Abstract
Cartilage repair tissue is usually accompanied by chondrocyte hypertrophy and osseous overgrowths, and a role for parathyroid hormone-related protein (PTHrP) in inhibiting chondrocytes from hypertrophic differentiation during the process of endochondral ossification has been demonstrated. However, application of PTHrP in cartilage repair has not been extensively considered. This review systemically summarizes for the first time the inhibitory function of PTHrP on chondrocyte hypertrophy in articular cartilage and during the process of endochondral ossification, as well as the process of mesenchymal stem cell chondrogenic differentiation. Based on the literature review, the strategy of using PTHrP for articular cartilage repair is suggested, which is instructive for clinical treatment of cartilage injuries as well as osteoarthritis.
Highlights
Articular cartilage injuries and osteoarthritis (OA) are commonly encountered in joint diseases
This review presents, compares and discusses the inhibitory function of parathyroid hormone-related protein (PTHrP) on chondrocyte hypertrophy in articular cartilage and during the process of endochondral ossification, as well as the process of mesenchymal stem cell (MSC) chondrogenic differentiation
Mizuta and colleagues [24] demonstrated that a 2-week treatment with PTHrP for fullthickness articular cartilage defects resulted in successful regeneration, while a 4-week treatment resulted in an inferior repair, the effect on hypertrophy inhibition in repair tissue was not assessed in this study
Summary
Articular cartilage injuries and osteoarthritis (OA) are commonly encountered in joint diseases. This review presents, compares and discusses the inhibitory function of PTHrP on chondrocyte hypertrophy in articular cartilage and during the process of endochondral ossification, as well as the process of MSC chondrogenic differentiation. The normal articular chondrocytes enter hypertrophic differentiation, resembling the process of endochondral bone formation [11,12], which can cause the upper cartilage to become calcified and a relatively thin repair tissue to be formed [1,9].
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