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1 CE credit
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written for dentists,
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and assistants.
Antibacterial Agents in
Dental Hygiene Care
A Peer-Reviewed Publication
Written by Dr. Howard M. Notgarnie, RDH, EdD
Abstract
Dental hygiene care incorporates antimicrobial agents as
adjunct services with nonsurgical periodontal therapy, and
as a measure to reduce the risk of hematogenous infection
subsequent to oral tissue manipulation. Knowledge of
antimicrobial properties provides practitioners the ability to
make sound decisions when diagnosing conditions treated
by dental hygiene intervention and choosing antibiotics
dentists prescribe for administration. Antimicrobial agents
inhibit structural or metabolic functions of microorganisms,
but also render adverse effects to patients. Bacterial mutation
and acquisition of genetic material enables development of
strains resistant to antibiotics. Understanding the interplay
of host, microorganism, and antimicrobials fosters advances
in therapeutic choices and delivery systems when treating
periodontal disease, as well as when responding to the risk of
hematogenous infection of endocardium or prosthetic joints.
Educational Objectives
At the end of this self-instructional education activity the
participant will be able to:
1. Explain antibiotic effectiveness as a function of selective
toxicity
2. Associate antibacterial agents with their antimicrobial
mechanisms
3. Describe how bacteria acquire and exercise antibiotic
resistance
4. Describe mechanisms of targeted antimicrobial therapy
5. Choose antimicrobial agents appropriate to periodontal
conditions
6. Identify conditions at risk of hematogenous infection
7. Choose agents appropriate for antibiotic prophylaxis
8. Discuss the research pertaining to antimicrobials as
adjunctive and prophylactic care
Author Profiles
Dr. Howard M. Notgarnie has been practicing
clinical dental hygiene for 20 years, currently
in Colorado. He has eight years experience in
professional association leadership and five
years teaching experience. He can be contacted
at howardrdhedd@gmail.com.
Author Disclosure
Dr. Howard M. Notgarnie has no commercial
ties with the sponsors or providers of the unrestricted educational grant for this course.
Go Green, Go Online to take your course
Publication date: July 2013
Expiration date: June 2016
Supplement to PennWell Publications
PennWell designates this activity for 1 Continuing Educational Credit.
Dental Board of California: Provider 4527, course registration number CA#:01-4527-13070
“This course meets the Dental Board of California’s requirements for 1 unit of continuing education.”
The PennWell Corporation is designated as an Approved PACE Program Provider by the
Academy of General Dentistry. The formal continuing dental education programs of this
program provider are accepted by the AGD for Fellowship, Mastership and membership
maintenance credit. Approval does not imply acceptance by a state or provincial board of
dentistry or AGD endorsement. The current term of approval extends from (11/1/2011) to
(10/31/2015) Provider ID# 320452.
This educational activity was developed by PennWell’s Dental Group with no commercial support.
This course was written for dentists, dental hygienists and assistants, from novice to skilled.
Educational Methods: This course is a self-instructional journal and web activity.
Provider Disclosure: PennWell does not have a leadership position or a commercial interest in any products or
services discussed or shared in this educational activity nor with the commercial supporter. No manufacturer or third
party has had any input into the development of course content.
Requirements for Successful Completion: To obtain 1 CE credit for this educational activity you must pay the
required fee, review the material, complete the course evaluation and obtain a score of at least 70%.
CE Planner Disclosure: Heather Hodges, CE Coordinator, does not have a leadership or commercial interest with
products or services discussed in this educational activity. Heather can be reached at hhodges@pennwell.com.
Educational Disclaimer: Completing a single continuing education course does not provide enough information to
result in the participant being an expert in the field related to the course topic. It is a combination of many educational
courses and clinical experience that allows the participant to develop skills and expertise.
Image Authenticity Statement: The images in this educational activity have not been altered.
Scientific Integrity Statement: Information shared in this CE course is developed from clinical research and
represents the most current information available from evidence based dentistry.
Known Benefits and Limitations of the Data: The information presented in this educational activity is derived from the
data and information contained in reference section. The research data is extensive and provides direct benefit to the patient
and improvements in oral health.
Registration: The cost of this CE course is $20.00 for 1 CE credit.
Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by
contacting PennWell in writing.
