This document provides information about antibiotics used in dentistry. It begins with definitions of antibiotics and a brief history of their discovery. It then discusses classifications of antibiotics based on mechanisms of action and spectrum of activity. The principles of antibiotic therapy and factors considered in antibiotic selection are explained. Commonly used antibiotics in dentistry are outlined, including penicillins, cephalosporins, macrolides, metronidazole, and clindamycin. Clinical uses and properties of penicillin and amoxicillin are described in more detail.

1. CH. SUMA PRIYANKA
PG STUDENT, DEPT. OF
PERIODONTICS
GUIDED BY: DR. P. SURESH, MDS
PROFESSOR & HOD
DEPT. OF PERIODONTICS

2. CONTENTS
• DEFINITION
• HISTORY
• CLASSIFICATIONS
• PRINCIPLES OF ANTIBIOTIC THERAPY IN DENTAL INFECTIONS
• SELECTION OF AN ANTIBIOTIC AGENT
• COMMONLY USED DRUGS IN DENTISTRY

3. • B-LACTAMS
• NITROIMIDAZOLES
• TETRACYCLINES
• AMINOGLYCOSIDES
• MACROLIDES
• ANTI-FUNGAL & ANTI-VIRAL AGENTS
• ANTIBIOTIC PROPHYLAXIS FOR INFECTIVE ENDOCARDITIS

4. • ANTIBIOTICS IN PERIODONTICS
• ANTI-PLAQUE & ANTI-GINGIVAL AGENTS
• ANTI-CARIES AGENTS
• DISCLOSING AGENTS
• FAILURE OF ANTI MICROBIAL THERAPY
• REFERENCES

5. DEFINITION
Anti=against; Bios=life
• Antibiotics are the chemical substances produced by
micro-organisms, which selectively suppresses the
growth of or kill the other microbes at very low
concentrations. { Waksman;1942}

6. HISTORY
EARLY HISTORY
 3500 BC the Sumerian doctors would give patients
‘Beer soup’ mixed with snakeskins and turtle shells.
Babylonian doctors would heal eyes by using an ointment
made of frog bile and sour milk.
Greeks & Indians used many herbs to heal ailments.
All of these “Natural” treatments contained some sort of
antibiotics.

8. MODERN HISTORY
• ‘Louis Pasteur’ was one of the 1st
recognized physicians who observed
that bacteria could be used to kill
other bacteria.
• The term “Antibiosis”-JEAN PAUL
VUILLEMIN in 1877.
• Renamed as “Antibiotics” by- SELMAN
WAKSMAN in 1942.

9.  ‘Alexander Fleming’-Penicillin in
1928.
 ‘Gerhard Domagk’-1st
Sulfonamide in 1932.
 Penicillin was commercially
available from 1941-”Golden
age of antibiotics”.
 Chlortetracycline-1948.

10. BASED ON MECHANISM OF ACTION

11. BASED ON SPECTRUM OF ACTIVITY
Narrow spectrum: PenicillinG, Streptomycin,
Erythromycin
Broad spectrum: Tetracyclines,
Chloramphenicol

12. BASED ON TYPE OF ACTION
1rly Bacteriostatic: Sulfonamides,
Tetracyclines, Chloramphenicol,
Erythromycin, Ethambutol,
Clindamycin, Linezolid.
1rly Bactericidal: Penicillins,
Cephalosporins, Aminoglycosides,
Vancomycin, Polypeptides,
Ciprofloxacin, Rifampacin,
Metronidazole, Cotrimoxazole

13. • Some static drugs may become Cidal at higher concentrations.
eg: Sulfonamides, Erythromycin, Nitrofuratoin.
• Some Cidal drugs may only be static under low
concentrations.
Eg: Cotrimoxazole, Streptomycin .

14. PRINCIPLES OF ANTIBIOTIC THERAPY
• Once the decision has been made to use antibiotics as an adjunct
to treat infection, antibiotics must be selected properly. The
following guidelines are useful:
1. Identification of causative organism.
2. Determination of antibiotic sensitivity.
3. Choice of antibiotics.
Upon culture and sensitivity report, there may be a
choice of 4-5 antibiotics. Selection should be based on
consideration of several factors like:

15. i. Patient’s with previous history of allergy.
ii. Antibiotics with narrow spectrum.
iii. Drug that causes few adverse reactions.
iv. Drug that is least toxic.
v. Bactericidal drug rather than bacteriostatic.
vi. Less expensive still effective antibiotic.
vii. Combination antibiotics.

16. SELECTION OF AN ANTIMICROBIAL AGENT
• Choice of an antimicrobial agent depends on:
a. Patient factors
b. Organism-related considerations
c. Drug factors.

17. PATIENT FACTORS:
•Age
•Renal & hepatic function
•Local factors
•Drug allergy
•Impaired host defence
•Pregnancy
•Genetic factors.

19. • ORGANISM-RELATED CONSIDERATIONS:
• Ideally, the identity and antimicrobial sensitivity of the
infecting bacteria should be determined before instituiting
systemic anti-bacterial therapy.
• However, this is impractical for most dental infections
which are acute in nature, being time consuming and
expensive, and treatment cannot be delayed.
• Oro dental infections are often mixed bacterial infections.
Therefore, the drugs mostly selected are like
Penicillin/Amoxicillin/some Cephalosporins like
Cefuroxime/Cefaclor which are active on anaerobes.

