1. MICROBIOLOGY OF PERIODONTAL DISEASE
Broadly categorized into gingivitis and periodontitis
Clinical features of plaque-related gingivitis are
redness, edema and bleeding
Periodontitis usually develops from a pre-existing
gingivitis
Not every gingivitis leads to periodontitis

2. Acute necrotizing ulcerative gingivitis

3. MICROBIOLOGY OF PERIODONTAL DISEASE
• Periodontitis can be classified into two main groups:
• Chronic (the most prevalent form)
• Aggressive
Localized and generalized
Rapidly progressive
Prepubertal

4. MICROBIOLOGY OF PERIODONTAL DISEASE
Initial lesion: Plaque at junctional epithelium, increased flow of GCV, migration of neutrophils due to acute inflammation. Mostly Gram + cocci
Early lesion: Gingival infiltrate dominated by lymphocytes (75%) and macrophages, with some plasma cells at the periphery. Actinomyces, spirochetes and capnophilic organisms

5. MICROBIOLOGY OF PERIODONTAL DISEASE

6. MICROBIOLOGY OF PERIODONTAL DISEASE
Established lesion: Predominance of plasma cells and B lymphocytes. P. gingivalis and Prevotella intermedia
Advanced lesion: Activated complement and osteoclast activating factor (secreted by T lymphocytes) stimulate bone resorption

7. Gross periodontal disease

8. MICROBIOLOGY OF PERIODONTAL DISEASE
Microorganisms in:
Healthy gingival sulcus:
Gram-positive and facultative anaerobic organisms
Chronic periodontitis:
~75% Gram-negative (90% strict anaerobes)
Motile rods and spirochetes

9. Predominant plaque bacterial morphotypes in
health, gingivitis and periodontitis

10. MICROBIOLOGY OF PERIODONTAL DISEASE
Currently recognized key Gram-negative
periodontopathogens include:
Porphyromonas gingivalis
Prevotella intermedia
Bacteroides forsythus
Actinobacillus actinomycetemcomitans
Fusobacterium nucleatum
Capnocytophaga species

11. MICROBIOLOGY OF PERIODONTAL DISEASE
Disease activity in periodontal disease ranges from
Slow, chronic, progressive destruction
Brief and acute “episodic bursts” with varying
intensity and duration

12. MICROBIOLOGY OF PERIODONTAL DISEASE
Localized or generalized aggressive periodontitis
is strongly associated with Actinobacillus
actinomycetemcomitans, either alone or
synergistically with
Capnocytophaga species and
Porphyromonas gingivalis

13. MICROBIOLOGY OF PERIODONTAL DISEASE
Necrotizing ulcerative gingivitis is a specific,
anaerobic, polymicrobial infection due to the
combined activity of fusobacteria
(Fusobacterium nucleatum), and oral spirochetes
(Treponema spp.)
“Fusospirochaetal complex”

14. MICROBIOLOGY OF PERIODONTAL DISEASE
Porphyromonas gingivalis
• Gram-negative rods, non-motile, obligatory anaerobes
• Growth requirements: Anaerobic conditions,
hemin (which carries iron and protoporphyrin)
& vitamin K
• Virulence factors: Capsular polysaccharides,
collagenase, trypsin-like proteases (gingipain),
keratinase, hemolysins, fibrinolysins,
hyaluronidase and phospholipase

16. MICROBIOLOGY OF PERIODONTAL DISEASE
Actinobacillus actinomycetemcomitans
• Gram-negative coccobacilli, facultative anaerobic
• Colonizes buccal mucosa & plaque
• Virulence factors
Leukotoxin kills human neutrophils (-> release of
lysosomal enzymes) & macrophages
Immunosuppressive factor inhibits B-cell growth
LPS activates the alternate complement pathway

17. MICROBIOLOGY OF PERIODONTAL DISEASE
Prevotella intermedia
• Gram-negative, pleomorphic rods, strict anaerobes
• Require vitamin K & hemin for growth
• Associated with chronic periodontitis &
dentoalveolar abscess
• Virulence factors
Phospholipase A, IgA/IgG proteases, mercaptans,
hydrogen sulfide

18. MICROBIOLOGY OF PERIODONTAL DISEASE
Spirochetes
• Long, thin, corkscrew-like, Gram-negative, anaerobic,
highly mobile bacteria
• Killed by oxygen, difficult to grow in media
• Virulence factors
Endotoxin
Ability to penetrate tissue
A factor that inhibits lymphocyte activation
Block fusion of phagosomes with lysosomes

19. ROLE OF BACTERIAL PRODUCTS
Endotoxin (all Gram-negative organisms)
Cytotoxicity, bone resorption, complement
activation, local inflammation
Activated complement > macrophage activation and
secretion of prostaglandins > PGE causes stimulated lymphocytes to produce osteoclast activating factor > bone resorption

21. ROLE OF BACTERIAL PRODUCTS
Collagenase (P. gingivalis, Aa, Bacillus spp.)
Disrupts connective tissue
Hyaluronidase (Strep. mitis, Bacteroides fragilis,
some Gram-positive rods)
Destroys sulcus attachment, increases tissue
permeability

22. ROLE OF BACTERIAL PRODUCTS
Protease (Porphyromonas, some fusobacteria)
Damages cell membranes
Phospholipase A (Pg, Prevotella intermedia)
Damages cell membranes, induces prostaglandin-
mediated bone resorption
Nuclease (Fusobacterium nucleatum, some
streptococci)
Degrades nucleic acids

23. ROLE OF BACTERIAL PRODUCTS
IgA/IgG proteases (Pg, P. intermedia, Capnocytophaga)
Degrades immunoglobulins
Catalase (Actinomyces viscosus, Aa)
Decreases PMN peroxide killing
Mercaptans (Pg, P. intermedia)
Causes cytotoxicity

