RESEARCH

Introduction

Tooth decay or dental caries is an oral disease with a complex aetiology influenced by a large number of factors. The enamel of a tooth is the hardest of all tissues and, paradoxically, the hardest of all tissues is so susceptible to dental caries in the living humans while it is almost indestructible in the dead. The name "Civilisation dystrophy" for dental caries etiologically is connected with damage caused by civilisation, seems quite justified. In the book Colour Atlas of a New Concept of Enamel Caries, Dr L.K. Bandlish presents a pictorial synopsis of a new concept in the natural history of enamel caries. Tooth surface may be divided into two parts; that is, one part where there is attrition and the other part where there is plaque. The term 'Attrition' used in its broadest sense to include attrition and the scouring effect of food. It has been seen that the enamel caries occurs where these two parts meet. Dental plaque, attrition and fluoride play a very important role in the causation control and prevention of enamel caries. It is generally believed that the locus of initial approximate caries lesion is situated just apical to the contact area and is situated on the sites covered with plaque. Dr L.K Bandlish suggests that in practically all cases the lesion begin at the actual point of contact of a tooth with its neighbour. Dr L.K. Bandlish is convinced that the locus of the initial approximate carious lesion is situated mostly at the contact area, and the carious lesion, in general, are situated on sites with least attrition and least plaque.

Concept of Enamel Caries

Dental caries involves demineralisation of enamel over a period of time by organic acids produced by bacterial fermentation of carbohydrates. Enamel is ectodermal in origin and is the hardest of all tissues. One of the ways it protects itself is by shedding its superficial layers through attrition and/or abrasion. The skeletal records tell us that the primitive man seldom lost teeth. They could become worn with advancing age to the point where the roots were left in the jaws but the dentition still functioned. In other words, dental decay seems to be a rather recent phenomenon and it flourished in the nourished population due to lack of attrition. In other words, caries occurs where there is the least attrition. Oral fluids protect the enamel by providing a protective covering on the enamel surface. This protective covering is always invaded by bacteria except under strict experimental conditions and is known as dental plaque. It has been seen that there is little topographical relationship between dental plaque and carious lesion. Enamel caries occurs where there is least plaque and least attrition. Attrition makes the fissures wider and removes the superficial layer of the enamel along with the initial carious lesions, if present. The new layer of enamel becomes protective again with the help of oral fluids on it. Where the oral fluids cannot reach, that is the contact areas, the new surface layer of enamel cannot be made protective against the carious attack. Attrition and plaque must be regarded as defence mechanisms against caries. Organic acids produced by the bacterial fermentation of the carbohydrates cause subsurface demineralisation of the enamel without the penetration of the bacteria through the intact enamel surface. Some of the products which are removed as a result of demineralisation are recycled into the enamel during the process of remineralisation. Demineralisation and remineralisation continue with time, but caries occurs only where there is more demineralisation. Dental caries occurs at the contact area because the contact area is not exposed to the protective action of the oral fluids and the protective action of the plaque. The area below the contact area is covered by plaque. The organic acids from the plaque attack the perimeter of the contact area. The carious lesion starts at the perimeter of the contact area. The perimeter-area ratio of square and circular areas. Smaller the area more the perimeter per unit area, as the area becomes larger, the perimeter per unit area falls. Similarly smaller the contact area, more the perimeter per unit area. As the contact area becomes greater with attrition, the perimeter per unit area falls. All other factors remaining constant the intensity of the acid attack on the contact area depends on the length of the perimeter per unit area. Greater the length of the perimeter per unit area, the stronger the acid attack on it. As the length of the perimeter per unit area falls with the increase in the size of the contact area so does the strength of the acid attack. Even with a small amount of attrition, the size of the contact area increases considerably.