Education Objectives
At the end of this self-instructional education activity the participant will be able to:
1. Explain antibiotic effectiveness as a function of selective
toxicity
2. Associate antibacterial agents with their antimicrobial
mechanisms
3. Describe how bacteria acquire and exercise antibiotic
resistance
4. Describe mechanisms of targeted antimicrobial therapy
5. Choose antimicrobial agents appropriate to periodontal
conditions
6. Identify conditions at risk of hematogenous infection
7. Choose agents appropriate for antibiotic prophylaxis
8. Discuss the research pertaining to antimicrobials as adjunctive and prophylactic care
Abstract
Dental hygiene care incorporates antimicrobial agents as adjunct services with nonsurgical periodontal therapy, and as a
measure to reduce the risk of hematogenous infection subsequent to oral tissue manipulation. Knowledge of antimicrobial
properties provides practitioners the ability to make sound decisions when diagnosing conditions treated by dental hygiene
intervention and choosing antibiotics dentists prescribe for
administration. Antimicrobial agents inhibit structural or
metabolic functions of microorganisms, but also render adverse
effects to patients. Bacterial mutation and acquisition of genetic
material enables development of strains resistant to antibiotics.
Understanding the interplay of host, microorganism, and antimicrobials fosters advances in therapeutic choices and delivery
systems when treating periodontal disease, as well as when responding to the risk of hematogenous infection of endocardium
or prosthetic joints.
Antimicrobial Agents in Dental Hygiene Care
Understanding antimicrobial agents is crucial to modern
dental hygiene practice. The properties of these agents influence the effectiveness of medications prescribed by dentists
or administered to patients. Dental practitioners use a variety
of antimicrobials as adjuncts to traditional mechanical dental
hygiene procedures. Although the effectiveness of antibiotic
prophylaxis has been questioned, dental professionals have a
history of attending to patients who might be at risk of hematogenous infections are protected using antibiotics. This article
will address properties of antimicrobials with their use in dental
hygiene therapy.
Properties of Antimicrobial Agents
Antimicrobials are chemicals that kill or suppress multiplication of microorganisms. Antibiotics are a subset of antimicrobials that have those antimicrobial effects on bacteria. Clinical
practitioners tend to use antibiotic and antimicrobial synony3 | rdhmag.com
mously. When using antimicrobials, health-care professionals
exploit their effects as anti-infective agents.
Antibiotic effectiveness is a result of its selective toxicity: the
metabolism of prokaryotic cells makes bacteria susceptible to the
toxic effects of antibiotics at far lower concentrations than the
concentrations that would adversely affect people, whose cells
are eukaryotic. An important factor in antibiotic effectiveness is
related to the cell wall structure. Gram-negative bacteria have cell
walls with less peptidoglycan than gram-positive bacteria have.
Instead, gram-negative bacteria have an extra layer of lipids that
protect them from many antibiotics.1
For most infections, the effectiveness of antibiotics does not
depend on whether the antibiotic is bactericidal or bacteriostatic.
However, endocarditis or meningitis caused by bacterial infection
and infections in some immunocompromised patients require
bactericidal antibiotics. An antibiotic’s spectrum refers to the
number of bacterial species the antibiotic inhibits or kills. There is
no clear definition of broad- and narrow-spectrum, but antibiotics
clinically effective against both gram-negative and gram-positive
bacteria are generally considered broad-spectrum.1
Antimicrobial Mechanisms
Antimicrobial agents have a variety of mechanisms of action.
Each mechanism inhibits a key structural or metabolic function.
Dental practitioners employ antiseptics such as chlorhexidine
(CHX) as antimicrobial agents. CHX exhibits its effects on cell
surfaces. The cationic nature of CHX gives it several valuable
properties: it sticks to anionic oral surfaces, it attaches to the anionic surfaces of bacteria targeted for treatment, and it does not
easily pass through skin and mucous membranes.2
Penicillins and cephalosporins, which contain the β-lactam
ring, inhibit synthesis of bacterial cell walls. Human cells do not
have these cell walls or the peptidoglycan of which cell walls are
composed. These drugs are bactericidal because they bind to
enzymes involved in formation of cell walls. With poorly formed
cell walls, the bacteria are susceptible to swelling and bursting.
As a class, these β-lactam antibiotics are effective against a broad
spectrum of bacteria because of the variety of synthetic forms
available.1
Quinolones (ciprofloxacin), rifamycins (rifampin), nitroimidazoles (metronidazole), and nitrofurans (nitrofurantoin) are
bactericidal because they inhibit nucleic acid production. Inhibition of DNA production prevents reproduction, and inhibition
of messenger RNA production prevents cells from making proteins necessary for metabolism. Metronidazole provides a good
example of the reason some antibiotic spectra are narrow. Metronidazole inhibits DNA synthesis only in the absence of oxygen;
thus only anaerobic bacteria are sensitive to metronidazole.1
An additional antibiotic mechanism is inhibition of ribosomes
synthesizing proteins. Tetracyclines inhibit the function of transfer
RNA, which carries amino acids to a ribosome building a protein.
