Characterization of Transcortical Porosities During Periodontal Disease in Rats
INTRODUCTION: Cortical bone microarchitecture exhibits a level of plasticity which adapts to changes in health status. In periodontal disease, bone loss can occur as a result of bacterial plaque induced inflammation around teeth. As we learn more about the mechanisms driving periodontal bone loss, one aspect that is not well understood are the changes in cortical bone and their role in alveolar bone remodeling. Previous studies utilizing long bones have recognized the importance of cortical bone microarchitecture in understanding disease pathogenesis, and preliminary evidence suggests similarities may exist in jaw bones as well. OBJECTIVE: The purpose of this �CT study is to identify and characterize transcortical canal porosities in rat jaws, and to evaluate the anatomical changes in response to experimental periodontitis.
MATERIAL AND METHODS: 14 eight-week-old, Wistar Han rats underwent ligature placement, utilizing 4-0 silk sutures ligated around the left maxillary second molars, and 28-gauge stainless-steel wire around the left mandibular first molars. Contralateral molars served as non-ligated control teeth in each animal. Animals were monitored to ensure ligature presence, and randomly assigned to euthanasia 2 or 4-weeks after ligature placement. Maxillae and mandibles were trimmed, placed in 10% formalin for 48-hours, then stored in 70% ethanol for �CT imaging at 15�m and 5�m resolution. CTan imaging software was used to quantify vertical bone loss circumferentially at 15�m resolution. A global threshold was applied to segment transcortical canal spaces at 5�m resolution, in order to quantify number and size of canals.
RESULTS: At 15�m resolution, three-dimensional reconstructions of the buccal cortical bone exhibited increased porosity in the presence of ligature-induced experimental periodontitis, over healthy non-ligature molars. Further analysis of selected binarized slices at 5�m resolution, revealed an increase in number and volumetric percentage of intracortical porosities in experimental periodontitis molars compared to non-ligature controls.
CONCLUSIONS: Our observations demonstrate a complex network of canals exists within the cortical jaw bones of healthy rats. After 2-weeks of experimental periodontitis, an increase in the size and number of transcortical canals was observed, indicating that cortical bone morphology is highly dynamic in response to oral disease. These results enhance our current understanding of bone microstructure and disease driven adaptation. Our ongoing studies are directed at further interrogating the role of intracortical canals in oral inflammatory bone remodeling.