antibiotics, antimicrobial, periodontics,

1. ANTI-MICROBIAL
THERAPY
PRESENTED BY- DR K. ABHILASHA
MODERATED BY- DR SHOBHA
Department of Periodontics, MRADC
1

2. CONTENT
 INTRODUCTION
 HISTORY
 RATIONALE OF ANTIBIOTIC THERAPY IN
PERIODONTICS
 GUIDELINES FOR USE OF ANTIBIOTICS IN
PERIODONTICS
 CLASSIFICATION
 ANTIBIOTICS
 BETA LACTAM
 TETRACYCLINES
 CHLORAMPHENICOL
 NITROIMIDAZOLE
 LINCOSAMIDE
PART 1
2

3. CONTENT
 ANTIBIOTICS
 MACROLIDE
 SULFONAMIDE
 CHLORAMPHENICOL
 AMINOGLYCOSIDES
 SELECTION OF ANTIBIOTICS
 PRINCIPLES OF ANTIBIOTIC DOSING
 INDICATIONS OF ANTIBIOTICS IN PERIODONTAL THERAPY
 MEDICAL CONDITION THAT NEED PRE-OPERATIVE
ANTIBIOTIC
 ANTIBIOTIC RESISTANCE
 ANTIBIOTIC SENSITIVITY TEST
 SUPERINFECTION
 COMBINATION THERAPY
 CONCLUSION
 REFERENCES
PART 2
3

4. SYSTEMIC
ANTIBIOTICS
BETA LACTAM
NITROIMIDAZOLE
QUINOLONE
TETRACYCLINE
LINCOSAMIDE
SULFONAMIDE
CHLORAMPHENICOL
AMINOGLYCOSIDES
MACROLIDE
4

5. MACROLIDE
 These are antibiotics having a macrocyclic lactone
ring with attached sugars.
 Erythromycin is the first member discovered in the
1950s.
 Roxithromycin, Clarithromycin and Azithromycin
are the later addition.
ERYTHROMYCIN:
 It was isolated from Streptomyces erythreus in 1952.
5

6. ERYTHROMYCIN
Mechanism of action:
 Bacteriostatic at low but bactericidal (for certain
bacteria only) at high concentrations.
 Sensitive gram-positive bacteria accumulate
erythromycin intracellularly by active transport.
 Inhibits bacterial protein synthesis.
 It combines with 50S ribosome subunits and
interferes with ‘translocation’
6

7. ERYTHROMYCIN
Antimicrobial spectrum:
 It is narrow, includes mostly gram-positive and a few
gram negative bacteria.
 Erythromycin is highly active against Str. pyogenes
and Str. pneumoniae, N. gonorrhoeae, Clostridia, C.
diphtheriae and Listeria.
 Penicillin-resistant Staphylococci and Streptococci
are now resistant..
7

8. ERYTHROMYCIN
Resistance:
Can acquire resistance to this antibiotic by:
 By acquiring the capacity to pump it out.
 Alteration in the ribosomal binding site for
erythromycin by a plasmid encoded methylase
enzyme.
Bacteria that develop resistance to erythromycin
are cross resistant to other macrolides as well.
8

9. ERYTHROMYCIN
 PERIODONTAL USAGE
1. An extremely safe drug that has often been recommended as an
alternative to penicillin for allergic patients.
2. Gingival fluid levels suggest that only a small portion reaches
the periodontal pocket by oral route.
Principle limitation of erythromycin is its poor tissue absorption.
Preparations for systemic administration are available as pro-drugs
(erythromycin estolate, erythromycin stearate or erythromycin
ethylsuccinate) to facilitate absorption. The pro-drug has little
antibacterial activity until hydrolyzed by serum esterases.
9

