Mechanism Research Of Osteotendinous Junction Injury Induced By Different Exercise Intensity

Purpose:Osteolendinous junction injures are common clinical problems for both athletes'training and recreational individuals common life. Overuse is a main cause of osteotendinous junction injuries. But the pathogenesis is poorly understood. The extracellular matrix has played an important role in resisting mechanical forces and restoration following injury. The purposes of this study are to elucidate the carly structural, cellular, and molecular changes in the osteotendinous junction following exposure to cyclic loading. It reveals the injury mechanisms and evaluates the dose of load required to induce an injury with the cyclic loading in vivo.Method:Forty-eight New Zealand rabbits were divided into6groups with eight rabbits per group. One group was the control; the others were electrically simulated to contract repetitively for2hours per day,3days a week.30%of peak titanic force was the100%cyclic loading group, other groups were simulated at20%,40%,60%,80%of this force respectively and defined as L20, L40, L60, L80. After4weeks, samples were used for haematoxyl i ne and eosion and immunohistochenii stry of major proteoglyeans and collagens and growth factor.Results:There were considerable differences in morphology between control group and cyclic loading groups. An increase in tendon cell density was observed in high loading groups after4-week cycl ic loading. The thickness of fibrocartilage and the expression of aggrecan were unaffected by four-week cyclic loading. The expression of collagen type III increased in the60%to100%cyclic loading groups compared to the control,20%, and40%cyclic loading groups. Tenascin-C decreased at60%cyclic loading, and increased at80%and100%cyclic loading comparing to the control,20%,40%cyclic loading groups respectively. The expression of TGF increased from20%to100%cyclic loading. The correlation coefficient analysis showed the cell density has strong correlation to the collagen type III and TGF respectively (R=0.46,0.71). There are moderate correlations in TGF and collagen type III and Tenascin-C (R=0.43,0.36)Conclusion:1. The considerable pathological changes in L60, L80, L100groups after4-week cyclic loading indicating this low-intensity cyclic loading can induce the injury of osteotendinous junction.2. The changes of morphological structure and composition with increasing exercise intensity elucidates the degree of osteotendinous junction injury is directly related to the intensity of exercise.3. The collagen type III and Tenasin-C have increased significantly and demonstrates that the extracellular matrix plays an important role during the osteotendinous junction injury process.4. TGF has increased significantly and is correlated to the collagen type III and Tenascin-C. This indicates TGF is an important regulating factor during the osteotendinous junction injures process.