Transcript Many filamentous bacteria is present

Calculus
Hanadi Baeissa
Hanadi Baeissa
Dental calculus
a) Supragingival
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b) Subginival
• Harder
Friable
Readily removed by scaling • Coloured (often green)
Unpigmented
• Present in smaller deposits,
Form in greatest amounts
on the lower incisors & upper which are not localized near
molars i.e. near the orifices of the salivary ducts
the main salivary ducts
• Composition less site
Composition varies in
dependent
different sites
• non-salivary (serum) origin
Salivary origin
Composition of Supragingival Calculus
Inorganic
(~ 80%)
Organic
(~ 20%)
• Derived from saliva &
bacteria
• Brushite
CaHPO4.2H2O detectable in all
deposits after 14 days of development - Largely protein with carbohydrate
attached (12-20%)
- GAG (CS, HA & HS) from the
Octa calcium
Wetlockite Ca3 (PO4)2
gingivae
phosphate
With some magnesium -Lipids (3%) perhaps bacterial
Ca8 (HPO4)2 (PO4)4
Instead of calcium
origin
Especially in the presence
Of fluoride
apatite
Composition of Supragingival Calculus
- ( continue)
F¯ is also present at ≤ 400 ppm (more in old
calculus)
 Many filamentous bacteria is present
(example: leptotrichia buccalis)
 Formation is intermittent
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Theories of calculus formation:
1.
2.
Carbon dioxide loss:
CO2 loss from saliva, as it equilibrates with low
CO2 tension in the month ppt of calcium salts
pH change by ammonia formation:
Urea NH3
pH, thus favoring ppt of calcium
phosphate
3.
The phosphatase theory:
Bacterial
pyrophosphatase
PPi
2Pi
mineralization of plaque
not much evidence to this
4.
encourage
Seeding theory:
A seeding process
calculus
This does not explain individual variations in
formation
Steps in calculus formation
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Two stages
1.
Matrix deposition (derived from plaque)
Mineralization: reason unknown yet but
provision of seed by plaque or bacteria is
likely (mainly filamentous bacteria)
2.
Notes:
Calculus is higher in smokers.
 There is variation between different people in
amount of calculus formed
 First stage of calculus formation (matrix
deposition) occurs readily in both slow and rapid
calculus formers
 The difference lies in the power to mineralize the
matrix
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Possible factors effecting calculus
formation
1.
Differences in plaque
a) composition:
- increase Ca & P
more mineralization
- decrease methyl pentose & hexosamine
b) increased rate of plaque formation in heavy
calculus formers
- therefore, the early stages, rather than the
mineralization , differed in the two groups
2.
Differences in saliva composition:
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increase protein, Ca & phosphate
calculus
increase activities of acid phosphatase,
pyrophosphatase, esterase
more calculus
increase urea
more calculus
increase lysozyme activity
less calculus
presence of low molecular weight protein
adsorbed to apatite & might act as seed
calculus
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3.
The acidic protein of saliva said to prevent Ca
ppt is either deficient or more rapidly broken
down by bacteria
calculus
High viscosity of saliva less calculus
Smoking leads to increased formation
Periodontal Disease
Two most frequently occurring forms:
1- Gengivitis
• Limited to the gingival or soft tissues,
surrounding the teeth
• Results in bleeding of gums, and
possibly change in color, shape, size,
surface texture and consistency
• Reversible on restoration of hygiene,
does not result in destruction of
tissues supporting the teeth
2- Periodontitis
• Extension of the inflammatory process
from the gingival to the supporting
periodontal tissue & destruction of
these tissues
• Can be controlled but not reversed
•Chronic peridontitis result in loss of
bone supporting the teeth
mobility
tooth loss
The effect of plaque on the gingivae
It was first thought that calculus caused
gingivitis
 Volunteers not brushing for days developed
gingivitis without calculus formation
 Conclusion: Old plaque (> 48 hours)
periodontal disease, but calculus help by
providing mechanical irritation
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The nature of toxins in plaque
causing Gingivitis
Plaque contains substances which
diffuse into the gingival tissues and
irritate them: ex.
 Proteolytic enzymes from bacteria
broken
release of a.a down amines + ammonia,
H2S and mercaptans (all potential
irritants)
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Plaque antigens such as bacterial
endotoxins, enter the gingival and induce
antibodies in the local lymph tissues.
 The interaction between antibodies &
antigens is beneficial, but it activates
complement which in turn causes the
release of substances contracting the
smooth muscles of arterioles and
increasing vascular permeability
(cytokines
edema)
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This is part of the inflammatory
response
destruction of bone and
periodontal fibers