10. SPIRAMYCIN
 It is excreted in high concentrations in saliva.
 The results of various clinical trials have revealed good efficacy
of spiramycin in the treatment of periodontitis and meta-
analysis of these studies revealed high levels of evidence
supporting its efficacy.
 It has been shown to reduce gingival crevicular fluid volume,
pocket depth and subgingival spirochete levels.
Herrera et al. in a meta analysis evaluating spiramycin, amoxicillin
plus metronidazole, and metronidazole showed a statistically
significant additional effect of spiramycin in comparison to other
antibiotics with regard to probing pocket depth reduction for sites with
initial probing depth of more than 6 mm.
10

11. AZITHROMYCIN
1. Effective against anaerobes and gram negative bacilli.
2. After an oral dosage of 500 mg o.d for 3 days, significant levels of
azithromycin can be detected in most tissues for 7-10 days.
3. Therapeutic use requires a single dose of 250 mg/day for 5 days after
initial loading dose of 500 mg.
4. It has been proposed that azithromycin penetrates fibroblasts and
phagocytes in concentrations 100-200 times greater than that of
extracellular compartment. The azithromycin is actively transported to
sites of inflammation by phagocytes, then directly released into the sites
of inflammation as phagocytes rupture during phagocytosis.
Jolkovsky DL, Ciancio S. Chemotherapeutic agents. In: Carranza FA, Newman
MG, Takei HH, Klokkevold PR, editors. Clinical periodontology
. 10th ed. Philadelphia: WB Saunders; 2006. pp. 798–812.
11

12. The use of systemic azithromycin adjunctive to SRP was evaluated by Oteo et al. in
Porphyromonas gingivalis-positive moderate chronic periodontitis. This systemic
antimicrobial was chosen because of its convenient dosage, and the results showed
significant benefits in both clinical and microbiological outcome variables after 6
months. These results, however, were not corroborated in a similar study done without
selecting the patients based on a specific microbiological profile; no adjunctive effect
was observed after 1 year.
12

13. SYSTEMIC
ANTIBIOTICS
BETA LACTAM
NITROIMIDAZOLE
QUINOLONE
TETRACYCLINE
MACROLIDE
SULFONAMIDE
CHLORAMPHENICOL
AMINOGLYCOSIDES
LINCOSAMIDE
13

14. SULFONAMIDE
Sulfonamides were the first antimicrobial agents (AMAs)
effective against pyogenic bacterial infections.
Classification
 Short acting (4–8 hr) : Sulfadiazine.
 Intermediate acting (8–12 hr) : Sulfamethoxazole.
 Long acting (~7 days) : Sulfadoxine,
Sulfamethopyrazine.
 Special purpose sulfonamides: Sulfacetamide sod.,
Mafenide, Silver sulfadiazine, Sulfasalazine.
14

15. SULFONAMIDE
ANTIBACTERIAL SPECTRUM:
 Sulfonamides are primarily bacteriostatic against
many gram-positive and gram-negative bacteria.
 However, bactericidal concentrations may be attained
in urine.
 Streptococcus pyogenes, Haemophilus influenzae,
Vibrio cholerae.
15

16. SULFONAMIDE
16

17. SULFONAMIDE
USES:
 Systemic use of sulfonamides alone (not combined
with trimethoprim or pyrimethamine) is rare now.
 Chronic urinary tract infection.
 Streptococcal pharyngitis.
 Combined with trimethoprim (as cotrimoxazole)
sulfamethoxazole is used for many bacterial
infections.
 Along with pyrimethamine, used for malaria and
toxoplasmosis.
 Topical silver sulfadiazine or mafenide are used for
preventing infection on burn surfaces.
17

18. SYSTEMIC
ANTIBIOTICS
BETA LACTAM
NITROIMIDAZOLE
QUINOLONE
TETRACYCLINE
MACROLIDE
SULFONAMIDE
CHLORAMPHENICOL
AMINOGLYCOSIDES
LINCOSAMIDE
18

