journal of dentistry 36 (2008) 95103

available at www.sciencedirect.com

journal homepage: www.intl.elsevierhealth.com/journals/jden

Dis-

Review

Bacterial resistance and the dental professionals

role to halt the problem

Mohammed Al-Haroni *
Department of Oral Sciences Oral Microbiology, Faculty of Dentistry, University of Bergen, Norway

article info abstract

Article history: Objectives: In the present review, background information on bacterial antibiotic resistance
Received 26 September 2007 is presented to dental practitioners. The review provides practical advice for dental profes-
Received in revised form sionals to combat and halt bacterial resistance.
12 November 2007 Data: Antibiotic use over time has led to the emergence of infectious bacteria that are
Accepted 16 November 2007 resistant to several antibiotics. Bacterial resistance is now considered a major threat to
public health, and control of resistance is an international priority. Here, we present the
current basic knowledge on bacterial antibiotic resistance to dental professionals, and
Keywords: discuss their role in combating and halting resistance.
Antibiotics use Sources: The material presented in this review is primarily based on peer-reviewed litera-
Bacterial resistance ture searches in Medline using the phrase antibiotic resistance and the following key
Dentists words: natural, acquired, mechanisms, use, dentists, and role.
Role Conclusions: Antibiotic resistance is a global problem, and dentists must be involved in
halting it. Prudent and judicious use of antibiotic by dentists is an essential method for
combating bacterial resistance. Health authorities are encouraged to monitor trends in
antibiotic prescriptions by dentists and measure antibiotic consumption in order to assess
and limit antibiotic use.
# 2007 Elsevier Ltd. All rights reserved.

1. Introduction Over the years, antibiotic use led to the emergence of

Since their introduction early in the last century, antimicrobial
drugs have revolutionized the treatment of infectious dis-
eases. Sir Alexander Fleming discovered the first antibiotic,
penicillin, in 1928, and 10 years later, sulfonamide was
discovered. Between the 1950s and the early 1990s, new drug
discoveries led to an explosive in antibiotic development.
Following the discovery of antibiotics active against both
Gram-positive and Gram-negative bacteria, surgeons believed
that the ongoing, ancient fight between humans and infec-
tious diseases was nearing its end.
infectious bacteria that are resistant to one or more antibiotics.
As a result, there are strains of bacteria today for which only one
effective drug treatment is available, and in some cases, there
are no treatments available.1 Antimicrobial resistance is now a
major threat to public health, and controlling antimicrobial
resistance is an international priority.2,3
Antibiotic resistance of oral microbes has become an
increasing problem when treating dental infections. In the
recent years, dentists have reported a shift from narrow-
spectrum to broad-spectrum antibiotic prescriptions due to
increasing antibiotic resistance.4 In the present review, an

