The Animal Model And Study On The Pathomechanism Of Temporomandibular Jonit Osteoarthrosis

Temporomandibular joint osteoarthrosis is a progressive noninfective disease, which is one of the most common forms of temporomandibular disorders. It includes sterile and chronic synovitis, the formation of pannus and the degeneration of cartilage and bone of condyloid. The disease can not been found easily in the initial stage. All kinds of therapy were used, but the effect is not satisfied. With the development of arthroendoscope, people have got more knowledge about histopathologic changes of OA. However, the questions of etiopathogenisis, pathomechanism and therapy methods of osteoarthrosis remain a point of controversy.It is available and effective to set up animal models for studying temporomandibular joint osteoarthrosis. In the experiment, eighteen adult New Zealand rabbits were used. We drilled two holes in right head of rabbit, one in the posterior part of the zygomatic arch (upper jaw) and the other in the anterior edge of the masseter tuberosity (lower jaw). A wire was passedthrough the holes, and a spring with a force was applied to initiate postero-superior displacement of the mandible. These rabbits were killed at 1,2,3,4 and 6 weeks after operation respectively. Then the histopathologic change on the TMJ was observed through hematoxylin and eosin stain and Alcian blue stain. In the early stage of post-operation, we can find the chondrocyte clusters forming and the extracellular matrix of cartilages being changed. And in the late one, articular cartilage splitting, osteophyte were observed, subchondralbone and calcified cartilage became irregular. There were synovitis and degeneration of articular disk in most temporomandibular joint of operated animals. These changes are the same as people's, which prove the OA animal model made through unilateral backward-upward mandible traction is successful.Parathyroid hormone-related protein (PTHrP) is a peptide which was first identified because of its biologic effects in the setting of malignancy. When produced in prodigious amounts by tumors, PTHrP, by virtue of its ability to bind to and activate the G protein-coupled PTH/PTHrP receptor in bone, is the humoral factor responsible for marked bone resorption and hypercalcemia in this setting. However, in the absence of malignancy, PTHrP is produced in many organs, where it acts locally, rather than systemically. More recently, PTHrP has also been identified as a member of the cytokines during the destruction and reparation of articular cartilage.We found that PTHrP expressed all layers chondrocytes plasm of articular cartilage including surface fiber layer, proliferation cell layer, hypertrophy cell layer and calcified cartilage layer , and in surface fiber layer, proliferation cell layer, upper hypertrophy cell layer stronger in theearly TMJOA. And it express weaker in mid stage, but stronger near the chondrocyte clusters and the proliferating chondrocyte in the disk stronger. But in the synovial membrane, PTHrP expressed in extracellular matrix. It is suggested that PTHrP as an autocrine or paracrine cytokine can regulate the reparation of articular cartilage. This mechanism is possibly the same as the enchondral bone formation.Based on these findigs, our study provide a scientific and reasonable animal model for TMJOA and investigate the regulation mechanism of PTHrP in the reparation of articular cartilage, however, the details in the pathway need more work to solve it.