MICROBIOLOGY OF PERIODONTAL DISEASE

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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
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Acute necrotizing ulcerative gingivitis
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MICROBIOLOGY OF PERIODONTAL DISEASE
Periodontitis can be classified into two main
groups Chronic (the most prevalent form)
Aggressive Localized and generalized Rapidly
progressive Prepubertal
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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
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MICROBIOLOGY OF PERIODONTAL DISEASE
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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
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Gross periodontal disease
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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
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Predominant plaque bacterial morphotypes
in health, gingivitis and periodontitis
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MICROBIOLOGY OF PERIODONTAL DISEASE
Currently recognized key Gram-negative periodontop
athogens include Porphyromonas
gingivalis Prevotella intermedia Bacteroides
forsythus Actinobacillus actinomycetemcomitans Fus
obacterium nucleatum Capnocytophaga species
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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
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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
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MICROBIOLOGY OF PERIODONTAL DISEASE
Necrotizing ulcerative gingivitis is a
specific, anaerobic, polymicrobial infection due
to the combined activity of fusobacteria (Fusobact
erium nucleatum), and oral spirochetes (Treponema
spp.) Fusospirochaetal complex
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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, colla
genase, trypsin-like proteases (gingipain), kerati
nase, hemolysins, fibrinolysins, hyaluronidase
and phospholipase
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MICROBIOLOGY OF PERIODONTAL DISEASE
Actinobacillus actinomycetemcomitans
Gram-negative coccobacilli, facultative
anaerobic Colonizes buccal mucosa plaque
Virulence factors Leukotoxin kills human
neutrophils (-gt release of lysosomal enzymes)
macrophages Immunosuppressive factor inhibits
B-cell growth LPS activates the alternate
complement pathway
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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
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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
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ROLE OF BACTERIAL PRODUCTS
Endotoxin (all Gram-negative organisms) Cytotoxici
ty, bone resorption, complement activation, local
inflammation Activated complement gt macrophage
activation and secretion of prostaglandins gt PGE
causes stimulated lymphocytes to produce
osteoclast activating factor gt bone resorption
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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
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ROLE OF BACTERIAL PRODUCTS
Protease (Porphyromonas, some fusobacteria) Damage
s cell membranes Phospholipase A (Pg, Prevotella
intermedia) Damages cell membranes, induces
prostaglandin- mediated bone resorption Nuclease
(Fusobacterium nucleatum, some streptococci) Degra
des nucleic acids
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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
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ROLE OF BACTERIAL PRODUCTS
Hydrogen sulfide (Fusobacterium nucleatum,
Pg, Pi, Wolinella) Causes cytotoxicity Fibrinolys
in (Pg, some spirochetes) Destroys fibrin
barrier Leukotoxin (Aa) Leukocyte cytotoxicity
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ROLE OF BACTERIAL PRODUCTS
Chemotaxis inhibitors (Pg) Decreases PMN
defense Capsules Decrease phagocytosis Immunosup
pressive factors (Aa, Treponema denticola, F.
nucleatum, T. socranskii) Inhibit lymphocyte
proliferation
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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
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MICROBIOLOGY OF PERIODONTAL DISEASE
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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
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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
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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
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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
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MICROBIOLOGY OF PERIODONTAL DISEASE
The presence of putative periodontopathogens can
be detected by Microscopy Microbial
cultures Enzymes liberated by the organisms
DNA/RNA probes
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MICROBIOLOGY OF PERIODONTAL DISEASE
Periodontal disease can be treated by Plaque
control Root surface debridement Periodontal
surgery Prudent use of antimicrobial agents
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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)
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DENTOALVEOLAR INFECTIONS

Pathways by which microorganisms may invade the
pulp and periapical tissues
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DENTOALVEOLAR INFECTIONS
Tooth fracture Traumatic exposure during dental
treatment Through the periodontal ligament Via
the pulpal blood supply (anachoresis)
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DENTOALVEOLAR INFECTIONS

Usually polymicrobial in nature Endogenous in
origin With a predominance of strict anaerobes
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DENTOALVEOLAR INFECTIONS
Facultative anaerobes Streptococcus milleri, S.
sanguis, S. anginosus Actinomyces
species mutans streptococci Lactobacillus
species Haemophilus species

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

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DENTOALVEOLAR INFECTIONS

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

Pathways by which pus may spread from an acute
dentoalveolar abscess
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DENTOALVEOLAR INFECTIONS
Extension of periapical infection from the upper
canine tooth to the infraorbital region

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DENTOALVEOLAR INFECTIONS
Ludwigs 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

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DENTOALVEOLAR INFECTIONS

Periodontal abscess Suppurative osteomyelitis of
the jaws Cervical actinomycosis
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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
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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
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ORAL MUCOSAL INFECTIONS
Classic disease triad of oral candidiasis
Pseudomembranous (thrush) Erythematous
Hyperplastic
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ORAL MUCOSAL INFECTIONS
Other common Candida-associated lesions
Denture stomatitis Angular cheilitis Median
rhomboid glossitis