dental calculus and other predisposing factors
TRANSCRIPT
Dental Calculus and other Predisposing Factors
Calculus
Mineralized bacterial plaque that forms on tooth surface and dental prostheses
Divided into Supragingival and Subgingival Calculus in relation to gingival margin
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Supragingival calculus
White or Whitish yellow in color
Hard with clay like consistency
Can be eaisly detached from
tooth surface
Color can be influenced by
contact with tobacco and food
pigment
Two most common locations are
buccal surface of maxillary molars
and lingual surface of mandibular
anterior teeth
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Subgingival calculus
• Located below the crest of marginal gingiva
• Not visible on routine clinical examination
• Location and extent can be evaluated by careful tactile examination using explorer
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Subgingival calculus
Typically hard and dense
Dark brown or greenish black in color
Firmly attached to tooth surface
Microscopic studies show that subgingival calculus
may extend nearly to base of periodontal pockets
but do not reach junctional epithelium
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• Supragingival calculus and subgingival calculus
generally occur together, but one may be present
without other
• When gingival tissue recede, subgingival calculus
becomes supragingival
• Thus supragingival calculus can be composed of
both supragingival and previous subgingival
calculus
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Both Supragingival
and Subgingival
calculus can be seen
on radiographs
However sensitivity of
calculus detection by
radigraphs is low
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Composition
• Supragingival calculus consists of
Inorganic(70-90%) and Organic components
1. Inorganic components
– 75.9 %CaPO4, 3.1% CaCO3, Traces of
Mg3(PO4)2
• Principal inorganic components are
– Ca (39%), P (19%), CO2(3.1%), Mg (0.8 %),
Traces of Na, Zn, Sr, Br, Cu, Mn, Au, Al, Si, Fe, F,
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• At least two-third of inorganic component is
crystalline in structure in 4 types
– Hydroxyapatite (58%)
– Magnesium Whitlockite (21%)
– Octacalcium Phosphate (12%)
– Brushite (9%)
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• Hydroxyapatite and Octacalcium phosphate are
detected most frequently (97 to100% of all
supragingival calculus)
• Brushite in mandibular anterior region
• Magnesium Whitlockite in posterior region
• The incidence of the four crystal varies with age of
deposit
• Dental calculus, salivary duct calculus and calcified
dental tissue are similar in inorganic composition
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2.Organic component
• Consists of mixture of Protein- polysacchride
complexes, desquamated epithelial cells,
leukocytes and various types of
microorganisms
• Carbohydrate(1.9-9.1%) consists of galactose,
glucose, rhamnose, mannose, glucouronic acid,
galactosamine and sometimes arabinose,
galactouronic acid and glucosamine
– All these are present in salivary glycoprotein except
arabinose and rhamnose
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• Salivary protein account for 5.9% to 8.2% of
the organic components of of calculus and include
most of the amino acids
• Lipids account of 0.2% of the organic
component in the form of neutral fats, free fatty
acids, cholesterol, cholesterol ester and
Phospholipids
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ComparisionContents: Supra gingival calculus Sub gingival calculus
Hydroxyappatite:
Octa Calcium Ph :
Mg white:
brushite:
ratio of Ca/Ph:
sodium contents:
salivary proteins
Equal.
More.
Less.
More.
Low.
Increase with the
depth of PD pocket.
Yes
Equal
Less.
More
Less.
Higher.
No.
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4 modes of attachment of calculus
• Organic Pellicle
• Mechanical locking into surface irregularities such as resorption lacunae
• Close adaptation of calculus undersurface depression to gently sloping mounds of unaltered cemental surface
• Penetration of calculus into cementum (Calculocementum)
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Calculus formation
Calculus is the dental plaque that undergoes
mineralization.
Calcification starts 4-8 hrs after plaque
formation.