20. • Most dentists initiate empirical therapy with
Amoxicillin+Metronidazole. Further therapy is modified on the
basis of clinical response.
• In few situations like ANUG, clinical diagnosis itself indicates
infecting organism and directs the choice of drug.
• Penicillin/Doxycycline + Metronidazole—ANUG
• Nystatin/Clotrimazole—THRUSH

21. DRUG
FACTORS:
• Spectrum of activity
• Type of activity
• Relative toxicity
• Pharmacokinetic profile
• Route of administration
• Evidence of clinical efficacy
• Cost.

22. MINIMUM INHIBITORY CONCENTRATION [MIC]:
• Lowest concentration of an antibiotic which prevents visible
growth of a bacterium.
CONCENTRATION-DEPENDENT INHIBITION:
Inhibitory effect depends on the ratio of peak concentration to the
MIC.
Eg; Same daily dose of Gentamicin produces better action when given as
a single dose than divided in 2-3 portions.
TIME-DEPENDENT INHIBITION:
Antimicrobial action depends on the length of time the
concentration remains above MIC. Here the division of daily dose has
better effect.
Eg; B-Lactams, Vancomycin, Macrolides.

23. • Penetration to the site of infection also depends on the
pharmacokinetic property of the drug.
• Drug which penetrates better and attains higher
concentration is likely to be more effective.
• Penetration of AMA’s into bone is generally poor, but
Clindamycin penetrates very well and is a good choice for
‘Purulent osteitis’.
• Penicillins and Aminoglycosides penetrate poorly into CSF
unless meninges are inflamed.

24. DENTAL PROCEDURES REQUIRING ANTIBIOTIC
COVERAGE
• All procedures that involves manipulation of gingival tissue and periapical
region of the teeth.
• Extractions
• Suturings
• Periodontal procedures {SRP, Surgery}
• Implant placement & reimplantation of avulsed tooth.
• Endodontic instrumentation or surgery beyond apex.
• Subgingival placement of antibiotic strips or fibres.
• Intra ligamentary LA injections
• Biopsies.

25. COMMONLY USED DRUGS IN DENTISTRY
• B-lactams
• B-lactamase inhibitors
• Macrolides
• Tetracyclines
• Metronidazole
• Clindamycin.

27. Penicillin was the 1st
antibiotic to be used
clinically in 1941.
Originally obtained from a
fungus “Penicillium
notatum”, but present
source is a high yielding
mutant of P.chrysogenum.

28. CHEMISTRY & PROPERTIES:
• Penicillin nucleus consists of fused Thiazolidone and b-lactam
rings to which side chains are attached to an amide linkage.
• PenicillinG, “ GOLD STANDARD PENICILLIN” having a benzyl side
chain [R] is the original penicillin used clinically. This side chain
can be split off by an amidase to produce 6-aminopencillianic
acid.
• Salt formation takes place with Na+ & K+ at the Carboxyl group
attached to thiazolidone ring. These salts are more stable than
parent acid.

30. • UNITAGE: 1U of crystalline sod.benzyl pencillin=0.6ug of the standard
preparation.
1g=1.6 million units.
MECHANISM OF ACTION:
All b-lactams interfere with the SYNTHESIS OF BACTERIAL CELL
WALL.
• Bacteria synthesize UDP-N-acetyl muramic acid pentapeptide, called
“Park nucleotide” and UDP-N-acetyl glucosamine.
• The peptidoglycan residues are linked together forming long strands
and UDP is split off.
• Final step is the cleavage of the terminal D-alanine of the peptide
chains by trans-peptidases.

31. • The energy so released is utilized for the
establishment of cross linkages between
peptide chains of the neighboring strands. This
cross linkages provide stability and rigidity to
the cell wall.
• B-Lactams inhibit transpeptidases so that
crosslinking doesn’t take place.

32. • When bacteria divide in the
presence of a b-lactam antibiotic,
cell wall deficient forms{CWD} are
produced. As the interior of the
bacterium is hyperosmotic CWD
forms swell and burstbacterial
lysis.
• In gram+ve bacteria, cell wall is
almost entirely made of
peptidoglycan; while –ve bacteria
consists of alternating layers of
lipoprotein and peptidoglycan. This
may be the reason for higher
susceptibility of gram+ve
organisms to PnG.

34. PHARMACOKINETICS:
• PnG is acid labile destroyed by gastric acids.
• Absorption of Sod.PnG from i.m site is rapid and complete.
• Distributed mainly extracellularly; reaches most body fluids, but
penetration in serous cavities and CSF is poor.
• Plasma T1/230mins.
• Renal excretion.
• Tubular secretion of PnG is blocked by Probenicid higher and
long lasting plasma concentrations are achieved.

35. USES:
DENTAL: Parenteral pnG remains effective in majority of
common infections caused by both aerobic and anaerobic
bacteria such as—
Streptococci
Peptostreptococci
Eubacterium
Prevotella
Porphyromonas
Fusobacterium.

