Systemic antibiotics in periodontal therapy

© Ramaiah University of Applied Sciences
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Faculty of Dental Sciences
©M. S. Ramaiah University of Applied Sciences
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Presented by:
Dr Safiya
Guided by:
Dr Bhavya

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CONTENTS
• Introduction
• Rationale
• Classification of antibiotics
• Penicillins
• Tetracyclines
• Macrolides
• Clindamycin
• Metronidazole
• Ciprofloxacin
• Resistance to antibiotics
• Drug interactions
• Serial and combination antibiotic therapy
• Antibiotics in periodontal diseases
• Antibiotic prophylaxis
• Sequencing of antibiotic therapy
• Conclusion
• References

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INTRODUCTION
An antibiotic is a naturally occurring, semisynthetic, or synthetic type of anti-infective
agent that destroys or inhibits the growth of selective microorganisms, generally at low
concentrations.

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RATIONALE
Pathogenic
microbiota Patient Drug

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Prime candidates for systemic antibiotic
therapy
Patients who exhibit continuing loss of periodontal attachment despite diligent
conventional mechanical periodontal therapy.
Patients with aggressive types of periodontitis.
Patients with medical conditions predisposing to periodontitis.
Patients with acute or severe periodontal infections.

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Factors determining the efficacy of
periodontal antibiotic therapy
Drug binding to
tissues.
Protection of pathogens through
binding, consumption, or
degradation of the drug by non-
target microorganisms.
Subgingival plaque
biofilm protecting the
pathogens.
Total bacterial load relative
to the maximum achievable
antibiotic concentration.
Effectiveness of the
host defenses.
Pathogens in periodontal
tissues, root surfaces, and
extra-dental oral sites not
affected by the therapy.

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ADVANTAGES
• Simple, easy administration of the drug to multiple sites
of disease activity.
• Eliminate or reduce pathogens colonizing on oral mucosa
and on other extra-dental sites including the tongue and
tonsilar areas.
• Reduce the risk for future translocation of organisms and
recolonization of the periodontal pocket, reducing the
risk for recurrent disease progression.
DISADVANTAGES
• Inability of systemic drugs to achieve high GCF
concentration as compared to locally applied
antimicrobial agents.
• Increased risk of adverse drug reactions.
• Increased antibiotic resistance.
• Uncertain patient compliance.

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CLASSIFICATION
Inhibit cell wall synthesis:
• Penicillin,
Cephalosporins,
Vancomycin
Cause leakage from cell
membrane:
• Polymyxins, Colistin,
Bacitracin, Amphotericin B
Inhibit protein synthesis:
• Tetracycline,
Chloramphenicol
Cause misreading of m-RNA
code and affect permeability:
• Streptomycin, Gentamicin
Inhibit DNA gyrase:
• Fluoroquinolones
Interfere with DNA function:
• Rifampin, metronidazole
Interfere with DNA synthesis:
• Acyclovir, zidovudine
Interfere with intermediary metabolism:
• Sulfonamides, Trimethoprim,
Pyrimethamine
I. BASED ON MECHANISM OF ACTION

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II. BASED ON SPECTRUM OF ACTIVITY
Broad spectrum Narrow spectrum
III. BASED ON TYPE OF ACTION
Bacteriostatic Bactericidal

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PENICILLINS
• Penicillins are natural and semisynthetic derivatives of broth cultures of Penicillium mold.
• They inhibit bacterial cell wall production and therefore are bactericidal.
PENICILLIN
Natural
E.g. Penicillin G,
Penicillin V
Semi-synthetic

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Amoxicillin
• Amoxicillin is a semi-synthetic penicillin with an extended anti-infective spectrum that
includes gram-positive and gram-negative bacteria.
• Susceptible to penicillinase.
• Amoxicillin may be useful for the management of patients with aggressive periodontitis
in both localized and generalized forms.
• The recommended dosage is 500 mg three times daily for 8 days.
Kunihira et al, 1985: Root planing, flap surgery and maintenance therapy every 3 months
provide an effective treatment for juvenile periodontitis, but treatment results were not
enhanced by oral administration of penicillin (250 mg qid for 10 days).

