Plaque and calculus Flashcards

1
Q

Current classification

A
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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2
Q

Plaque induced gingivitis

A

> 90% population have this

Without adequate self-performed plaque control there is no control

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3
Q

Aetiology of periodontal diseases

A

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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4
Q

Pathogenesis of Human Periodontitis (look at slides)

A

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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5
Q

Plaque

A

Bacterial aggregations on teeth and other solid or oral structures

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6
Q

Features of plaque

A

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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7
Q

Structure of plaque

A

70% micro organisms

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

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8
Q

Inter-bacterial matrix

A

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

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9
Q

Bacteria

A
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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10
Q

Stages of plaque formation: 0-20 mins

A

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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11
Q

Important first colonisers on pellicle

A

S. sanguis, S. oralis

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12
Q

Important first colonisers on pellicle

A

S. sanguis, S. oralis

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13
Q

Plaque stages A-E

A
A reversible adhesion
B colonisation
C co-adhesion
D multiplication
E detachment and recolonisation
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14
Q

Subgingival plaque

A

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

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15
Q

Pathogenicity of plaque

A

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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16
Q

Mouthwash

A

Doesn’t wash away plaque

Kills off some bacteria

17
Q

Calculus

A

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
18
Q

Types of calculus

A
Supra-gingival 
-white, yellow or stained
-formed rapidly, easier to remove
Subgingival
-darker harder, more difficult to remove
-slower to form
19
Q

Detection of calculus

A

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

20
Q

Composition of calculus

A

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

21
Q

Structure of calculus

A
Layered (resting lines in histological sections)
Varying amounts of calcification
Random arrangement of crystals
Outline of calcified micro-organisms
Plaque on the surface
22
Q

Formation of calculus

A

Always preceded by plaque

23
Q

3 theories of calculus formation

A

CO2 hypothesis
Ammonia production hypothesis
Nucleation hypothesis

24
Q

Balance

A

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

25
Q

Plaque biofilm maturation: 1-2 days

A

Attachment

  • formation of dental pellicle
  • selective colonisation of salivary and planktonic organisms, primarily gram +ve cocci
26
Q

Plaque biofilm maturation: 2-4 days

A

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
27
Q

Plaque biofilm maturation: 4-7 days

A

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
28
Q

Plaque biofilm maturation: 7-14 days

A

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
29
Q

Plaque biofilm maturation: 14 days onwards

A

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
30
Q

Stages of plaque formation: 3-8 hours

A

10^3 organisms per mm3

90% gram +ve cocci and rods, actinomyces species

31
Q

Plaque flora: gingivitis

A

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

32
Q

Plaque flora: periodontitis

A

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

33
Q

Attachment of calculus to tooth surface

A

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

34
Q

CO2 hypothesis

A

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

35
Q

Ammonia production hypothesis

A

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

36
Q

Nucleation hypothesis

A

Nucleation of crystal formation by unknown compounds

37
Q

Pathogenicity of calculus

A

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