Aminoglycosides (streptomycin) cause errors in the translation
of messenger RNA into protein, thereby causing the resultant
RDH | July 2013
protein to malfunction. Macrolides (erythromycin) bind to part
of the ribosome, preventing that ribosome from building proteins.
These antibiotics’ stronger attraction to bacterial ribosomes than
to human ribosomes results in their selective effects on bacteria.1
Sulfonamides provide one more mechanism by which antibiotics are toxic to bacteria. This class of compounds inhibits folate
synthesis.1 Folate participates in several enzyme functions in human metabolism, including the formation of nucleotides. Without
adequate function of folate and its metabolites, a person is at risk
of neurological and vascular disorders.3 Potential for toxic effects
on humans is one reason health professionals and patients should
use antibiotics cautiously.
Antibiotic Resistance
Another reason to use caution when considering antibiotics is
bacterial resistance. A prime mechanism of antibiotic resistance
development is characteristic of natural selection. Most bacteria
exposed to an unfamiliar antibiotic will perish, but a few will carry
a mutation giving them antibiotic resistance, which future generations will carry. Another method of acquiring antibiotic resistance
is incorporating plasmids, small segments of genetic material
contributed from a nearby bacterium. The fast reproduction of
bacteria leads researchers to fear a time limit to today’s antibiotics
and seek new compounds.
Bacteria can resist antibiotics by creating an enzyme that
destroys or deactivates an antibiotic such as penicillinase, which
reduces the effectiveness of penicillins. Bacteria can also develop
resistance by a change in the receptor molecule by which an antibiotic gains access to those bacteria. A change in a bacterial cell
wall can prevent an antibiotic from reaching that receptor. Finally,
bacteria can resist an antibiotic using a protein that pumps out
that compound. Given concerns of toxicity, allergy, secondary
infections, and resistance, an appropriate antibiotic choice accommodates the patient as well as the particular species of bacteria.1
Furthermore, the practitioner should ensure the antibiotic use
is cost-effective. A formulary developed through collaboration
among health-care team members, such as that of the Cleveland
Clinic, can help health practitioners confidently administer or
prescribe antibiotics that efficiently serve patients’ needs.4
Therapeutic Uses of Antibiotics
Antibiotics have been an essential component of care for dental infections, characterized by fever and swollen, tender lymph nodes.5
Removal of deposits has been the signature of nonsurgical periodontal therapy. However, a growing body of research provides
evidence supporting antimicrobial administration or prescription
to patients undergoing nonsurgical periodontal therapy. Targeted
or systemic antimicrobial agents can be effective adjuncts to the
traditional mechanical treatment.
Targeted Therapy
There are two mechanisms of targeting antibiotic application.
Antibiotics can target bacteria metabolically. Metabolically tarRDH | July 2013
geted antibiotic therapy involves laboratory testing of bacteria for
sensitivity to antibiotics, thereby allowing clinicians to prescribe
or administer antibiotics that will most effectively kill or inhibit
the particular species present in the patient’s infection.1 Testing of
oral flora and choosing an antibiotic regimen based on the patient’s
plaque composition is a promising method for metabolically targeted antibiotic therapy.6
The other mechanism of targeted antibiotic application is by
site specificity. Effective administration requires materials holding
the antimicrobial agent to withstand moisture, heat, and motions
of the mouth. Furthermore, a substrate that remains in place for
an extended time must be less than 1mm thick, soft, and flexible
so as not to irritate the patient.7 In a systematic review, CHX used
as a mouth rinse reduced plaque and gingivitis scores compared
with placebo but caused an increase in staining.2 CHX in a sustained delivery system improved ease of compliance. Reduced
risk of adverse effects, and continuous administration balanced
the lack of uniformity in dosage associated with the slow release
of the drug. This sustained delivery of CHX reduced the load
of bacterial plaque and adhesion of the fungus Candida albicans
while improving patient experience associated with the taste and
staining of CHX mouth rinses.7
A widely studied targeted delivery system for nonsurgical
periodontal treatment is the subgingival application of minocycline. In a systematic review, pocket depth and attachment of the
periodontium improved more with minocycline or doxycycline
than with placebo. This improvement occurred despite no significant difference in plaque index or bleeding on probing. Thus,
