Effect of load reduction on the calcification of rat tibial tuberosity: Focus on calcification factors and chondrocyte mechanosensors

Abstract

Abstract The tibial tuberosity has a superficial patellar tendon-embedded portion and a deep uncalcified cartilage portion. Osgood–Schlatter disease occurs because of suppressed calcification of the tibial tuberosity. The tibial tuberosity calcifies with aging, and load reduction degrades the cartilage matrix and promotes calcification. This suggests that reducing mechanical stimulation of the tibial tuberosity promotes calcification; however, this is yet to be clarified. Therefore, we aimed to investigate the effects of mechanical stimulation reduction on the tibial tuberosity tissue structure and calcification mechanism. We examined the effect of load reduction on tibial tuberosity calcification in 20 male 7-week-old Wistar rats classified into two groups: hind-limb suspension (HS, n = 10) and control (CO, n = 10). We observed superficial and deep tibial tuberosities in both groups. The tibial tuberosity in the HS group had narrower areas of deep portions than those in the CO group (p = 0.000539), and immature bone tissue was observed in addition to cartilage tissue. Enpp1 expression did not differ significantly between the groups (p = 0.804). In contrast, Alpl (p = 0.001) and Mmp3 (p = 0.006)expression in HS increased, whereas Timp3expression decreased (p = 0.002). This gene expression was similar to that in a murine join instability model of osteoarthritis with articular cartilage calcification and ossification. The HS tibial tuberosity also showed immature bone tissue. In conclusion, reduced mechanical stimulation caused tibial tuberosity calcification and pathological changes. These findings highlight the importance of optimal exercise to avoid premature pathological structural changes in bones/joints.