Intra-articular autologous uncultured adipose-derived stromal cell transplantation inhibited the progression of cartilage degeneration.

The role of uncultured adipose-derived stromal cells for osteoarthritis treatment remains unclear despite sporadic reports supporting their use in clinical settings. This study aimed to evaluate the therapeutic effects of autologous uncultured adipose-derived stromal cell transplantation in a rabbit osteoarthritis model. Uncultured adipose-derived stromal cells isolated from rabbits were administered via intra-articular injection into the knees after osteoarthritis onset. Animals were sacrificed at 8 and 12 weeks after osteoarthritis onset to compare the macroscopic, histological, and immunohistochemical characteristics between the uncultured adipose-derived stromal cell and control groups. Co-culture assay was also performed. The chondrocytes isolated from the model were co-cultured with adipose-derived stromal cells. The cell viability of chondrocytes and expression of chondrocyte-specific genes in the co-culture (uncultured adipose-derived stromal cell) group were compared with the mono-culture (control; chondrocytes only) group. In macroscopic and histological analyses, the uncultured adipose-derived stromal cell group showed less damage to the cartilage surface than the control group at 8 and 12 weeks after osteoarthritis onset. In immunohistochemical and co-culture assay, the uncultured adipose-derived stromal cell group showed higher expression of collagen type II and SRY box-9 and lower expression of matrix metalloproteinase-13 than the control group. The cell viability of chondrocytes in the uncultured adipose-derived stromal cell group was higher than that in the control group. Intra-articular autologous uncultured adipose-derived stromal cell transplantation inhibited the progression of cartilage degeneration in a rabbit osteoarthritis model by regulating chondrocyte viability and secreting chondrocyte-protecting cytokines or growth factors, which promote anabolic factors and inhibit catabolic factors. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.