24. ROLE OF BACTERIAL PRODUCTS
Hydrogen sulfide (Fusobacterium nucleatum, Pg,
Pi, Wolinella)
Causes cytotoxicity
Fibrinolysin (Pg, some spirochetes)
Destroys fibrin barrier
Leukotoxin (Aa)
Leukocyte cytotoxicity

25. ROLE OF BACTERIAL PRODUCTS
Chemotaxis inhibitors (Pg)
Decreases PMN defense
Capsules
Decrease phagocytosis
Immunosuppressive factors (Aa, Treponema
denticola, F. nucleatum, T. socranskii)
Inhibit lymphocyte proliferation

26. ROLE OF NEUTROPHILS Respond to bacterial and chemotactic factors in
the sulcus
Attracted by C5a & lymphokines (T-lymphocytes)
Tissue destruction
Lysosomal leakage while digesting bacteria
Release of endotoxin from digested bacteria
Release of collagenase

27. MICROBIOLOGY OF PERIODONTAL DISEASE

28. SPECIFIC & NON-SPECIFIC PLAQUE HYPOTHESES
The specific plaque hypothesis
Particular species are responsible for causing each
type of periodontal disease
Large numbers of spirochetes in tissues from
acute necrotizing ulcerative gingivitis
A. actinomycetemcomitans in localized juvenile
periodontitis
P. gingivalis in adult periodontitis

29. SPECIFIC & NON-SPECIFIC PLAQUE HYPOTHESES
The non-specific plaque hypothesis
Bacteria collectively have the total complement of
virulence factors required to cause destruction of
periodontal tissues
Some microorganisms can substitute for others
The wide range of species that have been associated
with periodontal disease supports this view

30. SPECIFIC & NON-SPECIFIC PLAQUE HYPOTHESES
The plaque ecology hypothesis
Conditions within the periodontal pocket allow the
overgrowth of certain microorganisms already
present
This shift in balance predisposes the site to disease
If the right ecological conditions within a site
allow the production of virulence factors that
overwhelm host defenses, a period of disease
activity & tissue destruction ensues

31. MICROBIOLOGY OF PERIODONTAL DISEASE
Microbiological tests used in the management of
periodontal disease:
help identify sites of active tissue destruction
monitor efficacy of therapy
decide recall intervals

32. MICROBIOLOGY OF PERIODONTAL DISEASE
The presence of putative periodontopathogens
can be detected by:
• Microscopy
• Microbial cultures
• Enzymes liberated by the organisms
• DNA/RNA probes

33. MICROBIOLOGY OF PERIODONTAL DISEASE
Periodontal disease can be treated by:
• Plaque control
• Root surface debridement
• Periodontal surgery
• Prudent use of antimicrobial agents

34. DENTOALVEOLAR INFECTIONS
Usually develop by the extension of the initial
carious lesion into dentine, and spread of the
bacteria to the pulp via dentinal tubules
Acute inflammation (pulp necrosis)
Chronic localized abscess (pulp viable)

35. DENTOALVEOLAR INFECTIONS
Pathways by which
microorganisms
may invade the pulp
and periapical
tissues

36. DENTOALVEOLAR INFECTIONS
Tooth fracture
Traumatic exposure during dental treatment
Through the periodontal
ligament
Via the pulpal blood supply
(anachoresis)

37. DENTOALVEOLAR INFECTIONS
Usually polymicrobial in nature
Endogenous in origin
With a predominance of strict anaerobes

38. DENTOALVEOLAR INFECTIONS
Facultative anaerobes
Streptococcus milleri, S. sanguis, S. anginosus
Actinomyces species
mutans streptococci
Lactobacillus species
Haemophilus species

39. DENTOALVEOLAR INFECTIONS
Obligate anaerobes
Peptostreptococcus species
Prevotella intermedia, P. melaninogenica, P. oralis
Porphyromonas gingivalis, P. endodontalis
Fusobacterium nucleatum
anaerobic cocci

40. DENTOALVEOLAR INFECTIONS
Drainage of pus is the mainstay of treatment
of dentoalveolar and periodontal abscesses
Elimination of the infective focus and
antibiotic therapy should be considered
on an individual basis

41. DENTOALVEOLAR INFECTIONS
Pathways by which pus may spread from an acute dentoalveolar abscess

42. DENTOALVEOLAR INFECTIONS
Extension of periapical infection from the upper canine tooth to the infraorbital region

43. DENTOALVEOLAR INFECTIONS
Ludwig’s angina
A spreading, bilateral infection of the sublingual
and submandibular spaces
Causes swelling of the tissues at the front of the neck
Life-threatening infection
High-dose systemic antibiotic therapy essential
i.v. penicillin +/- metronidazole

44. DENTOALVEOLAR INFECTIONS
Periodontal abscess
Suppurative osteomyelitis of the jaws
Cervical actinomycosis

45. ORAL MUCOSAL INFECTIONS
Oral candidiasis is the most common oral
fungal opportunistic infection in humans
It is usually seen in the very young, the very
old and the very sick

46. ORAL MUCOSAL INFECTIONS
Oral candidiasis classified as a superficial
(as opposed to systemic) mycosis is broadly
divided into primary and secondary disease
Primary: Confined to the oral cavity
Secondary: Oral and other superficial sites

47. ORAL MUCOSAL INFECTIONS
Classic disease triad of oral candidiasis:
• Pseudomembranous (thrush)
• Erythematous
• Hyperplastic

48. ORAL MUCOSAL INFECTIONS
Other common Candida-associated lesions:
• Denture stomatitis
• Angular cheilitis
• Median rhomboid glossitis