IADR Abstract Archives
Parathyroid Hormone Attenuates TMJ Osteoarthritis Through Regulating TGF-β Signaling Pathway
Objectives: The present study aimed to investigate the therapeutic effect of administration of parathyroid hormone (PTH) on osteoarthritis (OA) of the temporomandibular joint (TMJ) and to explore the role of TGF-β signaling pathway in this process.
Methods: Abnormal dental occlusion (ADO) was created in 8-week-old female SD rats, which were then treated with vehicle, TGF-β inhibitor, PTH. After 30 days, the temporomandibular joint was dissected and fixed. Condylar cartilage degeneration was graded using the Osteoarthritis Research Society International (OARSI) modified Mankin criteria. microCT (μCT) was performed to detect the change of microarchitecture in condylar subchondral bone of TMJ. Histology analysis was taken by HE staining, Sarfranin-O staining and TRAP staining. Immunostaining was conducted to detect relative protein expression.
Results: Condylar subchondral bone loss and cartilage degeneration were detected in TMJ of AOD rat model. And TGF-β signaling is abnormally increased in subchondral bone in response to altered mechanical loading. Inhibition of TGF-β activity reduced the subchondral bone lesions and degeneration of TMJ. Compared with vehicle-treated ADO controls , PTH-treated ADO substantially reduced the OARSI scores. PTH treatment increased the bone volume ratio, trabecular thickness (Tb.Th) ,bone mineral density (BMD) and reduced the trabecular separation (Tb.Sp) of condylar subchondral bone of TMJ OA rats. In parallel, PTH decreased matrix metalloproteinase-13,collagen X expression and increased Osterix, type-II collagen and aggrecan expression in the condylar. And we found that the expression of p-Smad 2/3 was decreased in subchondral bone of PTH-treated TMJ OA rats.
Conclusions: PTH exerted protective effects in part by suppressing Smad 2/3 dependent TGF-β signalling pathway in condylar subchondral bone as a potential preventive therapy for TMJ OA.
Methods: Abnormal dental occlusion (ADO) was created in 8-week-old female SD rats, which were then treated with vehicle, TGF-β inhibitor, PTH. After 30 days, the temporomandibular joint was dissected and fixed. Condylar cartilage degeneration was graded using the Osteoarthritis Research Society International (OARSI) modified Mankin criteria. microCT (μCT) was performed to detect the change of microarchitecture in condylar subchondral bone of TMJ. Histology analysis was taken by HE staining, Sarfranin-O staining and TRAP staining. Immunostaining was conducted to detect relative protein expression.
Results: Condylar subchondral bone loss and cartilage degeneration were detected in TMJ of AOD rat model. And TGF-β signaling is abnormally increased in subchondral bone in response to altered mechanical loading. Inhibition of TGF-β activity reduced the subchondral bone lesions and degeneration of TMJ. Compared with vehicle-treated ADO controls , PTH-treated ADO substantially reduced the OARSI scores. PTH treatment increased the bone volume ratio, trabecular thickness (Tb.Th) ,bone mineral density (BMD) and reduced the trabecular separation (Tb.Sp) of condylar subchondral bone of TMJ OA rats. In parallel, PTH decreased matrix metalloproteinase-13,collagen X expression and increased Osterix, type-II collagen and aggrecan expression in the condylar. And we found that the expression of p-Smad 2/3 was decreased in subchondral bone of PTH-treated TMJ OA rats.
Conclusions: PTH exerted protective effects in part by suppressing Smad 2/3 dependent TGF-β signalling pathway in condylar subchondral bone as a potential preventive therapy for TMJ OA.