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Calculus

Hanadi Baeissa

Hanadi Baeissa

Dental calculus
a) Supragingival

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

: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

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

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:

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

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
Gengivitis- 1
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

Periodontitis- 2

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

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)

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)

This is part of the inflammatory


response
destruction of bone and
periodontal fibers