19. CHLORAMPHENICOL
 Chloramphenicol was initially obtained from
Streptomyces venezuelae in 1947.
 It is a yellowish white crystalline solid, aqueous
solution is quite stable, stands boiling, but needs
protection from light.
 The nitrobenzene moiety of chloramphenicol is
probably responsible for the antibacterial activity
as well as its intensely bitter taste.
19

20. CHLORAMPHENICOL
 MECHANISM OF ACTION
At high doses, it can inhibit mammalian mitochondrial protein synthesis as
well. Bone marrow cells are especially susceptible.
20

21. CHLORAMPHENICOL
Antimicrobial spectrum:
 Chloramphenicol is primarily bacteriostatic, though high
concentrations have been shown to exert cidal effect on
some bacteria.
 It is a broad-spectrum antibiotic, active against nearly
the same range of organisms (gram-positive and
negative cocci and bacilli, rickettsiae, mycoplasma) as
tetracyclines.
Pharmacokinetics:
 Rapidly and completely absorbed after oral ingestion.
 Very widely distributed.
 It freely penetrates serous cavities and blood-brain
barrier.
 It crosses placenta and is secreted in bile and milk.
 Plasma t½ is 3–5 hours in adults.
21

22. CHLORAMPHENICOL
Preparations and administration:
 The commonest route of administration of
chloramphenicol is oral—as capsules.
 250–500 mg 6 hourly (max. 100 mg/kg/ day).
 Children 25–50 mg/kg/day.
Indications of chloramphenicol are:
 Pyogenic meningitis.
 Anaerobic infections caused by Bact. fragilis and
others.
 Intraocular infections.
 Topically In conjunctivitis, external ear infection -
chloramphenicol 0.5–5.0% is highly effective.
22

23. CHLORAMPHENICOL
PRECAUTIONS
 Risk of serious (though rare) bone marrow aplasia:
 Never use chloramphenicol for minor infections or
those of undefined etiology.
 Do not use for infections treatable by other safer
antimicrobials.
 Avoid repeated courses.
 Daily dose not to exceed 2–3 g; duration of therapy to
be < 2 weeks, total dose in a course < 28 g.
 Regular blood counts (especially reticulocyte count)
may detect dose-related bone marrow toxicity.
23

24. SYSTEMIC
ANTIBIOTICS
BETA LACTAM
NITROIMIDAZOLE
QUINOLONE
TETRACYCLINE
MACROLIDE
SULFONAMIDE
CHLORAMPHENICOL
AMINOGLYCOSIDES
LINCOSAMIDE
24

25. AMINOGLYCOSIDE
 Streptomycin was the first member discovered in
1944 by Waksman and his colleagues.
 Great importance because it was active against
tubercle bacilli.
 These are a group of natural and semisynthetic
antibiotics having polybasic amino groups linked
glycosidically to two or more amino sugar.
25

26. AMINOGLYCOSIDE
MECHANISM OF ACTION
26

27. AMINOGLYCOSIDE
PHARMACOKINETICS:
 Neither absorbed nor destroyed in the g.i..t.
 Absorption from injection site in muscles is rapid:
peak plasma levels are attained in 30–60 minutes.
 They are distributed only extracellularly.
 Cross placenta and can be found in foetal
blood/amniotic fluid.
 Not metabolized in the body and are excreted
unchanged in urine.
 The plasma t½ ranges between 2–4 hours.
27

28. MECHANISM OF RESISTANCE:
 Resistance to aminoglycosides is acquired by one of
the following mechanisms:
 Acquisition of cell membrane bound inactivating
enzymes.
 Mutation decreasing the affinity of ribosomal
proteins.
 Decreased efficiency of the aminoglycoside
transporting mechanism:
28

29. Toxicity:
1. Ototoxicity:
a. Vestibular.
b. Cochlear.
2. Nephrotoxicity.
3. Neuromuscular blockade.
● Avoid during pregnancy: risk of foetal ototoxicity.
● Avoid concurrent use of other nephrotoxic drugs, e.g. NSAIDs,
amphotericin B, vancomycin, cyclosporine and cisplatin.
● Cautious use in patients >60 years age and in those with kidney
damage.
● Cautious use of muscle relaxants in patients receiving an
aminoglycoside
● Do not mix aminoglycoside with any drug in the same
syringe/infusion bottle.
29

