1. Calculus
Hanadi Baeissa

2. Hanadi Baeissa

3. Dental calculus Supragingival b) Subginival Friable Harder
Readily removed by scaling
Unpigmented
Form in greatest amounts
on the lower incisors & upper
molars i.e. near the orifices of
the main salivary ducts
Composition varies in
different sites
Salivary origin
b) Subginival
Harder
Coloured (often green)
Present in smaller deposits,
which are not localized near
the salivary ducts
Composition less site
dependent
non-salivary (serum) origin

4. Composition of Supragingival Calculus Especially in the presence
Organic
(~ 20%)
Inorganic
(~ 80%)
Derived from saliva &
bacteria
Largely protein with carbohydrate
attached (12-20%)
GAG (CS, HA & HS) from the
gingivae
Lipids (3%) perhaps bacterial
origin
Brushite
CaHPO4.2H2O detectable in all
deposits after 14 days of development
Octa calcium
phosphate
Ca8 (HPO4)2 (PO4)4
Wetlockite Ca3 (PO4)2
With some magnesium
Instead of calcium
Especially in the presence
Of fluoride
apatite

5. 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

7. Theories of calculus formation:
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 NH pH, thus favoring ppt of calcium phosphate

8. Seeding theory: The phosphatase theory:
PPi Pi encourage mineralization of plaque
not much evidence to this
Seeding theory:
A seeding process calculus
This does not explain individual variations in formation
Bacterial
pyrophosphatase

9. Steps in calculus formation
Two stages
Matrix deposition (derived from plaque)
Mineralization: reason unknown yet but provision of seed by plaque or bacteria is likely (mainly filamentous bacteria)

10. 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

11. Possible factors effecting calculus formation
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

13. 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

14. 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

15. Two most frequently occurring forms:
Periodontal Disease
Two most frequently occurring forms:
1- Gengivitis
2- Periodontitis
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
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

16. 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

17. 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 release of a.a amines + ammonia, H2S and mercaptans (all potential irritants)
broken
down

18. 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)

19. This is part of the inflammatory response destruction of bone and periodontal fibers