the authors supported targeted subgingival antibiotic therapy as
an adjunct to mechanical removal of deposits.8 Liu and Yang emphasized the direct antimicrobial effects on periodontal pathogens
Porphyromonas gingivalis, Porphyromonas intermedius, Eikenella
corrodens, and Fusobacterium nucleatum. An additional benefit of
targeted delivery of these tetracycline derivatives is the reduction
in the destructive effects of the immune response. These medications modulate several immune responses, including macrophage
activity that produces tumor necrosis factor-α. Such modulation
improves indications of periodontal health.9
Systemic Therapy
Bowen recommended including amoxicillin and metronidazole as a
bivalent prescription at the initial phase of nonsurgical periodontal
treatment of generalized aggressive periodontitis (GAP). Patients
with GAP exhibit rapid destruction of periodontal tissues despite
being generally healthy systemically. Their neutrophils and serum
antibodies function abnormally. Differential diagnosis of GAP
includes loss of attachment and bone around first molars, mandibular incisors, and at least three other teeth; deposits that do not
befit the periodontal destruction; and a family history suggesting
susceptibility to GAP. GAP often begins under the age of 30. For
GAP patients with pockets up to 6mm, the outcomes of bivalent
antibiotic treatment during initial nonsurgical periodontal therapy
are better than deciding on systemic antibiotic treatment during
rdhmag.com | 4
Table 1. Antibiotic Regimens for Infective Endocarditis Prophylaxis
Administration
By Mouth
Unable to Take by Mouth
Age
Adult
Child
Adult
Child
Standard—Penicillins
2g amoxicillin
50mg/kg amoxicillin
2g ampicillin IV or IM
50mg/kg ampicillin IV
or IM
600mg clindamycin
20mg/kg clindamycin
600mg clindamycin IV
20mg/kg clindamycin IV
500mg azithromycin or
clarithromycin
15mg/kg azithromycin or
clarithromycin
2g cephalexin
50mg/kg cephalexin
1g cephazolin or ceftriaxone IV or IM
50mg/kg cephazolin or
ceftriaxone IV or IM
Penicillin Allergy—
Clindamycin or Macrolides
Penicillin Allergy—Cephalosporins*
*Not for those with immediate-type penicillin allergic reaction
the maintenance phase. Cases beyond that severity usually require
surgical intervention to control periodontitis. Limitations of this
bivalent antibiotic regimen are clinical significance of improved
pockets, adverse reactions to medications, and bacterial resistance.
In addition, differentiating GAP from chronic periodontitis is important because systemic antibiotics are not warranted for initial
therapy of chronic periodontitis. The recommended protocol is
amoxicillin and metronidazole, each 500 mg three times per day
for 7 to 10 days.10
Antibiotic Prophylaxis to Avert
Sequelae of Bacteremia
Frequently, patients have used antibiotics to reduce the risk of
hematogenous infection. Bod et al. explained the purpose of
antibiotic prophylaxis is to reduce the number of bacteria at the
treatment site and to reduce the ability of bacteria to colonize.
When using antibiotic prophylaxis, the practitioner should ensure
an effective concentration of antibiotic from the beginning of
treatment to the end of bacteremia, effectiveness of the antibiotic
for the bacteria likely to enter the bloodstream, avoiding multiple
doses that might lead to resistant bacterial strains, and the patient’s
potential for adverse reactions.11 Nevertheless, researchers widely
question the value of antibiotic prophylaxis. For example, case
reports have inferred prosthetic joint infection of oral origin, yet
no known studies have shown a genetic match. Maintaining good
oral health reduces risks associated with bacteremia.12
in patients under 70 and 14.5/100,000 in patients 70 to 80 years
of age. Prosthetic heart valves and degenerative heart disease have
supplanted rheumatic heart disease as underlying risk factors for
IE. New risk factors for IE include use of intravenous drugs and
catheters. Moreover, antibiotic prophylaxis does not seem to be
cost-effective. Consequently, only people with a high risk for IE
undergoing high risk procedures should have antibiotic prophylaxis. These high risk situations include manipulation of gingival
tissues on patients with prosthetic heart valves, a history of IE,
cyanotic heart disease that has not been repaired or that has been
repaired with a prosthesis less than six months ago, or heart disease
repaired with a prosthesis near which a defect remains.13
The American Heart Association explained that except in cardiac patients with the highest risk, the relative risks and effectiveness of antibiotic prophylaxis make routine use of those antibiotics
difficult to justify. Infectious endocarditis involves interplay of
clotting and immune factors with bacteria in the bloodstream.