30. SYSTEMIC
ANTIBIOTICS
BETA LACTAM
NITROIMIDAZOLE
QUINOLONE
TETRACYCLINE
MACROLIDE
SULFONAMIDE
CHLORAMPHENICOL
AMINOGLYCOSIDES
LINCOSAMIDE
30

31. 31

32. SelectionOf
Antibiotics
Age of the patient
Renal and Hepatic Functions
Local factors
Drug allergy
Impaired host defense
Pregnancy
Organism related considerations
Drug factors
32

33. SelectionOf
Antibiotics
 The microbial composition of subgingival plaque varies
considerably from patient to patient.
 The description of the Gram stain reaction and the
anaerobic requirement of the infectious periodontal
microbiota provided the first guidelines for selection of
antimicrobial therapy.
 Delineation of the type of periodontal infection
(exogenous/endogenous) may be important in selecting
a proper strategy for antimicrobial therapy in
periodontics.
 Two critical factors should be specifically considered in
selecting a systemic antibiotic in periodontal therapy:
 Gingival fluid concentration and
 Minimum inhibitory concentration (MIC).
33

34. SelectionOf
Antibiotics
 The gingival fluid concentration (CGCF) provides information
on the peak levels achieved by systemic delivery at the
primary ecological niche for periodontal pathogens, the
periodontal pocket.
 The 90% minimum inhibitory concentration (MIC90) is an in
vitro determination of the concentration that will inhibit
growth of 90% of the bacterial strains of a species that are
tested. Antimicrobial activity can be defined as a relationship
between CGCF and MIC90
 100 (CGCF/MIC90) = antimicrobial activity expressed as a
percentage for each antibiotic and each organism.
 Antibiotics that can achieve 90% inhibition of growth of an
organism appear on the 100% line. The most effective
antibiotics for treatment of a particular periodontal pathogen
are those that equal or exceed the 100% value.
34

35. PrinciplesOf
Antibiotic
Dosing
Employ high doses for a short duration: Antibiotic
success depends on maintaining the blood and
tissue concentrations above the minimal inhibitory
concentration for the target organism.
Use an oral antibiotic loading dose: Without a loading
dose, it takes 6-12 hours to achieve maximum
therapeutic blood and tissue levels via oral
administration.
Achieve blood levels of the antibiotic at 2-8 times the
minimal inhibitory concentration: Such blood levels
are necessary to compensate for the tissue barriers
that impede antibiotic penetration to the site of the
infection.
35

36. PrinciplesOf
Antibiotic
Dosing
Use frequent dosing intervals: This is important
with the older beta-lactam antibiotics such as
penicillin V and the first generation cephalosporins
(cephalexin, cephradine) so as to maintain
relatively constant blood levels.
Determine the duration of therapy by the remission
of disease: The antibiotic is terminated when the
patient host defenses have gained control of the
infection and the infection is reasonably certain to
resolve or has resolved. Systemically administered
bacteriostatic antibiotics characteristically require
longer periods of administration to be effective as
compared with their bactericidal counterparts.
36

37. INDICATIONS OF
ANTIBIOTIC IN
PERIODONTAL
THERAPY
1. In severe cases both of acute necrotizing ulcerative gingivitis and
periodontitis, especially if there are signs of systemic involvement,
METRONIDAZOLE can quickly alleviate the
symptoms, which then permits through mechanical
debridement to be carried out.
2. Occasionally, the local infection of a periodontal abscess can spread
within tissue planes to cause marked facial swelling and
systemic involvement.
 In these cases, BROAD-SPECTRUM ANTIBIOTICS
should be prescribed to control the infection.
 Careful Clinical And Radiographic Examinations must
be done to establish whether the lesion is wholly
periodontal in origin or whether there is pulpal
involvement of the associated teeth.
37

