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Microbiology of periodontal disease (Formation of plaque: (They adhere to…
Microbiology of periodontal disease
Bacteria
Bacterial lifestyles
Attached/biofilm
Resistant to antibiotics
Planktonic
Sensitive to antibiotics
Oxygen requirements
Anaerobic
Facultative anaerobic
Aerobic
Capnophilic
requires > [CO2]
Virulence: disease producing potential/
virulence factors:
Ability to invade tissues
Proteolytic enzymes (collagenases, gelatinases, hyaluronidases, fibrolysin, immunoglobin proteases
Toxin production
Exotoxins like leukotoxins produced by Aa kill leukocytes
Endotoxins (LPS)
Released from cell wall at death
Activation of inflammatory response
induction of bone resporption
Ability of microbial adhesion to host
Fimbria, pili
Capsule
Ability to evade host defences
capsule
Break down of host tissue (immunoglobulin proteases)
Dosage required to cause disease
Dental plaque
On the surfaces of teeth, prostheses, etc...
Consists of polysaccharide protein matrix of bacterial end products, enzymes, food debris, desquamated cells and calcium and phosphate
Organized mass of microorganisms that communicate and share different bacterial end products
Resistant to antibiotics
Formation of plaque:
They adhere to the enamel pellicle and use carbohydrates from the saliva as nutrients
They express receptors that allow 2º colonizers to attach
Early colonizers are aerobic Gram + Cocci
2º colonizers are capnophilic/facultative anaerobic Gram +& - rods that are also saccharolytic
As the bacterial plaque gets bigger and approaches the root surface, the level of oxygen decreases
Fusobacterium nucleatum adheres and allows late colonizer to attach
Late colonizers are anaerobic gram - rods that are proteolytic and get their nutrients from GCF
Types of plaque
Supra-gingival plaque
Nutrients come from saliva
Critical in calculus formation and root caries
multilayered
Gram + cocci and short rods predominate the tooth surface
Gram - rods, filament and spirochetes on the outer surface of mature plaque
Called marginal plaque when in direct contact w the gingival margin (prime role in gingivitis)
Distribution from > to <
Inter proximal areas of posterior teeth (molars and premolars)
Inter proximal surfaces of the anterior teeth & facial surfaces of posterior teeth
Lingual surfaces accumulate the least amount of plaque
Effective and complete plaque control at intervals of 48hr is compatible with no clinical signs of inflammation (pt should brush teeth at least 2x daily, brushing is not complete plaque control)
Found @ or coronal to the gingival margin
Sub-gingival plaque
Composition depends on pocket depth
Capable of invading dentinal tubules
is a source of bacteria in sub gingival spaces following tx of PD
Found apical to the gingival margin b/w the tooth and sulcular epithelium
Environment of sub gingival plaque
Local availability of blood products
Presence of crevicular fluid
By products of inflammation during PD may one day be used as biomarkers for periodontal condition
estimated flow:
Intermediate pocket: 20µl/hr
Deep pocket: 44µL/hr
Healthy crevice: 3µl/hr
Complex mixture of substances derived from:
Leukocytes
Structural cells of periodontium and oral bacteria
Serum
Anaerobic
Bacterial counts/ distribution of sub-gingival plaque
Buccal had > bacteria than lingual samples
Posterior tooth samples > bacteria than anterior samples
Distobuccal contains > bacteria than buccal samples
Maxillary samples > bacteria than mandibular samples
Types (classical theme):
Tooth associated sub-gingival plaque
Critical in calculus formation & root caries
Tooth associated cervical sub gingival plaque
Adheres to root cementum
Dominated by G+ rods and cocci
Strept. sanguis
Actinomyces viscosus
Streptococcus mitis
Tooth associated sub gingival plaque (deeper part of the pocket)
[G-] anaerobic rods
Apical border of plaque is separated from JE by leukocytes
Soft tissue associated sub-gingival plaque
Important in tissue destruction
bacteria sometimes found in host tissue
Contains 1ºly anaerobic G- rods, cocci and spirochetes
Porphyromonas gingivalis
Prevotella intermedia
Tannerella forsythia
4 layers of architecture
Basal layer of rod shaped bacteria (Actinomyces spp.) attached + to the tooth surface
Intermediate layer: many spindle-shaped cells –> F. nucleatum and tannerella forsythia
Top layer: many putative periodontal pathogens: P. gingivalis, P. intermedia
4th layer: unattached cells–> mostly spirochetes
Factors that modify plaque growth
Restoration overhangs (influence on the composition rather than amount of sub gingival plaque
Gingival tissue inflammation
Presence of gingivitis (inflammation) increases the
plaque formation rate so that more complex bacterial composition
is attained earlier
Individuals with gingivitis formed more plaque than individuals w healthy gingiva
Plaque forms more on tooth surfaces adjacent to areas with gingivitis
Surface roughness/ presence of calculus
Criteria for IDing Periopathogens
based off of Koch's postulates
Pathogen forms a cellular or humoral host response
Causes disease in animal models
Elimination of the organism with tx
Mechanisms of pathogenicity: the pathogen demonstrates virulence factors
Association with disease
increased # of pathogens @ diseased sites
Revelations of cluster analysis among sub-gingival spp.
Early colonizers are yellow, green , purple, blue, 75% G +
plaque closer to the root surface consists of these
Present in health
Strept sanguis, Stept. mitis (both yellow)
More green in pre-clinical inflammation
2º colonizers/ orange complex bridge yellow to red complex
44% G -
dominate in gingivitis
provide nutrients for red complex
Prevotella intermedia
Involved in Pregnancy associated gingivitis
Uses steroid hormones from GCF as growth factor
with Spirochetes causes Necrotizing PD (spirochetes can invade epithelium + CT and replicate in them)
F. nucleatum
red complex: late colonizers, G -
plaque closest to epithelium of pocket wall
75% G -, 90% anaerobic
Dominate in PD
Tannerella forsythia
Invades epithelial cells
Elevated subgingival proportions in active chronic PD lesions
10.4x > in PD pts
G- non motile, obligate anaerobic, spindle shaped rod
High affinity for crevicular epithelium
Produces proteolytic enzymes (trypsin-like proteolytic enzyme) that destroy immunoglobulins and complement factors
Spirochetes
Treponema denticola
Trypsin like proteolytic enzyme activity
Strong assoc. w Advanced Chronic Periodontitis & Recurrent Periodontitis
G-, motile, anaerobic, helical rods
Penetrates epithelium + CT
Porphyromonas gingivalis
12.3x > in PD pts
Aggressive
G-, non-motile, obligate anaerobic rod
Invades soft tissue
Transmittable w/i families
Fimbriae mediate adhesion, capsule defends against phagocytosis
Proteases: destroy immunoglobulins, complement factors and host cell collagenase inhibitor
Hemolysin: lysis RBCs
Collagenase: goes through CT
Aggregabacter (actinobacillus) actinomycetemcomitans (Aa): associated with aggressive PD
Associated with Localized Aggressive periodontitis (affects young individuals)
X biotypes and 5 serotypes (a-e)
Transmittable w/i families
Virulence factors:
Leukotoxin (forms pores in WBCs)
Collagenase
Endotoxin
Protease that cleaves IgG
G-, non-motile, anaerobic, small straight or curved rod
Presence of sub gingival EBV-1 (causes mononucleosis) and HCMV are associated with high levels of red complex pathogens (both may be altering saliva)