* Correspondence address: Laboratory of Oral Microbiology, Armauer Hansens Hus, N-5021, Bergen, Norway. Tel.: +47 55 97 5784;
fax: +47 55 97 4979.
E-mail address: Mohammed.Al-Haroni@odont.uib.no.
0300-5712/$ see front matter # 2007 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jdent.2007.11.007
96 journal of dentistry 36 (2008) 95103
overview of bacterial antibiotic resistance is presented to
dental practitioners with an emphasis on their role in halting
the global bacterial resistance problem.
2. Antibiotic resistance
Bacterial resistance to antimicrobials can be defined either
genotypically, where the bacteria carries certain genetic
resistance elements, phenotypically, where the bacteria can
survive and grow above a certain level of antibiotics in the
laboratory; or clinically, where the bacteria are able to multiply
in humans in the presence of drug concentrations during
therapy.5 Bacterial resistance to antimicrobial agents can be
either natural (inherent, intrinsic) or acquired.
2.1. Natural (inherent, intrinsic) resistance
In this type of resistance all isolates of a certain bacterial
species are not sensitive to the antimicrobial in question. This
could be because of a lack of certain structures in bacteria that
serve as the target molecules for the antimicrobial or the lack
of metabolic processes essential for the activation of the
antimicrobial. In agreement with this, bacteria without a cell
wall (e.g. the Mycoplasma species) are naturally resistant to
antimicrobial agents such as b-lactam antibiotics, having
activity against the cell wall.6 Intrinsic resistance attributable
to lack of metabolic processes is also noticed among oral
bacteria. For example, Actinomyces species, Streptococcus
species, and Aggregatibacter lack the enzyme nitroreductase
necessary to convert metronidazole to its active metabolites,
and are not affected by the drug at normal therapeutic
concentrations.7,8
2.2. Acquired resistance
In contrast to natural resistance, acquired resistance is
detected in only some bacterial species isolates. However,
the percentage of resistant isolates can be high. Acquired
resistance in bacteria evolves via two genetic mechanisms:
chromosomal mutation of the preexisting bacterial genome
or, most frequently, by horizontal gene transfer between
bacteria, either within or outside the species.5 Horizontal gene
transfer allows the bacterial population to develop antibiotic
resistance at a rate significantly greater than would be
afforded by mutation of chromosomal DNA. Indeed, horizon-
tal gene transfer is the most frequent pathway for the
dissemination of antibiotic resistance genes.
During horizontal gene transfer, a resistance gene can be
inserted into a transferable genetic element (plasmid, trans-
poson, or integron) and be linked to other resistance genes
contained in the element. The movement and introduction of
transferable genetic elements carrying antibiotic resistance
gene(s) into a bacterium can occur via three mechanisms,
namely, transformation, transduction, and conjugation.9 In
transformation, exogenous segments of DNA that carry resis-
tance genes are acquired by the bacteria from the environ-
ment. The bacteria enter an altered physiological state,
termed competence, during which the bacteria can take up
and integrate exogenous DNA from their environment.
Natural transformation was first demonstrated by Griffith in
Streptococcus pneumonia in 1928.10 Transformation occurs in
bacterial species that are naturally competent, such as
pneumococci, haemophilus, and some oral streptococci.11
Transformation is believed to be responsible for the develop-
ment of mosaic genes and the mosaic structure of Penicillin
Binding Proteins (PBP), which are responsible for penicillin
resistance in streptococci.12 Transduction, which was first
described in 1952,1315 is similar to transformation except
that the exogenous bacterial DNA is transferred from one
bacterium to another via a phage particle. The last mechanism
in horizontal gene transfer is conjugation, which was dis-
covered by Edward Tatum and Joshua Lederberg in 1947.16
After mixing two different strains of Escherichia coli, they
discovered recombinant types of bacteria that were different
from the two parental strains. This phenomenon resulted
from direct physical contact between the two strains, which
facilitated transfer of plasmid DNA from a donor to a recipient
bacterium. Many conjugative plasmids are resistant to a
variety of antibiotics, and they have the ability to transfer
resistance to a wide range of bacteria. Mobilizable plasmids
are not conjugative,17 but can be transferred to a recipient
when conjugative functions are provided by a separate, self-
transmissible plasmid in the donor. Mobilizable plasmids have
not been as thoroughly studied as conjugative plasmids, but
they may also play a role in the spread of antibiotic resistance
genes and the development of multidrug-resistant bacteria.17
Transposons and integrons are mobile DNA elements that
can be integrated into bacterial chromosomes or plasmids.
Transposons that are associated with antibiotic resistance fall
into three major classes based on their general structure and
method of insertion. The first two classes are composite and
noncomposite transposons, which integrate into the target
DNA by generating direct repeats in the target sequence.17
Composite and noncomposite transposons typically contain
genes that are not essential for transposition, such as antibiotic
resistance determinants, between flanking terminal insertion
sequences (composite) or inverted repeats (noncomposite).
Because transposition can involve excision and transfer of the
entire element, transposons are capable of spreading antibiotic
resistance genes.17 The third class of transposons are con-
jugative transposons, which are capable of excising from a
chromosome or plasmid in a donor cell and transferring the
DNA via conjugation into a recipient bacterium. Conjugative
transposons have a broad host range, which is not constrained
to closely related bacteria. For instance, the Tn916 and Tn1545
family can transpose into 50 different species and 24 genera of
both Gram-negative and Gram-positive bacteria.17 Conjugative
transposition begins with the excision of the transposon from
either the bacterial chromosome or plasmid DNA. The
transposon circularizes, and the single-stranded DNA copy is
transferred into the recipient cell by conjugation. A wide variety
of antibiotic resistance genes have been identified on large
conjugative transposons, and they are believed to significantly
contribute to the spread of antibiotic resistance in Gram-
positive bacteria.
The last type of mobile genetic element is the integron.
Integrons consist of an integrase gene, two promoters
transcribing in opposite directions, and an array of other
genes, which often include antibiotic resistance genes.17
 journal of dentistry 36 (2008) 95103 97