38. INDICATIONS OF
ANTIBIOTIC IN
PERIODONTAL
THERAPY
3. Multiple abscess formation and gross periodontal infection
 Administration of antibiotics
(METRONIDAZOLE and TETRACYCLINE).
4. 4. Antibiotic therapy is warranted in cases of periodontal disease,
which, despite through non surgical management and good plaque control,
continue to show breakdown and loss of attachment. These so called
refractory cases can benefit from a short course of antibiotic therapy.
 The drug of choice should be
determined from sampling the cultivable
pocket flora from which the predominant
populating organisms can be
identified.
5. Antibiotic therapy is recommended in the management of cases of AP
either in combination with flap surgery or a non-surgical treatment programme.
38

39. Medical
ConditionsThat
Need
Pre-operative
Antibiotic
 Some of the medical conditions where patients
are having greater risk of developing infection
after dental procedures due to
immunosuppression or decreased number of
immune cells.
 Uncontrolled diabetes,
 Organ transplantation,
 Bone marrow transplantation,
 Prosthetic joint replacement,
 Leukemia,
 Neutropenia,
 Thrombocytopenia
39

40. Medical
ConditionsThat
Need
Pre-operative
Antibiotic
 Chronic renal disease patients also need
antibiotic prophylaxis to prevent endarteritis of
the arteriovenous fistula or shunt
 To prevent infective endocarditis in patients
having previous history of infective endocarditis,
prosthetic cardiac valves, major congenital heart
disease, acquired valvular function, hypertrophic
cardiomyopathy, mitral valve prolapsed with
valvular regurgitation, thickened leaflets or both,
antibiotic prophylaxis is recommended
40

41. 41

42. 42

43. 43

44. 44

45. 45

46. ClinicalReasons
ForAntibiotic
Failure
1.Inappropriate choice of antibiotic
2.Emergence of antibiotic-resistant microorganisms
3.Too low a blood concentration of the antibiotic
4.Slow growth rate of microorganisms
5.Impaired host defenses
6.Patient noncompliance
7.Antibiotic antagonism
8.Inability of the antibiotic to penetrate to the site of the
infection
9.Limited vascularity or decreased blood flow
10.Unfavorable local factors (decreased tissue pH or oxygen
tension)
11.Failure to eradicate thesource of the infection (lack of
incision and drainage)
46

47. ANTIBIOTIC
RESISTANCE
 It refers to unresponsiveness of a microorganism to
an Antimicrobial agent.
 It can be:
 Natural / Intrinsic resistance.
 Acquired resistance.
 Cross resistance.
 The process of resistance may be developed by:
 Mutation
 Gene transfer.
47

48. Mutation:
● It is a stable and heritable genetic change that occurs spontaneously and
randomly among microorganisms.
● Any sensitive population of a microbe contains a few mutant cells.
● With time, a sensitive strain will be replaced by a resistant one.
● This is called vertical transfer of resistance.
● Relatively slow and usually of lower grade
48

49. It can be:
1. Single step (or point mutation):
E.g. enterococci to streptomycin
E. coli and Staphylococci to rifampin.
2. Multistep:
Resistance to erythromycin, tetracyclines and chloramphenicol is
developed by many organisms in this manner
49

50. Gene transfer (infectious resistance):
● The resistance causing gene is passed from one organism to the other; is called horizontal
transfer of resistance.
● Rapid spread of resistance can occur by this mechanism.
● High level resistance to several antibiotics (multidrug resistance) can be acquired too.
50

51. ● It can occur by:
● Conjugation:
Chloramphenicol resistance of typhoid bacilli,
Streptomycin resistance of E. coli,
Penicillin resistance of Haemophilus and gonococci
● Transduction:
Staph. aureus strains have acquired resistance by transduction.
● Transformation:
51

