Using a model of experimental occlusal trauma in mice, we investigated cytological kinetics of periodontal ligament by means of histopathological, immunohistochemical, and photographical analysis methods. Periodontal ligament cells at furcation areas of molar teeth in the experimental group on day 4 showed a proliferation tendency of periodontal ligament cells. The cells with a round-shaped nucleus deeply stained the hematoxylin and increased within the day 4 specimens. Ki67 positive nuclei showed a prominent increase in the group on days 4 and 7. Green Fluorescent Protein (GFP) positivity also revealed cell movement but was slightly slow compared to Ki67. It indicated that restoration of mechanism seemed conspicuous by osteoclasts and macrophages from bone-marrow-derived cells for the periodontal ligament at the furcation area. It was suggested that the remodeling of periodontal ligament with cell acceleration was evoked from the experiment for the group on day 4 and after day 7. Periodontal ligament at the furcation area of the molar teeth in this experimental model recovered using the cells in situ and the bone-marrow-derived cells.

The aim of this study was to establish a model, which can be used to investigate the response of periodontal tissues to excessive occlusal loading in mice by observing histopathological changes. The experiment was performed on ten 7-week-old ddY male mice. Under general anesthesia by intraperitoneal injection pentobarbital sodium, a micro-plus-screwpin (head part, 1.7mm in diameter, thickness 0.5mm thickness) was screwed into the pulp cavity of the upper-left-first molar. R_mCT images of the experimental site indicated the occlusal contact position between the upper-and lower-left-first molars during the experimental periods. A micro-plus-screwpin was maintained at a constant position on the occlusal surface throughout the experimental period. Histopathological changes of the periodontal ligament at the furcation lesion of the lower-left-first molar and its surrounding periodontal tissues were observed under a light microscope. The densities of deeply dyeing cells in hematoxylin staining with a round-shaped nucleus were increased in the periodontal ligament, with a peak effect of day 4. Multinucleated giant cells appeared in the central lesion of the periodontal ligament on day 7. The distribution of resorption on the surface of both of the cementum and the alveolar bone was accompanied by multinucleated giant cells, which expanded rapidly from day 7 to day 14. These results showed that histopathological changes of periodontal tissues to excessive occlusal load were observed at the furcation area of molar teeth. The present method confirmed the effectiveness of the experimental model to examine the occlusal trauma on periodontal tissues produced by excessive occlusal load.

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.

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