications given 1 hr
prior
40
(IAN) 1.8 ml of 2% Lido

with 1:80,000 epi
P=0.055
30 N=55/group
No pain upon access=

Successful
20 anesthesia
Irreversible pulpitis
teeth
10
0
Placebo Ibuprofen Dexamethsone
400 mg 0.5 mg
Shahi et al . Journal of Endodontics 2013;39(2):160-2.
90 Not Statistical Significance Despite the Trend 86.0
79.0
68
Placebo
Ibu 800mg /APAP 1,000mg
45 N=50/group. Man Molars

38.0
32.0
with
SIP
24.0 24.0
23 Analgesics taken 45min
prior injections
Success=no pain on access
0 and C&S
IAN block B. Infiltration Intraosseous
(2% Lido) (4% Articaine) (3% Mepi)
Simpson et al . Journal of Endodontics 2011;37(5):593-7.

80
N=50
mand molars with sip
60
Meds 1hr prior
to IAN block
40
3% Mepi/epi IAN block

Success=no pain on access
20
0
Placebo Ibuprofen
Noguera-Gonzales et al., 2013; IEJ.

N=1900 patients with hot lower molars
in 17 different trials
Conclusion is that despite heterogeneity

in the trials, preemptive analgesia
increased the odds ratio that successful
anesthesia is achieved
Summary of Preemptive
Analgesia and Anesthesia
NSAIDS (Ibuprofen 600-800mg) give 1hr prior to injection improved
anesthesia success rates in most studies.
Pre-medication with Ibuprofen may be advantageous to anticipate the
analgesic and anti-inflammatory effect of post-operatory NSAID regimen
Investigating the Assumed
Superiority of Articaine
How about different LA?
100 100
% of patients with no pain upon access

% of patients with no response to EPT
IAN block IAN block

80 80
60 60
40 40
20 20
0 0
Articaine Lidocaine Articaine Lidocaine
Tortamano et al., J Endodon 2009 Claffey et al., J Endodon 2004

Lido vs Articaine for IAN block
100 IAN block 100 IAN block
% of patients with no response to EPT
% of patients with no pain upon access

80 80
60 60
Even at double the concentration (4% vs 2%) Articaine has not been
40 40
found superior as primary LA in IAN block
20 20
0 0
Articaine Lidocaine Articaine Lidocaine
4% 2%
4% 2%
Tortamano et al., J Endodon 2009 Claffey et al., J Endodon 2004
Equal Dose Comparison
100
N=156
75
Lower Molars
with I.P
Success=no pain
50 on TX
25
0
4% Articaine 4% Lidocaine
Pooni et al., JOE 2011

Articaine as Supplemental
Injections
70
60
% Sucessful Anesthesia
50
40 N=98
Dx=I.P
30
Success=
No pain on TX
20
10
0
IAN Articaine Articaine+ Dexamethasone
ketorolac
Supplemental Buccal Infiltrations

Aggarwal et al.,JOE 2011
Suplemental
Suplemental
Articaine
Articaine Buccal Infiltration
Buccal Infiltration
80
70
70
N=57
N=57
60 Lower
53 LowerMolars
Molars
50 Dx=I.P
Dx=I.P
Success=no
Success=nopain
pain
40 ononTX
35 TX
30
20
18
10
0
0
IANB Lidocaine Articaine
IANB Infiltration Articaine infiltration
infiltration
Aggarwaletetal.,
Aggarwal al.,JOE
JOE 2009
2009
Suplemental
100
IANB
75
50
25
0
1st 2nd 1st 2nd
Molars Molars Premolars Premolars
Matthews et al., JOE 2009
248 cases of paresthesia in a
period of approx 10 years in US
1:1.3 million injections estimated

incidence
94.5% were associated with IAN

blocks (89% affected the lingual
nerve)
Articaine was 3.6X more likely to Articaine entered the U.S market in May 2000
result in paresthesia
Previous studies in Canada and

Denmark with similar results
Can long-lasting anesthesia
improve post-operative
discomfort ?
Bupivacaine Infiltration
80
Evoked Pain (Swallowing)
60
Saline
Pain (VAS)
40 **
20
Bupivacaine
**
**
0
0 2 4 6 8 10 12
Time (days)
Jebeles et al., Int J Ped Oto 25:149, 1998

Oraverse
(Phentoalamine Mestylate)
Non-selective alpha-adrenergic antagonist
Increase clearance of LA decreasing

bioavailability
Administered 1 carpule (0.4mg) for each LA

carpule used.
Oraverse
(Phentolamine Mesylate)
Surveyed 390 patients after the use of Oraverse and 51
dentists that currently employ Oraverse
Practice Builder
Would opt for OV in future
Practice Differentiator
Improved Dental Experience

Performs as Expected
Product
ReducedAddresses a Clinical Need
Time of Numbeness
0 23 45 68 90
70 78 85 93
% of Dentists' Positive Responses
% of Patients' Positive Responses
Saunders et al., 2011;Compendium
Oraverse
Maxillary
300 Mandibular
300
Maxillary
Time to Offset Anesthesia (min)
250 250
Mandibular
Time to Normal (min)

200 200
*
150 150 *
*
100
* 100
Sham Oraverse Sham Oraverse Sham Oraverse Sham Oraverse
N=46
Fowler et al., 2011; J Endodon

Oraverse
30min N=90
Elmore et al., 2013; J Endodon

Pharmacogenetics
of Local Anesthesia
Drug efficacy or toxicity may be
altered by patients DNA
Pharmacogenetics:
Red Heads & Lidocaine
11
saline
lidocaine (sc)
Maximum current tolerated (mA)
Mutation in the MC1R

8
involved in Red Hair
phenotype is also involved in
inflammatory pain
6
0
control red head
Liem et al., Anesthesiology 102:509, 2005 N = 60

Effect on MC1R mutation
on Endodontic Anesthesia
Disproven in an endodontic study of UNINFLAMMED teeth
N=~60
Droll et al., 2012; J Endodon

NaV1.7 SNPs are associated with
known painful conditions
Condition Sample size Rs6746030 allele P value
Cohort assoc with A allele
increased pain association
Osteoarthritis 578 A 0.016*

Sciatica 195 A 0.039*
Postamputation 100 A 0.011*
Postdiscectomy 179 A 0.088
Chronic 205 A=G 0.732
Pancreatitis
Reimann et al. PNAS 2010. 107(11):5148-53

Mutations on Nav 1.7 may make channel
insensitive to Lidocaine
% Inhibition of NaV1.7 sodium channels
Lidocaine Concentration (mM)
Sheets et al. J Physiol. 2007 ;581(3):1010-31

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Conclusions on Local
Anesthetics
Profound anesthesia is difficult to achieve
Intraosseous anesthesia is the only modification to demonstrate
a predictable significant improvement of anesthesia efficacy
Most studies have not demonstrated superiority of articaine for
anesthesia of symptomatic teeth for IANB, only a modest
increase in success when used as suplemental infiltrations
Clinicians must be aware of the increased risk of paresthesia
with Articaine
Genetic polymorphisms and epigenetic factors are likely to play
a role in anesthesia efficacy and deserves more investigation.
Management of Pre- and Post-
operative Endodontic Pain
Patient Expectations
Evidence-Based Decisions
35 Cochrane analyses were
included
45,000 patients in 350 studies
All randomized good quality

studies
Cochrane Review
NNT for >50% Dental Pain relief
Etoricoxib 120mg-1.6
Naprosyn 550mg 1.8
Ketoprofen 50mg 1.8
Etodolac 400 mg2.2
Ibuprofen 400mg2.3
Oxycodone 10mg/APAP 650- 2.3
Celocoxib 400mg2.5
Ibuprofen 200mg 2.7
Flurbiprofen2.8
Acetaminophen 1,000mg3.2
Codeine 60mg/APAP 650mg (Tylenol#4) 3.9
Codeine 60mg-21
Cochrane Review
% Achieving at least 50% Pain Relief
Etoricoxib 120mg-70%
Naprosyn 550mg 61%
Ketoprofen 50mg 62%

Etodolac 400 mg65%
Ibuprofen 400mg53%
Oxycodone 10mg/APAP 650- 65%
Celocoxib 400mg37%
Ibuprofen 200mg 47%

Acetaminophen 1,000mg41%
Codeine 60mg(same as placebo) 17%

NSAIDS
Steroids Endodontic
Pain
Opioids
Other
Classes
Acetaminophen Tramadol
Mechanism of Action of NSAIDS
NSAIDS
Phospholipase
Arachidonic
A2
Acid
Cyclooxygenases
Lipoxygenases
(COX1; COX2)
Prostaglandins
Leukotrienes
Thromboxane A2
Two Types of Cyclooxygenase
COX1 COX2
Constitutive Inducible
Present in stomach,
kidneys, platelets Synthesized in inflamed
tissue (IL-1, TNF, LPS)
Many traditional NSAIDs
preferentially inhibit
COX2 inhibitors should
COX1
have fewer GI & renal
side-effects
Contraindications for NSAIDs
GI Ulcers
Renal Disease/Failure
Coagulopathies
Asthma (specially with nasal polyps)
Hx of Stroke
Cox 2 vs 1 Selectivity
Cox-2 selective drugs

Warner and Mitchel, 2008; Lancet
NSAIDS and Cardiovascular
Risks
PGI2 (Prostacyclin) produced by
COX2 in the endothelial cells of Thrombotic
PGI2 TxA2
blood vessels keep them from Risk
contracting
Low dose
Loss of tone results in clumping of
Aspirin
platelets, formation of emboli and
increased risk for cardiovascular
incidents Conventional
NSAID
Selectively blocking COX-2 results
in more arachidonic acid available Selective
to COX-1 which potentially form COX-2
more Thromboxane A2 increasing inhibitor
aggregation of platelets
COX-2 selective drugs and Stroke
Rofecoxib
N=7,983
Naproxen
Diclofenac
Ibuprofen
Control
0 1.5 3 4.5 6
Ischemic Stroke Odds Ratio
Haag et al., 2008; JAMA internal Medicine

NSAIDS and Gastric Risks
NSAIDs
NSAIDS inhibit also COX-1
expressed in stomach leading
to loss of protective
prostaglandins and TxA2;
COX-1
resulting in increased gastric
damage, decreased platelet
aggregation (gastric bleeding)
and reduced blood flow (less
repair)
reduced
reduced Impaired Mucosal
mucus and
mucosal platelet Ulcer and
bicarbonate
blood flow aggregation Bleeding
secretion
Increased Cardiovascular Risk
Ro
fe
co
Ce xib
D i l co
clo xib
fe
na
Ib
up c
Na rofe
pr n
ox
As en
pi
Adapted from FitzGerald TIPS 2007.

rin
Adverse Effects of
Increased Gastrointestinal Risk

COX1 and COX2 Inhibitors
NSAIDS and Kidney Risks
Both COX-1 and Cox-2 promote glomerular blood flow in
the kidney by the productions of prostaglandins
Prolonged use of COX inhibitors decrease glomerular blood

flow. Interpreted as hypotension that through the renin
aldosterone system promote an increase in the blood pressure
This increase counteracts antihypertensive medication
Drugs excreted by the kidneys accumulate promoting kidney

damage and acute failure
Ibuprofen Dose Response
systematic Review
800
Ibuprofen Dose 600
400
200
100
0
8
NNT
NNT for >50% Pain Relief over 4-6 hours

Collins et al., 1998 Euro J Pain
Ibuprofen Dose Response
systematic Review
% of Patients with At Least 50% Pain Relief