36. • At ordinary doses {0.5-2MU i.m 6 hourly[sod.pnG] or 12-24
hours[Procaine pnG}, it can be used for Periodontal abscess,
Pericorinitis, acute suppurative pulpitis, ANUG etc;
• It can also be employed prophylactically to cover dental procedures in
predisposed patients.
GENERAL MEDICAL USES:
Streptococcal infections like pharyngitis, tonsillitis, bacterial
endocarditis etc;
Pneumococcal infections like pneumonia, meningitis.
Meningococcal meningitis and other infections.
Gonorrohea
Syphilis—Benzathine penicillin is DOC.
Diptheria, tetanus and other rare infections like gas gangrene, anthrax
etc;

37. PROPHYLACTIC USES:
• for Infective endocarditis
• to prevent recurrence of Rheumatic fever{benzathine pn DOC}
• Surgical prophylaxis combined with Gentamicin.
• To protect Agranulocytosis patients{ with Aminoglycosides}
INTERACTIONS:
• Hydrocortisone inactivates ampicillin if mixed in i.v solution. By
inhibiting colonic flora, it may interfere with metabolism of oral
contraceptives Failure of oral contraception.
• Probenicid retards renal excretion of penicillin.

38. AMOXICILLIN is a close congener of ampicillin, similar to it all
respects except:
Oral absorption is better; food doesn’t interfere with absorption,
higher and more sustained blood levels are produced.
Incidence of diarrohea is lower.
Less active against Shigella and H.influenza.
Amoxicillin + Clavulanic acid are used for periodontal
infections as they are mostly polymicrobial in nature.

39. PREPARATIONS & DOSAGE:
o Amoxicillins: Capsules-250mg,500mg
Oral suspension-125-250mg/5ml
Chewable-125,200,250,400mg
o Ampicillin: Oral-250,500mg capsules
Oral suspension-100mg/ml,125,250,500mg/5ml
Parenteral-125,250,500mg,1.2gm/vial.
o Amoxicillin/Pot.clavulanate-{500+125mg}
Oral-250,500,875mg tabs
Chewable-125,200,250,400mg
Oral suspension-125,200,250mg/5ml.

40. ADVERSE EFFECTS:
Local irritancy and direct toxicity.
Hypersenitivityrash, itching, utricaria, fever
 Wheezing, angioneurotic edema, Serum
sickness & exfoliative dermatitis are less common.
 Anaphylaxis is rare but fatal.
Intolerance
Superinfections eg; Candida
Jarisch-Herxheimer reaction on syphilitic patients treated with
penicillin.

41. NITROIMIDAZOLES
• Metronidazole
• Tinidazole
• Secnidazole
• Ornidazole
• Satranidazole

42. METRONIDAZOLE:
The prototype member of this class; introduced in
1959 for “Trichomonas vaginitis” and later found to be a Broad
spectrum anti-protozoal drug against Entamoeba histolytica and
Giardia.
SPECTRUM:
• Fusobacteruim
• Cl.difficle
• Prevotella
• Campylobacter
• H.pylori
• Spirochetes.

44. MECH.OF ACTION:
 Selectively toxic to anaerobes.
After entering the cell by diffusion, its nitro group is reduced by
certain redox proteins to a highly reactive “Nitro radical” which
exerts cytotoxicity.
Nitro radical can acts as an electron sink, which competes with
the biological electron acceptors of the anaerobic organisms for
the electron generated by the Pyruvate:Ferredoxin
oxidoreductase{PFOR} enzyme pathway of pyruvate oxidation.
Thus the energy metabolism of anaerobes is disrupted.

45. PHARMACOKINETICS:
 Almost completely absorbed from small intestines; little
unabsorbed reaches the colon.
Widely distributed in the body, attaining therapeutic
concentration in vaginal secretion, semen, saliva, CSF.
Plasma t1/2 8hrs.
Metabolized in liver primarily by Oxidation & Glucuronide
conjugation.
Excreted in urine.

46. ADVERSE EFFECTS:
 Anorexia, nausea, bitter/metallic taste and abdominal cramps
are the most common.
 Headache, glossitis, dryness of mouth, dizziness, rashes and
transient neutropenia are less frequent.
 Prolonged administration may cause Peripheral neuropathy and
CNS effects.
 Thrombophlebitis of the injected vein on i.v.

47. USES:
oMetronidazole in a dose of 200-400mg TDS{15-30mg/kg/day}
is extensively used for Orodental infections, because anaerobic
bacteria are frequently involved.
oDOC for ANUG, which is often combined with PencillinV,
Amoxicillin, Erythromycin/ Tetracycline for 5 days.
oPeriodontitis, pericoronitis, acute apical infections, and some
endodontic infections also respond well for 5-7 days.
oDOC for antibiotic associated “Pseudomembranus enterocolitis”
caused by Cl.difficle.

48. oMetronidazole is a component of “Triple drug therapy” for
eradication of H.pylori in Peptic ulcers when used along with
Clarithromycin/Amoxicillin and a Proton pump inhibitor.
oDOC for all forms of amoebic[Protozoal] infections like Dysentry,
chronic intestinal amoebiasis and liver abscess.

49. CONTRA-INDICATIONS:
 Neurological diseases
 Blood dyscrasias
 1st trimester of pregnancy
 Chronic alcoholism.

50. INTERACTIONS:
Disulfuram- like intolerance to alcohol.
Enzyme inducers like Phenobarbitone, Rifampacin may reduce
its therapeutic effects.
Cimetidine can decrease the metabolism of metronidazole.
Metronidazole enhances Warfarin action by inhibiting its
metabolism; Prothrombin time of patients taking Warfarin
should be monitored when Metronidazole is prescribed.