Bacteria attach to thrombi on cardiac endothelium and reproduce
in a vegetation at the attachment site. Turbulence initiates those
thrombi.14 Correcting dental problems before prosthetic heart
valve replacement, maintaining good oral health, and avoiding
procedures that result in bacteremia help avoid IE.13
Windle and Kulkarni (2012) noted antibiotic prophylaxis for
IE aims at the most common pathogen for that sequel, Streptococcus viridans. The antibiotic is indicated 30 to 60 minutes prior to
beginning care. Table 1 displays antibiotic choices.15
Infective Endocarditis
Common signs and symptoms of infective endocarditis (IE) are
fever, heart murmur, chills, weakness, and difficult breathing.
Treatment of IE depends upon identifying the pathogen and that
pathogen’s antimicrobial susceptibility profile. Surgical intervention is often necessary as well. Although Staphylococcus aureus and
Streptococcus species are predominant pathogens, other bacterial
species, parasites, and autoimmune processes may also cause endocarditis. Changes in recommendations for antibiotic prophylaxis reflect a change in epidemiology of IE. Antibiotic overuse has
led to bacterial resistance in strains endemic to human environments. Incidence of IE has been very low—less than 10/100,000
Prosthetic Joint Replacement
Benoit and Pickett showed the evolution of antibiotic prophylaxis
recommendations over the past two decades to demonstrate lack of
a clear rationale for antibiotic prophylaxis:
• In 1985, a survey reflected that most orthopaedic surgeons
did not believe there was a significant relationship between
oral procedures and infection of prosthetic joint replacements,
yet they recommended antibiotic prophylaxis.12 The most
common recommendation was a cephalosporin.16 However,
concerns over bacterial resistance to antibiotics led many
health professionals to question this practice of antibiotic
prophylaxis.
5 | rdhmag.com
RDH | July 2013
• In 1997, the American Dental Association (ADA) and
American Academy of Orthopaedic Surgeons (AAOS) jointly
issued a statement recommending selective antibiotic prophylaxis, which they later updated, in 2003. The guidelines for
antibiotic prophylaxis addressed time since placement of the
prosthesis, systemic health problems, medications, history of
complications with the prosthesis, and comorbidities.
• In 2009, the AAOS recommended antibiotic prophylaxis
of all patients with a total joint replacement for any oral
procedures. AAOS did not consult with ADA for this recommendation.
• In 2011 the American and Canadian Dental Associations
recommended no antibiotic prophylaxis if joint replacement is
more than two years old unless the patient has a history of infection in a prosthetic joint or the patient has a compromised
immune system. However, AAOS did not rescind its 2009
recommendations.12
Most recently, the AAOS and ADA issued three recommendations based on a systematic review of extant research
regarding risk of infection to joint implants. These recommendations are 1) consider discontinuing routine antibiotic
prophylaxis; 2) they are “unable to recommend for or against”
rinsing with an antimicrobial agent before dental care; and
3) maintenance of oral health is suitable to patients with
prosthetic joints. Several peer organizations, including the
American Dental Hygienists’ Association, reviewed the recommendations. Studies in the systematic review, informing
the first two recommendations, did not show an association
between bacteremia and implant infection. In fact, although
implant infections are mostly Staphylococcus species, bacteremias associated with dental procedures are mostly Streptococcus species. The third recommendation was a consensus
statement based on the benefit of current practices toward
good oral health and on evidence that a healthy oral condition
reduces bacteremia.17
Similarly, in 2008 British health officials recommended
against antibiotic prophylaxis for patients with a risk of IE
because there is no evidence of efficacy. There is no evidence
that antibiotic prophylaxis reduces infections of prosthetic
joints, yet bacteremia after brushing teeth and eating is
comparable to that of dental care.12 Berbari et al. showed that
dental procedures were not risk factors for prosthetic hip or
knee infections.18 Thus the low, 2% prevalence of prosthetic
joint space infection is inconsistent with the theory that those
infections originate from oral procedures. Furthermore, antibiotic prophylaxis does not prevent bacteremia.12
With the mounting evidence against effectiveness of antibiotic prophylaxis, Olsen, Snorrason, and Lingaas (2010) advised against antibiotic premedication for dental procedures
on patients with joint replacements except in those patients
with a high risk for infection. When practitioners prescribe
antibiotic prophylaxis for prosthetic joints, Olsen et al. recommended a regimen consistent with that in Table 1.19
RDH | July 2013
Bod et al. recommend antibiotic prophylaxis for dental procedures when the prosthetic joint is less than two years old, the
patient has a compromised immune system, or the patient has
a history of prosthetic joint infection. Vancomycin is indicated
only when there is a recognizable risk of infection with methicillinresistant Staphylococcus aureus.11
It is valuable to note that patients with prosthetic joints or a
high risk of IE are trying to reduce the risk of an infection subsequent to manipulation of oral tissues. The presumed critical event
is bacteremia, which is not associated with the misperception of
hierarchy. Thus it would be prudent to question a physician’s
rationale when prescribing antibiotic prophylaxis “for fillings but
not for cleanings.”
