Abstract: Objective：To evaluate the effect of chondrocyte mitochondrial dysfunction on the development of cartilage degeneration. Methods: In the study, 10 cartilage samples of the knee joint were collected during total knee arthroplasty surgery because of OA from April to October of 2012 in Peking University First Hospital. All the tissues were taken from transmission electron microscope (TEM) observation grouped by Outerbridge classification. Then, TEM observation, quantitative detection of mitochondrial respiratory chain enzyme complex 1,2,2+3,4 and ATPase activity, detection of the mitochondrial membrane potential by JC-1 method were taken with cultured normal and OA chondrocytes. Healthy chondrocytes from 10 normal cartilage samples were divided into 2 groups: the normal control group and rotenone group. The ultrastuctrure alterations of mitochondria, mitochondrial membrane potential, apoptosis rate and collagen Ⅱ content were compared. Results: With the aggravation of cartilage degeneration, mitochondria swelling, outer membrane rupture, cristae destruction and disappearance were observed in both the tissue and cell TEM examinations. JC-1 staining showed a decreased membrane potential in OA chondrocytes which had a lower red/green fluorescence ratio of 1.50 than that of the normal chondrocytes of 2.58. mitochondrial respiratory chain (MRC) enzyme complex 1,2,2+3,4 and ATPase activity of the OA chondrocytes also represented a decreased tendency compared with the normal chondrocytes although the difference was not significant (P=0.109,0.197,0.098,0.169,0.145). The mitochondria in the Ro group cells showed OA-like changes morphologically by TEM detection. JC-1 staining showed a decreased mitochondrial membrane potential in the Ro group chondrocytes which had a lower red/green fluorescence ratio of 1.78 than that of the normal ones of 2.58. Apoptosis examination represented a higher apoptosis rate of 7.53% in the Ro group chondrocytes than that of the normal ones of 4.38%. Collagen Ⅱ content of the chondrocytes in the Ro group was (44.63±7.11) μg/L , significantly lower than (72.88±24.3) μg/L in the control group (P=0.044). Conclusion: Mitochondrial function is impaired in OA chondrocyte. Mitochondrial function destruction results in an increased chondrocyte apoptosis rate and a decreased collagen Ⅱ secretion.

Key words: Osteoarthritis, Chondrocytes, Mitochondria, Rotenone