Integrons differ from transposons because they do not possess
a site-specific recombination system and cannot randomly
excise or insert into DNA regions. Many antibiotic resistance
genes have been identified in integrons, and these gene
cassettes are capable of insertion and excision from other
mobile genetic elements or the bacterial chromosome. Thus,
the antibiotic resistance genes that are present on some
transposons and plasmids may be the result of integron
insertion.17
3. Mechanisms of antibiotic resistance
Specialized defence mechanisms, encoded by resistant genes,
are utilized by bacteria for their survival in an environment in
which antimicrobials are designed to kill them. Generally, one
or more of four principal ways are utilized by bacteria to
render antimicrobials ineffective.5 These are the following:
(i) The target molecules are structurally altered to prevent
antibiotic binding. An example of this includes the
alteration of ribosomal target sites in the DNA gyrase/
topoisomerase genes that are the targets of fluoroquino-
lones. Modification of the PBPs may occur through
mutation in the chromosomal genes encoding the enzymes
or through the acquisition of foreign homologous genes or
fragments of genes from related species encoding new
PBPs, a mechanism which is prevalent in Gram-positive
cocci but seen less frequently in Gram-negative bacteria.
Methicillin-resistant Staphylococcus aureus (MRSA) is known
to produce an alternative PBP (2a) that bypasses the effect of
the antibiotic. Resistance to b-lactam antibiotics might be
caused by the production of low-affinity PBPs. This
resistance mechanism is widespread among the oral
viridans streptococci, such as, Streptococcus oralis, Strepto-
coccus sanguis, and Streptococcus mitis.18
(ii) Antibiotics are excluded from cell entry. Several anti-
biotics utilize porin channels when entering Gram-
negative bacteria. So, the decreased expression of porins
results in impermeability or decreased uptake that often
leads to antibiotic resistance.
(iii) Antibiotics are pumped out of the cell through a mechan-
ism known as efflux pump. The bacteria can actively efflux
the antimicrobial agent. Five major families of the efflux
system are present. These are MFS: Major Facilitator
Superfamily; RND: Resistance Nodulation-Division; SMR:
Small Multidrug Resistance; ABC: ATP-Binding Cassette;
and MATE: Multidrug and Toxic Extrusion.
(iv) Antibiotics are inactivated, for example, through enzy-
matic degradation. The most common example of this
mechanism is resistance against b-lactam antibiotics
because of b-lactamases. These enzymes present resis-
tance to the most widely used antimicrobials in medical
and dental practice, that is, b-lactams. Therefore, a special
account, with some detailed information, for these
enzymes is given.
Table 1 summarizes the mechanisms of action, antimi-
crobial spectra and main antimicrobial resistance mechan-
isms of the antimicrobials mostly used in dental practice.
3.1. b-Lactamases
More than 300 b-lactamases from various bacteria have been
described, which differ in their substrate profiles, potential for
inhibition, and physiological characteristics. These enzymes
catalyze the hydrolysis of the b-lactam ring in b-lactam
antibiotics, rendering them inactive. Several classification
schemes for b-lactamases have been proposed.2528 The
simplest scheme is composed of four distinct molecular
classes (A, B, C, and D) based on amino acid sequences.28
Classes A, C, and D are evolutionarily distinct groups of serine
enzymes, and class B contains the zinc types. The molecular
class B b-lactamases are the most threatening because they
inactivate nearly all b-lactam drugs, including carbapenem
antibiotics.19,26 Additionally, extended spectrum b-lactamases
(ESPLs) have evolved from mutations around the active sites in
the class A and D parental b-lactamases, which allowed these
enzymes to hydrolyze a larger panel of b-lactam antibio-
tics.19,29 The genes encoding for the production of b-lactamase
can be either chromosomal or inserted on a mobile genetic
element.17,19
Constitutive or induced b-lactamase production by bac-
teria can be copious.19,27 The b-lactamases of Gram-positive
bacteria are generally excreted in large amounts. Therefore, in
mixed infections, they may also protect other organisms that

