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Chondrocytes are indispensable for the development, maintenance, and repair of the cartilaginous ECM. The components of articular cartilage are the extracellular matrix (ECM) with sparsely distributed specialized cells called chondrocytes, collagen fibers (mainly type II and IX), proteoglycans, water, and a small volume of non-collagenous proteins and glycoproteins such as fibronectin ( Sophia Fox et al., 2009).
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It coordinates with the synovial membrane and associated synovial fluid to bring about frictionless movement. Cartilage and Associated ComponentsĪrticular cartilage is a highly specialized connective tissue that ensures normal function and optimal load-bearing capacity ( Sophia Fox et al., 2009). OA is also a multifaceted disease based on recent findings that, apart from cellular and molecular mechanisms, inflammation, metabolic processes, and epigenetic modifications ( Shen et al., 2017) are involved in the pathogenesis and progression of the disease ( Blanco and Rego-Perez, 2014 Ishijima et al., 2014 Courties et al., 2015). Understanding of OA has progressed from what was regarded as a condition affecting articular cartilage to the concept that the disease process has broader consequences affecting all joint tissues, including the synovium and ligaments as well as the underlying subchondral bone ( Gupta et al., 2012 Barry and Murphy, 2013) and is characterized as a whole-joint disease. With the disease predominantly affecting the aging population, the impact of OA is set to increase exponentially in coming decades ( Kim et al., 2015). Osteoarthritis (OA) is the most common musculoskeletal disorder impacting life quality of patients with about 35–40 million Europeans and ~355 million affected worldwide ( Barry and Murphy, 2013 Mobasheri, 2013). This review also addresses key inflammatory factors in synovial inflammation, epigenetics, and chondrocyte fate, and how agents that inhibit epigenetic mechanisms like DNA methylation and histone modifications could aid in development of long-term treatment strategies for the disease.
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Data highlighted here have identified critical inflammatory genes involved in OA and how these factors impact chondrocyte hypertrophy in the disease. Studies conducted over the last decade have focused on three key aspects in OA inflammation and the immune response, genome-wide association studies that have identified important genes undergoing epigenetic modifications, and finally how chondrocytes transform in their function during development and disease. As well as a genetic input, recent data have highlighted epigenetic factors as contributing to disease. Synovial inflammation is also a pivotal element of the osteoarthritic, degenerative process: influx of pro-inflammatory cytokines and production of matrix metalloproteinases accelerate advanced cellular processes such as synovitis and cartilage damage. However, extrinsic factors such as injury to the joint or intrinsic alterations to the chondrocytes themselves can lead to an altered phenotype and development of OA. Chondrocytes, the cellular component of cartilage, reside in an avascular environment and normally have limited potential to replicate. Osteoarthritis (OA), a degenerative disease of diarthrodial joints, is influenced by mechanical and inflammatory factors with aging, obesity, chronic injuries, and secondary diseases thought to be major factors driving the process of articular cartilage degeneration.