51. PREPARATIONS:
 Flagyl, Metrogyl, Aristogyl.
200-400mg tabs.
200mg/5ml oral suspensions.
500mg/100ml i.v infusion.

52. TETRACYCLINES
• Obtained from soil Actinomycetes.
• 1st to be introduced was Chlortetracycline in 1948.
• Broad-spectrum antibiotic.
• All are slightly bitter solids which are slightly water soluble, but
their hydrochlorides are more soluble.

53. AVAILABLE ARE:
 Tetracycline
 Oxytetracycline
 Demeclocycline
 Doxycycline
 Minocycline.

54. MECHANISM OF ACTION

55. Primarily Bacteriostatic.
• INHIBIT PROTEIN SYNTHESIS by binding to 30s ribosomes in
susceptible organisms; following attachment of aminoacyl t-RNA
to the m-RNA—ribosome complex is interfered. As a result,
peptide chain fails to grow.

56. PHARMACOKINETICS:
• Older tetracyclines are incompletely absorbed from GIT, i.e;
better absorbed if taken in empty stomach.
• Doxycycline & Minocycline are completely absorbed.
• Have Chelating property forms insoluble and unabsorbable
complexes with Ca and other metals.
• Milk, iron preparations, non-systemic antacids & Sucralfate
reduce their absorption.
• Widely distributed in the body[Vol. of dist.>1L/kg]
• Concentrated in liver, spleen, gingival tissue and bind to the CT
in bone & teeth. Intracellularly, bind to Mitochondria.

57. • Primarily excreted in Urine; dose has to be reduced in renal
failure. Doxycycline is an exception.
• Enterohepatic circulation to some extent.
• Secreted in milk in amounts sufficient enough to affect the
suckling infant.

58. ADMINISTRATION:
• Mostly Oral; capsule should be taken 1/2hr before or 2hrs
after food.
• Not recommended by i.m as it is painful and absorption from
injection site is poor.

59. USES:
 Benefit certain forms of Periodontal diseases by their Broad-
spectrum action as well as by Suppressing the activity of matrix-
metalloproteinases derived from neutrophils and fibroblasts that
contribute to gingival inflammation. These enzymes are Ca
dependent and tetracyclines chelate Ca.
 May benefit periodontal inflammation by scavenging free radicals.
 Acc.to GORDAN & WALKER, systemic administration of tetracycline
in conjunction with Conventional therapy provides better response
than mechanical scaling alone.
 In refractory periodontitis, 2week tetracycline{1gm/day} or
Doxycycline{0.1-0.2mg/day} therapy controls gingival
inflammation and helps to normalize the periodontal microflora.

60.  Highly active against Actinobacillus sp. Responsible for
destruction of gums and bone loss in Juvenile periodontitis.
 Apart from dental, also used for;
• Venereal diseases– Lymphogranuloma venereum
• Atypical pneumonia
• Cholera
• Brucellosis
• Relapsing fever
• Urinary tract infections
• Community-acquired pneumonia.

61. ADVERSE EFFECTS:
• Irritant property; cause epigastric pain, nausea, vomiting,
diarrohea.
• i.m is very painful & i.v may cause thrombophlebitis.
DOSE-RELATED TOXICITY:
 Kidney damage
 Anti-anabolic effect
 Phototoxicity
 Increased intracranial pressure
 Diabetis insipidus

62.  Liver damage
 Dentition & bones
 Fanconi syndrome
 Vestibular toxicity
 Hypersensitivity
 Superinfections

63. • When given from mid-pregnancy to 5 months of extrauterine
life, Decidous teeth are affected; brown discoloration, ill-formed
teeth.
• When given from 3months-6years crown of permanent
anterior dentition.

64. PRECAUTIONS:
 Avoided during Pregnancy, lactation & in children.
 Avoided in patients on diuretics blood urea may rise.
 Used cautiously in hepatic or renal insufficiency.
 Never used beyond their expiry date.
 Do not mix injectable tetracyclines with Penicillins
inactivation occurs.

65. AMINOGLYCOSIDES
Polybasic amino groups linked amino
glycosidically to 2/more amino sugar
residues.

66. • MECHANISM OF ACTION:
• Transport of aminoglycoside through the
bacterial cell wall and cytoplasmic membrane.
• Binding of ribosomes resulting in Inhibition of
protein synthesis.

68. • Once inside the bacterial cell, Streptomycin binds to 30s subunit,
but others bind to 50s as well as 30s-50s interface.
 Freeze initiation of protein synthesis
 Prevents polysome formation
 Prevent their disaggregation into monosomes.
• Binding of Aminoglycoside to 30s-50s junction causes distortion
of mRNA codon recognition resulting in mis-reading of codon
1/more aminoacids are entered into the peptide chainpeptides
of abnormal length are produced.

69. PROPERTIES:
• All are used as Sulfate salts, which are highly water soluble;
solutions are stable for months.
• They ionize in solution; not absorbed orally; distribute only
extracellularly; do not penetrate brain/CSF.
• Excreted unchanged in urine by glomerular filtration.
• All are primarily active against aerobic gram-ve bacilli and do
not inhibit anaerobes.
• Relatively narrow margin of safety.
• All exhibit Ototoxicity and nephrotoxicity.

