After a tooth extraction, several options are available for administering antibiotics or antimicrobial drugs. Oral administration is generally the most convenient and economical route but may result in incomplete drug absorption in the gastrointestinal tract. Parenteral routes like intravenous and intramuscular injection allow for more rapid and precise dosing but are more invasive and require more medical skill. Topical administration can help minimize systemic side effects. Selection of the appropriate antibiotic considers the infection severity, ability to drain the infection source, and patient's immune status, aiming to use the narrowest spectrum drug with the lowest toxicity. Antimicrobial resistance is an increasing problem promoted by misuse and overuse of antibiotics.

1. Pharmacological Drugs Used
After Tooth Extraction
Dr. Wael M. Talaat

2. Antibiotic/Antimicrobial
• Antimicrobial agent: Chemical
that kills or inhibits the growth of
microorganisms

3. Antibiotic Spectrum of Activity
• No antibiotic is effective against all
microbes

4. Common routes of administration
Parentral intravenous (i.v) & intramuscular
(i.m)
Rectal
Enema, Ointments & Suppositories
Oral
Capsule, Tablet & Solution
Topical Cream, Ointment & Transdermal
patch

5. Parentral
Rectal
rapid
rapid
precise
precise
•toxicity
•invasive
•skill
avoid
avoid first-pass
Oral
Oral not
recommended
Oral
Convenient
Convenient
economical
economical
non-invasive
non-invasive
safer
safer route
Topical
 minimize side
effects
•Incomplete ab.
(pH)

6. TREATMENT of INFECTION
• Remove the cause of infection is the most
important of all, by either spontaneously or
surgically drain the pus.
• Antibiotics are merely an adjunctive therapy.
Drainage
Host defense
Antibiotics

7. INDICATIONS for ANTIBIOTICS
1. Severity of the infection
• Acute onset
• Diffuse swelling involves fascial spaces
2. Adequacy of removing the source of infection
• When drainage can’t be established immediately
3. The state of patients’ host defense
• When the patient is febrile
• Compromised host defenses
• For prophylaxis

8. MICROBIOLOGY
• Most oral infections are mixed in origin
consisting of aerobic and anaerobic gram
positive and gram negative organisms
• Anaerobes predominant (75%)

9. SELECTION of A/B
• Use the narrowest spectrum antibiotics
• Use the antibiotics with the lowest toxicity
and side effects
• Use bactericidal antibiotics if possible
• Be aware of the cost of antibiotics

10. Mechanisms of
Antimicrobial Action
• Bacteria have their own enzymes
for
– Cell wall formation
– Protein synthesis
– DNA replication
– RNA synthesis
– Synthesis of essential
metabolites

11. Mechanisms of
Antimicrobial Action
• Viruses use host enzymes inside
host cells
• Fungi and protozoa have own
eukaryotic enzymes
• The more similar the pathogen and
host enzymes, the more side
effects the antimicrobials will have

12. Modes of Antimicrobial Action

13. Antibacterial Antibiotics
Inhibitors of Cell Wall Synthesis
• Penicillin (over 50 compounds)
– Share 4-sided ring (β lactam ring)
• Natural penicillins
• Narrow range of action
• Susceptible to penicillinase (β
lactamase)

14. Prokaryotic Cell Walls

15. Penicillins
Fig 20.6
Figure 20.6

16. Penicillinase (β Lactamase)
Figure 20.8

17. Semisynthetic Penicillins
• Penicilinase-resistant penicillins
• Carbapenems: very broad
spectrum
• Monobactam: Gram negative
• Extended-spectrum penicillins
• Penicillins + β-lactamase inhibitors

18. Other Inhibitors of Cell Wall
Synthesis
• Cephalosporins
– 2nd, 3rd, and 4th
generations
more effective
against gramnegatives
Figure 20.9

19. Other Inhibitors of Cell Wall
Synthesis
• Polypeptide antibiotics
– Bacitracin
• Topical application
• Against gram-positives
– Vancomycin
• Glycopeptide
• Important "last line" against
antibiotic resistant S. aureus

20. Other Inhibitors of Cell Wall
Synthesis
• Antibiotics
effective against
Mycobacteria:
interfere with
mycolic acid
synthesis or
incorporation
– Isoniazid (INH)
– Ethambutol

