An established lesion can persist for years.

The transition to
an advanced lesion signals the change to a chronic and successful defensive reaction to a destructive immunopathological mechanism, or periodontitis. Two schools of
thought seek to explain this progression: (1) involvement
of a host immune response and (2) involvement of a specific
microorganism in the plaque or a change in the organisms
virulence. The factors responsible for destructive periodontitis developing from reversible gingivitis are unknown.
Advanced periodontal lesions include pocket formation,
ulceration of the pockets epithelium, destruction of the
collagenous periodontal ligament, and bone resorption.
Teeth become mobile and can be lost. The inflammatory
infiltrate extends apically and laterally, reducing collagen
content and accumulating a dense population of lymphocytes, plasma cells, and macrophages. Reparative fibrosis is
noted peripherally, with destruction of the epithelial barrier
between plaque and periodontal connective tissue. As a
result, the loss of attachment becomes irreversible, with
loss of the periodontal ligament and bone and increased
pocket formation. Gingival crevicular fluid contains high
concentrations of IgG, IgA, IgM, complement, and polymorphs. Other notable changes include the inconsistent
invocation of antibodies that seem unable to protect from
disease, rising antibody titers during treatment related to
instrumentation inoculating antigens, and intrinsic mitogenicity or immunogenicity of plaque antigens rather than a
concentration of a single organism as the cause of disease.
The mediation of tissue damage relies more on
hypersensitivity-like responses such as antibody-mediated
cellular cytotoxicity and IgE-mediated hypersensitivity-like
reactions.
Bacteria can directly or indirectly damage tissues. Tissue
destruction can be caused by cytotoxic cellular immune responses to self or pro-inflammatory responses, such as the
release of interleukin 1b (IL-1b), tumor necrosis factor a
(TNF-a), and interleukin 6 (IL-6).

Conclusions.A complex interaction between host

and microbial factors is involved in the pathogenesis of periodontal disease. Targets for treatment include efforts to
improve the hosts ability to prevent microorganisms
from attaching to teeth and restorations, thus keeping
them from colonizing the oral cavity; eliminating pathogenic microbial species; and interrupting the process of biofilm establishment early in the process, before periodontal
processes can develop. Suggested courses of action include
diminishing the humoral response by altering the
pro-inflammatory/anti-inflammatory antibody responses
so plasma cell differentiation is reduced or absent, and
regulating the complex cytokine networks, which would
limit damage at sites of inflammation, among other
interventions.

Clinical Significance.Future treatment strategies should take advantage of all that has
been learned about the pathogenesis of periodontal disease. Because the disease appears
to involve an imbalance between host and microbial influences, efforts should be made to
bolster host immune responses and other factors that will reduce the pathogenicity of oral
microorganisms. Many other possible courses
of action also suggest ways to avoid tissue
destruction and promote a healthy oral
environment.

Hasan A, Palmer RM: A clinical guide to periodontology: Pathology

of periodontal disease. Br Dent J 216:457-461, 2014
Reprints available from RM Palmer, Implant Dentistry and Periodontology, Kings College London Dental Institute, London; e-mail:
rich.m.palmer@gmail.com

Oral Medicine
Lyme disease
Background.The multisystemic inflammatory condition Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried on ticks and transmitted via their
bite. The facts about this disease are useful to dentists who
may be called on to manage oral manifestations (Table 1).
Incidence and Prevalence.Between 1992 and 1998
the US Centers for Disease Control and Prevention (CDC)

recorded 88,967 cases of Lyme disease occurring in 49

states and the District of Columbia. The annual number
of cases increased from 9896 in 1992 to 16,802 in 1998, reflecting most likely a true increase in cases in high-risk areas
as well as more complete reporting overall. Lyme disease
has been seen in North America, Europe, and Asia. New
York, Connecticut, Pennsylvania, Massachusetts, Rhode Island, New Jersey, Wisconsin, and Minnesota have reported

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Table 1.Facts About Lyme Disease



Lyme disease is a bacterial illness that is spread by tick bites.

Lyme disease can affect the skin, joints, heart, and nervous
system.
 Lyme disease occurs in phases, the early phase beginning at the
site of the tick bite with an expanding ring of redness.
 Lyme disease is diagnosed based on the patients clinical signs of
illness and the detection of Lyme antibodies in the blood.
 Lyme disease is treated with antibiotics.

viremia-like syndrome with fever, malaise, nausea, myalgia,

fatigue, headache, and arthralgias.

(Courtesy of Rhodus NL: Lyme disease. Northwest Dent 93:23-25, 2014.)

90% of the US cases. The clinical presentation of the disease

may result from differences in the organism and the immunogenetics of the affected population.
Pathophysiology, Clinical Manifestations, and Laboratory Results.Although the exact mechanism of Lyme disease is unknown, it is suspected that B burgdorferi activates
proteolytic enzymes and induces spirochetemia. Host
response mechanisms produce local inflammation. Peripheral neuropathy may be related to vasculitis. A vascular
lesion resembling endarteritis obliterans has been seen in
meninges and synovium in Lyme disease patients.
Clinical manifestations of Lyme disease occur in three
phases, and patients may not be identified until they reach
the later phases. In the early localized phase, erythema migrans is seen in 50% to 80% of patients within a month of
being bitten by a tick, although only about 30% recall
such a bite. The target or bulls eye lesions of erythema
migrans (Fig 1) are usually found in or near the axilla or
waist. The lesion is usually asymptomatic but may itch,
burn, or hurt. Typically the lesion enlarges over a few
days, and about half of all patients have multiple lesions.
Other early localized phase symptoms include an acute