70. USES:
• Gentamicin 2mg/kg i.m/i.v is used to supplement Amoxicillin/
Vancomycin for prophylaxis of bacterial endocarditis following
dental surgery in patients with Prosthetic heart valves.
• Prevents and treats respiratory infections in critically ill patients.
• In pseudomonas, Proteus or Klebsiella infections.
• Meningitis caused by gram-ve bacilli.
• SABE to accompany pencillin.

71. ADVERSE EFFECTS:
 Ototoxicity Cochlear & vestibular damage.
Neomycin.
 Nephrotoxicity
 Neuromuscular blockade Neomycin & Streptomycin.

72. PRECAUTIONS & INTERACTIONS:
• Avoid during pregnancy; risk of foetal ototoxicity.
• Avoid concurrent use of other ototoxic drugs.
eg; high ceiling diuretics, Minocycline.
• Avoid concurrent use of other nephrotoxic drugs.
eg; AmphotericinB Vancomycin, Cyclosporine &
Cisplatin.
• Cautious use of muscle relaxants in patients receiving an
aminoglycoside.
• Do not mix an aminoglycoside with any drug in the same
syringe/ infusion bottle.

73. MACROLIDES
Antibiotics having a Macrolytic lactone ring with attached
sugars.
 Erythromycin
 Roxithromycin
 Clarithromycin
 Azithromycin.

74. ERYTHROMYCIN:
Isolated from Streptomyces erythreus in 1952 and is
widely employed, mainly as an alternative to Penicillin.
MECHANISM OF ACTION:
• Bacteriostatic at low but Cidal at high concentrations.
• Acts by Inhibiting bacterial protein synthesis. It combines
with 50s subunit and interferes with “Translocation”.

76. ANTIMICROBIAL SPECTRUM:
• S.pyogenes
• S.pneumoniae
• N.gonorrhea
• Clostridia
• C.diptheriae
• Listeria
• Campylobacter
• Legionella

77. PHARMACOKINETICS:
• Given as enteric coated tablets to protect it from gastric acid.
• Widely distributed in body, enters into abscesses, crosses
placenta but not BBB.
• 70-80% plasma protein bound, partly metabolized & excreted
primarily in bile in active form.
• T1/21.5hrs.

78. DOSAGE:
250-500mg 6hrly{max. 4gm/day}
Children-30-60mg/kg/day

79. USES:
• 2nd choice drug to Penicillins for Periodontal/periapical abscess,
Necrotizing ulcerative gingivitis, post extraction infections etc;
• Particularly valuable for patients allergic to penicillins or those
with Penicillin-resistant infections.
• Less effective than penicillins as it is bacteriostatic.
• Pharyngitis, tonsillitis and other respiratory/ENT infections.

80. ADVERSE EFFECTS:
• Mild to severe epigastric pain
• Very high doses Reversible hearing impairment
• Hypersensitivity

81. CLINDAMYCIN
Lincosamide antibiotic with spectrum of activity
similar to Erythromycin with which it exhibits partial cross
resistance.
MECH.OF ACTION:
Inhibits protein synthesis by binding to 50s ribosomes.

82. PHARMACOKINETICS:
• Oral absorption is good. Penetration into most skeletal and soft
tissues, but not brain and CSF., accumulates in neutrophils and
macrophages.
• T1/23 hrs.
• Excreted in urine & bile.
• Penetrates good into Bone, suited for “Dentoalveolar abscess”
and other bone infections caused by Staphylococci /
Bacteroides.

83. ADVERSE EFFECTS:
• Rashes, Utricaria, abdominal pain
• Diarrohoea
• “Pseudomembranous enterocolitis” due to Cl.difficle
superinfection.

84. SULFONAMIDES

85. MECHANISM OF ACTION

86. QUINOLONES

87. CEPHALOSPORI
NS

88. WHY CEPHALOSPORINS??
Broad-spectrum of activity
Stability to B-lactamase
Oral & parenteral preparations
Widely accepted
Treats ‘Day to day’ as well as ‘serious infections’
High safety profile.

89. CEPHALOSPORINS ADVANTAGES OVER PENICILLINS:
• Increased acid stability compared to penicillins
• Better absorption
• Broad spectrum
• Increased activity against resistant microbes
• Decreased allergenicity
• Increased tolerance

90. ADVERSE EFFECTS:
• Pain
• Diarrhoea
• Nephrotoxicity
• Bleeding

91. ANTI-FUNGAL DRUGS

92. ANTI-VIRAL DRUGS

94. ANTIBIOTICS IN
PERIODONTICS
INTRODUCTION:
• During the past 2 decades, Dentists &
Microbiologists have embraced
periodontal antibiotic therapy as a
powerful adjunct to conventional
mechanical debridement for
therapeutic management of the
disease.
• The concept of the therapy centers
upon:
i. Pathogenic microbiota
ii. Patient
iii. Drug

95. PERIODONTAL MICROBIOTA:
• 500 bacterial taxa
• Usually a constellation of putative pathogens rather than a
single pathogenic species.
• Most putative are:
 Gram –ve anaerobic rods

96. ASSOCIATION B/W PUTATIVE PERIODONTAL PATHOGENS & PERIODONTITIS:

97. RATIONALE:
• The microbial etiology of inflammatory periodontal diseases
provides the use of antimicrobial medication in periodontal
therapy.
• Despite diligent periodontal therapy, some individuals continue
to experience periodontal breakdown due to some major
pathogens which may reside in inaccessible areas like furcations
or due to poor host defense mechanisms.