Table 1 Main antibiotics used in dentistry, mechanisms of action, their spectra, and main bacterial resistance
mechanisms involved
Drug Mechanism of action Spectrum Main resistance mechanism(s)

Phenoxymethylpenicillin Inhibition of cell wall synthesis Aerobic G+, anaerobic G+, Enzymatic (b-lactamases), alteration
anaerobic G (narrow-spectrum) of the target site (mosaic PBP) [12,19]
Amoxicillin, Ampicillin Inhibition of cell wall synthesis As above plus haemoghilus spp. As above
(broad-spectrum)
Metronidazole Inhibition of RNA synthesis Strict anaerobic bacteria, some Enzymatic (5-nitroimidazole reductase) [20]
facultative anaerobes
Erythromycin Inhibition of protein synthesis Mainly G+ Target site modification, enzymatic
inactivation, and active efflux [21,22]
Clindamycin Inhibition of protein synthesis As above plus additional activity As above
on anaerobes
Tetracycline Inhibition of protein synthesis Many G+ and G Active efflux, enzymatic inactivation,
ribosomal protection proteins [23,24]
98 journal of dentistry 36 (2008) 95103
are present at the infection site. This has clinical relevance in
biofilm-associated diseases, such as periodontal diseases. The
membrane permeability characteristics may act in concert
with b-lactamase production to protect the microorganism
from b-lactam antibiotics. Therefore, decreased permeability
of antibacterial agents can allow small amounts of strategi-
cally located b-lactamase to present high resistance.30
Previous studies showed that oral bacteria, recovered from
subgingival plaque samples, had high penicillin susceptibility
(9099%).31,32 In the 1980s, reports emerged, describing the
clinical failure of penicillin therapy for the treatment of
oro-facial infections, and penicillin-resistant, b-lactamase-
producing oral Bacteroides, Capnocytophaga, Veillonella, and
Streptococcus strains were isolated.3335 In addition, b-lacta-
mase-producing Bacillus and Pseudomonas species were iso-
lated from subgingival plaque in patients with chronic
periodontitis.36 The Prevotella species has been reported to
be the most frequent b-lactamase-producing species found in
periodontal pockets and saliva,3638 and it is frequently
detected in infants and healthy young children.38,39 Isolates
of Fusobacterium nucleatum were shown to produce significant
amounts of b-lactamase in patients suffering from tonsilli-
tis.40 In addition, Kononen et al. demonstrated that penicillin
resistance caused by b-lactamase production by oral strains of
F. nucleatum frequently occurs in childhood.41 Prophyromonas
gingivalis isolates were reported to be 100% susceptible to
penicillins, and it was believed that the bacterium did not
carry b-lactamase enzymes.37,4244 However, when Nagy et al.
investigated 183 clinical isolates of Bacteroides, Porphyromonas,
and Prevotella species from severe infections after abdominal,
gynaecological, and oral surgery, 47% of the b-lactamase
producing Porphyromonas were P. gingivalis strains.45 In addi-
tion, Prieto-Prieto et al. referred to a study conducted in Spain
in which 59% of Porphyromonas species were resistant to
penicillin G.46
The first molecular characterization of the b-lactamases
produced by oral bacteria began in 1991 when Lacroix et al.
sequenced a b-lactamase gene (TEM-1) from E. corrodens,
which was isolated from the periodontal pocket.47,48 Further
studies characterized the b-lactamases produced by oral
bacteria, mainly in Bacteroidaceae, since members of this
family were implicated in the aetiology of acute oral infections
and periodontal disease.49,50 More recently, the b-lactamase
genes in subgingival oral bacteria, which were isolated from
patients with refractory periodontitis, were characterized.51,52
The CfxA b-lactamase gene was shown to be prevalent in the
Prevotella and Capnocytophaga species.51,52 In our lab, we
detected a class D b-lactamase produced by F. nucleatum
strains in isolates from dental patients.53
4. Use of antibiotics and development of
resistance
Antibiotic therapy, if indiscriminately used, may turn out to be a
medicinal flood that temporarily cleans and heals, but ultimately
destroys life itself Felix Marti-Ibanez, 1955.
The resistance development is a natural biological outcome
of antibiotic use.54 It represents a particular aspect of the
general evolution of bacteria that is genetically determined
and presents a survival advantage. The selection pressure
applied on bacterial population when antimicrobials are used
is the driving force for resistant bacteria to emerge.5456
Therefore, resistant bacterial clones are continuously selected
as an evolutionary response to the use of antibiotics. The