100
50
0
100 200 400 600 800
Ibuprofen Dose (mg)
Collins et al., 1998 Euro J Pain

Sniffing out Pain
N=21
Turner et al. J Endod 2010; 37(4):439-44

Synergism between Ibuprofen and
Tylenol
N=57
Hx of spontaneous pain:
~ 70% of IP
30% of pulp necrosis
72% reduction in
pain intensity with Endo alone
Menhenick et al., 2004 IEJ 37:531-41

No effect on another Endodontic
Study
1. Patients were instructed to take medication as needed (prn) not

by the watch (qid)
1. There was no placebo control group. Therefore, there is the

possibility for flooring effect
1. It contradict every present clinical trial and experimental studies

on the synergism of Ibuprofen and Acetaminophen
Wells KL., Drum M., Nusstein, J ., Reader, A., Beck, M. J Endod 2012 (12):12608-12
Ibuprofen/Acetaminophen
Synergism
Mehlisch et al. 2010. Clin Ther.32(6):1033-49

Ibuprofen/Acetaminophen
Synergism Post-Operatively
80
% Patients Requiring Rescue
60
Medication
40
Placebo
Ibu (400mg)
20 APAP (1,000 mg)
Ibu (400 mg)/APAP (1,000 mg)
0
1 2 3 4 5 6 7 8
Hours After Dental Sx
Moore et al. ,2011. Pain, 152 (5):982-9

Acetaminophen
Acetaminophen
Relatively weak analgesic
for dental pain
Good antipyretic
Very poor anti-

inflammatory
Mech of Action is mainly

in the CNS
Acetaminophen (APAP) mechanism of
action
Previously thought to acts through
the inhibition of COX3.
More recently, the hypothesis that

it acts by promoting the
accumulation of endocannabinoids
in the central nervous system is
more accepted
Kis et al 2005. J Pharmacol Exp Ther; 315:1-7

APAP Mechanism of Action:
1. APAP is Converted to AM404
Conversion Primarily Brain
FAAH
AM404 = N-acyl phenolamine Hogestatt et al., J Biol Chem

280:31405, 2005
Acetaminophen and Liver Risks
47 - 62% 25 - 36%
It is the leading cause of liver failure in
the U.S.
10%
Unintentional overdose is very

common
Its that are drug users, alcoholics and

malnourished are at increased risk
Alcohol
Because acetaminophen is metabolized
in the liver by cytochrome 450
enzymes, this pathway can be
overwhelmed and NAPQI accumulates
leading to liver failure
New FDA guidelines
Not as safe in pregnancy as

previously thought.
Long term use interferes with

warfarin , risk of bleeding
exists (decrease dose to max
2,000mg/day)
Increase risk of Asthma in

children and young adults
OPIOIDS
DEA Schedules
Schedule I -Illicit drugs with no medicinal benefit (eg. Ecstasy, Methamphetamines, marijuana etc)
Schedule II- Drugs with high potential for abuse, with use potentially leading to severe
psychological or physical dependence. Example: Combination products with less than 15mg
hydrocodone (Vicodin, Norco), cocaine, methamphetamine, methadone, oxycodone (OxyContin),
fentanyl, Dexedrine, Adderall, and Ritalin
Schedule III-Drugs with moderate to low potential for physical and psychological
dependence.Examples: Combinations with less than 90 milligrams of codeine per dosage unit
(Tylenol III and IV), ketamine, anabolic steroids, testosterone.
Schedule IV-Drugs with a low potential for abuse and low risk of dependence. Examples: Xanax,
Darvocet, Valium, Ambien, Tramadol
Schedule V-Drugs with lower potential for abuse than Schedule IV and consist of preparations
containing limited quantities of certain narcotics. Examples: antidiarrheal, antitussive, and analgesic
purposes such as Lomotil, Robitussing AC and Lyrica, respectively.
https://www.dea.gov/druginfo/ds.shtml
Opioid Medication Mechanism of
Action
Act on pre-synaptic neurons
inhibiting neurotransmitter release
and post-synaptically by inhibiting
neuronal excitation
Act on their putative receptors Mu,

Kappa and Delta Opioid Receptors
Not Good for Chronic Pain
In addition to reduced effectiveness
or tolerance, Long term opioid use
leads to release of pro-inflammatory
mediators pre-synaptic and
activation of spinal microglial cells
resulting in release of inflammatory
mediators resulting in neuro-
inflammation and opioid-induced
hyperalgesia
Opioids
Combination drugs
Most of the analgesia is due to the non-narcotic
Most of the side effects is due to the opiate narcotic
The minimal effective dose of codeine for the average

healthy patient is 60mg
Analgesic Effect of Codeine 30 mg
1.0
Aspirin 650/Cod
0.8
Aspirin
0.6
Pain (category
Codeine
0.4
Placebo
0.2
0.0
0 1 2 3
Time
N = 128
al.
From: Cooper et al., Pharmacotherapy 2:162, 1982
Analgesic Effect of 60 mg Codeine
1.0
Pain Intensity Difference Score
0.8 Ibuprofen 400

0.6
0.4 APAP 600/Cod 60

APAP 600
0.2
APAP 300/Cod 30
0.0
-0.2
Placebo
-0.4
0 1 2 3 4
Time (hours) N = 203
From: Cooper et al.

Effects of Opioids
DESIRABLE: UN-DESIRABLE:
Analgesia Nausea and Vomiting
Antitussive Respiratory Depression

Constipation
Histamine Release
(itching, rash)
Tolerance &
Dependence
New FDA guidelines for
hydrocodone
The U.S. (4.5% of worlds
population) consumes 99% of
worlds hydrocodone
131 million prescriptions for

Vicodin were issued in 2011
It is the most abused drug in the

U.S.
It is now the same schedule as

oxycodone
(source: International Narcotics Control Board)

Distribution of Opioid Rx/
Specialty
Non-medical use of opiods
among 12th graders
Hydrocodone (e.g., Vicodin, Lorcet) 50
Codeine (e.g., Tylenol with codeine) 38
Oxycodone (e.g., OxyContin, Percocet) 14
Propoxyphene (e.g., Darvon, Darvocet) 10
0 20 40 60
% use
Source: McCabe, Cranford, Boyd & Teter, 2007"Addict Behav 2006\7

Effect of Oxycodone Dose
on Ibuprofen 400mg Analgesia
Opioid-induced
side effects were
dose depended
80
% Pain Relief
60
Ibu
Ibu + 2.5 Oxy
40 Ibu + 5 Oxy
Ibu + 10 Oxy
20
0
0 15 30 45 60 120 180 240 300 360
Neither 2.5 nor 5mg
Time (min) Oxycodone increased
Ibuprofen analgesia
Dionne JOMS 57:673, 1999

ABE Diplomates
Prescription Habits
5% Ibuprofen
Survey, N=232 13% Vicodin
Acetaminofen
Percocet
56%
26%
Lee et al., 2009. J Endodon

Tramadol
An atypical drug- It acts as an opioid and
antidepressant
It binds to u-opioid (mu) receptor and

inhibits the reuptake of serotonin and
nor-adrenaline in the pre-synaptic
terminals in the CNS
Its side effects are mimic the same of

opioid drugs
Not often used Endodontics but it has

been shown to have synergistic effects in
one endodontic study (Doroschak, Bowles and
Hargreaves. 1999 J Endodon)
Commonly Prescribed Analgesics
for Dental Pain
DRUG Brand Name Dosage Max Dose OTC or RX (Sch)
Ibuprofen Advil, Motrin, Nuprin 400-600mg every 4-6 3,200mg/day OTC 200mg
hours Rx>200mg
Tylenol 325-500mg every 4 to 6 3,000mg/day OTC

Acetaminophen
hours
Aleve, Naprosyn 1-2 tabs every 4-6 hours 1,000-1,100mg/day OTC 220mg
Naproxen
Rx>220mg
Ultram (50mg) 1-2 tablets every 4-6 400mg/day Rx (Sch III)
Tramadol
hours
Tylenol with Codeine 1-2 tablets every 4-6 3,000mg Rx (Sch III)
Acetaminophen with
#3 hours acetaminophen/day and
Codeine #3
360mg codeine /day
Ultracet 1-2 tablet every 4-6 3,000mg Rx (Sch III)
Acetaminophen with
(37.5mg tramadol/325 hours acetaminophen/day and
Tramadol
mg Tylenol) 400mg tramadol/day
Vicodin-5 1-2 tablets every 4-6 3,000mg Rx (Sch II)
Acetaminophen w/
(5mg hydrocodone and hours acetaminophen/day and
Hydrocodone
300mg acetaminophen) 60mg hydrocone /day
Percocet-5 1-2 tablet every 4-6 3,000mg Rx (Sch II)
Acetminanophen with (5mg oxycodone/325mg hours acetaminophen/day and
Oxycodone acetaminophen) 60mg hydrocone /day
Flexible Pain Control
NSAIDs indicated NSAIDs not indicated
APAP 650-975mg
mild
Ibuprofen 200-400mg, qid

Max 3,000mg/day

moderate
APAP 625mg-975mg
+ Tylenol 500mg-1,000 mg with Hydrocodone

severe
APAP 1,000mg
+ Tylenol or Tylenol/Oxycodone
with oxycodone 10mg
10mg
Thanks for the
Attention!
Biography
Dr. Donna Ma scheck received her D.M.D. from the University of Kentucky in 1992. She completed a
GPR (general practice residency) at Northwestern Memorial Hospital and a Fellowship in Orofacial Pain
at the University of Kentucky. She received her certicate in endodontics from the University of Iowa in
1996 and has been a Diplomate of the American Board of Endodontics since 2000.
She served as predoctoral director of endodontics at the University of Minnesota for eight years. In 2001
she received the Edward M. Osetek Educator Award. She has served on several commi ees for the
American Association of Endodontists including Educational A airs and Regenerative Endodontics and
the Special Commi ee on Fractured Tooth Initiative. Additionally, she served as treasurer on the AAE
Foundation and their liaison to the Research and Scientic A airs Commi ee.
Dr. Ma scheck is a past President and Director of the American Board of Endodontics, the only
certifying board for the specialty of endodontics. She has given numerous invited presentations both
here and abroad and has co-authored a chapter in Pathways of the Pulp.
She joined Advanced Endodontics in Tigard, Oregon in the fall of 2010.