98. INDICATIONS:
• Patients who do not respond to conventional periodontal therapy.
• Patients with acute periodontal infections with systemic
manifestations.
• Prophylaxis in medically compromised patients.
• As an adjunct to surgical & non-surgical periodontal therapy.
AJ Van Winkelhoff, TE Rams, J Slots. Systemic antibiotics in periodontics.
Periodontol2000.1996;10:45-78

99. GUIDELINES FOR USE OF ANTIBIOTICS IN PERIODONTAL DISEASE:
 The clinical diagnosis and situation dictate the need for
possible antibiotic therapy.
 Continuing disease activity even after SRP.
Antibiotics are selected based on the patient’s medical & dental
status, current medications, and results of microbial analysis, if
performed.
 Microbial plaque samples may be obtained from individual
pockets or from pooled subgingival sites.
 Studies have shown that systemic antibiotics can improve
attachment levels when they are used as adjuncts to SRP in
chronic & aggressive periodontitis.

100.  Disruption of bacterial “Biofilm” is a must, so that antibiotic
agents can have access to subgingival pathogens.
 Debridement of root surfaces, optimal oral hygiene, and
frequent periodontal maintenance therapy are important.
 Slots et.al; described a series of steps using anti-infective agents
for enhancing regenerative healing. They recommend to start
antibiotics 1-2 days before surgery and continuing for at least 8
days.
However, the value of this regimen has not been well
documented.

103. FACTORS THAT PLAY A ROLE IN THE EFFICACY OF ANTIBIOTIC :
 Drug binding to tissues.
 Protection of key organism thru binding and/or consumption of
the drug by non-target organisms.
 Microbial invasion of periodontal tissues and root surfaces.
Total bacterial load in the pocket.
 Subgingival plaque biofilm
 Effectiveness of the host defenses.

104. ANTIBIOTIC DOSING PRINCIPLES:
 Employ high doses for a short duration of time.
 Use an oral antibiotic loading dose.
 Achieve blood levels of the antibiotic 2-8times the MIC.
 Use frequent dosing intervals.
 Determine duration of therapy by the remission of the disease.

105. 2 critical factors should be considered in selecting a
systemic antibiotic:
 Gingival fluid concentration {CGCF}
 Minimum inhibitory concentration {MIC90}
CGCF provides info. on the peak levels achieved by
systemic delivery at the periodontal pocket.
90% MIC is an in vitro determination of the ‘Concentration’
that will inhibit growth of 90% of the bacterial strains that are
tested.
Antimicrobial activity can be defined as a relationship
b/w CGCF & MIC.

106. PERIODONTAL CONDITIONS REQUIRING ANTIBIOTIC THERAPY:
Chronic periodontitis
Aggressive periodontitis
Necrotizing periodontal diseases
Periodontal abscess
Perio-endo lesions.

107. ADMINISTRATION:
i. Systemic administration
ii. Local administration

108. ADVANTAGES OF SYSTEMIC THERAPY:
 Simple, easy administration of drug to multiple sites of disease
activity
 Eliminate or reduce pathogens on oral mucosa & extra-dental
sites.

109. DISADVANTAGES:
 Inability to achieve high GCF concentrations
 Increased risk of adverse reactions
 Increased development of multiple antibiotic resistant microbes
 Uncertain patient compliance.

110. ANTIBIOTICS IN PERIODONTICS:
Tetracycline
Minocycline
Doxycycline
Erythromycin
Clindamycin
Ampicillin
Amoxicillin
Metronidazole

111. There are 5 daunting problems that have slowed progress of
antibiotic therapy:
• Periodontal diseases are heterogenous
• Clinical diagnoses are made on the basis of clinical signs, not
molecular pathology
• Actual causal factor have not been definitely identified.
• No microbiological sampling
• Only few well designed, RCT that test the efficacy of these
protocols are available.

112. SEQUENTIAL SYSTEMIC THERAPY:
• Bacteriostatic antibiotics – rapidly dividing microbes
• Interrupted function – with a bactericidal agent
• When both are required, they are best given ‘Serially’, but not in
combination, to avoid un favourable interactions.

113. In one such study, 6 patients with ‘Recurrent progressive
periodontitis’ were given the usual dosage of Doxycycline for 4
days  Augmentin {Amoxicillin + clavulanic acid} for 5 days.
• 6 similar patients were given Doxycycline alone for 10 days.
• After 25weeks, patients receiving the sequential combination
had significantly “Greater pocket depth reduction” than those
receiving Doxycycline alone.

114. COMBINATION THERAPY:
• Beneficial – Mixed infections.
 Metronidazole + Amoxicillin {250mg+250mg TID,3
days} A.a, P.gingivalis infections.
 Ciprofloxacin+ Clindamycin {500mg+300mg BID,8
days} anaerobes
 Metronidazole + Ciprofloxacin {500mg+500mg BID,8
days}  A.a

115. In a study by Winkel et.al, it was observed that patients
with subingival P.gingivalis at baseline who were treated with
Metronidazole + Amoxicillin showed reduction of app. Half the
number of >5mm pockets after therapy compared with those
given a placebo.
 Guerreo et.al, used a comparable treatment protocol in
patients with Aggressive periodontitis and showed significantly
better improvement of all periodontal parameters in the
antibiotic treated patients compared to placebo treated subjects
6 months post-treatment.
 Antibiotics result in better resolution of periodontal
inflammation, better probing depths, and attachment loss
reduction.