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Amoxicillin-clavulanate potassium
• Resistant to penicillinase enzymes,
• Useful for the management of patients with LAP or refractory periodontitis.
• Available as 375 mg or 625 mg, tablet which contain 250 mg and 500 mg of amoxicillin,
respectively, and 125 mg clavulanic acid.
NSPT with adjunctive use of Augmentin (750 mg/day for 2 weeks) may reduce the incidence
of attachment loss for at least 12 months in individuals who previously had been refractory to
treatment. [Magnusson et al, 1989]

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TETRACYCLINES
Tetracyclines at a low GCF concentration (i.e., 2
μg/ml to 4 μg/ml) are very effective against
many periodontal pathogens. [Baker et al, 1985]
The average GCF concentration of tetracycline
varies between 0 and 8 μg/ml explaining the
variability in response to systemic tetracyclines.
[Sakellari et al, 2000]
Effective in inhibition of gram-negative
facultative anaerobes i.e., A.a, C. rectus, E.
Corrodens, and Capnocytophaga.
Used to treat refractory periodontitis, including
localized aggressive periodontitis (LAP).
Inhibit microbial protein
synthesis.
Binds specifically to 30S
sub-unit of ribosome.
Bacteriostatic, effective against
rapidly multiplying bacteria.

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ADDITIONAL
PHARMACOLOGICAL
PROPERTIES OF
TETRACYCLINES
Collagenase
inhibition
Anti-proteolytic
property
Inhibition of
bone
resorption
Anti-
inflammatory
actions
Enhance
fibroblast
attachment
Substantivity
Reduce
adherence and
co-aggregation
of P. gingivalis
and P.
intermedia

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Systemic tetracycline can eliminate tissue bacteria, and arrest bone loss and suppress A.
actinomycetemcomitans levels in conjunction with scaling and root planing.
[Slots et al, 1990]

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Minocycline,taken orally (700 mg for 7 days), can improve gingival health and can
markedly change, both quantitatively and qualitatively, the subgingival microflora
for a prolonged period. The greatest effect was seen when minocycline was given
as an adjunct to SRP. [Ciancio et al, 1982]
Doxycycline (100 mg/day for 6 weeks) was effective in achieving an overall gain of
clinical attachment as well as reduction of gingival inflammation for upto 24 weeks
duration following SRP. [Veronica W-K Ng et al, 1998]
Surgery plus doxycycline (100 mg/day for 14 days) effectively eliminated Aa from
periodontal pockets and this elimination resulted in clinical improvement and
attachment gain at 3 and 12 months following surgery. [Mandell et al, 1988]

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MACROLIDES
• Macrolides can be bacteriostatic or bactericidal, depending on the concentration of the
drug and the nature of the microorganism.
• The macrolide antibiotics commonly used for periodontal treatment include
spiramycin, clarithromycin and azithromycin.
Spiramycin (1,500,000 IU, bid for 14 days), as an adjunct to thorough SRP, provides a
statistically significant improvement in PD for up to 24 weeks when compared with SRP alone.
[Bain et al, 1994]
With spiramycin (1 g twice a day for 14 days) the microflora shifted to a typical microbial
population associated with healthy gingiva and the inflammation could be readily controlled.
There was a prompt significant decrease in PD, while GI, PI and Crevicular Fluid reduction
became significant at 4 wk examination. [Sznajder et al, 1987]

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Pradeep et al, 2011: The utilisation of CLM (500 mg b.i.d. for 3 days) in
combination with SRP improves the efficacy of NSPT in reducing PD,
improving CAL and in lessening microbial loads.
Andere et al, 2017: Adjunct use of CLM (500 mg, every 12 hours for 3 days) to
FMUD leads to better reduction of deep pockets and Pg at 6 months compared
with FMUD alone.

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Azithromycin is a member of the azalide
class of macrolides.
Effective against anaerobes and gram-
negative bacilli.

