Journal
OSTEOARTHRITIS AND CARTILAGE
Volume 12, Issue 7, Pages 586-596Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.joca.2004.04.008
Keywords
osteochondral defect; chondrogenic repair; fibroblast growth factor
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Objectives: In full-thickness articular defects, fibroblast growth factor-2 (FGF-2) participates in the chondrogenic repair response which occurs in a defect-size dependent manner. Here we demonstrate that FGF-2 plays a critical role in the proliferation of pre-chondrogenic mesenchymal cells during chondrogenic induction. Methods: Three-millimeter- or 5-mm-diameter cylindrical defects were created in the femoral trochlea of the rabbit knee. The defects received sterile saline or FGF-2 (50 pg/h) via an osmotic pump for the initial 2 weeks. We assessed the proliferative capacity of undifferentiated mesenchymal cells in the reparative tissue with the anti-proliferating cell nuclear antigen (PCNA) monoclonal antibody. Using a total of 180 rabbits, we performed three sets of experiments. Results: In the 3-mm-diameter defects, undifferentiated mesenchymal cells spontaneously initiated chondrogenic differentiation within 2 weeks, resulting in the regeneration of surfacing articular cartilage concomitantly with the repair of subchondral bone. No evidence of chondrogenesis was seen in the 5-mm-diameter defects, whereas application of FGF-2 promoted successful regeneration of articular cartilage. In the 3-mm-diameter defects and in the FGF-2-treated 5-mm defects, PCNA immunoreactivity was widely detected in undifferentiated cells in the reparative tissue at 1 and 2 weeks after creation of the defects. In contrast, in the 5-mm-diameter defects without FGF-2 treatment, the PCNA-positive cells were found at a significantly lower incidence. Conclusions: Active expansion of undifferentiated cell population mediated by FGF-2 is required to initiate and support a chondrogenic repair response in full-thickness defects of articular cartilage. Endogenous FGF-2 could not meet the requirements of growth signaling in the center of larger sized defects. (C) 2004 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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