Biography Dr. George Bruder Nov. 2016
George A. Bruder, D.M.D. Dr. Bruder was the founding Chair of the Department of
Endodontics and Director of the Advanced Specialty Education Program in Endodontics at Stony
Brook University School of Dental Medicine from 2006 2015. In 2012, Dr. Bruder was
awarded the prestigious Edward M. Osete Educator Award from the American Association of
Endodontists and is also a member of Omicron Kappa Upsilon, National Dental Honor Society.
Dr. Bruder is a Diplomate of the American oard of Endodontics and the Coordinator of icro-
Endodontics and Endodontic Technologies in the Advanced Graduate Program in Endodontics
at Harvard School of Dental Medicine.
Dr. Bruder has delivered more than 750 lectures both nationally and internationally and
published numerous articles on icro-Endodontics and Endodontic technologies. In addition,
he has authored and co-authored numerous text boo chapters including the chapter on non-
surgical icro-Endodontic Retreatments with Dr. Robert R. White in Color Atlas of Endodontics,
by Dr. William Johnson.
Currently, Dr. Bruder divides his time between his family, private practice in anha an, ,
and providing the ultimate in hands-on participation continuing education programs held in
Palm Beach Gardens, , at the facility he co-founded with Dr. Sergio Ku ler, International
ental nstitute Forever Learning (IDI-FL). Dr. Bruder serves as CFO and Director at IDI-FL.
02/12/2017
Periradicular Surgery and Repair
Direc tor, Mic ro-Endodontic s and Endodontic Tec hnologies

Adv anc ed Spec ialty Educ ation Program in Endodontic s
Diplom ate of the Am er ican Boar d of Endodont ics
gbruder@IDIFL.com
George_ Bruder@hsdm.harvard.edu
Retreat or Surgery:
Decision Planning Dilemmas
The impact of emerging technology on endodontists care
Of those surveyed, 33.3% felt as though their

endodontic training in surgery was inadequate, and Practitioners Ability to Develop
47.95% went on to acquire additional training in
surgery postresidency. Skills and Comfort Level-
Guide Treatment Options
Learning Curves
Learning Line
Key Learning Points
1
02/12/2017
Guideline 1: When the initial endodontic obturation is inadequate, when Guideline 3: Tooth must have sufficient structure and ferrule integrity in
coronal microleakage is suspected, and when the tooth structure can order to predictably save it and to predictably restore it.
sustain disassembly, then nonsurgical retreatment over surgical treatment
maybe the optimal choice. Guideline 4: If coronal leakage is suspected, then NSRCT and a new
crown should be chosen over SRCT retreatment.
Guideline 2: If Finding is confined apically, and the previous endodontic
treatment is reasonably sufficient, and if nonsurgical retreatment were Guideline 5: If a gingival black triangle or unaesthetic incision is a
to compromise the structural integrity of the tooth, then surgical high risk, review microsurgical techniques (incisions/suturing) and
correction is the treatment of choice. NSRCT retreatment options.
Blo g Created : Su n d ay , 0 1 Ap ril 2 0 0 7 0 0 :0 0 Hits: 8 6 6 Blo g Created : Su n d ay , 0 1 Ap ril 2 0 0 7 0 0 :0 0 Hits: 8 6 6
What are the alternatives to retreatment? Friedman, S. The prognosis and expected outcome of apical surgery.
Endodontic Topics 2005;11:219-262.
If nonsurgical retreatment is not an option, then

endodontic surgery should be considered. This surgery
involves making an incision to allow access to the tip of
the root. Endodontic surgery may also be recommended
in conjunction with retreatment or as an alternative.
Toronto (Friedman) 74% healed; 91% functional

Rubinstein, Kim 97% (3-12 mo.); 92% (5-7yrs.)
Outcome Studies
Surgical Root Canal Treatment
Author % Healed # Cases Follow-up Date

period
There is no difference in outcome between surgical and non- Dorn 95 488 6mos-10years 1990
Friedman 44 136 6mos-8 years 1991
surgical therapy for endodontic re-treatment of teeth with Frank 58 104 15 years 1992
periapical disease. ... August 63 39 10 years 1996
Testori 85 302 6 years 1999
Rubinstein 92 59 5 years 2002
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Outcome Studies Outcome Studies
Prognostic Factors in Endodontic Microsurgery. J Endod 2011;37:927- Prognostic Factors in Endodontic Microsurgery. J Endod 2011;37:927-
933. 933.
Conclusions: Under the control of the significant variables in

logistic regression, the potential prognostic factors on the outcome
were:
sex
tooth position
lesion type
root-end filling material
On the other hand, the tooth position was a pure predictor of an

endodontic lesion affecting the clinical outcome.
Cohn, S. Treatment choices for negative outcomes with non-surgical root canal treatment:
non-surgical retreatment vs. surgical retreatment vs. implants. Endodontic Topics 2005;4:-24.
Therapy
Endodontic Therapy vs. Implant Placement
Indications and contraindications
Factors affecting success / failure
Procedures and techniques involved
Criteria for success / failure
3
02/12/2017
EVIDENCED-BASED DENTISTRY
The evidence is lacking!
Endodontic Therapy vs. Implant Therapy
Placement Levels of Evidence (LOE)
* LOE 1-5 based on trustworthiness
When comparable criteria are applied to outcomes, the survival rates * Few Level 1 RCTs
of endodontic treatment and implant placement are the same. * Most evidence is lower level
* Case series
Cohn, S. Endodontic Topics 2005;11:4-24.
* Anecdote
Endodontists should be trained in implantology to assist patients and referring * Bench top studies
colleagues in making informed treatment decisions. Must use best available evidence
Paik et al, J Endod 11.2004
JOURNAL OF ENDODONTICS Printed in U.S.A.
Copyright 2004 by The American Association of Endodontists VOL. 30, NO. 11, NOVEMBER 2004
CLINICAL RESEARCH
Levels of Evidence for the Outcome of Endodontic

Retreatment
Stephen Paik, DDS, Christopher Sechrist, DDS, Mahmoud Torabinejad, DMD, MSD, PhD
Not Level 1 prospective randomized, double-blind, controlled clinical trials

The purpose of this investigation was 2-fold: (a) to of the entire root canals in a few days (59). This occurs as a result
Much of oursearch
complete a thorough cited literature
of published literature in ofEndodontics is unfortunately,
either the presence of voids between the dentinal walls and the
related to clinical studies on the success and fail- filling materials used to obturate the root canal system, and/or
of
ure a lower retreatment,
of nonsurgical LOE, mostly retrospective
and (b) to assign LOE 3 and 4 studies.
washing out of the root canal sealers.
The preferred treatment of failing endodontic cases is nonsur-
levels of evidence to these publications. Clinical
gical retreatment. According to Bergenholtz et al. (10), Molven
studies related to success and failure of retreat-
and Halse (11), Allen et al. (12), Sjogren et al. (13), and Friedman
ment since 1970 were identified using both elec-
Paik S, Sechrist C, Torabinejad
tronic and manual literature searches. After iden-
M. Levels
et al. (14), this treatment usuallyofresults
evidence for outcomes.
in successful the outcome
The success rate of endodontic retreatment ranges between 40 to
tification of pertinent literature, of endodontic
each articleretreatment.
100% (Table J Endod. 2004;30:745-50.
1). With this wide range of data, clinicians do not
received a level of evidence (LOE) from one (high) have consistent information upon which to base their clinical
to five (low). Thirty-one clinical studies and six retreatment choices.
view articles related to this subject were identified. In an effort to provide patients with the most recent, highest
There was no LOE 1 Randomized Control Trials quality and predictable treatment modalities for dental care, clini-
(RCT). There were three LOE 2 RCTs, one LOE 2 cians must be well informed of the outcome of proposed treatment.
Cohort, and two LOE 3 Case Control Studies. Thir- In cases refractory to initial root canal therapy in which a decision
is made to perform nonsurgical retreatment, the patient has the
teen Case Series (LOE 4), which comprise the most
right to know the prognosis of the proposed treatment as a com-
highly quoted success and failure data, were ponent of informed consent. Clinicians must be able to provide this
found. Twelve Case Reports (LOE 5) and six review information to the patient based on the best available data.
articles (LOE 5) were found. Based on these find- Since the 1990s, there has been a paradigm shift to evidence-
ings, it appears that few high level studies have based medicine. The Center for Evidence Based Medicine (www.
been published in the past 34 yr related to the cebm.net) is an organization providing criteria for what constitutes
success and failure of endodontic retreatment. evidence-based research. As in medicine, dentistry has shifted to
this new thinking. The American Dental Association defines evi-
dence-based dentistry (EBD) as an approach to oral healthcare that
requires the judicious integration of systematic assessments of
clinically relevant scientific evidence, relating to the patients oral
Complete cleaning and filling of root canals should result in and medical condition and history, with the dentists clinical ex-
resolution of periradicular lesions after nonsurgical root canal pertise and the patients treatment needs and preferences (15). The
therapy. The degree of success following root canal therapy has EBD process consists of four steps. The first step is the formulation
been reported as high as 98.7% (1) and as low as 45% (2). The of a relevant question related to a specific clinical application.
Washington study reports a success rate of 95% (3) of all treated Well-formulated clinical questions usually contain four elements
endodontic cases, which compares favorably with other reports of (PICO): the patient or the problem, the intervention, the compar-
success. An examination of failed cases from the Washington ison of the intervention with alternative treatments, and the treat-
study (3) showed that over two-thirds of these failures were related ment outcome (16). This process will allow the researcher or
to incomplete cleaning and obturation of root canals. Harty et al. clinician to find the best available evidence related to the treatment
have also reported that the majority of nonsurgical endodontic of the patient. Best available evidence may include randomized
procedures that fail do so because of inadequate apical seal (4). controlled clinical trials, nonrandomized controlled clinical trials,
Implant Survival Rates

In addition to the factors cited in the above studies, a number of cohort studies, case-control studies, cross over studies, cross-sec-
recent investigations have shown that the exposure of the coronal tional studies, case studies, or consensus opinions of experts in the
parts of filled root canals to oral flora results in total contamination field. The second step includes gathering of the data through
745
Various bone grafting / implant treatments Indications and contraindications

10 clinical studies 3344 implants Procedures and techniques involved
Mean 86.8% Factors affecting success / failure
Criteria for success / failure
-ADA Council on Scientific Affairs J Endod 2008;34:1316 -1324

JADA Jan 2004 Developed at Univ. Nebraska- easier to use and understand than Sussmans in 1998
4
02/12/2017
Types
Surgical Complications Implant Therapy
Implant Loss
Bone Loss * Longer Follow-up
Soft Tissue Complications * Criteria
Mechanical Complications
Esthetic / Phonetic Complications * Excluded Patients
* Success <86.7%
Goodacre
J Prosthet Dent Papaspyridakos, Chen, Singh, Weber, Gallucci
Volume 90, Issue 2, Pages 121-132, August 2003 J Dent Res 91(3):242-248, 2012
Da Silva, J. et al., JADA 2014;145(7):704-713 Da Silva, J. et al., JADA 2014;145(7):704-713
Other Implant Considerations
Systemic Factors
* Diabetes Test for Diabetes-
Hemoglobin A1c (HbA1c)
* Immune disorders
Normal range 4% and 5.6%
Environmental Factors Increased risk 5.7%-6.4%
Diabetes >6.5%
* Smoking Goal for diabetics <7.0%
Diabetes Fiorellini, Nevins & Nevins

Int J Periodontics & Restorative Dentistry 2000
5
02/12/2017
Endodontic Residents Typical Clinical Experience Endodontic Residents Typical Clinical Experience
communications@AAE.org
Endodontic Residents Typical Clinical Experience Endodontic Residents Typical Clinical Experience
Important Dates
Written Examination- May 17, 2017
Application Deadline- January 27, 2017
http://www.collegeofdiplomates.org
http://www.aae.org/board
6
02/12/2017
Important Dates
Written Examination- - May 17, 2017
Application Deadline- - January 27, 2017*
Case History- - May 1, 2017

- September 1, 2017
Oral Examination- St. Louis, MO

- March 24 & 25, 2017
- October 21, 22, & 23, 2017
http://www.collegeofdiplomates.org
http://www.aae.org/board
Johnson B., J En d o d VOL. 26, NO. 8, AUGUST 2000
www.collegeofdiplomates.org http://www.aae.org
7
02/12/2017
http://www.aae.org/Board/
Practitioners Ability to Develop Skills and Comfort