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Smith et al, 2002: Azithromycin (500 mg once daily for 3 days) may be a useful adjunct in
the treatment of adult periodontitis, particularly where deep pockets are present.
Mascarenhas et al, 2005: The utilization of AZM in combination with SRP improves the
efficacy of NSPT in reducing probing depth and improving attachment levels in smokers with
moderate to advanced attachment loss.
Haas et al, 2008: Better clinical outcomes including higher PPD reduction and CAL gain were
obtained with the adjunctive use of azithromycin (500 mg daily for 3 days) than placebo in
patients with AgP.

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CLINDAMYCIN
Effective against
anaerobic bacteria
and it has a strong
affinity for osseous
tissue.
Effective in case
patient is allergic
to penicillin.
Diarrhea or
cramping that
develops during
clindamycin therapy
may be indicative of
pseudomembranous
colitis.

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METRONIDAZOLE
Metronidazole is a nitroimidazole compound developed to
treat protozoal infections.
Disrupts bacterial DNA synthesis and is bactericidal to
anaerobic organisms.
Effective against A. actinomycetemcomitans when it is used in
combination with other antibiotics and also against anaerobes
such as P. gingivalis and P. intermedia. [Greenstein et al, 1993]
Used clinically to treat gingivitis, ANUG, chronic periodontitis,
and aggressive periodontitis.
Adult dosage of metronidazole is 200-400 mg 3 times a day.
Metronidazole has a disulfiram (Antabuse) effect when alcohol
is ingested.
Metronidazole also inhibits warfarin metabolism.

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QUINOLONES
Broad-spectrum agents that act on DNA gyrase.
• Ciprofloxacin is effective against a wide
range of both gram-positive and
gram-negative micro-organisms.
• The adult dosage is 500 mg bid.
Fluoroquinolones are effective against the pasteurellaeae family, to which A.
actinomycetemcomitans belongs. [Tanner et al, 2000]
Systemic ofloxacin in conjunction with open flap surgery was able to suppress A.
actinomycetemcomitans below detectable levels for a period of 12 months.
[Kleinfelder et al. 2000]

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CEPHALOSPORINS
It acts by inhibition of cell wall
synthesis.
Penicillins are superior to cephalosporins with
regard to their range of action against
periodontal pathogenic bacteria.
It can effectively inhibit growth of gram-negative
obligate anaerobes (P. Gingivalis, P. Intermedia,
Fusobacterium. Sputigena, B. Forsythus.) but may fail to
inhibit gram-negative facultative anaerobes. [Goodson
et al, 1994]
Patients who are allergic to
penicillins must be considered
to be allergic to all β-lactam
products.

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ANTIBIOTIC RESISTANCE
Mutations in
common resistance
genes that extend
their spectrum of
activity;
Exchange of genetic
information among micro-
organisms in which
resistance genes are
transmitted to new hosts;
Development of environmental
conditions in hospitals and
communities that facilitate the
development and spread of
resistant organisms;
Proliferation and spread, in some
cases globally, of resistant clones of
bacteria;
Inability of some laboratory
testing methods to detect
emerging resistance phenotypes.

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Suboptimal dosage of antibiotics,
caused by either inadequate
prescribing or poor patient
compliance, favors the emergence of
antibiotic‐resistant bacterial clones.
A randomized trial conducted by Schrag et al, 2001 in children receiving antibiotic
prescriptions for upper respiratory tract infections demonstrated the advantage of
short‐course, high‐dose outpatient antibiotic therapy to minimize the impact of antibiotic
use on the spread of drug‐resistant pneumococci.

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ADVERSE REACTIONS

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SERIAL AND COMBINATION THERAPY
Mixed” infections can include a variety of aerobic,
microaerophilic, and anaerobic bacteria, which may
be both gram negative and gram positive.
Therefore, it may be necessary to use more than one
antibiotic, either serially or in combination.
The periodontal pathogens being treated must be
identified and antibiotic-susceptibility testing
performed.
Helps to broaden the
anti-microbial range of
therapeutic regimen
beyond that attained by any
single antibiotic.
Prevents the emergence of
bacterial resistance by using
agents with overlapping
anti-microbial spectra.
Lowers the dose of
individual antibiotic by
exploiting possible synergy
between 2 drugs against
targeted organisms.