116. ADVANTAGES OF COMBINATION THERAPY:
 Empirical treatment of severe infections
 Treatment of polymicrobial infections
 Prevention of the emergence of bacterial resistance
 Increased effectiveness from antibiotic synergism.

117. DISADVANTAGES:
 Increased adverse reactions
 Antagonistic drug interactions with improperly selected
antibiotics
 Superinfections with Candida or other microbes.

118. ANTIBIOTIC PROPHYLAXIS:
Recommended when the patients undergo procedures that are at
risk for producing bacteremia.
Incidence of infections such as IE ranges from 5.0 to 7.9 in
100,000 person/year with a significant increasing trend among
women.

119. MEDICAL CONDITIONS REQUIRING ANTIBIOTIC PROPHYLAXIS DURING
DENTAL PROCEDURES:
 Uncontrolled Diabetes
 Infective endocarditis
 Organ transplantation
 Previous late artificial joint infection
 Patients undergoing treatment of severe and spreading oral infections
 Patients with increased susceptibility for systemic infections
 Congenital or acquired immunodeficiency
 Patients at a significant risk for medication-related Osteonecrosis of
the jaw.

120. PROCEDURES DO NOT NEED PROPHYLAXIS:
• Routine anesthetic injections through non-infected tissue
• Taking dental radiographs
• Prosthetic joint replacements
• Placement of removable prosthodontic or orthodontic appliances
• Adjustment of orthodontic appliances
• Placement of orthodontic brackets
• Shedding of deciduous teeth
• Bleeding from trauma to the lips or oral mucosa

121. ANTIBIOTIC PROPHYLAXIS FOR INFECTIVE ENDOCARDITIS :

122. ADDITIONAL CONSIDERATIONS:
 “If the dosage of antibiotic is inadvertently not administered
before the procedure, the dosage may be administered up to 2
hours after the procedure.”
 Patients who require prophylaxis but are already taking
antibiotics for another condition; In these cases, the guidelines for
infective endocarditis recommend that the dentist select an
antibiotic from a different class than the one the patient is already
taking.

123. LOCAL DRUG DELIVERY
Goodson et al, in 1979 first proposed the concept of “Site-
specific delivery” in the treatment of periodontitis.
• The 1st delivery devices involved hollow fibers of Cellulose acetate
filled with “Tetracycline”.
• Devices with minimal control of drug release.
• However ,Tetracycline fibers are no longer commercially available.

124. • Provides long-term retention of a highly concentrated drug at the
base of the periodontal pocket.
• Periodontal pockets provide natural reservoir bathed by gingival
crevicular fluid that is easily accessible for the insertion of a
delivery device.
• Controlled drug delivery  more prolonged availability and
sustained action.

125. IDEAL REQUISITES OF LOCALLY APPLIED DRUG:
Acc. to Greenstein & Tonetti--
 Must reach the intended site of action.
 Must remain at an adequate concentration.
 Should last for a sufficient duration of time.

126. INDICATIONS FOR LDD:
As an adjunct to Scaling and Root planing
Periodontal maintenance therapy
Medically compromised patients for whom surgery is not an
option.
To halt the progression of periodontal disease in patients with
moderate periodontitis.

127. CONTRA-INDICATIONS:
 Hypersensitivity to the drug
 Susceptible to IE
 Ultrasonic device based drug delivery in cardiac pacemakers,
asthmatics, TB etc;

128. BASED ON DURATION OF ACTION: Greenstein & Tonetti in 2000
i. Sustained release devices
ii. Controlled delivery devices.
BASED ON DEGRADABILITY:
i. Non-degradable
ii. Degradable
BASED ON APPLICATION: Rams & slots in 1996
i. Personally applied (in patient home)
ii. Professionally applied ( in dental office)
CLASSIFICATI
ON

130. ADVANTAGES OF LOCAL DRUG DELIVERY:
• Attains 100-fold higher concentrations of an antimicrobial agent
in sub gingival sites.
• No potential danger of resistant strains and super imposed
infections
• No risk of adverse drug reactions and dependence of patient
compliance
• May employ antimicrobial agents not suitable for systemic
administration.

131. DISADVANTAGES:
 Difficulty in placing into deeper parts of periodontal pockets and
furcation lesions.
 Lack of adequate manual dexterity
 Time-consuming and labor-intensive.
 Do not markedly affect periodontal pathogens residing within
adjacent gingival connective tissues and on extra pocket oral
surfaces, which increases the risk of reinfection.

