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|dc.title||Patterns of diabetic periodontal wound repair: A study using micro-computed tomography and immunohistochemistry|
|dc.identifier.citation||Chang, P.-C., Chung, M.-C., Wang, Y.-P., Chien, L.-Y., Lim, J.C., Liang, K., Chong, L.Y., Kuo, Y.-P., Chen, C.-H., Chiang, H.-C. (2012). Patterns of diabetic periodontal wound repair: A study using micro-computed tomography and immunohistochemistry. Journal of Periodontology 83 (5) : 644-652. ScholarBank@NUS Repository. https://doi.org/10.1902/jop.2011.110325|
|dc.description.abstract||Background: Diabetes is known to impair wound healing and deteriorate the periodontal condition. There is limited information about the patterns and events associated with periodontal wound repair. In this study, we evaluate the dynamics of periodontal wound repair using micro-computed tomography (microCT) and immunohistochemistry. Methods: Thirty-six male rats were used, and diabetes was induced by streptozotocin. The maxillary first molars were extracted, and a tooth-associated osseous defect was created in the extraction area. Animals were sacrificed after 7, 14, and 21 days. Volumetry and distribution of bone trabeculae were evaluated by microCT imaging. The patterns of healing and collagen alignment were evaluated by histology. Advanced glycation end-product (AGE) deposition and expression of the receptor for AGEs (RAGE), tartrate-resistant acid phosphatase, and proliferating cell nuclear antigen were evaluated by histochemical and immunohistochemical staining. Results: Diabetic animals demonstrated a significantly reduced bone volume and trabecular number as well as thinner trabeculae and more trabecular separation in osseous defects. The early stage was characterized by significantly reduced cellular proliferation and prolonged active inflammation without evident bone resorption, whereas delayed recovery of collagen realignment, matrix deposition, and bone turnover was noted in later stages. Although AGEs and RAGE were present during healing in diabetes and controls, a stronger and more persistent level of expression was observed in the group with diabetes Conclusions: Diabetes significantly delayed osseous defect healing by augmenting inflammation, impairing proliferation, and delaying bone resorption. The AGE-RAGE axis can be activated under metabolic disturbance and inflammation. © 2012 American Academy of Periodontology. All rights reserved.|
|dc.subject||Glycosylation end products, advanced|
|dc.description.sourcetitle||Journal of Periodontology|
|Appears in Collections:||Staff Publications|
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