Faculty Bibliography

The Sonicare sonic toothbrush and a traditional manual toothbrush were compared for efficacy in improving periodontal health in young orthodontic patients with existing gingival inflammation. A 4-week, single-blind clinical trial was employed. Twenty-four subjects, ages 11-17 years, who were fully bonded and banded with fixed orthodontic appliances were selected. Subjects were randomly assigned to use either the manual or the Sonicare toothbrush, instructed in its use, and asked to brush each morning and evening for 2 minutes. Plaque index, gingival index, percentage of sites which bled on probing, pocket depth, and total gram-negative bacteria in a subgingival plaque sample were assessed at baseline and 4 weeks around the banded teeth. The results demonstrate that the Sonicare brush was significantly more effective than the manual brush in all clinical parameters. Sonicare was statistically superior to the manual brush in supragingival plaque reduction (57% vs. 10%, respectively; p < 0.001). Gingival Index scores fell by 29 percent in the Sonicare group, but only 3 percent in the manual group. Reduction of bleeding on probing was significantly greater in the Sonicare group than in the manual group (p < 0.001). The Sonicare group decreased from 78% bleeding sites at baseline to 24.5% after 1 month. In the manual group there was only a slight reduction in bleeding on probing (70% of sites at baseline and 64.6% sites after 1 month). Mean pocket depths were significantly reduced compared to baseline values in both the Sonicare and the manual groups (p < 0.001). Pocket depth reduction in the Sonicare group was, however, significantly greater than in the manual group (28% vs. 6%, respectively: p < 0.001). Total gram-negative bacteria in subgingival plaque samples from banded test teeth of a subset of patients were reduced in the Sonicare group (p < or = 0.05), but increased in the manual group. These results clearly demonstrate that the Sonicare sonic toothbrush is superior to a manual toothbrush in improving periodontal health in adolescent orthodontic patients with existing gingivitis.

Short-chain carboxylic acids (SCCA; C < or = 5; e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacterial presence; SCCA concentration; and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r > or = 0.47; all p < or = 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (-0.31 < or = r < or = 0.39; 0.08 < or = p < or = 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.

The cadherins are a family of cell membrane proteins that mediate calcium-dependent cell-cell adhesion. E-cadherin is required for the formation, differentiation, polarization and stratification of epithelia; P-cadherin is also expressed on many epithelia. We report here the first study of cadherin expression in immortalized human gingival epithelial cells (IHGK) and examine the role of cadherins in growth regulation of these cells. We found that the IHGK cells are similar to normal gingival epithelial cells in their cadherin expression and density-dependent inhibition of growth. The IHGK cells proliferate more rapidly at low calcium concentration (0.15 mM) than at physiological concentrations of calcium (1.8 mM) and magnesium (0.65 mM; Ca/Mg medium) suggesting that calcium is required for density-dependent regulation of proliferation. To evaluate the possibility that cadherin function is required for contact inhibition in these cells, we grew them in Ca/Mg medium in the presence of adhesion-blocking anti-cadherin monoclonal antibodies. At anti-E-cadherin concentrations sufficient to disrupt cell-cell adhesion, the proliferation of the IHGK cells was similar to that observed in medium containing 0.2 mM EDTA. Anti-P-cadherin had a much weaker effect on cell proliferation than anti-E-cadherin, and cells grown in medium containing both antibodies grew at intermediate rates. The increased proliferation of the IHGK cells in either low calcium medium or Ca/Mg medium containing adhesion-blocking anti-cadherin antibodies suggests that cadherin-mediated adhesion is required for density-dependent regulation of growth of these cells.