Initiation and progression of dental-stimulated temporomandibular joints osteoarthritis

Temporomandibular joint (TMJ), a site that is often impacted by osteoarthritis (OA), is biomechanically linked with dental occlusion. Tissue responses in TMJ condyle to biomechanical stimulation could be investigated by intervention of the dental occlusion in animals. Unilateral anterior crossbite, an experimental malocclusion, has been demonstrated to induce TMJ-OA lesions, showing primarily as enhanced cartilage calcification and subchondral cortical bone formation at the osteochondral interface, causing the osteochondral interface thickening and stiffening. The changed interface would worsen the local biomechanical environment. At the cartilage side, the matrix degenerates. In the case of insufficient restoration of the matrix, the cells in the deep zone flow into the ones undergoing autophagy, apoptosis, and terminal differentiation while the cells in the superficial zone are promoted to differentiate to supply the loss of the deep zone cells. At the meantime, the bone marrow stromal cells are stimulated to bone formation in the subchondral cortical region which is uncoupled with the sites of the osteoclast-mediated resorption process that is predominantly observed at the subchondral trabecular bone region. Overall, the thickening and stiffening osteochondral interface, due greatly to the enhanced endochondral ossification in deep zone cartilage, should be a central pathological process that links with cartilage decay and subchondral bone remodelling in OA joints. The residual chondrocytes locating in the cartilage superficial zone have the progenitor-like qualities that can proliferate, and also differentiate into the deep zone chondrocytes, thus should be critical in progression and rehabilitation of TMJ-OA. ? 2021 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

Automated summary

Research indicates that malocclusion can induce TMJ-OA lesions, resulting in enhanced cartilage calcification and subchondral cortical bone formation, leading to thickening and stiffening of the osteochondral interface, which worsens the local biomechanical environment.