In the early disseminated phase, which occurs a few

days to months after the tick bite, cardiac and neurologic
problems are likely. Eight percent of all Lyme disease patients experience some cardiac problems, but the carditis
begins to resolve in most cases without antibiotic treatment. The neurologic problems occur in about 10% of untreated Lyme disease patients and include lymphocytic
meningitis, cranial nerve palsy (often affecting the facial
nerve), and radiculoneuritis.
The late disease phase may occur months to years after
the infection with or without earlier manifestations. Musculoskeletal problems predominate and include intermittent,
migratory episodes of polyarthritis in about half of all patients. Chronic arthritis of the knee with erosion of bone
and cartilage is common. This phase may be marked by
chronic inflammatory joint disease lasting 5 to 8 years.
Tertiary neuroborreliosis, which consists of encephalopathy, neurocognitive dysfunction, and peripheral neuropathy, can develop late in the course of the disease.
Symptoms tend to be subtle, including headache, fatigue,
and disturbances of cognition, mood, and sleep. The diagnosis may be confirmed by neuropsychological testing.
Patients with Lyme disease often develop fibromyalgia.
The diagnosis of Lyme disease is based on these clinical
findings, but serologic testing may also be helpful. All
enzyme-linked immunosorbent assay (ELISA) results are
confirmed using Western blot analysis. Mimics of Lyme disease must be considered, including Epstein-Barr virus infection, systemic lupus erythematosus (SLE), and infective

Fig 1.Characteristic presentation of Borrelia burgdorferi tick bite. (Courtesy of Rhodus NL: Lyme disease. Northwest Dent 93:23-25, 2014.)

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Dental Abstracts

Table 2.Dental Management for the Patient with Lyme Disease

Patient Evaluation and Risk Assessment
 Evaluate and determine whether rheumatoid or joint disorder (which) exists.
 Obtain medical consultation if poorly controlled, undiagnosed, or if uncertain.
Potential Issues or Concerns
 Analgesics. If patient is raking NSA1DS, aspirin, or acetaminophen, be aware of dosing and the possibility of being refractory to some
analgesics; dosing and/or analgesic choices may need to be modified in consultation with the physician.
 Antibiotics. No need for antibiotic prophylaxis unless the patient has a prosthetic joint replacement; if so the decision should he based on
the ADA (2003) guidelines if within the past two years; or a compelling condition.
 Anesthesia. No issues.
 Anxiety. No issues.
 Allergy. Allergic reaction or lichenoid reactions possible in patients taking many medications.
 Bleeding. Excessive bleeding may occur if major surgery is performed on patients who take aspirin or NSAIDs, or who may be anemic.
Levels of bleeding are usually not clinically significant and can be controlled with local hemostatic measures.
 Blood pressure. No issues.
 Cardiovascular. In rare cases, heart block and myopericarditis could result and possibly lead to heart failure; therefore careful evaluation
for these conditions should be performed.
 Chair position. Ensure comfortable chair position. Consider shorter appointments and use supports as needed (pillows, towels, etc.).
 Devices. Patients having prosthetic joint replacement should be managed based on ADA (2003) guidelines.
 Drugs. Obtain blood cell count with differential and bleeding time if surgery is planned for patients taking gold salts, penicillamine,
antimalarials, or immunosuppressives. If patient is taking corticosteroids, secondary adrenal suppression is possible but typically is not
clinically significant for dental treatment.
 Equipment. None.
 Emergencies. If surgery is performed, supplemental techniques may be necessary to control bleeding.
 Follow-up. Routine.
(Courtesy of Rhodus NL: Lyme disease. Northwest Dent 93:23-25, 2014.)

carditis. Antibody responses may not be detected within the

first 6 weeks of infection. Most patients with late disease
symptoms are strongly seropositive, but early antibiotic treatment may make patients in the early phase seronegative.

may be present alone or combined with other neurologic

deficits. The parotid glands may also be involved.

Treatment.Patients should be treated promptly with

antibiotics when early symptoms are reported. This can prevent the progression to later stages of the disease. Doxycycline 100 mg given orally twice a day for 3 to 4 weeks is the
first-line treatment for patients in the early phase of Lyme
disease. Doses of 250 to 500 mg of tetracycline or amoxicillin given four times a day may also be effective. For
patients in the late disseminated phase, intravenous antibiotics may be needed, including cephalosporins, penicillin
G, or chloramphenicol. Some physicians treat pregnant
women only using intravenous agents. If the patient has
arthritis and is not responding to antibiotics, intraarticular corticosteroid injections or hydroxychloroquine
may be required. Neurologic damage can be difficult to
manage, with very slow recovery.

Clinical Significance.Dentists can take simple steps to help manage patients with Lyme
disease. Patients with suspicious symptoms
should be referred to their primary care provider for assessment. Patients who have been
diagnosed and are under treatment should
be asked about what medications they are taking and if their symptoms are sufficiently
controlled. Refractory responses to analgesics,
allergic reactions, excessive bleeding when
the patient is taking aspirin or non-steroidal
anti-inflammatory drugs, and the possibility
of cardiac disorders may complicate the delivery of dental care. Chair position may need to
be altered to make the patient comfortable. In
addition, surgical plans should include supplemental measures to control bleeding.

The dentists major role is the identification of unusual

symptoms with no clear medical cause (Table 2). Among
these are fatigue, malaise, arthralgia, neuritis, or neuralgia,
including facial palsy. If these conditions are identified, the
patient should be referred for medical diagnosis. Dentists
should also be aware that facial nerve palsy closely resembles Bells palsy caused by Lyme disease. The facial palsy

Rhodus NL: Lyme disease. Northwest Dent 93:23-25, 2014

Reprints available from NL Rhodus; e-mail: rhodu008@umn.edu

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