Conclusion
Dental practitioners and their patients benefit when practitioners
understand the pharmacology of antimicrobial agents. Dental
hygienists have a history of administering antimicrobials upon the
prescription of dentists as an adjunct to nonsurgical periodontal
care. Furthermore, dentists have a history of prescribing antibiotics as a risk-reduction measure for hematogenous infection.
Awareness of modern principles gives dental practitioners the
opportunity to offer state-of-the-art care to clientele by choosing
effective medications and avoiding those with risks outweighing
the benefits.
References
1. Kaufman G. Antibiotics: Mode of action and mechanisms
of resistance. Nursing Standard 2011; 29: 49-55.
2. van Strydonck DAC, Slot DE, Van der Velden U, Van der
Weijden F. Effect of a chlorhexidine mouthrinse on plaque,
gingival inflammation and staining in gingivitis patients: a
systematic review. Journal of Clinical Periodontology 2012;
39: 1042–1055. doi:10. 1111/j.1600-051X.2012.01883.x.
3. Fowler B. The folate cycle and disease in humans. Kidney
International 2001; 59: S221-S229.
4. Cleveland Clinic. Guidelines for antimicrobial usage. West
Islip, NY: Professional Communications. 2012.
5. Goldberg MH, Topazian RG. Odontogenic infections
and deep fascial space infections of dental origin. In RG
Topazian, MH Goldberg, & JR Hupp (eds.). Oral and
Maxillofacial Infections, 4th ed. pp. 158-187. Philadelphia,
PA: Saunders, 2002.
6.van Vinkelhoff AJ, Herrera D, Oteo A, Sanz M.
Antimicrobial profiles of periodontal pathogens isolated
from periodontitis patients in The Netherlands and Spain.
Journal of Clinical Periodontology 2005; 32: 893-898.
7. Fini A, Bergamante V, Ceschel GC. Mucoadhesive gels
designed for the controlled release of chlorhexidine in the
oral cavity. Pharmaceutics 2011; 2011: 665-679.
8.Matesanz-Pérez P, García-Gargallo M, Figuero E,
Bascones-Martínez A, Sanz M, Herrera D. A systematic
review on the effects of local antimicrobials as adjuncts
to subgingival debridement, compared with subgingival
debridement alone, in the treatment of chronic
periodontitis. Journal of Clinical Periodontology 2013; 39:
227-241. doi: 10.1111/jcpe.12026.
9. Liu D,Yang PS. Minocycline hydrochloride nanoliposomes
inhibit the production of TNF-α in LPS-stimulated
macrophages. International Journal of Nanomedicine
rdhmag.com | 6
2012; 7: 4769-4775. doi: 10.2147/IJN.S34036
10.Bowen DM. Treating aggressive periodontitis. Journal of
Dental Hygiene 2011; 85: 244-246.
11.Bod P, Kurtus I, Incze S, Moldovan R, Vâlcu A, Nagy Ö.
Clindamycin — An option for antibiotic prophylaxis in
arthroplasty. Acta Medica Marisiensis 2011; 57: 574-577.
12.Benoit G, Pickett FA. Antibiotic prophylaxis with
prosthetic joint replacement. What is the evidence?
Canadian Journal of Dental Hygiene 2011; 45: 103-108.
13.Baluta MM, Benea EO, Stanescu CM, Vintila MM.
Endocarditis in the 21st century. Maedica: A Journal of
Clinical Medicine 2011; 6: 290-297.
14.American Heart Association. Prevention of infective
endocarditis: Guidelines from the American Heart
Association. Circulation 2007; 116; 1736-1754.
15.Windle ML, Kulkarni R. Antibiotic prophylaxis regimens
for endocarditis 2012; Medscape article 1672902. Retrieved
February 5, 2013 on http://emedicine.medscape.com/
article/1672902-overview#a30.
16.Jaspers MT, Little JW. Prophylactic antibiotic coverage in
patients with total arthroplasty: current practice. Journal of
the American Dental Association 1985; 111: 943-948.
17. American Association of Orthopaedic Surgeons, American
Dental Association. Prevention of orthopaedic implant
infection in patients undergoing dental procedures:
Evidence-based guideline and evidence report. Rosemont,
IL: American Association of Orthopaedic Surgeons. 2012.
