Plaque and calculus Flashcards
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
Plaque induced gingivitis
> 90% population have this
Without adequate self-performed plaque control there is no control
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
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)
Plaque
Bacterial aggregations on teeth and other solid or oral structures
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)
Structure of plaque
70% micro organisms
30% inter-bacterial matrix including extra-cellular polysaccharides and host cells
Inter-bacterial matrix
Cuticle
Epithelial cells
Polymorphonuclear leucocytes
Carbohydrates, lipids (LPS), proteins, immunoglobulins, enzymes
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
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
Important first colonisers on pellicle
S. sanguis, S. oralis
Important first colonisers on pellicle
S. sanguis, S. oralis
Plaque stages A-E
A reversible adhesion B colonisation C co-adhesion D multiplication E detachment and recolonisation
Subgingival plaque
Derived from supra-gingival plaque
Low O2 levels favour anaerobes
Nutrients from crevicular fluids
Can survive without attachment to pellicle
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)
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
