Cyclosporine and nifedipine therapy produces gingival overgrowth in many patients. Neither the mechanism underlying this undesirable side effect nor the possibility of synergism between these drugs is known, although many renal transplant patients receive both drugs. This study compared the rates of 3H-glucosamine utilization by three groups of fibroblasts: untreated gingival fibroblasts, fibroblasts from gingival overgrowth tissue of a patient receiving both cyclosporine and nifedipine, and normal gingival fibroblasts exposed to cyclosporine-A in vitro. Significant differences in the rates of deposition of 3H-glucosamine into the extracellular matrix by each group of gingival fibroblasts were demonstrated, suggesting that increased rates of deposition of proteoglycans into the gingival extracellular matrix by fibroblasts should be further investigated as a biologic mechanism for gingival overgrowth.

(1)H magnetic resonance spectroscopy combined with multivariate methods of analysis can distinguish between normal and malignant squamous cell tissue, and this may lead to the development of an objective and noninvasive diagnostic procedure.

Nifedipine induces overgrowth of gingival tissues in some patients. However, other collagenous tissues in their body do not overgrow. The purpose of this study was to compare effects of serial dilutions of nifedipine on the in vitro metabolism of fibroblasts derived from normal gingiva, nifedipine-induced hyperplastic gingiva, knee capsular ligament, and dermis. The data suggested that nifedipine affects the metabolism of fibroblasts derived not only from gingiva, but also from other collective connective tissues. Thus, nifedipine-responder cells are present in tissues other than gingiva. There was an inverse relationship between in vivo tissue levels of IL-1-beta and in vitro responsiveness to nifedipine of fibroblasts derived from that tissue. Nifedipine-induced overgrowth of connective tissues, other than gingiva, probably does not occur either because of the relatively slow rate of collagenous protein synthesis by resident fibroblasts or because of alterations in collagen deposition/resorption within susceptible tissues produced by nifedipine on collagenase synthesis.

Reduced caries rates and an increased percentage of children with

Longitudinal microbiological examinations have been made of dental plaque from a site approximal to the upper central incisors of 10 8-year-old children living in an area with water fluoridation. Differential counts of viable bacteria, made using a selective medium containing various levels of fluoride (0 to 100 μg/ml) at pH levels of 7.0 to 5.5, demonstrated an effect of both pH and fluoride on the numbers and types of bacteria isolated. Strains of Streptococcus and Neisseria grew after only 16 h of incubation at pH levels as low as 6.0 with fluoride levels up to 50 μg/ml. The most commonly isolated streptococci were Streptococcus mitior and S. salivarius. S. mutans was isolated less frequently and was inhibited by 20 and 50 μg of fluoride per ml at pH 6.0 and 6.5, respectively. Veillonella strains were the most resistant isolates, being isolated after 16 h of incubation on media at pH 6.0 with 100 μg of fluoride per ml. Despite their known fluoride resistance, Actinomyces spp. were often only detected on the selective media after 72 h of incubation. The pH of the medium had a definite selective effect, as the number of colonies growing on the fluoride-free basal media at pH 6.0 was only 30% of that at pH 7.0. Representative strains of S. mutans, S. mitior, S. sanguis , and S. milleri were tested for their ability to utilize glucose at the pH and fluoride levels of the medium on which they were initially isolated. Fluoride reduced the initial glycolytic rate of the cells, but in 5 of the 13 strains tested the final amount of glucose used after 2 h of incubation was the same in the presence or absence of fluoride. The isolation of bacteria capable of growth in the presence of fluoride over a significant portion of the pH range that occurs in plaque in vivo could explain in part the finding that fluoride does not have a dramatic effect on the plaque community. Fluoride in plaque may reduce the ecological advantage afforded to aciduric S. mutans strains by carbohydrate substances. In the in vivo situation this could mean that, even with high carbohydrate intake, fluoride may permit S. mitior to compete with S. mutans within the plaque ecosystem.