132. LOCAL DRUG DELIVERY AGENTS:
•Tetracycline
•Doxycycline
•Minocycline
•Metronidazole
•Moxifloxacin
•Azithromycin
•Chlorhexidine

133. TETRACYCLINE CONTAINING FIBER:
 The 1st local delivery product
 Tetracycline fibers with 12.7mg per 9 inches, an ethylene/vinyl
acetate copolymer fiber 0.5mm diameter and 23 cm long
 Well tolerated in oral tissues and concentration reach 1300μg/ml
for 10 days
 No change in antibiotic resistance to tetracycline was found
 ACTISITE, PERIODONTAL PLUS AB
 These fibers are no longer commercially available

135. DOXYCYCLINE:
 A gel system using a syringe with 10% doxycycline (Atridox).
 Only local delivery system accepted by the American Dental
Association
 1500mcg/ml in 2 hrs and remains >1000mcg/ml through18 hrs.
 The combined use of systemically delivered Doxycycline
hyclate (20mg BID) + locally delivered Doxycycline hyclate gel
(10%) in combination with scaling and root planning provided
statistically significantly greater clinical benefits.

137. MINOCYCLINE:
• A locally delivered sustained release form of minocycline microspheres
(Arestin).
• The 2% minocycline is encapsulated into bioresorbable microspheres in
gel carrier.
 Grace et al; evaluated topical locally delivered minocycline as an
adjunctive to non-surgical periodontal treatment and found advantageous
outcome in terms of BOP, attachment level.

138. METRONIDAZOLE:
• A topical medication containing an oil based metronidazole 25%
dental gel. (glyceryl monooleate and sesame oil)
• Two 25% gel application at a 1- week interval have been used.
• Studies have shown that metronidazole gel is equivalent to scaling
and root planning.
• Bleeding on probing was reduced by 88% of cases.

139. MOXIFLOXACIN:
Fourth-generation synthetic fluoroquinolone
Broad-spectrum antibacterial
Antimicrobial activity against aerobic and anaerobic bacteria,
including a number of periodontal pathogens
Local delivery of 0.4% moxifloxacin may be of benefit as an
adjunct to scaling and root planning for the treatment of
periodontitis

140. AZITHROMYCIN:
 Has a wide antimicrobial spectrum of action towards an
aerobic bacteria & Gram-negative bacilli.
It is effective against periodontal pathogens such a s A.a & P.g
Tyagi et al investigated the clinical effectiveness of AZM at a
concentration of 0.5%In an indigenously prepared
bioabsorbable controlled release gel as an adjunct to non
surgical mechanical therapy in the treatment of chronic
periodontitis.
Although both treatment strategies seem to benefit patients,
the adjunctive use of 0.5%ofAZM showed better results.

141. CHLORHEXIDINE:
A resorbable delivery system resorbs in 7-10 days.
No signs of staining were noted in any of the studies!!
PERIOCHIP, PERIOCOL-CG 123
Studies have shown suppression of pocket flora for upto11 weeks
following treatment with periochip.
Largest effect on PPD reduction—tetracycline fibres, doxycycline,
minocycline
Highest effect for CAL gain—CHX

143. COMPARATIVE STUDY:
In a study, attempted to compare LDD devices,
Doxycycline polymer, Metronidazole gel, and PerioChip were
compared in 47 periodontal patients.
• The study found that all controlled-release polymer devices
increased gingival attachment levels but there was a slightly
greater improvement with the doxycycline polymer {Salvi GE,
Mombelli A, Mayfield L, et al}.

145. COMMON ANTI - FUNGALS IN DENTISTRY:
 Stops spread of infection
 In Candidiasis
 Desquamative gingivitis
Denture stomatitis
 Angular chelitis
In combination with anti-bacterial in case of an abscess.

146. ANTI-VIRALS COMMONLY USED IN DENTISTRY:
• Acyclovir & Valacyclovir Herpes, varicella, infectious
mononucleosis
• These drugs doesn’t cure the infection, but they do decrease the
signs & symptoms associated with the infection.
• Acts by inhibiting “Replication of viral DNA”.
• Nausea, vomiting, diarrhea can occur.

147. FAILURES OF ANTIBIOTIC THEPARY:
Inappropriate choice of antibiotic
 Emergence of antibiotic-resistant microorganisms
 Too low a blood concentration of the antibiotic
 Slow growth rate of microorganisms
 Impaired host defenses
 Patient noncompliance

148.  Antibiotic antagonism
 Inability of the antibiotic to penetrate to the site of the infection
 Limited vascularity or decreased blood flow
 Unfavorable local factors (decreased tissue pH or oxygen tension)
 Failure to eradicate the source of the infection {lack of incision
and drainage}

149. BIBLIOGRAPHY:
 Essentials of pharmacology for Dentistry- KD Tripathi 2nd ed;
 Basic and clinical Pharmacology- McGrawHill Lange 10th ed;
 Carranza’s Clinical Periodontology- 11th ed;
 Practical Periodontics- Kenneth Eaton & Philip Ower
Systemic antibiotic therapy in periodontics- Arie Jan Van Winkelhoff, Thomas.E.Rams,
Jorgan Slots; - Periodontology 2000 February 1996 - Vol. 10 Issue 1 Page 5-159
 Role of systemic antibiotics in the treatment of periodontal diseases- J Periodontal
2004;75:1553-1565
 Systemic antibiotic therapy in periodontics-Dental Research Journal,2012 sep-
oct:505-515
Highlights on role of antibiotics in periodontics- International journal of research
dentistry2016;24-27
Application of Local drug delivery in periodontics, A review- International journal of
scientific research, vol(6) January 2017
Local drug delivery in periodontics- International journal of research in health and
allied sciences, vol(3) July-August2017