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ANTIBIOTICS IN PERIODONTAL DISEASE

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ANTIBIOTICS IN PERIODONTAL ABSCESS
Antibiotic therapy is indicated for
periodontal abscesses with systemic
manifestations (fever, malaise,
lymphadenopathy).
Antibiotics for the treatment of
abscesses should be prescribed in
conjunction with surgical incision and
drainage.

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ANTIBIOTICS IN PERIODONTAL SURGERY
Loesche et al. 2002, demonstrated a reduced need for surgical therapy in patients who
were treated early with systemic metronidazole as an adjunct to SRP claiming sustained
benefits 5 years after initial antimicrobial therapy.
For subjects with generalized aggressive periodontitis, better clinical outcomes were achieved
if patients were given amoxicillin plus metronidazole immediately after initial SRP rather than
after retreatment of persisting pathology. (Kaner et al. 2007; Griffiths et al. 2011)

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SRP alone is able to resolve
a considerable amount of
periodontal pathology on
its own, this strategy may
help to restrict the
prescription of antibiotics
to a minimum.
[Heitz‐Mayfield et al.
2002; van der Weijden &
Timmerman 2002]
Given the restricted effects
of antibiotics on intact biofilm
and the known limitations of
non‐surgical mechanical
debridement, surgical
intervention may be needed
for access to assure complete
removal of subgingival biofilm
and calculus.
[Rabbani et al. 1981;
Buchanan & Robertson 1987]

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ANTIBIOTIC PROPHYLAXIS

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SEQUENCING OF ANTIBIOTIC THERAPY
Initial periodontal therapy should include thorough mechanical root
debridement followed by surgical access if needed.
Antibiotics may be prescribed on the basis of the clinical need for further
treatment, findings of microbiological testing, and the medical status and
current medications of the patient.
The clinical response should be evaluated 1-3 months after completion of
the mechanical therapy.
If periodontal inflammation does not resolve, a microbiological
examination of the subgingival microbiota may help determine the
presence and amount of remaining putative periodontal pathogens.

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1-3 months after systemic antimicrobial therapy, another microbiological
test may be needed to verify the subgingival elimination of target
pathogen(s).
High levels of subgingival viridans Streptococcus, Actinomyces, and
Veillonella species are suggestive of periodontal health or minimal
disease.
After resolution of the periodontal infection, the patient should be
placed on an individually tailored maintenance program to help prevent
recolonization by putative periodontal pathogens.
Recurrence of progressive disease may prompt repeated microbiological
testing and subsequent antibiotic therapy targeted against the specific
microorganisms detected.

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CONCLUSION
Systemic antibiotic therapy in periodontics aims to reinforce mechanical
treatment and to support host defenses in overcoming periodontal
infections by killing subgingival pathogens that remain after periodontal
instrumentation.
Systemic antibiotic therapy can provide greatest benefit to periodontitis
patients who do not respond well to mechanical periodontal therapy or
who are experiencing fever or lymphadenopathy. Prescription of any
systemic antibiotic therapy requires a careful analysis of patients’ medical
status and current medications.

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REFERENCES
• American Academy of Pediatric dentistry. 2014. Antibiotic Prophylaxis for Dental
Patients at Risk for Infection . Recommendations: Best Practices. Vol 40. Issue 6. Pg:
386-391.
• American Academy of Periodontology. 1996. Position paper. Systemic antibiotics in
periodontics. Journal of Periodontology. Vol 67. Pg: 831-838.
• Lang NP, Lindhe J. 2015. Clinical Periodontology and Implant Dentistry. 6th ed. India:
Wiley Blackwell.
• Newman M, Takei H, Klokkevold P, Carranza F. 2014. Carranza’s Clinical
Periodontology. 12th ed. Canada: Elsevier.
• Patil V, Mali R, Mali A. 2013. Systemic antimicrobial agents used in periodontal
therapy. Journal of Indian Society of Periodontology. Vol 17. Issue 2. Pg: 162-8.

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