Gordon Nikiforuk

Risk Factors for Dental Fluorosis in a Fluoridated Community

We conducted a case-control study to determine the sources of fluoride which are particular risk factors to dental fluorosis. Cases and non-cases were identified by the screening of 8-, 9-, and 10-year-old schoolchildren in the fluoridated community of East York, Ontario-Parents were interviewed about the childs first five years of residence and about diet and preventive caries practices. The Mantel-Haenszel odds ratio and associated chi-square tests were used to assess the association of fluorosis with several potential sources, controlling for other sources of fluoride and mothers education. The prevalence of mild fluorosis [1-4 on the Thylstrup and Fejerskov (1978) Index] was 13%. Those who brushed their teeth before the age of 25 months had 11 times the odds of fluorosis compared with those beginning toothbrushing later; prolonged use of infant formula (≥ 13 months) was associated with 3.5 times the risk of fluorosis, compared with no, or shorter duration of, formula use. We estimate that these factors were responsible for 72% and 22%, respectively, of the cases in our population. Dental fluorosis is not a public health problem in East York, but parents should be advised to supervise toothbrushing by children under 2 years of age.

The etiology of enamel hypoplasia: A unifying concept†

In a study of children with chronic disorders of calcium and phosphate homeostasis, enamel hypoplasia was found in hereditary vitamin D-dependency rickets and in hypoparathyroidism, conditions characterized by hypocalcemia, and was not found in X-linked hypophosphatemic rickets, a condition in which the plasma calcium concentration is normal. The occurrence of enamel hypoplasia bore no relation to the plasma phosphate concentration. Enamel hypoplasia has also been reported in other pediatric disorders in which hypocalcemia is a major sign (for example, vitamin D deficiency, prematurity, and neonatal tetany). The existence of enamel hypoplasia in a hypoparathyroid or rachitic patient, when correlated with the chronology of enamel mineralization, helps to establish the time of onset of hypocalcemia. The observations led us to the hypothesis that a low serum calcium concentration during enamel formation is a specific determinant of enamel hypoplasia. This hypothesis may be relevant to the etiology of linear enamel hypoplasia, an endemic lesion of primary teeth in children of many Third World countries that predisposes the teeth to dental caries. The hypothesis may therefore be relevant also in explaining the prevalence of caries in the primary teeth of children in many underdeveloped countries.

Etiology of Enamel Hypoplasia and Interglobular Dentin: The Roles of Hypocalcemia and Hypophosphatemia

Abstract In the course of a long-term investigation of children with three well-defined disturbances of calcium and phosphate homeostasis - hereditary vitamin D dependency rickets, X-linked hypophosphatemia and hypoparathyroidism - we have observed distinctive distributions of enamel hypoplasia and interglobular dentin that provide a clue to the pathogenesis of these dental lesions. Each of the 25 patients with X-linked hypophosphatemia had extensive interglobular dentin in the primary and permanent teeth but no enamel hypoplasia; these patients were normocalcemic but very hypophosphatemic. Each of ten patients with vitamin D dependency rickets had severe enamel hypoplasia in the permanent teeth, and in the 7 patients whose teeth were examined histologically moderate interglobular dentin was observed in each; these patients were hypocalcemic and, because of secondary hyperparathyroidism, also hypophosphatemic. Fifteen of 21 children with hypo parathyroidism had severe enamel hypoplasia but none had interglobular dentin; these patients were hypocalcemic and hypopphosphatemic. From these observations we have formulated a unifying hypothesis that enamel hypoplasia, in disturbances of calcium and phosphate homeostasis; is caused by hypocalcemia and interglobular dentin is caused by hypophosphatemia.

Chemical Determinants of Enamel Hypoplasia in Children with Disorders of Calcium and Phosphate Homeostasis

Studies of children with disorders of calcium and phosphate homeostasis indicate that hypocalcaemia, but not hypophosphataemia, is a significant and specific factor in the etiology of enamel hypoplasia. Only those teeth were affected that had developed during the hypocalcaemic episodes.

Staining Reactions Following Demineralization of Hard Tissues by Chelating and Other Decalcifying Agents

ALL the usual methods for demineralization of hard tissues require the m use of solutions with low pHs, with the exception of the method recommended by Kramer and Shipley2 using magnesium citrate. Because of the limited number of techniques available for decalcifying hard tissues at alkaline pHs, the present study was planned to observe the effects of using one of the chelating agents, the sodium salt of ethylenediaminetetraiicetic acid,* as a decalcifying medium, and to compare the effects with those of conventional acidulated solutions on the staining reactions of dental andosseous tissues following the use of hematoxylin and eosin. It is recognized that the procedures employed in histopathologic techniques are based as much on empiricism as on known scientific methods, and that the differences in color values and clarity of cytologic detail of different sections are necessarily assessed subjectively.

Calcific bridging of dental pulp caused by iatrogenic hypercalcemia: Report of a case

A case of renal osteodystrophy treated with high doses of vitamin D is presented. The treatment, carried out when the patient was between 3 1/4 and 6 years of age, induced hypercalcemia (up to 13.9 mg./dl.) which resulted in dentinal bridging corresponding chronologically to the part of the root developing at this age. Dentinal bridging associated with iatrogenic hypercalcemia has not been reported previously.

Posteruptive Effects of Nutrition on Teeth

At the outset, I must admit that the assignment I received has been a dilemma. The reason is simple-the most significant metabolic effects of food deficiencies or imbalances on teeth occur during the developmental phase and not after eruption. Although food components such as fluoride and sucrose play a significant role in the carious process, posteruptively, these items are covered in other sections. I was therefore left with an assignment that was reminiscent of the elusive Cheshire cat. Whenever I felt that I had a hold on some substantive material I found that, as in the case of the Cheshire cat, only the grin remained. I shall first attempt to delineate the mechanisms by which food may influence teeth, metabolically, during the posteruptive stage. In addition to metabolic effects, I have found it necessary to discuss some of the local effects of food on enamel and plaque. Food imbalances or deficiencies may influence teeth through the following mechanisms: blood elements, by affecting the pulp circulation and hence dentin metabolism and salivary composition, and direct, local effect on enamel and plaque. Figure 1 shows the interrelations of these mechanisms. Table 1 summarizes the posteruptive effects of nutritional factors on caries.