Level Guide Treatment Options
CASE #1

Case 1 Level Guide Treatment Options
Referrer: Patient had root canal done on lower left 15+ yrs. ago and is having pain
Chief Complaint:
* CC: Pain when I drink cold and occasional throbbing (Patient is holding lower left side)
Medical History:
* Medical Hx.- Patient denies all CV, GI, GU, Hematologic, Neuro, Musc/Skel, Derm or allergic
abnormalities. BP 118/70, Pulse 60, Respiration 14.
Past Dental History:
* Patient has had previous dental care including: exams, radiographs, cleanings, NSRCT and
restorations. Patient has had intermittent throbbing and cold sensitivity on the lower left for the
past month. Patient has no memory of trauma. Patient was referred by prosthodontists for
endodontic consult and possible retreatment of tooth #18 to a different endodontic office. The
patient came to our office where they remembered receiving treatment over 16 years ago.
8
02/12/2017

Case 1
Clinical Evaluation: (Diagnostic Procedures)
*Patient was ambulatory, alert and was holding her lower right jaw.
Extraoral and intraoral examinations revealed no sinus tracts, no
swelling or lymphadenopathy. Intact crown #18 and amalgam filling #19.
Test Results:
| CO2 Perc Palp Bite Perio Mobility |
| #18 - ++ - + 2-3mm - |
| #19 ++ L ++ - + 2-5mm - |
| #20 + NL - - - 2-3mm - |
| #30 + NL - - - 2-3mm - |
Practitioners Ability to Develop Skills and Comfort Practitioners Ability to Develop Skills and Comfort
Level Guide Treatment Options Level Guide Treatment Options
Radiographic Interpretation: (Imaging)

*Tooth #18- previous Crown and NSRCT which appears to be filled
short of apices with possible root resorption and extensive
periradicular radiolucency. No other pathology was evident upon
review of all imaging acquired. Tooth #19- Amalgam filling, caries
and periradicular radiolucencies noted. Crestal bone height intact
with no horizontal or vertical bone loss noted. No other pathology
was evident upon review of all imaging acquired.
PO-1999 December 2015

Cause:
Microorganisms
Kakehashi et al, 1965; Korzen et al, 1974; Sundqvist, 1976
9
02/12/2017
Kakehashi et al, 1965; Korzen et al, 1974; Sundqvist, 1976 Reeves OOO July 1966
Pretreatment Diagnosis: #19
* Pulpal- Symptomatic Irreversible Pulpitis
* Periradicular- Symptomatic Apical Periodontitis
Treatment Plan:
* NSRCT #19
* Restorative- Full Coverage Crown #19
Alternative:
* Extraction
* Extraction/Bridge 18-20
* Extraction/Implant
Treatment Plan Tooth #18? Intentional Replantation
ARS
RESULTS
10
02/12/2017
Pretreatment Diagnosis: #18
* Pulpal- Previously Treated
* Periradicular- Symptomatic Apical Periodontitis
Treatment Plan:
* Surgical Replantation #18
Alternative:
* NSRCT ReTx #18
* Extraction
* Extraction/Implants
In an artific ial env ironment outs ide a liv ing organis m.
11
02/12/2017
Intentional replantation was a viable treatment

option for teeth with previously failed non-surgical
root canal
12
02/12/2017

Pre-surgical Evaluation Program (PREP) Pre-surgical Evaluation Program (PREP)

Medical/Dental History
Diagnosis
Diagnosis
Reproduce the Chief Complaint Reproduce the Chief Complaint
Determine the Cause Determine the Cause
Eliminate the Cause Eliminate the Cause
Psychological (anxiety, behavioral observations) Pre-operat ive n on -st eroidal an t i-in flammat ory medicat ion s for t h e preven t ion of post operat ive den t al pain .
Pre-surgical Prophylaxis Jackson , Moore, Hargreaves. JADA, 1 9 8 9 ; 1 1 9 :64 1
Preoperative Medication Dru gs for pain man agemen t in Den t ist ry
Anatomical Considerations Hargreaves K, Abbot t PV. Au st Den t J. 2 0 0 5 Dec;5 0 (4 Su ppl 2 ):S1 4 -22 .
The 3-Ds
First, Do No Harm Hargreaves K, Abbott PV.
The Nature of the Disease

Diagnosis
Reproduce the Chief Complaint
Determine the Cause
Eliminate the Cause
Etiology
Pathogenesis
Dynamic diagnosis
Siquiera et al, OOOOE 2002
Colleagues for Ex cellence Winter 2015
13
02/12/2017
Trauma Incomplete removal of intracanal irritants

* Calcified Canals/ Ledges
Biopsy- * Mor phology
*Suspect/nonhealing lesions Accessibility issues
* Resor pt ion
Post-Treatment Disease Irretrievable materials blocking access to the apex, leads to incomplete removal of
intracanal irritants
Emergencies * Post s / Inst r ument s
Practical Lessons in Endodontic Surgery Practical Lessons in Endodontic Surgery

Quintessence Books 1998 Quintessence Books 1998
Gutmann J L, Harris on J W editor. Surgical endodontics. Gutmann J L, Harris on J W editor. Surgical endodontics.
Bos ton: Blac k well Sc ientific Public ations ; 1991;p. 736 Bos ton: Blac k well Sc ientific Public ations ; 1991;p. 736
Post Space Considerations

Apical seal
Post Space Considerations Endodontic Retreatment
*How much gutta-percha should be removed? Prognosis

Periradicular tissues
* Mattison et al. J Prosthet Dent 1984
* 3, 5 and 7mm apical gutta-percha left *Apical seal
* determined 5mm adequate *Adjacent teeth
* 4mm hard to get to *Isolation
* increased safety at 5mm
Post Space and Root Morphology

Post Space Considerations Reference Points Goodacre Root Thickness and Strength
Apical seal *Curves
*How much gutta-percha *Thin roots
should be removed? * How much dentin on
*Goodacre each side of post 1-2
* 4-5mm of gutta-percha mm?
from apex
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02/12/2017
Post Considerations
Diameter
Gates Glidden Drills *Keep diameter of the post as small as possible
* Decreases stresses on the root
* Sorensen & Engelman J Prosthet Dent 1990
*Only place in largest straightest canals

* Upper Molar Palatal
* Lower Molar Distal
* Abou-Rass et al JADA 1990
.50 .70 .90 1.10 1.30 1.50
Urban Legend:
Morgano showed that 62% of dentists over the age of 50 Restorability
believe that a post reinforces a tooth
Trauma
Morgano et al. Dent Clin North Am 2004
* Fractures
Mythbuster:
Diagnosis and Management
Not only do posts fail to add any additional reinforcement,
* Sealing of the root canal system
but furthermore the post space actually weakens teeth *Chronic irritants
Trope M et al. Endod Dent Traumatol 1985 * Post endodontic disease?
Biological Widths Biological Widths
Bur-958C
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What is the Ferrule? What is the Ferrule?

Importance of the ferrule
*1.5 - 2mm ferrule to prevent fracture Importance of the ferrule
*Results in a reduction of static load failure for *Increase ferrule Increase fracture resistance of tooth
the restored tooth * Stankiewicz Int Endod J 2002
* Barkhordar et al J Prosthet Dent. 1989 Ferrule
*Increase ferrule Increase fracture resistance of post
* Libman & Nicholls Int J Prosthodont 1995 * Torbjorner & Fransson Int J Prosthododnt 2004
* Morgano & Brackett J Prosthet Dent 1999
The finish line of a preparation must end in natural tooth structure. The finish line of a preparation must end in natural tooth structure.
Asepsis
Biological Widths
2010 Position Statement of the
American Association of Endodontists Crown Lengthening
http://www.aae.org
* Caries removal
* Isolation
Only dental dam isolation minimizes the
risk of contamination of the root canal
system by indigenous oral bacteria.
Biological Widths Biological Widths

Restorative margins should end
3mm coronal to alveolar crest
or 1mm coronal to JE
Gargiulo, J Perio 1961
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Biological Widths Restorative margins should end 3mm Flap Design

coronal to alveolar crest
or 1mm coronal to JE
Flap Design/Retraction Flap Design/Retraction
Endodontic therapy is not complete until the

tooth is restored to function
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When is the tooth being restored

*No more than 3 months between RCT and final crown Full Coverage Restorations
* Provision restorations will have marginal breakdown
* Coronal leakage will occur
* The root filling will become contaminated Full cuspal coverage
* Retreatment is recommended.
* Magura et al J Endo 1991
Tidmarsh J Endod 1976
*Fabricate restorations that overlay the cusps or a post, core and
crown
Full Coverage Restorations Are Endodontically Treated Teeth More Brittle?
Full cuspal coverage Sedgley & Messer J Endod1992

Aquilino & Caplan J Prosthetic Dent 2002 *Found no significant differences in biomechanical properties.
*Similarity between biomechanical properties of endodontically
*Six times greater rate of survival if restored with a full cuspal treated teeth and their vital pairs indicates that teeth do not
coverage restoration. become more brittle following endodontic treatment
Full Coverage Restorations

Endodontic therapy is not complete
until the tooth is restored to function
Are Endodontically Treated Teeth More Brittle?
Sedgley & Messer J Endod1992

*It is the cumulative loss of tooth structure from caries, trauma,
restorative and endodontic procedures (access and preparation)
that leads to susceptibility to fracture
Rapp, Brown & Newton 1991

Sig n ifican tly b etter h ealin g was seen with teeth th at were
p erman en tly resto red fo llowing surgery.
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Reversible pulpitis Irreversible pulpitis Irreversible pulpitis

(symptomatic) (asymptomatic)
Pulpal & Periradicular Diagnosis Non-lingering Spontaneous No clinical symptoms
(thermal tests)
Pain lingers after Inflammation
Not spontaneous stimuli (thermal tests) produced by:
Usually severe Caries
Caries excavation
Trauma, etc.
An inflammatory process in the periradicular tissues

Pulp necrosis Previous root Previously caused by microorganisms in the infected root canal
canal therapy initiated therapy
No response to Canals are Partial endodontic

thermal or obturated therapy
electrical stimuli (e.g. pulpotomy,
pulpectomy)
Sundqvist Scand J Dent Res, 1976 Nair P Periodontol 2000, 1997

Pathways of the Pulp 10th Ed., 2010
Assessment Periapical Diagnosis Assessment Periapical Diagnosis

Acute Chronic
Normal apical Symptomatic Asymptomatic apical abscess apical abscess
tissues apical periodontitis apical periodontitis
Localized swelling, Minimal or no pain
Asymptomatic, Pain to biting and Cannot elicit pain pain, pus formation
Pus drains from a
intact lamina dura percussion or altered sensation Tender to pressure sinus tract
May or may not Apical radiolucent Fever?
have associated area Lymphadenopat hy?
PA radiolucency
PA radiolucency?
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Note: Assessment Periapical Diagnosis

Inflammation does not always equal an infection Acute Chronic
apical abscess apical abscess
Aim: Localized swelling,

pain, pus formation
Minimal or no pain
Pus drains from a
Establish Drainage! Tender to pressure

Fever?
sinus tract
Lymphadenopat hy?
PA radiolucency?
Avanced Endodontics Advanced Endodontics