18.Berbari EF, Osmon DR, Carr A, Hanssen AD, Baddour
LM, Greene D, Kupp LI, Baughan LW, Harmsen WS,
Mandrekar JN, Therneau TM, Steckelberg JM, Virk A,
Wilson WR. Dental procedures as risk factors for prosthetic
hip or knee infection: A hospital-based prospective case–
control study. Clinical Infectious Diseases 2010; 50: 8–16.
doi: 10.1086/648676.
19.Olsen I, Snorrason F, Lingaas E. Should patients with
hip joint prosthesis receive antibiotic prophylaxis before
dental treatment? Journal of Oral Microbiology 2010; 2:
5265-5275. doi: 10.3402/jom.v2i0.5265.
Author Profiles
Dr. Howard M. Notgarnie has been practicing clinical dental
hygiene for 20 years, currently in Colorado. He has eight years experience in professional association leadership and five years teaching
experience. He can be contacted at howardrdhedd@gmail.com.
Author Disclosure
Dr. Howard M. Notgarnie has no commercial ties with the sponsors
or providers of the unrestricted educational grant for this course.
Notes
7 | rdhmag.com
RDH | July 2013
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Questions
1.Antibiotic resistance is not related to:
a. Bacterial mutations
b. Plasmid incorporation
c. Rate of bacterial reproduction
d. Human drug tolerance
2.Sulfonamides’ antibiotic effects are inhibiting
synthesis of:
a.DNA
b.Protein
c.Folate
d. Cell walls
3.Implant infections are mostly of what genus?
a.Staphylococcus
b.Candida
c.Porphyromonas
d.Streptococcus
4.The defining difference between antimicrobials
and antibiotics is:
a. Antibiotics are a subset of antimicrobials
b. One type affects eukaryotic cells, and the other affects
prokaryotic cells
c. They affect different types of cell walls
d. One type is bacteriostatic, and the other is bactericidal
5.Antibiotic prophylaxis for dental care is
intended to avoid:
a. Bleeding during dental procedures
b. Hematogenous infection of prosthetic joints and
endocardium
c. Bacteremia associated with brushing teeth and eating
d. Poor oral health
9.Antibiotics with a β-lactam ring act by binding
to:
a.Peptidoglycan
b. Anionic surfaces
c. Messenger RNA
d.Enzymes
10. A substrate for sustained, site-specific
antibacterials are more effective if they are:
a.Rigid
b. Thicker than 1mm
c. Kept dry
d. Heat tolerant
11. Each of the following directly affects protein
synthesis except:
a.Rifampin
b.Tetracycline
c.Streptomycin
d.Erythromycin
12. Bacteria may resist antibiotics by all of the
following except:
a. Preventing the antibiotic from entering the cell
b. Destroying the antibiotic
c. Pumping out the antibiotic
d. Influencing the antibiotic’s toxicity to the host
13. Metabolic antibiotic targeting involves all of
the following except:
a. Bacterial sensitivity testing
b. Plaque composition
c. Human sensitivity testing
d. Oral flora testing
6.A 7 to 10 day regimen of amoxicillin and
metronidazole has been found most effective
for which of the following:
a. Initial treatment of chronic periodontitis
b. Treatment of generalized aggressive periodontitis
during maintenance phase
c. Initial treatment of generalized aggressive periodontitis
d. Treatment when pockets are ≥7mm in depth
14. Baluta et al. recommended infective endocarditis prophylaxis if the patient has any of the
following conditions except:
a. Prosthetic heart valve
b. History of infective endocarditis
c. Prosthetic repair of heart disease with a remaining
defect
d. Cyanotic heart disease that was successfully repaired >6
months ago
7.Which of these statements about chlorhexidine
is true?
a. It is an anionic compound
b. Its effects are on cell surfaces
c. It does not interact with oral surfaces
d. It easily passes through mucous membranes
15. Targeted subgingival delivery of minocycline
does not affect:
a. Bleeding on probing
b. Human immune response
c. Pocket depth
d. Attachment of the periodontium
8.Bacteremia associated with dental procedures is
mostly of what genus?
a. Staphylococcus
b. Candida
c. Porphyromonas
d. Streptococcus
16. Typical presentation of a person with generalized aggressive periodontitis is:
a. Normal immune function
b. Under age 30
c. Systemic illnesses are apparent
d. Periodontal destruction consistent with deposits
RDH | July 2013
17. Changes in antibiotic prophylaxis for
infective endocarditis involve all the following
epidemiological changes except:
a. Rheumatic heart disease has become an increasing
concern
b. Incidence of infective endocarditis is very low
c. Antibiotic prophylaxis is not cost-effective
d. Antibiotic-resistant strains of bacteria are endemic to
human populations
18. Windle and Kulkarni named which
microorganism the most common pathogen for
infective endocarditis?
