Abstract
Kashin-Beck Disease (KBD) is an endemic, chronic and degenerative osteoarthropathy principally occurring in children. The characteristic pathological change of KBD is chondrocyte necrosis in hyaline articular cartilage. Proteoglycans are one of the major components in the extracellular matrix of articular cartilage, and disrupted proteoglycan metabolism and loss of proteoglycans in articular cartilage from KBD patients has been observed. In this mini-review, we discuss the close relationship between chondrocyte death including necrosis and loss of proteoglycan, and its potential mechanism during KBD onset and development, which may provide new clues for KBD research.
Highlights
Kashin-Beck Disease (KBD) is an endemic, chronic and degenerative osteoarthropathy affecting approximately 3 million people in China [1, 2]
A recent rat study in our lab has shown that the depletion of aggrecan induced by T-2 toxin and selenium deficiency was mainly localised to the focal areas where cell death occurred (Fig. 2), indicating a close relationship between PG loss and chondrocyte necrosis induced by mycotoxin
We investigated chondrocyte apoptosis in the articular cartilage from these experimental rats and found that it was selenium deficiency but not T-2 toxin that significantly induced cell apoptosis; there was no apparent correlation between the distribution of apoptotic chondrocytes and the localisation of aggrecan depletion
Summary
Kashin-Beck Disease (KBD) is an endemic, chronic and degenerative osteoarthropathy affecting approximately 3 million people in China [1, 2]. In contrast to PGs, mycotoxins did not significantly influence collagen metabolism in articular cartilage from these animal models, several recent in vitro studies have shown some mycotoxin-induced changes in type II collagen at gene and protein levels [51,52,53] This indicates that, similar with the other degenerative joint diseases such as OA, in KBD PGs are more vulnerable to loss and damage than the collagen networks, the causes of their initial stages of degradation may be different. A recent rat study in our lab has shown that the depletion of aggrecan induced by T-2 toxin and selenium deficiency was mainly localised to the focal areas where cell death occurred (Fig. 2), indicating a close relationship between PG loss and chondrocyte necrosis induced by mycotoxin. The related clinical trials on KBD patients are still ongoing
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