Diagnosis Diagnosis
Brynolf I. 1970
As additional radiographs are taken, diagnostic accuracy is increased.
73% accuracy with 1 film; 87% with 3 films. Take additional films as needed.
Information Technology
Digital Radiography/CBCT
20
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Dental X-rays Linked to Brain Tumors http://www.webmd.com/brain/news/20120410/dental-x-rays-l
Article Link: http://www.webmd.com/brain/news/20120410/dental-x-rays-linked-brain-tumors
Digital radiography has many benefits: Brain & Nervous System Health Center
* Less Radiation Dental X-rays Linked to Brain Tumors
* 55% less than D Speed Annual X-rays May Expose Patients to Unnecessary Risk
* 45% less than E Speed By Salynn Boyles
WebMD Health News
Reviewed by Louise Chang, MD
* Instant Radiographs Pre Op

April 10, 2012 -- Getting frequent dental X-rays appears to increase the risk for a commonly diagnosed brain
* Unlimited viewing options tumor, a new study finds.
* Conservation of time Exposure to ionizing radiation -- the kind found in X-rays -- is the biggest known environmental risk factor for
largely non-malignant meningioma brain tumors. Routine dental X-rays are among the most common sources of
* Changes in angulations without radiation for most healthy people in the U.S.
removing sensor Po st Op The new study suggests that performing frequent X-rays may expose patients to unnecessary risk.
* No chemical waste "These findings should not prevent anyone from going to the dentist," says lead researcher and neurosurgeon Elizabeth B.
Claus, MD, PhD, of Yale University School of Medicine and Boston's Brigham and Women's Hospital. "But it appears that a
large percentage of patients receive annual X-rays instead of every two to three years, which is the recommendation for
healthy adults."
Bruder G.A., et al. Dental X-ray, Benign Brain Tumors
J Endod. 1999 Apr;25(4):275-6. While the vast majority of meningiomas are non-malignant, they often grow to be very large and can cause a wide range of
potentially serious symptoms, including vision and hearing loss, frequent headaches, memory loss, and even seizures.
They are the most frequently diagnosed brain tumors among adults in the United States, accounting for about a third of all
primary brain and central nervous system tumors.
Several small studies have suggested a link between cumulative dental X-ray exposures and meningiomas, but the findings
were inconclusive.
In the newly published study -- the largest ever to examine the question -- people who reported having "bitewing" X-rays at
least yearly were found to have a 40% to 90% greater risk of meningioma.
The study shows an association but does not prove a cause-effect relationship.
The study included about 1,400 meningioma patients between the ages of 20 and 79 when they were diagnosed between the
spring of 2006 and the spring of 2011.
When the patients' self-reported dental histories were compared to adults with similar characteristics who did not have the brain
tumors, lifetime exposure to either bitewing or panoramic dental X-rays -- which include the upper and lower jaw -- was
significantly associated with meningioma risk. This risk was higher in people who received panoramic X-rays when they were
younger than 10.
The meningioma patients were more than twice as likely as the adults without brain tumors to have had dental X-rays at some
Recent Study Questions Safety of Dental X-rays - American Dental Associ... http://ada.org/6972.aspx point during their lives, Claus tells WebMD.
The study appears in the April 10 issue of the American Cancer Association journal Cancer.
Join/Renew Membership Find-a-Dentist Contact Us ADA e-Catalog Annual Dental X-rays Not Recommended
Claus tells WebMD that the American Dental Association recommends healthy adults receive routine mouth X-rays every two to
three years. Dental X-rays are recommended every one to two years for children and every 1.5 to three years for teens.
Children often require more X-rays than adults because of their developing teeth and jaws and increased likelihood for cavities.
HOME ADA NEWS MEDIA RESOURCES PRESS RELEASES RECENT STUDY QUESTIONS SAFETY OF DENTAL X-RAYS Neurosurgeon Michael Schulder, MD, agrees that the newly published findings make a good case for limiting the frequency of
dental X-rays whenever possible.
Schulder is vice chairman of the department of neurosurgery at the Cushing Neuroscience Institute, which is part of the North
April 10, 2012
Shore-LIJ Health System in Manhasset, New York.
Sign up for e-mail updates
Recent Study Questions Safety of Dental
Press Releases
Press Kits X-rays "The chance of these tumors arising in patients who were X-rayed yearly was low," he notes in a news release. "Nonetheless,
dentists and their patients should strongly consider obtaining X-rays less often than yearly unless symptoms suggest the need
Contact Information:
for imaging."
Telephone: 312-440-2806
E-mail: mediarelations@ada.org (Journalists) or Contact ADA (All Others) Top Picks
CHICAGO, April 10, 2012 The American Dental Association (ADA) is aware of a recent Seizures and Dupuytren's Contracture: What's the Link?
study that associates yearly or more frequent dental X-rays to an increased risk of
Early Signs of Alzheimer's
developing meningioma, the most commonly diagnosed brain tumor. The ADAs
long-standing position is that dentists should order dental X-rays for patients only when The Future of MS Treatment
necessary for diagnosis and treatment. Since 1989, the ADA has published Rehab Programs After Brain Injury
recommendations to help dentists ensure that radiation exposure is as low as reasonably
Treating Relapsing MS
achievable.
Cerebral Bypass Surgery
The ADA has reviewed the study and notes that the results rely on the individuals
memories of having dental X-rays taken years earlier. Studies have shown that the ability
to recall information is often imperfect. Therefore, the results of studies that use this
SOURCES:
design can be unreliable because they are affected by what scientists call "recall bias." Claus, E.B. Cancer, April 10, 2012.
Also, the study acknowledges that some of the subjects received dental x-rays decades Elizabeth B. Claus, MD, PhD, professor, department of epidemiology and public health, Yale
ago when radiation exposure was greater. Radiation rates were higher in the past due to University School of Medicine, New Haven, Conn; attending neurosurgeon, Brigham and Women?s
the use of old x-ray technology and slower speed film. The ADA encourages further
Hospital, Boston.
research in the interest of patient safety.
Michael Schulder, MD, vice chairman, department of neurosurgery, Cushing Neuroscience Institute,
As part of the ADAs recommendations to minimize radiation exposure, the ADA North Shore-LIJ Health System, Manhasset, N.Y.
encourages the use of abdominal shielding (e.g., protective aprons) and thyroid collars on
all patients. In addition, the ADA recommends that dentists use E or F speed film, the two
fastest film speeds available, or a digital x -ray.
In addition to the X-ray recommendations, the ADAs Council on Scientific Affairs will
publish clinical guidance on the use of cone-beam computed tomography in an upcoming
issue of The Journal of the American Dental Association. The ADA will share these
1 of 2 4/10/2
recommendations as soon as they are available.
Dental X-rays are valuable in helping dentists detect and treat oral health problems at an
early stage. Many oral diseases cant be detected on the basis of a visual and physical
examination alone, and dental X-rays are valuable in providing information about a patients
oral health such as early-stage cavities, gum diseases, infections or some types of tumors.
How often dental X-rays should be taken depends on the patients oral health condition,
age, risk for disease and any signs and symptoms of oral disease that the patient might be
experiencing.
The ADA encourages patients to talk to their dentists if they have questions about their
dental treatment. As a science-based organization, the ADA fully supports continuing
research that helps dentists deliver high-quality oral health care safely and effectively.
Additional information about dental x-rays is available on ADA.org.
About the American Dental Association
1 of 2 4/16/2012 9:35 AM
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Pre-surgical Evaluation Program (PREP)

Medical/Dental History
Diagnosis
Reproduce the Chief Complaint
Determine the Cause
Eliminate the Cause
Psychological (anxiety, behavioral observations)
Pre-surgical Prophylaxis
Preoperative Medication
Anatomical Considerations
First, Do No Harm
Anatomical Variations Anatomical Variations

Premolars
Root Canal Anatomy of the human permanent teeth.
Vertucci F . Oral Surg 1984;58:589 99
Brynolf I. 1970
As additional radiographs are taken, diagnostic accuracy is increased.
6% have three canals 73% accuracy with 1 film; 87% with 3 films. Take additional films as
needed.
Anatomical Variations Anatomical Variations
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Anatomical Variations
Pre-surgical Evaluation Program (PREP)
Comparison of Periapical Radiography and Limited Cone-Beam Computed

Tomography in Mandibular Molars for Analysis of Anatomical Landmarks before
Apical Surgery.
Michael M. Bornstein, Roland Lauber, Pedram Sendi, Thomas von Arx.
Journal of Endodontics Vol. 37, Issue 2 ,Pages 151-157
CBCT
Velvart 100% detection of apical lesions

Velv art P, Hec k erH, Tillinger G. Detection of the apic al lesion and the mandibular canal
in c onv entional radiography and c omputed tomography. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 2001;92:6828.
Randolph Todd, DMD

Past President: College of Diplomates of the American Board of Endodontics
CBCT
Denio D, Torabinejad M, Bak land LK. Anatomical relationship of the mandibular canal to its
surrounding structures in mature mandibles. J Endod. 1992;18:161165
An terio r Nasal Sp in e
In cisiv e Fo ssa
Can in e Emin an ace
Greater Palatin e Fo ramen
Men tal
23
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Microscopes
Microscopes
Anesthesia
Incisions
Osteotomy
Baumann RR.-
Hemostasis How may the dentist benefit from the
Root End Resection RER operating microscope?
Root End Preparation REP Quintessance Int 1977;5:17-8.

Root End Materials REM
Sutures
Complications of Treatment/Perforations
Magnification
Buhrley et al JOE April 2002
Dr Howard Selden- * Effect of Magnification on Locating the MB2 Canal in Maxillary 1 st

Th e sign ifican t redu ct ion in u n t reat able can als
Molars Molars
is probably micro-en dodon t ics
great est con t ribu t ion
* Scope - 71.1%
* Loupes - 62.5%
Pa Dent J May-June 1986 , 36-37. * No Mag -17.2%
Wit h micro-en dodon t ics mu ch of t h e in visible h as

been elimin at ed, an d mu ch great er precision
at t ain able, accomplish ed con siderably more gen t le
t o bot h pat ien t s an d t issu es.
1995 In Chicago
ZEISS USA OPMI PROergo Dentistry
ZEISS USA OPMI PROergo Dentistry
OPM I PROe r g o

OPM I PROe rgo

Pecora, Andreana
Use of Dental Operating Microscope OOO 1993;
75:751-758.
<PO Pain
<PO Swelling
Approximately 50 Post Graduate Endodontic

Chairmen voted to teach the use of Microscopes
in Conventional and Surgical Endodontics by January 1998.
24
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Proper positioning is a must...

*Equipment positioning
*Patient positioning
*Assistant positioning
*Surgeon positioning
Micro-Endodontic Education
25
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Anatomy/Positioning? Anatomy/Positioning?
Positioning is everything Surgeon Positioning Courtes y Steve Niemcz yk

Position yourself behind the patient?
Floor
26
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Adjustable surgeon s chair with armrest

*Arms/Hands: arm supports provide comfort and minimize
fatigue
Thighs should be at 10- 15
Hand Signals
*Index finger
*Number of fingers
*practice with your assistants
Microscopes
Anesthesia
Anesthesia Proper anesthesia and hemostasis is essential
Incisions * Location:
* Infiltration / Block
Osteotomy * 2-3mm. Below the Mucogingival Junction
Hemostasis * @ The Apex of Roots
Root End Resection RER
Root End Preparation REP
1:50,000 epinephrine
* Buckley 1984
Sutures
27
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Best hemostasis is achieved preoperatively Proper anesthesia and hemostasis is essential

*Correct placement and injection rate (minimize adrenergic * Location: at the apex of roots in addition to blocks and/or
response in skeletal muscle) infiltration's
*Sufficient time for diffusion (5-10 minutes) 1:50,000 epinephrine Milam SB
Gage TW
Adrenergic receptors Gutmann/Harrison
Kim S
Roberts, Sowray (1987) Local Anesthesia in Dentistry
*
Curtis, 1966
* 2
Beta effect-
* Restricted blood flow slowly returns
* Localized tissue hypoxia and acidosis caused by prolonged
vasoconstriction
How much blood is typically lost during endodontic surgery?
*Avg 9.5 ml; similar to tooth extractions
Yagiela- Pharmacology and Therapeutics for Dentistry *Time biggest factor
BLOOD LOSS DURING ENDODONTIC SURGERY

SELIM HA, EL DEEB ME, MESSER HH.
ENDOD DENT TRAUMATOL 1987;3:33-36
Microscopes
Anesthesia Incisions should not be closer than 4mm. to a bony defect...
Incisions
Incisions
Vertical incisions must be at least one tooth lateral to tooth
Osteotomy
being operated on...
Hemostasis
Root End Resection RER Flaps
Root End Preparation REP *Envelope
Root End Materials REM *Semilunar
Sutures *Submarginal Ochsenbein-Luebke
Complications of Treatment/Perforations *Intrasulcular
*Papilla based
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Microsurgical scalpels Microsurgical scalpels
Folke LE, Stallard RE.