21. Inhibitors of Protein Synthesis
• Broad spectrum, toxicity problems
• Examples
– Chloramphenicol (bone marrow)
– Aminoglycosides: Streptomycin,
neomycin, gentamycin (hearing, kidneys)
– Tetracyclines (Rickettsias & Chlamydia;
GI tract)
– Macrolides: Erythromycin (gram +, used
in children)

22. Injury to the Plasma Membrane
• Polymyxin B (Gram negatives)
– Topical
– Combined with bacitracin and
neomycin (broad spectrum) in overthe-counter preparation

23. Inhibitors of Nucleic Acid
Synthesis
• Rifamycin
– Inhibits RNA synthesis
– Antituberculosis
• Quinolones and fluoroquinolones
– Ciprofloxacin
– Inhibits DNA gyrase
– Urinary tract infections

24. Competitive Inhibitors
– Sulfonamides (Sulfa drugs)
• Inhibit folic acid synthesis
• Broad spectrum
Figure 5.7

25. Antifungal Drugs
• Fungi are
eukaryotes
• Have unique
sterols in their cell
walls
• Pathogenic fungi
are often outside
the body

26. Antiviral Drugs
• Viruses are composed of nucleic
acid, protein capsid, and host
membrane containing virus proteins
• Viruses live inside host cells and
use many host enzymes
• Some viruses have unique
enzymes for DNA/RNA synthesis or
protein cutting in virus assembly
Figure 20.16a

27. Antiviral Drugs
Nucleoside and Nucleotide Analogs
Figure 20.16a

28. Analogs Block DNA Synthesis
Figure 20.16b, c

29. Antiviral Drugs
Enzyme Inhibitors
• Inhibit assembly
– Indinavir (HIV)
• Inhibit attachment
– Zanamivir (Influenza)
• Inhibit uncoating
– Amantadine (Influenza)

30. Antiviral Drugs
Enzyme Inhibitors
• Interferons prevent spread of viruses
to new cells (Viral hepatitis)
• Natural products of the immune
system in viral infections

31. Antiprotozoan Drugs
• Protozoa are
eukaryotic cells
• Many drugs are
experimental and
their mode of
action is unknown

32. Measuring Antimicrobial
Sensitivity
• E Test
• MIC: Minimal
inhibitory
concentration

33. Measuring Antimicrobial
Sensitivity: Disk Diffusion

34. Antibiotic Resistance
Figure 20.20

35. Antimicrobial Resistance
• Relative or complete lack of
effect of antimicrobial against a
previously susceptible microbe

36. Mechanisms of Antibiotic
Resistance
• Enzymatic destruction of drug
• Prevention of penetration of drug
• Alteration of drug's target site
• Rapid ejection of the drug

37. Antibiotic Selection for
Resistant Bacteria

38. What Factors Promote
Antimicrobial Resistance?
• Exposure to sub-optimal levels
of antimicrobial
• Exposure to microbes carrying
resistance genes

39. Inappropriate Antimicrobial
Use
• Prescription not taken correctly
• Antibiotics for viral infections
• Antibiotics sold without medical
supervision
• Spread of resistant microbes in
hospitals due to lack of hygiene

40. Inappropriate Antimicrobial
Use
• Lack of quality control in
manufacture or outdated
antimicrobial
• Inadequate surveillance or
defective susceptibility assays
• Poverty or war
• Use of antibiotics in foods

41. Consequences of
Antimicrobial Resistance
• Infections
resistant to
available
antibiotics
• Increased
cost of
treatment

43. Proposals to Combat
Antimicrobial Resistance
• Speed development of new
antibiotics
• Track resistance data nationwide
• Restrict antimicrobial use
• Direct observed dosing (TB)

44. Proposals to Combat
Antimicrobial Resistance
• Use more narrow spectrum
antibiotics
• Use antimicrobial cocktails

45. The Future of
Chemotherapeutic Agents
• Antimicrobial peptides
– Broad spectrum antibiotics from
plants and animals
• Squalamine (sharks)
• Protegrin (pigs)
• Magainin (frogs)

46. The Future of
Chemotherapeutic Agents
• Antisense agents
– Complementary DNA or peptide
nucleic acids that binds to a
pathogen's virulence gene(s) and
prevents transcription