Plaque and calculus Flashcards by Rachel Sladden

Current classification

I. Gingival diseases
II. Chronic diseases
III. Aggressive periodontitis
IV. Periodontitis as manifestation of systemic disease
V. Necrotising periodontal diseases
VI. Abscesses of the periodontium
VII. Periodontitis associated with endodontic lesions
VIII. Developmental/ acquired conditions

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Plaque induced gingivitis

> 90% population have this

Without adequate self-performed plaque control there is no control

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Aetiology of periodontal diseases

1676 Antonin van Leewenhoek - detected ‘small animacules that moved’ in the coating removed from his own teeth
Löe H, Experimental Gingivitis in Man 1965 (experimented on dental students) - forefather of periodontal diseases

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Pathogenesis of Human Periodontitis (look at slides)

Environmental and acquired risk factors –> host immuno-inflammatory response (‘correct’ i.e. not pathogenic in itself) –> destructive mechanisms –> CT & bone metabolism –> microbial challenge –> clinical signs of disease initiation and progression
(both affected by genetic risk factors)

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Plaque

Bacterial aggregations on teeth and other solid or oral structures

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Features of plaque

Biofilm of organisms that develop on teeth, gingivae, oral appliances and restorations (Soft, concentrated mass consisting mainly of large variety of bacteria)
Present with microbial by-products, salivary consituents and food debris
Always present and rapidly reforms after cleaning
Cannot be removed by rinsing with water
Sucrose may speed up formation
Two types described, supra- and subgingival (food debris is separate)

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Structure of plaque

70% micro organisms

30% inter-bacterial matrix including extra-cellular polysaccharides and host cells

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Inter-bacterial matrix

Cuticle
Epithelial cells
Polymorphonuclear leucocytes
Carbohydrates, lipids (LPS), proteins, immunoglobulins, enzymes

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Bacteria

Prevotela intermedia
Porphyromonas ginginvalis (perio breath)
Eikonella corrodens
Tannerella forsythensis
Peptostreptococcus micros
Ag. actinomyc. (aggressive disease - use antibiotic because can hide in soft tissue when scaling)
Spirochaetes

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Stages of plaque formation: 0-20 mins

Pellicle/ cuticle
Formed by opposite charges in salivary macro-molecules
Large amounts of acidic amino-acids, and glycoproteins from saliva
Small amounts of basic and sulphur containing amino-acids

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Important first colonisers on pellicle

S. sanguis, S. oralis

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Important first colonisers on pellicle

S. sanguis, S. oralis

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Plaque stages A-E

A reversible adhesion
B colonisation
C co-adhesion
D multiplication
E detachment and recolonisation

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Subgingival plaque

Derived from supra-gingival plaque
Low O2 levels favour anaerobes
Nutrients from crevicular fluids
Can survive without attachment to pellicle

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Pathogenicity of plaque

Endotoxin - LPS induces bone resorption
Enzymes - metalloproteinases, collagenases, hyaluronidases etc.
Cytotoxic metabolites - volatile sulphides (H2S), urea, organic acids (e.g. lactic, pyuric)

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Mouthwash

Doesn’t wash away plaque

Kills off some bacteria

Calculus

The calcified, or calcifying deposits on teeth, or other solid structures present in mouth

buccal surfaces of upper molar teeth
lingual surfaces of lower anterior teeth

Types of calculus

Supra-gingival 
-white, yellow or stained
-formed rapidly, easier to remove
Subgingival
-darker harder, more difficult to remove
-slower to form

Detection of calculus

Visual - direct, airstream
Tactile - WHO probe/ curette
Radiography - must have been there for minimum of 6 months

Composition of calculus

70-80% inorganic/ crystalline: HAP, whitlockite, brushite, otocalcium phosphate
20% organic: proteins, carbohydrates, small amount lipids

Structure of calculus

Layered (resting lines in histological sections)
Varying amounts of calcification
Random arrangement of crystals
Outline of calcified micro-organisms
Plaque on the surface

Formation of calculus

Always preceded by plaque

3 theories of calculus formation

CO2 hypothesis
Ammonia production hypothesis
Nucleation hypothesis

Balance

If bacterial challenge not overwhelming in ‘healthy’ individual the balance is in favour of repair
Balance tipped away from repair by diseases, modifying factors, genes

Plaque biofilm maturation: 1-2 days

Attachment - formation of dental pellicle - selective colonisation of salivary and planktonic organisms, primarily gram +ve cocci

Plaque biofilm maturation: 2-4 days

Primary colonisation - cocci are predominant and there is > in gram +ve filamentous and rod shaped organisms - formation of ECM which provides attachment to tooth surface and protection

Plaque biofilm maturation: 4-7 days

Succession - >in no. of filamentous organisms - > in bacterial species forming mixed and diverse flora - thickening of biofilm around gingival margins - colonisations of gram -ve organisms such as vibrios and spirochaetes

Plaque biofilm maturation: 7-14 days

Secondary colonisation and proliferation - colonisation of more gram -ve bacteria and > no. of anaerobes - > expression of virulent factors by bacteria - formation of well organised biofilm colonies - clinical sign of gingival inflammation visible

Plaque biofilm maturation: 14 days onwards

Maturation - biofilm maturation takes place by proliferation of gram -ve organisms in deeper layers of plaque - organisms densely packed in biofilm with well organised protective ECM - clinical signs of gingival inflammation well established

Stages of plaque formation: 3-8 hours

10^3 organisms per mm3 | 90% gram +ve cocci and rods, actinomyces species

Plaque flora: gingivitis

25% streptococci]25% actinomyces 25% gram -ve rods (fusobacteria, bacteroides, wolinella) 2% spirochaetes 23% others

Plaque flora: periodontitis

>800 species have been isolated 90% anaerobes May be up to 50% spirochaetes

Attachment of calculus to tooth surface

Calcification of pellicle Intimate contact of crystals in calculus between the enamel, cementum or dentine, ionic attraction Micro-mechanical interlocking

CO2 hypothesis

High levels of CO2 in saliva as it leaves glands CO2 leaves saliva gives rise in pH, Ca and PO4 ions come out of solution Precipitation into plaque

Ammonia production hypothesis

Research showed that rapid calculus formers had > salivary urea > in pH Ca and PO4 ions come out of solution Precipitation into plaque

Nucleation hypothesis

Nucleation of crystal formation by unknown compounds

Pathogenicity of calculus

Calculus is associated with periodontal disease Calculus does not cause periodontal disease Calculus is a plaque retention factor May be viable bacteria within lacunae in calculus