J Periodontal Res. 1967;2(1):53-63
Folke LE, Stallard RE.
J Periodontal Res. 1967;2(1):53-63
RETRACTION
Air Force Flap

Rud J & Rud V. JOE 1998
Velvart Int Endod J. 2002
Int Endod J. 2004
J Endod. 2005
Endo Topics 2005
Lubow RM, Way man BE, Cooley RL. Endodontic flap design:
analysis and recommendations for current usage.
Oral Surg Oral Med Oral Pathol. 1984;58:207212
29
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Microscopes
Proper location:
Anesthesia
*Advanced Imaging
Incisions *locate pathology (where bone is thin)
Osteotomy
Osteotomy *measure location from radiograph and transfer using sterile file or rule
Hemostasis *measurement of the last file used during n.s. tx.
*cut small window and take radiograph
Use surgical handpiece to establish bony window ( osteotomy) with a #6 or
Root End Preparation REP #8 carbide bur or Molt
Molt
Sutures Copious irrigation to maintain bone temperature
Complications of Treatment/Perforations (Fister & Gross Oral Surg. 49;105, Feb., 1980)
Eberhardt, Torabinejad, Anatomical Considerations

Oral Su rg Oral Med Oral Path o l. 1 992 Mar;73(3):3 45-6.
30
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Osteotomy Approach
Microscopes
Anesthesia
Incisions
Osteotomy
Hemostasis
Hemostasis
Sutures
Ibarrola JL et al. JOE 1985

an alyzed bon e wax, Su rgicel, an d Gelfoam in
osseou s defect s an d fou n d t h at all t h ree were
associat ed wit h an inflammatory response that
impaired osseous regeneration
Proper Anesthesia
Bone wax (ethicon)
Hemostasis in Periradicular surgery Witherspoon DE & Nu Gauze (plain)
Gutmann JL(1996) Int Endodn J 29:135-149
Telfa
CollaTape/CollaPlug
Parameters of Achieving Quality Anesthesia and
Epidri
Hemostasis in Surgical Endodontics Gutmann JL (1993) Anesth
Hemodettes
Pain Control Dent 2: 223-226
CUT~TROL/Monsel
(Ferric Subsulfate)
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Telfa
CollaTape/CollaPlug
Hemodettes
Chemical
AlCl2 gel (Hemodette)
- necrosis, removal
FeSO4 (conc. 15.5%-20%)
Hemostasis
Proper Anesthesia Hemos tatic Effic acy and Cardiovascular Effec ts of Ph y sical
Agents Us ed During Endodontic Surgery
Bone wax (ethicon) Francine J. Vickers, J. Craig Baumgartner, Gordon Marshall. Calciu m su lfate
Nu Gauze (plain) Journal of Endodontics Vol. 28, Issue 4 ,Pages 322-323 Nu Gau ze (p lain )
KY jelly
Telfa Min i su ctio n tip
CollaCote
Epidri Ferric sulfate hemostasis: Ch emical
Effect on osseous wound healing. Part I & II FeSO 4 (co n c. 15 .5%-20%)
Hemodettes
AlCl2 g el (Hemo d ette)
Monsel s solution Ronald R. Lemon, Paul J. Steele, Billie G. Jeansonne.
Par t I -Journal of Endodontics Vol. 19, Issue 4 ,Pages 170-173 - n ecro sis, remo val
CUT~TROL Ph y sio lo g ic
Billie G. Jeansonne, William S. Boggs, Ronald R. Lemon
(Ferric Subsulfate) Par t II- Journal of Endodontics Vol. 19, Issue 4 ,Pages 174-176 Av iten e,Co llaPlu g /Co te
- p lacemen t, actio n (p latelet p lu g )
Microscopes
Proper Anesthesia Anesthesia
Bone wax (ethicon) Incisions
Nu Gauze (plain) Osteotomy
Hemostasis
Telfa Root EndResection
Root End ResectionRER
CollaTape/CollaPlug RER
Epidri Root End Materials REM
Sutures
Hemodettes
CUT~TROL/Monsels
(Ferric Subsulfate) Lin, Langeland, OOO 1991
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Root End Resection/Inspection
Resected Root Tip

*Apical 2-3mm
* Secondary Weller, Nimc z y k , Kim 1995
* Accessory Is thmus (c omplete or partial 100% time, MB Root)
*Removal of granulomatus tissue
*Irregular/incomplete outline may indicate
incomplete resection
Basic configurations
Unlimited variations
Affects ability to completely debride
and fill the canal system
Must understand to perform RCT
Hess and Zurcher 1925
33
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Gra phic Co urtesy of Stephen Niemczyk
Root End Resection/Inspection Tidmarsh, Arrowsmith (1989)

Apica l Dentin Permea bility a nd Micro lea ka g e Impact Air HP
Asso cia ted with Ro o t End Resectio n a nd
Retro g ra de Filling . Bevel related to tubule
exposure
Reverse bevel presents
Intact ++ +++ placement / finishing
Resected Root Tip
difficulties
*Apical 2-3mm 00
Velv art P, Peters CI
30
0
45 Impact Air HP
* Secondary Soft Tis s ue Management in Endodontic Surgery
H2O stream only
J Endod. 31(1) 4-16, 2005
* Accessory 45 angle offers greater
access flexibility
Gilhea ny , Fig do r and Tya s, J Endodon 20(1): 2 2-25, 1 99 4
Root End Inspection

Tidmarsh, Arrowsmith ( IEJ 1989)
Apica l Dentin Permea bility a nd Micro lea ka g e
Resected root tip
Asso cia ted with Ro o t End Resectio n a nd Impact Air HP * Removal of tissue
Retro g ra de Filling . Bevel related to tubule * Mirror image of
exposure resected surface
Reverse bevel presents * Irregular outline may
placement / finishing indicate incomplete
difficulties resection
Impact Air HP
H2O stream only

45 angle offers greater
Gilhea ny , Fig do r and Tya s, J Endodon 20(1): 2 2-25, 1 99 4 access flexibility Gutmann & Harrison 1985
In tern atio n al En do don tic Jo urnal (19 85) 18 , 8-34
34
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Root End Resection/Inspection
Root End Resection/Inspection Root End Resection/Inspection

Staining RER
Ho
Thaw nk
is yyour
o u,
resectio n?
Stev e
Root End Resection/Inspection Root End Inspection

Cambruzzi JV, Marshall FJ, Pappin JB
Methylene Blue Dye: An Aid to Endodontic Surgery
J Endodon 11(7): 311-314, 1985
Methylene Blue Dye
Outlines roots
Delineates root dentin
from bone
Isthmus
Extra canals
Incomplete resection
Outlines cyst for
enucleation
35
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Root End Inspection Root End Resection/Inspection

Cambruzzi JV, Marshall FJ, Pappin JB
Methylene Blue Dye: An Aid to Endodontic Surgery
J Endodon 11(7): 311-314, 1985
Methylene Blue Dye
Outlines ro o ts
Delinea tes ro o t dentin Resected Root Tip

fro m bo ne *Apical 2-3mm
Isthmus * Secondary Weller, Nimc z y k , Kim 1995
Ex tra ca na ls * Accessory Is thmus (c omplete or partial 100% time, MB Root)
Inco mplete resectio n
*Removal of granulomatus tissue
Outlines cy st fo r
enuclea tio n
*Irregular/incomplete outline may indicate
incomplete resection
Fra ctures
Microscopes
Anesthesia
Incisions
Richman, (1957)
Osteotomy
Serota & Krakow 1983 ultrasonic chisel
Hemostasis
*Discussed if good conventional cleansing and obturation have not Root End Resection RER
been accomplished prior to surgery, additional efforts must be
expanded during the surgical procedure to debride clean and Root End Preparation REP
obturate the canal from the apex, prior to creating an apical Root End Materials REM Carr, G. (1992)
seal. Sutures
Rud et al. 1972 Complications of Treatment/Perforations
* Showed that not doing so lead to a higher incidence of failure
APICAL PREPARATION
Root End Preparation
Alignment
Long axis /root: mark on
osseous surface
Tip angle / Handle (standard
vs. back-action)
Diamond vs. Smooth
Engle, Steiman (1995) JOE
Preliminary Investigation of Navarre, Steiman (2002) JOE
Ultrasonic Root-End Preparation Vol. 28, No. 4: 330-332
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ROOT END PREPARATION ROOT END PREPARATION
Alignment Alignment
Long axis /root: mark on osseous surface Long axis /root: mark on osseous surface
Tip angle / Handle (standard vs. back-action) Tip angle / Handle (standard vs. back-action)
Surgical Endodontics
Apical Preparations
Surgical Endodontics
REP Cleaning ?
Craig KR, Harrison JW.
Wound healing following demineralization of resected
root ends in periradicular surgery. J Endod 1993.
37
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Microscopes
Drying Preparations Anesthesia
Stropko Irrigator
Incisions
Osteotomy
Hemostasis
Sutures
Chapman-Huffman (Irrigator Complications of Treatment/Perforations
Regulator Kit, Part #17-050-00) 5-7lb/in 2
38
02/12/2017
Amalgam Zinc-free Amalgam Zinc-free

Super EBA Omnell,1959 Super EBA Omnell,1959
MTA Moodnik et al. 1975 MTA Moodnik et al. 1975
Tenca, JOE, 2:25, Jan., 1976 Tenca, JOE, 2:25, Jan., 1976
EndoSequence- Oynick, JOE 1976 EndoSequence- Oynick, JOE 1976
Root Repair Mat er ial Root Repair Mat er ial
High Copper High Copper
Phillips & Isler 1983 Phillips & Isler 1983
Dorn SO, Gartner AH. Retrograde filling materials: a retrospective success-

failure study of amalgam, EBA, and IRM. J Endod 1990.
Friedman S, Retrograde Approaches in Endodontic
Therapy, Endod Dent Traumatol 1991; 7:97-107.
75% for amalgam, 91% for IRM, and 95% for SuperEBA
Less irrita ting
Fran k LF, Glick DH, Patterso n SS, Wein e FS.