52. Resistant organisms can broadly be of the following three types:
● Drug tolerant: Loss of affinity of the target biomolecule of the microorganism for a particular
AMA.
● Drug destroying: The resistant microbe elaborates an enzyme which inactivates the drug,
● Drug impermeable: Many hydrophilic antibiotics gain access into the bacterial cell through
specific channels formed by proteins called ‘porins’, or need specific transport mechanisms.
These may be lost by the resistant strains.
52

53. Prevention of drug resistance:
● No indiscriminate and inadequate or unduly prolonged use of AMAs should be made
● Prefer rapidly acting and selective (narrow spectrum) AMAs whenever possible
● Use combination of AMAs whenever prolonged therapy is undertaken.
● Infection by organisms notorious for developing resistance must be treated intensively.
53

54. Antibiotic
SensitivityTest
54

55. ● Broth cultures with break-point concentration:
○ Concentration that demarcates between sensitive and resistant
bacteria of antibiotics.
○ Break-point concentrations are related to clinically attainable serum
concentrations of the antibiotic.
55

56. Minimum inhibitory concentration (MIC):
The lowest concentration of an antibiotic which prevents visible growth of a bacterium
after 24 hours incubation in microwell culture plates using serial dilutions of the antibiotic.
56

57. Minimum bactericidal concentration (MBC):
● The concentration of the antibiotic which kills 99.9% of the bacteria.
● Determined by subculturing from tubes with no visible growth.
● If the organism is killed, no growth will occur, but if it was only inhibited in the
parent culture—it will grow on subculturing in antibiotic-free medium.
● A small difference between MIC and MBC indicates that the antibiotic is primarily
bactericidal.
● A large difference indicates bacteriostatic action.
57

58. Postantibiotic effect (PAE):
● After a brief exposure if the organism is placed in antibiotic-free medium, it starts multiplying
again, but after a lag period which depends on the antibiotic as well as the organism.
● This lag period in growth resumption is known as ‘postantibiotic effect’ and is the time required
for reattainment of logarithmic growth.
● It is generally calculated from the time required to attain 10 fold increase in bacterial count in
the culture for antibiotic exposed and unexposed tubes.
● A longer PAE is seen in fluoroquinolones,
aminoglycosides and rifampin
58

59. Kirby-Bauer disc diffusion:
59

60. E TEST:
60

61. Automated instrument systems
61

62. SUPERINFECTION
Superinfection (Suprainfection)
 This refers to the appearance of a new infection as a
result of antimicrobial therapy.
 The pathogen has to compete with the normal flora
for nutrients to establish itself.
 Lack of competition may allow even a normally non
pathogenic component of the flora, which is not
inhibited by the drug (e.g. Candida), to predominate
and invade.
62

63.  Commonly associated with the use of
broad/extended-spectrum antibiotics.
 Tetracyclines are more liable than chloramphenicol.
 Ampicillin is more liable than amoxicillin to cause
superinfection diarrhoeas.
 More common when host defence is compromised.
 Sites involved in superinfection are those that
normally harbour commensals, i.e. oropharynx,
intestinal, respiratory and genitourinary tracts;
occasionally skin.
63

64. 64

65. The organisms frequently involved, the manifestations
and drugs for treating superinfections are
 Candida albicans: monilial diarrhoea, thrush,
vulvovaginitis; treat with nystatin or clotrimazole.
 Resistant staphylococci: enteritis; treat with
cloxacillin or vancomycin/linezolid.
 Clostridium difficile: pseudomembranous
enterocolitis associated with the use of clindamycin,
tetracyclines. Metronidazole and vancomycin are the
drugs of choice.
 Proteus: Urinary tract infection, enteritis. Treat with
a cephalosporin or gentamicin.
 Pseudomonas: Urinary tract infection, enteritis.
Treat with carbenicillin, piperacillin, ceftazidime,
cefoperazone or gentamicin.
65

