Transplantation of dedifferentiated fat cell-derived micromass pellets contributed to cartilage repair in the rat osteochondral defect model.

BACKGROUND: Mature adipocyte-derived dedifferentiated fat (DFAT) cells possesses the ability to proliferate effectively and the potential to differentiate into multiple linages of mesenchymal tissue; similar to adipose-derived stem cells (ASCs). The purpose of this study is to examine the effects of DFAT cell transplantation on cartilage repair in a rat model of osteochondral defects. METHODS: Full-thickness osteochondral defects were created in the knees of Sprague-Dawley rats bilaterally. Cartilage-like micromass pellets were prepared from green fluorescent protein (GFP)-labeled rat DFAT cells and subsequently transplanted into the affected right knee of these rats. Defects in the left knee were used as a control. Macroscopic and microscopic changes of treated and control defects were evaluated up to 12 weeks post-treatment with DFAT cells. To observe the transplanted cells, sectioned femurs were immunostained for GFP and type II collagen. RESULTS: DFAT cells formed micromass pellets expressing characteristics of immature cartilage in vitro. In the DFAT cell-transplanted limbs, the defects were completely filled with white micromass pellets as early as 2 weeks post-treatment. These limbs became smooth at 4 weeks. Conversely, the defects in the control limbs were still not repaired by 4 weeks. Macroscopic ICRS scores at 2 and 4 weeks were significantly higher in the DFAT cells-transplanted limbs compared to those of the control limbs. The modified O'Driscol histological scores for the DFAT cell-transplanted limbs were significantly higher than those of the control limbs at corresponding time points. GFP-positive DAFT cells were detected in the transplanted area at 2 weeks but hardly visible at 12 weeks post-operation. CONCLUSIONS: Transplantation of DFAT cell-derived micromass pellets contribute to cartilage repair in a rat osteochondral defect model. DFAT cell transplantation may be a viable therapeutic strategy for the repair of osteochondral injuries.

Effect of increased iliotibial band load on tibiofemoral kinematics and force distributions: a direct measurement in cadaveric knees.

STUDY DESIGN: Controlled laboratory study using cadaveric knee specimens and a repeated-measures design. OBJECTIVES: To investigate the effect of increased iliotibial band load (assumed to represent increased tensor fascia latae and gluteus maximus strength) on tibiofemoral kinematics and force distribution on the tibiofemoral articulation. BACKGROUND: Owing to the difficulty in measuring in vivo joint loading, there is limited evidence on the direct relationship between increased iliotibial band load and force distribution in the tibiofemoral articulation. METHODS: Eight fresh-frozen cadaveric knee specimens were used in this study. A robotic testing system assessed tibiofemoral kinematics under 3 simulated loading conditions: (1) 300-N quadriceps load, 100-N hamstrings load, 0-N iliotibial band load; (2) 300-N quadriceps load, 100-N hamstrings load, 50-N iliotibial band load; and (3) 300-N quadriceps load, 100-N hamstrings load, 100-N iliotibial band load. The load distribution in the medial and lateral tibiofemoral articulation was also measured under these loading conditions by using piezoelectric pressure sensors. Data were collected and analyzed at full extension and at 5°, 10°, 15°, 20°, 25°, and 30° of knee flexion. RESULTS: The loads transmitted through the medial tibiofemoral articulation significantly decreased when the load on the iliotibial band was increased, with a concomitant significant increase in lateral tibiofemoral articulation load. Greater iliotibial band load also increased anterior tibial translation and valgus tibial rotation, and decreased the amount of internal tibial rotation and medial tibial translation. CONCLUSION: The present study demonstrated that an increase in iliotibial band load, when tested in a non-weight-bearing condition in a cadaveric model, can significantly decrease the loads transmitted through the medial tibiofemoral articulation.

Osteogenic effects of dedifferentiated fat cell transplantation in rabbit models of bone defect and ovariectomy-induced osteoporosis.

We have previously reported that mature adipocyte-derived dedifferentiated fat (DFAT) cells have a high proliferative activity and the potential to differentiate into lineages of mesenchymal tissue similar to bone marrow mesenchymal stem cells (MSCs). In the present study, we examined the effects of autologous DFAT cell transplantation on bone regeneration in a rabbit bone defect model and an ovariectomy (OVX)-induced osteoporosis model. The formation of tissue-engineered bone (TEB) was observed when rabbit DFAT cells were loaded onto a ß-tricalcium phosphate (TCP)/collagen sponge and cultured in an osteogenic differentiation medium for 3 weeks. Autologous implantation of DFAT cell-mediated TEB constructs promoted bone regeneration in a rabbit tibial defect model. Regenerated bone tissue induced by transplantation of DFAT cell-mediated TEB constructs was histologically well differentiated and exhibited higher bone strength in a three-point bending test compared to that induced by the ß-TCP/collagen sponge alone. In OVX-induced osteoporosis model rabbits, DFAT cells were obtained with the osteogenic activity similar to cells from healthy rabbits. Intrabone marrow injection of autologous DFAT cells significantly increased the bone mineral density (BMD) at the injected site in the OVX rabbits. Transplanted DFAT cells remained mainly on the injection side of the bone marrow by at least 28 days after intrabone marrow injection and a part of them expressed osteocalcin. In conclusion, these results demonstrate that autologous implantation of DFAT cells contributed to bone regeneration in a rabbit bone defect model and an OVX-induced osteoporosis model. DFAT cells may be an attractive cell source for cell-based bone tissue engineering to treat nonunion fractures in all patients, including those with osteoporosis.