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

Acute necrotizing ulcerative gingivitis

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

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

MICROBIOLOGY OF PERIODONTAL DISEASE

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

Gross periodontal disease

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

Predominant plaque bacterial morphotypes in health, gingivitis and periodontitis

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

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

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

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”

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

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

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

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

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

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

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

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

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

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

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

MICROBIOLOGY OF PERIODONTAL DISEASE

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

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

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

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

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

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

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)

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

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

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

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

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

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

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

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

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

DENTOALVEOLAR INFECTIONS Periodontal abscess Suppurative osteomyelitis of the jaws Cervical actinomycosis

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

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

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

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