66. To minimize superinfections:
 Use specific (narrow-spectrum) AMA whenever
possible.
 Do not use antimicrobials to treat self-limiting or
untreatable (viral) infections.
 Do not unnecessarily prolong antimicrobial therapy.
66

67. Combination
Therapy
 There are five daunting problems that have slowed progress of
antibiotic therapy are:
1. Periodontal diseases are heterogeneous;
2. Clinical diagnoses are made on the basis of clinical signs, not
molecular pathology;
3. The actual causal factor(s) have not been definitively identified;
4. No microbiological sampling.
5. There are many different antibiotic protocols but few well
designed, randomized controlled trials that test the efficacy of
these protocols.
Periodontal infections may be considered as mixed infections, in which a variety of aerobic, microaerophilic,
and anaerobic bacteria, both gram negative and gram positive, sensitive to different drugs are involved.
Therefore, it seems better to use more than one antibiotic to cover all the periodontal
pathogens in some clinical situations.
67

68. A combination of metronidazole and amoxicillin (MA) has shown to be an effective antibiotic regime to combat
Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis-associated periodontal infections.
One important clinical finding in a study by Winkel et al.,was the observation that patients with subgingival P.
gingivalis at baseline who were treated with metronidazole+amoxicillin showed approximately half the number of >5
mm pockets after therapy compared with P. gingivalis positive patients treated with 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.
These studies have revealed that, in chronic as well as in aggressive periodontitis, the antibiotics result in better
resolution of the periodontal inflammation, better probing depths, and attachment loss reduction.
68

69. Metronidazole ciprofloxacin combination is effective against A. actinomycetemcomitans. Metronidazole targets
obligate anaerobes, and ciprofloxacin targets facultative anaerobes. This is a powerful combination against mixed
infections. Studies of this drug combination in the treatment of refractory periodontitis have documented marked
clinical improvement
Metronidazole and clindamycin appear to be more efficient in eradicating the anaerobic periodontopathic bacteria
than doxycycline or mechanical therapy alone.
69

70. Conclusion
 In the present review, different aspects of the use of
systemic antimicrobials in the treatment of
periodontitis have been addressed, especially focusing
on the fact that the target pathogens are organized in
biofilms.
 But if not prescribed properly, we may soon face a new
breed of oral microorganisms with heightened defenses
that will ensure the survival of the species, allows for
greater pathogenicity and transfer genetic material
coding for increased virulence and antibiotic resistance
to other oral and nonoral microorganisms
 Antimicrobial agents against periodontal disease
should be used intelligently.
70

71. References
.
 Textbook of pharmacology, K D Tripathi 7th ed
 Jolkovsky DL, Ciancio S. Chemotherapeutic agents. In:
Carranza FA, Newman MG, Takei HH, Klokkevold PR,
editors. Clinical periodontology . 10th ed. Philadelphia: WB
Saunders; 2006. pp. 798–812
 Patil V, Mali R, Mali A. Systemic anti-microbial agents
used in periodontal therapy. Journal of Indian Society of
Periodontology. 2013 Mar;17(2):162.
 Kapoor A, Malhotra R, Grover V, Grover D. Systemic
antibiotic therapy in periodontics. Dental research journal.
2012 Sep;9(5):505.
71

72.  Herrera D, Alonso B, León R, Roldán S, Sanz M. Antimicrobial therapy in periodontitis: the
use of systemic antimicrobials against the subgingival biofilm. Journal of clinical
periodontology. 2008 Sep;35:45-66.
 Paddmanabhan P. Antimicrobials in treatment of periodontal disease-A review. IOSR J Dent
Med Sci. 2013;4:19-23.
 Agnihotri R, Gaur S. Chemically modified tetracyclines: novel therapeutic agents in the
management of chronic periodontitis. Indian Journal of Pharmacology. 2012 Mar;44(2):161.
 Tong DC, Rothwell BR. Antibiotic prophylaxis in dentistry: a review and practice
recommendations. The Journal of the American Dental Association. 2000 Mar 1;131(3):366-74.
72

73. 73