Abstract
Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. This issue arises, in part, due to the complex processes occurring in the microenvironment of articular cartilage that lead to osteoarthritic changes. Gaining a better understanding of these processes is crucial in developing a viable therapy for OA. A recent report in Journal of Bone Mineral Metabolism by Janune et al. (J Bone Miner Metab 35:582–597, 2016) suggests a novel role for CCN3 in maintaining the differentiated phenotype of articular cartilage. This report suggests that CCN3, a member of the CCN family of matricellular proteins, is important for proteoglycan accumulation, as well as expression of type II collagen, tenascin C, and lubricin in vitro. Furthermore, exogenous CCN3 increased tidemark integrity and lubricin protein expression in a rat model of OA. These results implicate the regulation of CCN3 as a potential therapeutic target in patients with OA.
Highlights
Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist
It has been shown that osteoarthritic changes occur in articular cartilage of mice lacking CCN3 protein, suggesting that CCN3 may play a role in the underlying mechanisms of OA pathogenesis (Roddy and Boulter 2015)
The authors aimed to investigate the reciprocal regulation of CCN3 during osteoarthritic changes in a monoiodoacetic acid (MIA)-induced model of OA, as well as evaluate the in vitro effects of CCN3 overexpression on articular chondrocytes
Summary
Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. Phases of osteoarthritis (OA) development often involve re-initiation of endochondral ossification, a process that occurs in embryos and children but ceases into adulthood, resulting in degradation of articular cartilage and osteophyte formation (Saito et al 2010). There is a lack of information on factors governing the regulatory processes that maintain the healthy articular cartilage phenotype, as well as factors that cause re-initiation of endochondral ossification in osteoarthritic cartilage.
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