MICROBIOLOGY OF PERIODONTAL DISEASE Broadly categorized into gingivitis and periodontitis Clinical...

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


• Periodontitis can be classified into two main groups:

• Chronic (the most prevalent form)

• AggressiveLocalized and generalizedRapidly progressivePrepubertal


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


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


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


Currently recognized key Gram-negativeperiodontopathogens include:

Porphyromonas gingivalisPrevotella intermediaBacteroides forsythusActinobacillus actinomycetemcomitansFusobacterium nucleatumCapnocytophaga species


Disease activity in periodontal disease ranges from

Slow, chronic, progressive destruction

Brief and acute “episodic bursts” with varyingintensity and duration


Localized or generalized aggressive periodontitisis strongly associated with Actinobacillusactinomycetemcomitans, either alone orsynergistically with

Capnocytophaga species andPorphyromonas gingivalis


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



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


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


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


Collagenase (P. gingivalis, Aa, Bacillus spp.)Disrupts connective tissue

Hyaluronidase (Strep. mitis, Bacteroides fragilis,some Gram-positive rods)Destroys sulcus attachment, increases tissuepermeability


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


IgA/IgG proteases (Pg, P. intermedia, Capnocytophaga)Degrades immunoglobulins

Catalase (Actinomyces viscosus, Aa)Decreases PMN peroxide killing

Mercaptans (Pg, P. intermedia)Causes cytotoxicity


Hydrogen sulfide (Fusobacterium nucleatum, Pg,Pi, Wolinella)Causes cytotoxicity

Fibrinolysin (Pg, some spirochetes)Destroys fibrin barrier

Leukotoxin (Aa)Leukocyte cytotoxicity


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

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


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


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


Microbiological tests used in the management ofperiodontal disease:

help identify sites of active tissue destruction

monitor efficacy of therapy

decide recall intervals


The presence of putative periodontopathogenscan be detected by:• Microscopy• Microbial cultures• Enzymes liberated by the organisms• DNA/RNA probes


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)


Pathways by whichmicroorganismsmay invade the pulpand periapicaltissues


Tooth fracture

Traumatic exposure during dental treatment

Through the periodontalligament

Via the pulpal blood supply(anachoresis)


Usually polymicrobial in nature

Endogenous in origin

With a predominance of strict anaerobes


Facultative anaerobes

Streptococcus milleri, S. sanguis, S. anginosus

Actinomyces species

mutans streptococci

Lactobacillus species

Haemophilus species


Obligate anaerobes

Peptostreptococcus species

Prevotella intermedia, P. melaninogenica, P. oralis

Porphyromonas gingivalis, P. endodontalis

Fusobacterium nucleatum

anaerobic cocci


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


Pathways by which pus may spread from an acute dentoalveolar abscess


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


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


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 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


Classic disease triad of oral candidiasis:

• Pseudomembranous (thrush)

• Erythematous

• Hyperplastic


Other common Candida-associated lesions:

• Denture stomatitis

• Angular cheilitis

• Median rhomboid glossitis

MICROBIOLOGY OF PERIODONTAL DISEASE Broadly categorized into gingivitis and periodontitis Clinical...

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