Vitamin D along with parathyroid hormone and calcitonin play primary roles in regulating the concentration of calcium and inorganic phosphate in the plasma and extracellular fluids, in regulating the movement of these ions into and out of cells and in controlling the mineralization of bones and teeth. Until recently it was believed that vitamin D was the active hormonal compound that cured rickets. It is now clearly established that vitamin D has to be converted by a controlled mechanism to a hormone that regulates calcium and phosphorus metabolism.
The chemistry of vitamin D and its derivatives has been slowly elucidated. Vitamin D2 is derived by radiation of the naturally occurring substance ergosterol and has for many years been the major synthetic form of vitamin D used for the prevention and cure of rickets in main. Subsequently, the form of vitamin D occurring in the human body, namely D3 or cholecalciferol (CC), was produced by radiation of 7- dehydrocholesterol, which is present in the skin. It is known that both vitamin D2 and D3 are themselves inactive in vivo. They must first be converted to a hormonal end product by means of two enzymatic hydroxylations before they can exert physiological actions at a target cell. The first metabolic step which takes place in the liver is the conversion of vitamin D to 5-hydroxy vitamin D ( 25-OH-D3) by a specific enzyme, vitamin D-25- hydroxylase. The 25-OH-D3 subsequently undergoes conversion to 1,25 dihydroxy D3(1,25(OH)2D3) in the kidney by the enzyme, D-25- hydroxy vitamin D-1- hydroxylase. Of the metabolites identified to date, 1;25 (OH)2D3 has the greatest and most rapid effect on the transport of calcium. This compound has all the characteristics of a hormone in that it is produced in the kidney, is transported by the blood t to its target tissues ( small intestine, bone and kidney) where it has specific effects (calcium and phosphate regulation) and its production is under precise fee back regulation.
Along with the elucidation of the chemistry considerable progress has been made in the understanding of the physiological functions of the vitamin. It is now well established that small amounts of vitamin D are essential for normal calcium homeostasis. One action that has been conclusively demonstrated is that vitamin D specifically improves intestinal absorption of calcium probably by increasing the synthesis of a calcium- binding protein in the mucosa which is concerned with calcium absorption.
In vitamin A-deficient animals, atrophic changes in the ameloblasts, subsequent abnormalities in tooth morphology and a reduced number of salivary acini in the major and minor salivary glands has been observed. Addition of vitamin A to the diet of animals, posteruptively, does not affect the number or extent of the carious lesions. In a study of persons with vitamin A deficiency sufficiently severe cause xerophathalmia, slight hypoplasia was found in only one quarter of the sample and many had perfectly formed teeth in spite of their deficiency. Evidently in man, severe vitamin A deficiency during tooth formation does not necessarily lead to defective enamel.
Other Vitamins & Caries - The only member of the Vitamin B complex which has been associated with caries is pyridoxine (vitamin B6). This vitamin has been stated to reduce caries in rats but the effects was not confirmed on monkeys [Cole et al 1980]. Very high doses (some 10times the normal dose) have been reported in two small scale experiments in human subjects (pregnant women and school children) to reduce caries. It is not suggested that a deficiency of pyridoxine is responsible for caries but that large unphysiological dose, in which pyridoxine is being used as a drug rather than as a vitamin, reduced caries by modifying the oral flora.
Lipids - Deficiency of essential fatty acids in man is rare and evaluation of the role of these nutrients on caries is not available. As more food is processed it is possible that nutritional deficiencies may increase in the population that subsist primarily on such foods.
Fat Fat consumed post eruptively in diets of animals, has been correlated with caries reduction. The mechanism of action of fats in reducing caries may be due to a combination of several factors. The enamel surface may be protected from demineralization by the formation of fatty films but this is unlikely in approximate areas. Another factor may be that contact between carbohydrate foods and bacteria is reduced in the presence of fat.
Protein Deficiency Gross protein deficiencies are rare in modern industrialized countries but occur in many economically deprived regions where kwashiorkor is prevalent. The caries rate of this population is considerably less than in populations on an adequate diet. This is probably related to the low intake of cariogenic food, and reduced frequency of eating of refined carbohydrate. It is almost certain that the last word has not been written about optimal nutrition in man and its role in host (tooth and salivary secretions) resistance to caries. This statement is supported by evidence that severe nutritional deficiencies in experimental animals are known to affect development of teeth and salivary glands and increase their susceptibility to dental caries.
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