Calculus Hanadi Baeissa

Hanadi Baeissa

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

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

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: 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

Seeding theory: The phosphatase theory: PPi 2Pi 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

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)

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 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

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

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

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

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

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