Sakata, Kenichiro Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Furumatsu, Takayuki Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Miyazawa, Shinichi Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Okada, Yukimasa Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Fujii, Masataka Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Ozaki, Toshifumi Okayama Univ, Dept Orthopaed Surg, Grad Sch Med Dent & Pharmaceut Sci
Loose fragments in osteochondritis dissecans (OCD) of the knee require internal fixation. On the other hand, loose fragments derived from spontaneous osteonecrosis of the knee (SONK) are usually removed. However, the difference in healing potential between OCD- and SONK-related loose fragments has not been elucidated. In this study, we investigated proliferative activity and redifferentiation potential of normal cartilage-derived and loose fragment-derived chondrocytes. Cells were prepared from normal articular cartilages and loose fragment cartilages derived from knee OCD and SONK. Cellular proliferation was compared. Redifferentiation ability of pellet-cultured chondrocytes was assessed by real-time PCR analyses. Mesenchymal differentiation potential was investigated by histological analyses. Positive ratio of a stem cell marker CD166 was evaluated in each cartilaginous tissue. Normal and OCD chondrocytes showed a higher proliferative activity than SONK chondrocytes. Chondrogenic pellets derived from normal and OCD chondrocytes produced a larger amount of safranin O-stained proteoglycans compared with SONK-derived pellets. Expression of chondrogenic marker genes was inferior in SONK pellets. The CD166-positive ratio was higher in normal cartilages and OCD loose fragments than in SONK loose fragments. The OCD chondrocytes maintained higher proliferative activity and redifferentiation potential compared with SONK chondrocytes. Our results suggest that chondrogenic properties of loose fragment-derived cells and the amount of CD166-positive cells may affect the repair process of osteochondral defects.
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