Lo n g -term ev alu atio n o f su rg ically p laced amalg am fillin g s.
J En d o d 1 9 9 2 ;1 8 :3 9 1 8 .
ROOT END FILLING MATERIALS

ProRoot MTA Benefits
Ron Lemon
On Sealability
MTA provides a better apical seal as a root-end filling material than Amalgam, IRM or
Super-EBA .
Particles suspended in a liquid
medium exhibit friction
Compression of a slurry mixture
Fisher, E. et al J Endod Vol 24 Num 3 tends to force out the liquid and
March 1998 , pp176-179 leave the particulate
Vibration of a slurry reduces friction Hoover Dam Construction
of the particulate = flow
39
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TOOTH #8 SURGICAL RETREATMENT

A Question of Scale
How to Make a Slurry Flow is Known
n Particles suspended in a
liquid medium exhibit
friction
n Compression of a slurry
mixture tends to force out
the liquid and leave the
particulate
n Vibration of a slurry
reduces friction of the Hoover Dam Construction
particulate = flow
Ron Lemon
Microscopes
Silk: 4.0 , 5.0 , 6.0
Anesthesia
GORE-TEX: Suture is a microporous, non-absorbable
Incisions monofilament made of expanded polytetrafluoroethylene (ePTFE).
Osteotomy
Hemostasis
Becker, Vicryl (polyglactin) little
Root End Resection RER inflammatory response
Root End Materials REM Kim, Remove sutures in 2-3 days .
Sutures
Sutures Gutmann, Harrison, Surgical Endodontics, 1991
PS2 & FS2 P3
Suturing
Deklene: The strong, smooth, pliable Deklene
polypropylene suture provides superior handling,

accurate knot placement and knot security.
Tevdek II: Impregnated polyester material with the
characteristics of silk and the bacterial colonization
resistance of Gore-tex (PTFE coating)..
40
02/12/2017
Suturing
Epithelial seal at 2 days
Harrison and Jurosky

Kim
Harrison and Jurosky J En d o d VOL. 17, NO. 9, SEPTEMBER 1991
Microscopes
Anesthesia
Incisions
Osteotomy
Hemostasis
Sutures
Complications
Complications ofof
Treatment/Perforations
Treatment/Perforations
Harrison and Jurosky J En d o d VOL. 17, NO. 9, SEPTEMBER 1991
Nonsurgical vs. Surgical Endodontics Proper Anesthesia

Bone wax (ethicon)
Complications of Nu Gauze (plain)

Telfa
CollaTape/CollaPlug
Treatment Epidri
Hemodettes
CUT~TROL/Monsel s
(Ferric Subsulfate)
41
02/12/2017
Fuss Z, Trope M., Endod Dent Traumatol. 1996 Dec;12(6):255-64.

Root perforations: classification and treatmentchoices based on prognostic factors .
Perforation of Schneiderian Membrane

Lin, Langeland, J Endodon. 1985; 11: 40-44
Complications of Treatment
Perforation Repairs
Management of instrument perforations in the
periodontal ligament space during endodontic or
restorative procedures is an ongoing problem in
dentistry. The introduction of microscopes, new
instruments and materials has resulted in more
controllable and predictable surgical and non-
surgical outcomes. This paper discusses some of
the newer techniques and materials used to
manage perforations effectively.
George A. Bruder III, D.M.D.; Seymour F riedman, D.D.S.
May 1999, Volume 65, Number 5 Lemon, R.R.- Dent Clin North Am. 1992 Apr ;36 (2):439-57
Regan JD, Witherspoon DE, Foyle DM. Surgical repair of root and Prognostic Factors in Endodontic Microsurgery. J Endod 2011;37:927-933.
tooth perforations. Endodontic Topics 2005;11:152-178.
42
02/12/2017
Friedman, S. The prognosis and expected outcome of apical surgery.

Prognostic Factors in Endodontic Microsurgery. J Endod 2011;37:927-933. Endodontic Topics 2005;11:219-262.
Conclusions: Under the control of the significant variables in

logistic regression, the potential prognostic factors on the outcome
were:
sex
tooth position
lesion type
root-end filling material
On the other hand, the tooth position was a pure predictor of an

endodontic lesion affecting the clinical outcome. Toronto (Friedman) 74% healed; 91% functional
Rubinstein, Kim 97% (3-12 mo.); 92% (5-7yrs.)
Endodontic therapy is not complete

until the tooth is restored to function
If you can dream it, you can do it.
Walt Disney
Rapp, Brown & Newton 1991

Sig n ifican tly b etter h ealin g was seen with teeth th at were
p erman en tly resto red fo llowing surgery.
43
Dr. arry Myers c rrently serves as the grad ate endodontic rogram director at irginia
Commonwealth University in ichmond, irginia. e com leted his dental school
ed cation at the University of Te as ealth Science enter at San Antonio in .
Following grad ation Dr. Myers entered the USA here he served for fo r years as a
general dentist before entering the endodontic residency rogram at ilford all Medical
Center at Lac land AFB also in San Antonio. In 1 after serving on active d ty for 3
years, Dr. Myers left the USA to enter rivate ractice in lym ia, ashington here he
racticed for the ne t years. n the s mmer of 14, f ll time ed cation entered the
ict re hen Dr. Myers acce ted a osition at CU where he no or s. Dr. Myers has
been active in organized dentistry having served as the resident of the ashington State
Association of Endodontists in - and he is c rrently the resident-elect for the
American Association of Endodontists having been involved over the last nine years with
vario s committees of the AAE as ell as serving on the Board of Directors. e has s o en
internationally in both Ja an and atemala as ell as serving as a scientiic oster dge
at the recent AD meeting in Brisbane, A stralia.
UTHSC San Antonio, Texas
- Dentistry
Traumatic Dental Injuries
& Root Resorption
an endodontic perspective
USAF Dental Corp
Private Practice
My background
Olympia, WA
Garry L. Myers, DDS
The relationship between traumatic dental injuries Traumatic dental injuries

and root resorption
Traumatic dental Root resorption

injuries
I. Crown fractures
II. Luxations
III. Avulsions
IV. Root fractures
Traumatic Dental Injuries

For every force (action), there is an equal and
opposite force (reaction).
Root resorption
I. External root resorption

II. Internal root resorption
III. Cervical root resorption
1
Crown fractures Complicated crown fractures
assess pulpal vitality / root development
I. Enamel-dentin fractures Tx options
II. Complicated crown fractures I. Pulp cap
III. Crown-root fractures II. Shallow pulpotomy (Cvek)
III. Complete pulpotomy
IV. Root canal therapy
Treatment options:
DiAngelis AJ, et al
Dent Traumatol 2012
The Cvek pulpotomy Crown-root fractures

Complex injuries
3 year recall
Remove the coronal segment
Restore if possible
Crown lengthening prn
Surgical or orthodontic extrusion
Pulpotomy or RCT prn
March 1999 July 1999 June

July
2000
2002 DiAngelis AJ, et al
Dent Traumatol 2012
Cvek, M J Endod, 1978
Cvek, M J Endod, 1983
Fuks AB, et al Pediatr Dent 1993
Luxations Luxations
I. Lateral luxations
- treatment principles
II. Intrusive luxations
Reposition the tooth
III. Extrusive luxations
Splint / stabilize the tooth
IV. (Concussions/subluxations)
Vitality testing
Follow up and treat as needed
Andreasen JO
2
Luxations Intrusive luxations
- prognosis of these injuries
Maximum damage to pulp and PDL
Pulp necrosis or calcific metamorphosis Can reposition surgically, orthodontically or
allow to re-erupt on their own
Extrusive and lateral luxations of mature roots: Long term prognosis often unfavorable
- 55-60% develop pulp necrosis within 1 year.
- if an open apex, only 5% become necrotic,
but 35% experience pulp canal obliteration.
Intrusions: mature roots 85% develop pulp necrosis.

open apex 50% develop pulp necrosis.
(Dentaltraumaguide.org)
Avulsion injuries Avulsion injuries

- critical factors
Time out of the socket
Storage medium
Splinting type and duration
Stage of root formation
-- Andreasen, JO

- consequences of avulsions - case reports
Attachment damage Avulsed #8, luxated #9 replanted within 10 minutes
Pulpal necrosis and bacterial ingress
Root resorption inflammatory & replacement
Mature roots with closed apices:

Replanted within 5 min 5-10% resorption
Replanted within 1 hour 25-60% resorption
Replanted over an hour 35-75% resorption
9-20-2006 10-30-2006 8-8-2011
Eval Obturated 5 year recall
(Dentaltraumaguide.org)
3
- case reports - case reports
Avulsed #8 on Xmas eve, kept in milk for 4 hours 7 y/o avulsed #8 & 9 playing football, unknown time
out of mouth, but were stored in milk.
9-29-2015
12-28-11 1-31-2013
7-18-2012 9-5-2013 7-27-2015 8-3-2015 11-11-2015
(Courtesy Dr. Cyrous Ardalan)
Horizontal Root Fractures

Horizontal root fractures
These can be sub-classified on the basis of:
Location of fracture line
(cervical, middle, apical)
Extent of fracture (partial or complete)
Number of fracture lines
(simple, multiple, comminuted)
Position of coronal segment
(displaced or non-displaced)
Root fractures Root fractures

- horizontal root fractures - four modes of healing
Teeth must be repositioned & Healing with calcified tissue

stabilized Interposition of connective tissue
Rigid or flexible splint 4 weeks Interposition of bone & connective tissue
to 4 months Interposition of granulation tissue
RCT / CaOH tx of coronal (Andreasen & Hjorting-Hansen, 1967)
segment if pathosis develops
4
Case report: History of trauma 3 months earlier, Case report: Trampoline accident 4 days earlier, tooth
root fracture stabilized and splint removed 2 weeks later. splinted that day. Tooth #8 non-responsive to cold.
Patient presents now with pain on biting down on #9.
Sep 1, 2016 Oct 14, 2016 Dec 1, 2016
On Dec 1, tooth #8 responded to cold testing!
(Courtesy Dr. Nick Schroeder) (Courtesy Dr. Laura Garden)
Splinting teeth Dentaltraumaguide.org

- requirements
Passive placement
Stabilize teeth in position
Easy to make/place
Does not interfere with occlusion
Allows endodontic access
Allows good oral hygiene
Easily removed
(Neaverth & Goerig, 1980)
Take home points regarding traumatic dental

injuries: One common sequelae to many of the more
significant dental injuries...........
Get a good history of the traumatic event!
Young pulps have a great capacity to heal. A non-
responsive pulp does not imply pulp necrosis.
Infection related resorption progresses very rapidly in
immature teeth!
Endo tx is NOT a 1st priority in root fracture cases.
Every traumatic injury is its own individual injury!
Multiple injuries to a tooth decrease the prognosis. Root Resorption
5
I. Historical background
II. Mechanisms of resorption
III. External root resorption
IV. Cervical root resorption
V. Internal root resorption
I. Historical Background
1951 Henry & Weinman

1894 Gaskill Histological study of extracted teeth
Case report of internal > 90% showed some type of evidence related to
resorption w/ a pink spot external root resorption
1930 Gottlieb & Orban

Described internal root
resorption
1966 Andreasen &

Hjorting-Hansen 1979 Harrington &
Natkin
Studies with replanted teeth
defined 3 types of external First described post-
resorption: bleaching cervical
- surface resorption
- inflammatory
- replacement
6
1981 Al Frank
First described extracanal invasive resorption Heithersay 1999
Invasive Cervical
Resorption
Quintessence Int 1999,

Endo Topics 2004
1982 Present
.but,
Primary teethwhen
resorbpermanent teeth resorb,
physiologically..
Many reports/studies on root resorption since
it is pathologic.
1982
Root Resorption
How does root resorption take place?
Responsible cells: odontoclasts / osteoclasts

