A study of correlation between posterior palatal seal width and soft palatal angulation with palatal contour.

CONTEXT: The spatial relationship of posterior palatal seal (PPS) width and vibrating lines varies among individuals. Such variability could be related to contour of the palate. AIMS: The study was carried out to evaluate the relationship between PPS width of the patient intra-orally and cephalometric tracing of the same patient. Second part of the study was formulated to determine whether the anterior and posterior vibrating lines can be distinguished as two separate lines by different observers. MATERIALS AND METHODS: A lateral cephalogram was made to trace the hard and soft palatal contour, and the angle of the palatal contour was measured with the v-ceph program. Correlation analysis was conducted to examine the relationship between the distance from anterior to posterior vibrating lines and the angle of the palatal contour at the junction of the hard and soft palate. STATISTICAL ANALYSIS USED: The data were analyzed using the Karl Pearson Correlation test. RESULTS: Correlation of the angle of the palatal contour to PPS width, showed perfectly positive value; whereas, correlation of angle between anterior nasal spine-posterior nasal spine (ANS-PNS) and PNS-Uvula (U) to PPS width showed partially positive value. CONCLUSION: The correlation of angle between hard tissue and soft tissue to PPS width, and the angle between ANS-PNS and PNS-U to PPS width, increases with an increase in PPS width.

Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling.

BACKGROUND: Type 1 diabetes mellitus (T1DM) and periodontitis have long been thought to be biologically connected. Indeed, T1DM is a risk factor for periodontal disease. With the population of diabetic individuals growing, it is more important than ever to understand the negative consequences of diabetes on the periodontium and the mechanisms. The aim of this study was to find out the early effects of T1DM on the periodontium without any experimentally induced periodontitis. METHODS: We established the streptozotocin (STZ)-induced diabetic mouse model and examined the periodontium 8 weeks later by histology, molecular and cellular assays. Microcomputed tomographic (𝜇CT) imaging and in vivo fluorochrome labeling were also used to quantify bone volume and mineral apposition rates (MAR). RESULTS: The histologic appearance of epithelium tissue, connective tissue, and periodontal ligament in the diabetic condition was comparable with that of control mice. However, immune cell infiltration in the gingiva was dramatically elevated in the diabetic mice, which was accompanied by unmineralized connective tissue degeneration. Bone resorption activity was significantly increased in the diabetic mice, and quantitative 𝜇CT demonstrated the bone volume, the ratio of bone volume over tissue volume, and cemento-enamel junction to alveolar bone crest (CEJ-ABC) in the diabetic condition were equivalent to those in the control group. In vivo fluorochrome labeling revealed increased MAR and bone remodeling in the diabetic mice. Further investigation found the diabetic mice had more osteoprogenitors recruited to the periodontium, allowing more bone formation to balance the enhanced bone resorption. CONCLUSIONS: STZ-induced T1DM mice, at an early stage, have elevated gingival inflammation and soft tissue degeneration and increased bone resorption; but still the alveolar bone was preserved by recruiting more osteoprogenitor cells and increasing the rate of bone formation. We conclude that inflammation and periodontitis precede alveolar bone deterioration in diabetes.