Garciadiego CD

Language: Spanish
References: 91
Page: 7-17
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ABSTRACT

Articular cartilage unlike the growth plate cartilage, is a specialized tissue to keep uncalcified. However, the mineralization of articular cartilage is a common process in the osteoarthritis (OA) and aging complications. Some studies shows similarities in the mechanisms of growth plate differentiation and articular cartilage degeneration. These include chondrocyte proliferation, hypertrophy, extracellular matrix (ECM) mineralization and apoptosis. The growth plate development is regulated by certain growth factors signaling and interactions of chondrocytes with extracellular matrix molecules. Related Protein Parathyroid Hormone (PthrP) and Indian hedgehog (Ihh) are central mediators of endochondral bone development, PthrP is abundant in the synovial fluid of OA patients but decreased the expression of Ihh in the cartilage with OA . Furthermore, PthrP is known to induce the proliferation of chondrocytes, while the Fibroblast Growth Factor 18 (Fgf-18) negative regulates it and their application intra-synovial in OA rats results in the generation of cartilage. Wnt signaling plays an important role in the differentiation of chondrocyte growth plate, Wnt-5a promotes chondrocyte prehipertrofia but simultaneously inhibits cartilage hypertrophy, on the contrary Wnt-4 induces chondrocyte hypertrophy and from the early stages of OA increases its expression in the articular cartilage. Moreover, the imbalance of matrix turnover during the OA cartilage results in increased deposition of collagen type I and X characteristics of hypertrophic cartilage, while decreasing the expression of collagen type II and IX. That is, although the chondrocyte is the cellular unit of articular cartilage and growth plate that share several characteristics, have an important difference, the rate of chondrocyte hypertrophy is higher in OA articular cartilage, than in healthy articular cartilage and recapitulates the signaling of cartilage growth plate. But, what is the signal that makes the difference? We think the answer is in the embryonic origin of these two types of cartilage, right in the formation of joints for the skeletogenesis.

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