Osteoclasts are attracted to specific proteins
present on calcium salt crystals in mineralized
II. Mechanisms of resorption tissues such as bone and dentin.
Under normal circumstances, the mineralized
tissues of permanent are resistant to resorption.
7
Two things that need to happen before root A. Protective layers against resorption
resorption can occur --- what are they?
A. loss/alteration of protective layer

B. inflammation present next to dentinal surface
Cementum and pre-dentin Odontoclasts are considered a variant of the

both are unmineralized layers osteoclast. A vast amount of our knowledge
both are resistant to the resorptive process regarding these cells comes from studies of
bone physiology and pathology.
Levin & Trope, Quintessence, 2002
Osteoclasts will not adhere to NOR resorb B. Inflammation

unmineralized matrix
Destructive phase
acidic environment
-clastic cells active
will continue as long as
stimulus is present
8
External root resorption:
--- A physiologic or pathologic process
resulting in the loss of dentin or cementum
which initially begins in the periodontium and
affects the external or lateral surfaces of a tooth.
-- AAE Glossary of Terms
A. Apical/ lateral root resorption

B. Cervical root resorption
A. Apical/lateral root resorption

1. Surface Resorption
1. Surface
2. Inflammatory
3. Replacement
(Andreasen)
Henry & Weinmans study ?

Transient stimulus followed by cemental healing
2. Inflammatory Resorption 3. Replacement Resorption
pulpal bacteria / infection Ankylosis

sulcular bacteria Trauma most common etiology
Pressure - impacted teeth, ortho tx Bone replacing tooth structure
9
Treatment principles
In osseous replacement resorption, bone is
for external root resorption
undergoing a normal physiological process,
thus is essentially untreatable.
A. Apical/lateral inflammatory resorption

Remove the etiology!
RCT
CaOH
therapy
Prognosis
Pre-tx film 18 month recall
Avulsion injuries
How does CaOH work? - case report
Antibacterial 2-25-2003 2-17-2004 7-20-2009
Influences pH in dentin referral film MTA #9, GP #10 5 year recall
Possibly stimulates repair on root surface
10
B. Replacement resorption Replacement resorption
Treatment principles in adults:

RCT (?) Can maintain in the absence of
CaOH (?) symptoms, however the root will
Prognosis (?) gradually resorb away as it is
replaced with bone ultimately
resulting with the crown of the tooth
fracturing away from the ridge.
The tooth preservation phase:

In kids, two principles to consider:
If you can preserve these teeth beyond the
1. Tooth preservation phase
individuals growth phase,
2. Ridge preservation phase consider it a success!
Hypothesis: if inflammation can be minimized,

could resorption then be reduced?
RCT may be beneficial.
Ledermix paste?
The ridge preservation phase: Decoronation
If the tooth becomes in infraposition of

2mm or more, the tooth will not erupt and
the ridge will not grow! 5/2009 5/2009
Treatment Decoronation
Goal: to preserve a good osseous ridge for
implant placement after the growth
phase is complete!
5/2012
-- Malmgren
11
Summary of treatment principles
1. Inflammatory root resorption is very treatable

remove the etiology!
2. Replacement resorption is a result of normal cells
performing their normal function, thus is not
treatable, but can/should be managed.
3. Replacement resorption can be a rapid or very slow
progressive process.
Extracanal invasive resorption

Cervical root resorption (aka)
Typically asymptomatic
1. post-bleaching resorption Histologically similar to
2. Invasive cervical resorption other inflammatory
3. extracanal invasive resorption defects
resorption Pulp tissue plays no role
4. Sub-epithelial external in process
inflammatory resorption Cervical region of the
5. And other related terms root is invaded by
fibrovascular tissue from
the PDL
Southan, 1967 Post-bleaching resorption

- reported 5-10% incidence where enamel and cementum do
Harrington & Natkin, 1979
NOT meet in cervical area
younger patients
history of trauma
history of RCT & N-V bleaching
Gap Flush Overlap

Neuvald, et al, J Endod, 2000
Cervical region prone to resorption
12
Pre-disposing factors to cervical resorption:
Heithersay 2004
Orthodontics
Invasive Cervical Trauma
Resorption Bleaching
Endo Topics 2004,7,73-92 Surgery
No identifiable factor
Heithersay, 1999
(Good summary article.)
Potential predisposing factors to ICR Other proposed etiologic factors:
Playing wind instruments?
Contact with cats?
Asymptomatic tooth #11

If long standing, granulation tissue in the dentin can referred for evaluation for
be seen undermining enamel pink tooth. internal root resorption
Often misdiagnosed as internal resorption!
13
Giannopoulou, et al, 2008, J Clin Periodontol
Llamas-Carreras, et al, 2010, Int Endo J
29 premolars orthodontically tipped buccally
for 8 weeks => 27 of 29 showed clear signs Compared root resorption in endo-treated
of buccal cervical resorption. teeth vs their contralateral teeth with vital pulps
during orthodontic treatment.
18 contralateral premolars served as controls
no ortho tx => only 1 of 18 showed buccal No significant differences were found.
cervical resorption.
Can we remove the cause if it is sulcular bacteria?

Treatment options for cervical resorption:
1. RCT / internal repair

2. Surgical repair
3. Combined RCT / surgical tx
4. Orthodontic extrusion
5. Do nothing observe
Frank & Torabinejad, 1998

Heithersay, 1999
2. Surgical repair
1. RCT / internal repair
Case #1
8-13-2012 8-30-2012
8-30-2012 8-30-2012
14
3. Combined RCT / surgical tx
4. Orthodontic extrusion (& repair)
The concept here ------

extrude the entry point(s) above bone
and restore the resorptive defect.
For Heithersay Class I & II cases: For Heithersay Class III & IV cases:
1. Reflecting a flap starts by disrupting the Use of Trichloracetic acid

blood supply to the area.
Heithersay, 1999 non-surgical tx using
2. Clean out both the tooth and bony defects. a topical application of 90% aqueous solution
of trichloroacetic acid for 1-2 minutes.
3. Restore the tooth.
Theory that this causes coagulation necrosis
4. Monitor tooth vitality post-op of the resorptive tissues.
5. Do nothing & follow

Summary of treatment principles
for cervical resorption
1. Stop the continuation of the process.

2. Restore unprotected root surface with
restorative material.
2-8-05 8-31-06 3. When extensive, long term prognosis is
questionable.
8-29-07
8-13-09
8-15-11
15
The use of CBCT in root resorption cases Patel, et al, 2009 CBCT had better sensitivity than PA films.
Cohenca, et al, 2007, Dental Traumatology CBCT and extracanal invasive resorption
discussed and illustrated clinical applications of
cone beam computed tomography for the
diagnosis and treatment planning of root
resorption.
Estrela, et al, 2009 CBCT detected root resorption Case report: 61 y/o female referred to evaluate
much more frequently than PAs.
#21, sensitivity noted to brushing in area.
CBCT and external inflammatory resorption
(Courtesy Dr. Eshwar Arasu)
IV. Internal root resorption
Internal root resorption
described in 1930 by
Gottlieb & Orban
rare in permanent teeth
16
Gaskill, 1894 and Mummery, 1920 Internal Root Resorption
Both presented case reports of Internal
resorption showing pink spots.
Nice review article by Haapasalo & Endal
Endodontic Topics 2006,14,60-79.
In retrospect, it may have been that both of these
Estimated prevalence: 0.01-1%
cases were external resorption in origin.
Diagnostic features to distinguish from external

root resorption
usually asymptomatic Change angles of films, lesion stays centered
oval shaped normal canal shape not visible thru defect
enlargement of pulp
space
part of pulp tissue must
be vital
D. Internal root resorption

RCT
Clean, shape and obturate the
canal space
I. Historical background
II. Mechanisms of resorption
V. Internal root resorption
(Courtesy Dr. Husain Karashi)
17
Thank you for your
Summary attention!
Questions?
18

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2017 Endodontic Board Review and Scientific Update

DAY 1: Friday, February 10, 2017

7 a.m. Registration and Breakfast

7:45 a.m. Welcome

8 a.m. Top 20 Questions on the Top 20 Prescribed Drugs

9:30 a.m. Break

10 a.m. Radiology in Endodontics

11 a.m. Pathology and Endodontics

12:30 p.m. Lunch

3:15 p.m. Microbiology of Endodontic Disease

4:45 p.m. Break

5 p.m. ABE Boardwalk

6 8 p.m. Wine and Cheese Reception

DAY 2: Saturday, February 11, 2017

8 a.m. The Current Best Evidence for Endodontic Treatment Outcomes

9:30 a.m. Break

9:45 a.m. Inflammation and Immunology

11:15 a.m. Break

1:45 p.m. Regenerative Endodontics, Analgesics, Anesthetic Review on Regenerative Endodontics

3:15 p.m. Break

3:30 p.m. Pain Management: Anesthetics and Analgesics

5 6 p.m. Oral Board Exam: Strategies in Preparation and Execution

DAY 3: Sunday, February 12, 2017

8 a.m. Periradicular Surgery and Repair

9:30 a.m. Break

11:30 a.m. Closing Remarks

11:45 a.m. Program Conclusion

B. Ellen Byrne, DDS, PhD

Dr. B. Ellen Byrnes academic background includes a BS in Pharmacy,

She is currently a professor of Endodontics and Senior Associate Dean of

Top 20 questions about the Top 20

#19 warfarin (Coumadin)

#14 atenolol (Tenormin)

#18 clopidogrel (Plavix) #13 zolpidem (Ambien)

#17 citalopram (Celexa) #12 furosemide (Lasix)

#16 montelukast (Singulair) #11 atorvastatin (Lipitor)

Top 20.... and the # 1 prescribed drug is...

#7 omeprazole (Prilosec) 53.4M #3 lisinopril (Zestril) 87.4M

#6 azithromycin (Z-pak) 53.8M #2 simvastatin (Zocor) 94.1M

Drug Abuse Drug Abuse

Drug overdose death rates by state (2008)

Hydrocodone changed schedules.... tramadol (Ultram,Ultram ER, Ultracet)

tramadol (Ultram, Ultracet) tramadol (Ultram,Ultram ER, Ultracet)

Morphine poisoning in a breastfed neonate of a codeine-prescribed

Acetaminophen (N-acelyl-p-aminophenol or APAP) Dosage forms (OTC)

Acetaminophen (N-acelyl-p-aminophenol or APAP) Acetaminophen (N-acelyl-p-aminophenol or APAP)

Combine OTC ex. sleep aid which 1990-1998

Toxicity Acetaminophen (N-acelyl-p-aminophenol or APAP)

Therapeutic Index Acetaminophen

Caffeine 1:100 six 500 mg tablets or 3000 mg/day

Acetaminophen (APAP) Acetaminophen

Red Flags that might indicate substance

Red Flags that might indicate substance

Some interesting facts Some dos and donts.....

Some dos and donts..... Patient information

Many types of pain medication and opioid medication is only one

Disposal of unused medications Statins

Statins #3 lisinopril ( Prinivil, Zestril)

#3 lisinopril ( Prinivil, Zestril) Effects of Elevated BP

#4 levothyroxine (Synthroid) #5 amlodepine (Norvasc)

calcium channel blocker

#6 azithromycin (Zithromax Z-pak) #6 azithromycin (Zithromax Z-pak)

#6 azithromycin (Zithromax Z-pak) #7 omeprazole (Prilosec)

PPI....whats the problem(s)? PPI....whats the problem(s)?