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)