Aim Cellular and molecular immunoinflammatory changes in gingival tissues drive alveolar bone loss in periodontitis. Since aging is a risk factor for periodontitis, we sought to identify age-related gingival transcriptome changes associated with bone metabolism in both healthy and in naturally-occurring periodontitis. Materials and Methods Adult (12–16 years) and aged (18–23 years) non-human primates (M. mulatta) (n=24) were grouped into healthy and periodontitis. Gingival tissue samples were obtained and subjected to microarray analysis using the Gene Chip Macaque Genome Array. Gene expression profiles involved in osteoclast/osteoblast proliferation, adhesion, and function were evaluated and compared across and between the age groups. QPCR was also performed on selected genes to validate microarray data. Results Healthy aged tissues showed a gene profile expression that suggest enhancement of osteoclastic adhesion, proliferation/survival and function (SPP1, TLR4, MMP8, and TFEC) and impaired osteoblastic activity (SMEK3P and SMAD5). The gingival transcriptome in both adult and aged animals with naturally-occurring periodontitis (FOS, IL6, TLR4, MMP9, MMP10 and SPP1 genes) was consistent with a local inflammatory response driving towards bone/connective tissue destruction. Conclusion A pro-osteoclastogenic gingival transcriptome is associated with periodontitis irrespective of age; however; a greater bone-destructive molecular environment is associated with aging in healthy tissues.

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Understanding the differences between animal models and their adaptation biology as it relates to OTM is key to make valid conclusions. The rodent model can be used to understand the initial phases of tooth movement. Unlike the dog model, the rodent model does not lend itself to understand prolonged adaptation in response to bodily tooth movement. Extrapolation of rate of tooth movement to humans is more challenging from rodent model data.

Purpose The primary objective of this study was to analyze the thickness and height of alveolar bone around the maxillary and mandibular incisors. Additionally, this study aimed to compare bone parameters between Caucasian (CC) and African American (AA) female patients. Materials and Methods In this retrospective pilot study, 50 female subjects (25 CC and 25 AA) were included. The inclusion criteria were AA or CC women between the ages of 18 and 50 with a normo-divergent facial pattern and Angle's class I, end-on class II, or mild class III malocclusion. The distance from the cementoenamel junction (CEJ) to the buccal and lingual alveolar crest; the alveolar ridge thickness at the mid-root and apex; and the buccal and lingual bone thickness at 3, 6, and 9 mm from the CEJ were measured. Results No significant difference was found ( P >0.05) in the cortical bone thickness at 3 mm, 6 mm, or 9 mm from the alveolar crest between CC and AA populations for most measurements. A significant difference in bone thickness was found ( P <0.05) for the lingual surface of the central incisor, with maxillary bone thickness found to be higher than mandibular bone thickness. The measurements of lingual thickness were larger than those of buccal thickness for both races. Conclusion There were no differences in maxillomandibular anterior alveolar bone measurements between normo-divergent adult AA and CC women, except for a few parameters at varying locations. However, future studies can be planned based the current pilot study data, which may provide valuable information.

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