TMD in osteoporosis and occlusional disorder using animal model

Objectives: Aging and impaired occlusion caused by tooth loss may result in temporo-mandibular joint disorder or dysfunction (TMD). Both osteoporosis and osteoarthritis are belong to senile diseases characterized by decreasing bone mass and/or erosion of cartilage tissue on the surface of joint, and result higher risk for developing fractures and pain at joint sites. Although both diseases damage to cartilage tissue, the mechanisms remain poorly understood. Since Wnt/β-catenin signaling is essential for skeletal and cartilage tissue development included membranous and endochondral ossification, we studied its possible roles in TMD using senile model of rats through osteoporosis and senescence accelerated mice 8 (SAMP8). Methods: 10 weeks old Wistar rats (baseline control without operated, SHAM, and osteoporosis induced by operation of ovary extraction, OVX) and 4 weeks old SAMP8 mice with and without extraction of the bilateral molar teeth of maxilla were used. Animals were anesthetized and euthanized after experimental term with normally feeding, processed to histological analysis. We performed Hematoxylin/Eosin (HE), Safranin-O/Fast green (SF) staining and immunohistochemistry (IHC) for β-catenin. Results: In OVX rats, histological and immunohistochemical analysis revealed that fibrous layer of TMJ condylar head surface was thickened and their proliferating, prehypertrophic and hypertrophic layer chondrocytes were not well organized. In SAMP8 mice with teeth extracted, SF staining revealed that apparently decreasing of cartilage tissue chondrocytes and extracellular matrix. Immunohistochemically β-catenin of both animals localized in the prehypertrophic layer chonrocytes, and their number also was decreased. Conclusions: In this study, both OVX rats and SAMP8 cartilage prehypertrophic chondrocytes showed decreased number of β-catenin. Thus, Wnt/β-catenin signaling is an essential not only for bone formation but also in cartilage tissue of senile TMJ.