Int J Med Sci 2016; 13(4):248-254. doi:10.7150/ijms.14129 This issue
1. Department of Oral Health Promotion, Matsumoto Dental University Graduate School of Oral Medicine, Shiojiri, Japan
2. Department of Hard Tissue Research, Matsumoto Dental University Graduate School of Oral Medicine, Shiojiri, Japan
3. Department of Oral Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan
4. Department of Orthodontics, Matsumoto Dental University School of Dentistry, Shiojiri, Japan
5. Department of Oral and Maxillofacial Biology, Matsumoto Dental University Graduate School of Oral Medicine, Shiojiri, Japan
We carried out an experiment to induce traumatic occlusion in mice periodontal tissue and analyzed the expression of HSP47. Continuous traumatic occlusion resulted to damage and remodeling of periodontal ligament as well as increase in osteoclasts and bone resorption. Four days after traumatic occlusion, osteoclasts did not increase but Howship's lacunae became enlarged. That is, the persistent occlusal overload can destroy collagen fibers in the periodontal ligament. This was evident by the increased in HSP47 expression with the occlusal overload. HSP47 is maintained in fibroblasts for repair of damaged collagen fibers. On the other hand, osteoclasts continue to increase although the load was released. The osteoclasts that appeared on the alveolar bone surface were likely due to sustained activity. The increase in osteoclasts was estimated to occur after load application at day 4. HSP47 continued to increase until day 6 in experiment 2 but then reduced at day 10. Therefore, HSP47 appears after a period of certain activities to repair damaged collagen fibers, and the activity was returned to a state of equilibrium at day 30 with significantly diminished expression. Thus, the results suggest that HSP47 is actively involved in homeostasis of periodontal tissue subjected to occlusal overload.
Keywords: Occlusal trauma, Periodontal ligament, Immunohistochemistry, HSP47, Mouse