a. Streptococcus mutans
b. Staphylococcus aureus
c. Streptococcus viridans
d. Eikenella corrodens
19. Which of the following inhibits nucleic acid
production?
a.Penicillin
b.Ciprofloxacin
c.Sulfonamide
d.Tetracycline
20. Bod et al. recommended antibiotic prophylaxis for a prosthetic joint if the patient has any
of the following conditions except:
a. Prosthetic joint <2 years old
b. Pins or screws in a bone
c. History of infection in the prosthetic joint
d. Compromised immune system
21. Which of the following inhibits nucleic acid
production?
a.Penicillin
b.Ciprofloxacin
c.Sulfonamide
d.Tetracycline
22. Bod et al. recommended antibiotic prophylaxis for a prosthetic joint if the patient has any
of the following conditions except:
a. Prosthetic joint <2 years old
b. Pins or screws in a bone
c. History of infection in the prosthetic joint
d. Compromised immune system
rdhmag.com | 8
ANSWER SHEET
Antibacterial Agents in Dental Hygiene Care
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Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all
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you 1 CE credit. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 216.398.7822
If not taking online, mail completed answer sheet to
Educational Objectives
Academy of Dental Therapeutics and Stomatology,
1.Explain antibiotic effectiveness as a function of
selective toxicity.
5.Choose antimicrobial agents appropriate to
periodontal conditions.
2.Associate antibacterial agents with their antimicrobial
mechanisms.
6.Identify conditions at risk of hematogenous infection.
A Division of PennWell Corp.
7.Choose antimicrobial agents appropriate for antibiotic
prophylaxis.
3.Describe how bacteria acquire and exercise antibiotic
resistance.
8.Discuss the research pertaining to antibiotics as
adjunctive and prophylactic care.
4.Describe mechanisms of targeting antibiotic therapy.
Course Evaluation
Objective #2: Yes No
Objective #3: Yes NoObjective #4: Yes No Objective #5: Yes No
Objective #6: Yes NoObjective #7: Yes No
Objective #8: Yes No
2. To what extent were the course objectives accomplished overall?
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3. Please rate your personal mastery of the course objectives.
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5
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3
2
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5
4
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6. Please rate the instructor’s effectiveness.
5
4
3
2
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7. Was the overall administration of the course effective?
5
4
3
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8. Please rate the usefulness and clinical applicability of this course. 5
4
3
2
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9. Please rate the usefulness of the supplemental webliography.
4
3
2
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0
Yes
No
11. Would you participate in a similar program on a different topic?
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12. If any of the continuing education questions were unclear or ambiguous, please list them.
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___________________________________________________________________
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AGD Code 016
PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.
COURSE EVALUATION and PARTICIPANT FEEDBACK
We encourage participant feedback pertaining to all courses. Please be sure to complete the survey included
with the course. Please e-mail all questions to: hhodges@pennwell.com.
INSTRUCTIONS
All questions should have only one answer. Grading of this examination is done manually. Participants will
receive confirmation of passing by receipt of a verification form. Verification of Participation forms will be
mailed within two weeks after taking an examination.
COURSE CREDITS/COST
All participants scoring at least 70% on the examination will receive a verification form verifying 1 CE credit.
The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership
credit. Please contact PennWell for current term of acceptance. Participants are urged to contact their state
dental boards for continuing education requirements. PennWell is a California Provider. The California
Provider number is 4527. The cost for courses ranges from $20.00 to $110.00.
PROVIDER INFORMATION
PennWell is an ADA CERP Recognized Provider. ADA CERP is a service of the American Dental Association
to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP
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Concerns or complaints about a CE Provider may be directed to the provider or to ADA CERP at www.ada.
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The PennWell Corporation is designated as an Approved PACE Program Provider by the Academy of General
Dentistry. The formal continuing dental education programs of this program provider are accepted by the
AGD for Fellowship, Mastership and membership maintenance credit. Approval does not imply acceptance
by a state or provincial board of dentistry or AGD endorsement. The current term of approval extends from
(11/1/2011) to (10/31/2015) Provider ID# 320452.
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contact our offices for a copy of your continuing education credits report. This report, which will list all
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Completing a single continuing education course does not provide enough information to give the
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ANTIAG713RDH