magnitude of this selection is determined by the total
consumption of antibiotics. The correlation between the
antibiotic use and bacterial resistance is well established,
and bacterial resistance is considerably higher in countries
with a high antibiotic consumption.57
In any bacterial ecology, the proportion of bacteria that are
susceptible and resistant to antibiotics reach an equili-
brium.58 This equilibrium is determined by the relative
fitness of the resistant and sensitive strains, which includes
transmission ability, the genetic basis and stability of
resistance, and the magnitude of the antibiotic selection
pressure. Once equilibrium has been reached, it is difficult to
contain or potentially lower the resistance level.59 One widely
adopted strategy to curtail the emergence and dissemination
of resistance genes is restraining antibacterial drug use.6062
Despite the fact that many countries have adopted antibiotic
treatment guidelines, restricted antibiotic use outside human
medicine, and improved the diagnostic tools for bacterial
infections, global antibiotic resistance is still on the rise.
Globally, antibiotics are extensively overused. For example,
antibiotic use is often based on incorrect medical indications.
Misuse occurs when patients are given the wrong agent or
dose, and also when patients are given antibiotics by the
incorrect route or for the wrong treatment duration.63,64 In
developed countries, around 8090% of human antibiotic
consumption takes place in the community, and at least half
of this is based on incorrect indicators, mostly viral infec-
tions.3,64,65 In Europe, antibiotic consumption is four times
higher in France than in the Netherlands, although there is no
reason to believe that the burden of disease differs between
the two countries.57 Additionally, the ease of access to
antimicrobial agents is a large problem in several countries.
Nonclinical factors also influence the use of antibiotics, such
as cultural conceptions, patient demands, economic incen-
tives, and advertising to prescribers, consumers, and provi-
ders by the pharmaceutical industry.66,67 Consequently, the
patterns of antibiotic use differ substantially between and
within countries.57 In developing countries, a high infectious
disease burden commonly coexists with high antibiotic
consumption, resulting in the rapid emergence and spread
of microbial resistance.68,69 Risk factors for antibiotic resis-
tance are particularly pertinent to, but not limited to,
developing countries.68,69 These factors include misuse of
and easy access to antibiotics, poor quality antimicrobials,
and lack of patient compliance to the prescribed drug
regimen. In addition, the dissemination of resistant bacteria
in developing countries is facilitated by inadequate infection
control measures in health facilities and shortfalls in hygiene,
sanitation, and public health.68,70
In dental practice, prescriptions are biased toward certain
classes of antimicrobials, mainly penicillins and metronida-
zole. Penicillin and metronidazole prescriptions accounted for
about 68 and 26%, respectively, of the total antibiotic
prescriptions in a survey of 10% of the dentists working in
 journal of dentistry 36 (2008) 95103
England.71 Metronidazole prescriptions issued by dentists
accounted for 45% of all metronidazole prescriptions in the
United Kingdom.72 It was estimated that the total dentists
prescriptions were 79% of the total prescriptions issued for
the community.72,73 In Norway, dental prescriptions of 11
commonly used antibiotics contributed to approximately 8%
to the total antibiotic consumption in the country.74 On
average, 159 antibiotic courses per year are prescribed by each
dentist in the United Kingdom.4 The average number of
prescriptions per dentist per week ranged from three in the
United Kingdom to 4.45 in Canada.4,75 However, the average
number of prescriptions per dentist per week in Norway in
2004 and 2005 was 0.59.74
It is generally agreed that more the antimicrobials used,
the more is the selection pressure applied on bacterial
population, and resistant bacteria began to emerge. Resis-
tant bacterial populations can theoretically revert to become
susceptible, however; this possibility is a debatable issue,
and the probability of reversion differs greatly between the
hospital setting and the community. The rationale for
reversibility is that resistant bacteria have a disadvantage
over susceptible strains in environments lacking antibiotics,
since most resistance mechanisms reduce bacterial fitness.
For example, resistant bacteria can have slower growth
rates, reduced virulence or reduced transmission rates.7678
