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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)
• AggressiveLocalized and generalizedRapidly progressivePrepubertal
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 inhealth, gingivitis and periodontitis
MICROBIOLOGY OF PERIODONTAL DISEASE
Currently recognized key Gram-negativeperiodontopathogens include:
Porphyromonas gingivalisPrevotella intermediaBacteroides forsythusActinobacillus actinomycetemcomitansFusobacterium nucleatumCapnocytophaga species
MICROBIOLOGY OF PERIODONTAL DISEASE
Disease activity in periodontal disease ranges from
Slow, chronic, progressive destruction
Brief and acute “episodic bursts” with varyingintensity and duration
MICROBIOLOGY OF PERIODONTAL DISEASE
Localized or generalized aggressive periodontitisis strongly associated with Actinobacillusactinomycetemcomitans, either alone orsynergistically with
Capnocytophaga species andPorphyromonas gingivalis
MICROBIOLOGY OF PERIODONTAL DISEASE
Necrotizing ulcerative gingivitis is a specific,anaerobic, polymicrobial infection due to thecombined activity of fusobacteria(Fusobacterium nucleatum), and oral spirochetes(Treponema spp.)
“Fusospirochaetal complex”
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
MICROBIOLOGY OF PERIODONTAL DISEASE
Actinobacillus actinomycetemcomitans
• Gram-negative coccobacilli, facultative anaerobic• Colonizes buccal mucosa & plaque• Virulence factors
Leukotoxin kills human neutrophils (-> release oflysosomal enzymes) & macrophagesImmunosuppressive factor inhibits B-cell growthLPS 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
EndotoxinAbility to penetrate tissueA factor that inhibits lymphocyte activationBlock fusion of phagosomes with lysosomes
ROLE OF BACTERIAL PRODUCTS
Endotoxin (all Gram-negative organisms)Cytotoxicity, bone resorption, complementactivation, local inflammation
Activated complement > macrophage activation andsecretion 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 tissuepermeability
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, somestreptococci)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
CapsulesDecrease phagocytosis
Immunosuppressive factors (Aa, Treponemadenticola, F. nucleatum, T. socranskii)Inhibit lymphocyte proliferation
ROLE OF NEUTROPHILS
Respond to bacterial and chemotactic factors inthe sulcus
Attracted by C5a & lymphokines (T-lymphocytes)
Tissue destructionLysosomal leakage while digesting bacteriaRelease of endotoxin from digested bacteriaRelease of collagenase
MICROBIOLOGY OF PERIODONTAL DISEASE
SPECIFIC & NON-SPECIFIC PLAQUE HYPOTHESES
The specific plaque hypothesis
Particular species are responsible for causing eachtype of periodontal disease
Large numbers of spirochetes in tissues from acute necrotizing ulcerative gingivitis
A. actinomycetemcomitans in localized juvenileperiodontitis
P. gingivalis in adult periodontitis
SPECIFIC & NON-SPECIFIC PLAQUE HYPOTHESES
The non-specific plaque hypothesis
Bacteria collectively have the total complement ofvirulence factors required to cause destruction of periodontal tissues
Some microorganisms can substitute for othersThe 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 alreadypresent
This shift in balance predisposes the site to diseaseIf the right ecological conditions within a site
allow the production of virulence factors thatoverwhelm host defenses, a period of diseaseactivity & tissue destruction ensues
MICROBIOLOGY OF PERIODONTAL DISEASE
Microbiological tests used in the management ofperiodontal disease:
help identify sites of active tissue destruction
monitor efficacy of therapy
decide recall intervals
MICROBIOLOGY OF PERIODONTAL DISEASE
The presence of putative periodontopathogenscan 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 initialcarious lesion into dentine, and spread of thebacteria to the pulp via dentinal tubules
Acute inflammation (pulp necrosis)
Chronic localized abscess (pulp viable)
DENTOALVEOLAR INFECTIONS
Pathways by whichmicroorganismsmay invade the pulpand periapicaltissues
DENTOALVEOLAR INFECTIONS
Tooth fracture
Traumatic exposure during dental treatment
Through the periodontalligament
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 treatmentof dentoalveolar and periodontal abscesses
Elimination of the infective focus andantibiotic therapy should be consideredon 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 sublingualand submandibular spaces
Causes swelling of the tissues at the front of the neck
Life-threatening infection
High-dose systemic antibiotic therapy essentiali.v. penicillin +/- metronidazole
DENTOALVEOLAR INFECTIONS
Periodontal abscess
Suppurative osteomyelitis of the jaws
Cervical actinomycosis
ORAL MUCOSAL INFECTIONS
Oral candidiasis is the most common oralfungal opportunistic infection in humans
It is usually seen in the very young, the veryold and the very sick
ORAL MUCOSAL INFECTIONS
Oral candidiasis classified as a superficial(as opposed to systemic) mycosis is broadlydivided into primary and secondary disease
Primary: Confined to the oral cavitySecondary: 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
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