50 % become mineralized after 2 days
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60-90 % becomes mineralised after 12 days
All plaque do not necessarily undergo calcification
Plaque that does not develop into calculus
reaches a plateau of maximal mineral content
within 2 days
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Saliva is the source of mineralization for
Supragingival calculus whereas GCF furnishes
minerals for subgingival calculus
Plaque has the ability to concentrate calcium 2-
20 times its level in saliva
Phosphorous is more critical than Ca in plaque
mineralization
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Calcification entails the binding of Ca ions to
carbohydrate protein complex of the organic
matrix and the precipitation of crystalline
calcium phosphate salts
Crystals form first in the intercellular matrix, then
on bacterial surface and finally within bacteria
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Calcification begins along the inner surface of the
supragingival plaque and in the attached
component of subgingival plaque adjacent to
tooth
Separate foci of calcification increase in size and
coalesce to form solid masses of calculus
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Calcification of the plaque is accompanied by alteration in bacterial content and staining qualities
– Filamentous bacteria increase in number
– Staining of plaque change from basophilic to
eosinophilic
– Reduction in PAS positive stain
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– Sulfhydryl and amino groups are reduced
– Stain with toluidine blue which is intially orthochromatic becomes metachromatic and then disappears
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Calculus is formed in layers, which is often
separated by thin cuticle that become
embedded in the calculus as calcification
process progresses
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• The initiation of calcification and the rate of
calculus accumulation vary from person to
person, for different teeth, and at different
times in the same person
– Slight calculus former
– Moderate calculus former
– Heavy calculus former
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• The average daily increment in calculus formers is from 0.10% to 0.15% of dry weight
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Reversal phenomenon
Calculus formation continues until it reaches a
maximum after which it may be reduced in
amount
This decline from maximal calculus
accumulation is called reversal phenomenon
The time required to reach maximal level has
been 10 weeks and 6 months3/17/2020 Dr Saif Khan 25
Theories of calculus formation
The mechanism by which plaque becomes mineralized can beexplained by two theories
1. Mineral precipitation
Results from local rise in the degree of saturation of calcium and
phosphate ions which can occur through
• Increase in pH of saliva causes precipitation of CaPO4 by
lowering of precipitation constant
pH is elevated by loss of CO2 and formation of ammonia by dental plaque bacteria or by
protein degradation during stagnation
• Colloidal proteins in saliva bind Ca and Phosphate ions and
maintain supersaturated solution with respect to calcium
phosphate salts
with stagnation of saliva, colloids settle out and supersaturated solution is no longer
maintained leading to precipitation of calcium phosphate salts
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• Phosphatases liberated from dental plaque,desquamated
epithelial cells, or bacteria precipitates calcium phosphate by
hydrolyzing organic phosphate in saliva, thus
increasing the concentration of free phosphate ions
• Esterase another enzymes present in cocci and filamentous
organism, leukocyte, macrophages and dequamated
epithelial cells of dental plaque
Esterase may initiate calcification by hydrolyzing fatty
ester into fatty acids
The fatty acids form soaps with Ca and Mg that are later
converted into less soluble calcium phosphate salts
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2.Seeding agents
• Carbohydrate-protein complexes may initiate calcification by removing Ca from saliva(chelation) and binding with it to form nuclie that induce subsequent deposition of minerals
• Induce small foci of calcification that enlarge and coalesce to form calcified mass
• This concept is called epitactic concept or heterogenous nucleation
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Role of microorganisms in mineralization of calculus
• Bacterionema and Veillonella species have the ability to form intracellular apatite crystals
• Bacterial plaque may actively participate in mineralization of calculus by forming phosphates which change pH of the plaque and induce mineralization
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Etiologic significance
A positive correlation between presence of calculus and
the prevalance of gingivitis exists but this correlation is
not as great as between plaque and gingivitis
The non mineralised plaque on calculus surface is the
principal irritant, but underlying calcified portion may be
significant contributing factor
The incidence of calculus,gingivitis and periodontal disease
increases with age
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Other predisposing factors
1.Iatrogenic factorsi. Location of gingival margin for the restoration
ii. Space b/w margin of restoration and unprepared tooth
iii. Contour of restoration
iv. Occlusion
v. Material used in the restoration
vi. Restorative procedure itself
vii. Design of the RPD
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2.Malocclusion• Positive correlation between crowding and
periodontal disease
• Roots of teeth that are prominent in arch are associated with high frenal attachment and frequently exhibit reccession
• Tongue thrusting habit lateral pressure on anterior teeth resulting in spreading and tilting of anterior teeth leading to open bite
• Mouthbreathing may marginal and pappillary gingivitis in upper anterior region
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3.Periodontal complication associated with orthodontic therapy
A. Plaque retention and composition
• Increase in P melaninogenica, P intermedia and A
odontolyticus and decrease in in proportion of facultative
microorganisms were detected in gingival sulcus after
placement of orthodontic bands
• Decrease in proportion of facultative microorganisms
were detected in gingival sulcus was seen after placement
of orthodontic bands
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B. Gingival trauma and alveolar bone height
The mean alveolar bone loss per patient for
adolescent who went 2 years of orthodontic
care during 5 yr peroid range b/w 0.1 and
0.5mm
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C. Tissue response to orthodontic forces
Excessive orthodontic forces also increase the risk of apical
root resorption
Surgical exposure of impacted teeth and orthodontic- assisted
eruption may compromise the periodontal attachment on
adjacent teeth
Dento-alveolar gingival fibers located within the marginal and
attached gingivae are streched when teeth are rotated during
orthodontic treatment3/17/2020 Dr Saif Khan 35
4.Extraction of impacted third molars
Various clinical studies have suggested that
extraction of impacted third molars results in
creation of vertical defect distal to second
molars
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5.Habits and self-inflicted injuries
• Toothbrush trauma
• Chemical injury
• Trauma associated with oral jewelry
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6. Tobacco use
• Smokers are 2.6 to 6 times more likely to
develop periodontal disease than non-smokers
• Smokers have more pathogenic subgingival
microflora with increased virulence
• Smokers have negative effect on periodontal therapy
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7.Radiation therapy
– Oral mucositis
– Soft tissue ischaemia & fibrosis
– Irradiated bone is hypovascular and hypoxic
– Osteoradionecrosis
– xerostomia
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