Thus, decreasing antibiotic use should lead to lower
selection pressure and a reduction in the proportion of
resistant bacteria. In line with this, Feres et al. found that the
prevalence of amoxicillin-resistant subgingival bacteria
following a 14-day amoxicillin therapy decreased from
37% to the baseline value (0.5%) during a 90-day period.79
Therefore, resistant bacteria are replaced by susceptible
ones following removal of the antibiotic selective force.
However, the issue of reversibility is complicated by the fact
that resistant bacteria may reduce the biological costs
associated with resistance through compensatory evolu-
tion.80,81 Therefore, reversibility is difficult to achieve in
highly adapted resistant strains. In recent years, measure-
ment of antibiotic consumption is increasingly being
recognized as an important way to monitor emerging
antibiotic resistance.
4.1. Measuring antibiotic consumption
Antibiotic consumption measurements can describe the
extent of antibiotic use for a specific duration and/or in a
certain area (e.g. country, region, community or hospital).
Consumption can be presented as the defined daily doses
(DDDs) per 1000 inhabitants per day for outpatient antibiotic
use, or can be measured as the DDDs per 1000 bed-days for
inpatients.82 The DDD unit is defined as the average main-
tenance dose of the drug in adults. The number of DDDs/1000
inhabitants/day can be used to estimate the proportion of the
population exposed daily to a particular drug. Since this figure
is a rough estimate, it should be used with caution.
Dentistry-based antibiotic prescriptions are being surveyed
with greater interest. These data can be used to define the
type, quantity and location of antibiotics prescriptions.
Consumption data can also be used to implement and monitor
interventions that aim to prevent antibiotic overuse.
99
5. The role of dentists in halting antibiotic
resistance
Dental practitioners have the legal right to prescribe antibiotics.
Overall, there are fewer prescriptions by dentists than medical
practitioners; however, dentistry-based prescriptions of certain
antimicrobials can be very high. In Norway, for example, dental
prescriptions of b-lactam penicillin accounted for 13.5% of the
total consumption in that country.74 In the United Kingdom,
metronidazole prescriptions issued by dentists accounted for
45% of the total metronidazole prescriptions in the country.72
Therefore, an emphasis on the judicious use of antibiotics by
dentists is important.
There are three general strategies to prevent the develop-
ment of bacterial antibiotic resistance. The first strategy is to
prevent infections from taking place, which eliminates the
need for antibiotic use. Second, optimal use of antibiotics must
be ensured when these drugs are necessary. Third, optimal
infection control measures should be used to prevent the
spread of resistant clones or/and determinants.
Periodontitis and dental caries are the most prevalent
diseases in humans, and both are dental biofilm-mediated
diseases.83,84 Therefore, reduction of dental biofilm accumu-
lation is a primary goal to prevent and control these diseases.
This is achieved mainly through oral hygiene efforts by
patients coupled with regular professional help from dental
hygienists. Systemic antibiotic therapy has no effect on
reducing supragingival plaque accumulation and using anti-
biotics to control plaque-mediated periodontal diseases is not
appropriate.85
In general, antimicrobial prescriptions in dental clinics are
justified when they are used as a: (1) therapeutic aid to surgical
treatment of an acute or chronic infection, (2) therapy to treat an
active infectious disease, such as acute ulcerative gingivitis, and
(3) prophylactic to prevent a metastatic infection, such as
bacterial endocarditis.8690 It is worth noting that prophylaxis in
medically compromised patients (MCPs) who receive dental
treatment is not always a clear-cut matter, because of the
different guidelines, recommendations, and regimens for these
patients. Furthermore, these guidelines are often revised,
obligating dentists to update themselves regularly. Recently,
the American Heart Association (AHA) recommended that
some patients who had taken prophylactic antibiotics routinely
in the past should no longer take them as a preventive measure
before dental treatment. This includes patients with mitral
valve prolapse, rheumatic heart disease, bicuspid valve disease,
calcified aortic stenosis, and congenital heart conditions, such
as ventricular septal defect, atrial septal defect, and hyper-
trophic cardiomyopathy.91 The new guidelines regarding
cardiac conditions for which prophylaxis is recommended
with dental procedures are listed in Table 2. However, very
recently the National Institute for Health and Clinical Excel-
lence (NICE) issued a draft on clinical practice guideline on
antibiotic prophylaxis against infective endocarditis for use in
the NHS in England, Wales and Northern Ireland.92 The
recommendations are provisional and may change after
consultation. In the recommendations, antibiotic prophylaxis
is not recommended for patients at risk of infective endocarditis
undergoing dental procedures (recommendation number
1.3.2.2). The presence of different recommendations highlights
100 journal of dentistry 36 (2008) 95103
Table 2 Cardiac conditions for which antibiotic pro-
phylaxis is recommended (adapted from [91]) with dental
procedurea
Cardiac conditions for which antibiotic prophylaxis with
dental procedurea is needed
Prosthetic cardiac valve
Previous infective endocarditis
Congenital heart disease (CHD)
 Unrepaired cyanotic CHD, including 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 6 months after the procedure
 Repaired CHD with residual defects at the site or adjacent to the
site of a prosthetic patch or prosthetic device (which inhibit
endothelialization)
Cardiac transplantation recipients who develop cardiac
valvulopathy
a
Dental procedures that involve manipulation of gingival tissue or
the periapical region of teeth or perforation of the oral mucosa.
the need for international guidelines that are generally agreed
on and followed.
In dental practice, therapeutic antibiotic use should be
limited to treat active bacterial infections where local
measures alone are not sufficient. Clinical signs and symp-
toms of active infections that require antibiotic therapy
include tachycardia, facial swelling, limited mouth opening,
raised temperature, difficulty in swallowing, and regional
lymphadenitis. Antibiotics use should be directed against the
probable causative agent, based on local surveillance data, if
available, or preferably identified by microbiological testing.
According to the German Society for Periodontology and the
German Society for Dental, Oral, and Maxillofacial Medicine,
antibiotic prescriptions should be based on microbiological
testing for the following clinical diagnosis: aggressive period-
ontitis, generalized severe chronic periodontitis, periodontitis
exhibiting progressive attachment loss despite thorough and
adequate treatment, and severe periodontitis associated with
systemic diseases, for example, human immunodeficiency
virus.93 If infections do not respond to empirical antibiotic
treatment within 48 h, then the best clinical practice is to
change to another antibiotic treatment based upon micro-
biological testing. Whenever antibiotic prescription is
required, dentists should consider the pharmacological
characteristics of the antibiotic, patient safety, probable
infectious agent, drug cost, and the development of bacterial
resistance. Single or combined drug therapies have become
more important in dental practice, but whenever possible,
single drug therapies should be prescribed to reduce the
incidence of side effects, emergence of resistant bacteria, and
cost of therapy.
In the recent years, there were reports of potential cross-
contamination with MRSA in dental clinics.9496 This is a
particular concern for medically compromised patients where
resistant bacterial clones are a potential threat. It is essential
to revise infection control measures in dental practices to
accommodate these concerns. Kurita et al. found that MRSA
could be eliminated by using the following measures: ending
use of the airwater syringe, and using disposable covers for
the lights, headrests, instruments, tables, dental vacuum
suctions, and chair control switches instead of wiping them
with alcohol-soaked gauze.95
In conclusion, bacterial antibiotic resistance is a global
problem, and dentists play an essential role in halting
resistance. The prudent and judicious use of antibiotics is a
critical method to combat bacterial resistance. The local
patterns of oral bacterial antibiotic susceptibility and micro-
biological testing can help optimize antibiotic treatments and
restrict the use of broad-spectrum antibiotics when directed
therapies are superior. Finally, health authorities are encour-
aged to monitor trends in antibiotic prescriptions by dentists
and measure antibiotic consumption in order to assess and
limit antibiotic use.
Acknowledgment
This study was supported by a grant from the Lab of Oral
Microbiology, Faculty of Dentistry, University of Bergen.
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