Abstract
Osteoarthritis (OA), the most common degenerative and inflammatory joint disorder, is multifaceted. Indeed, OA characteristics include cartilage degradation, osteophytes formation, subchondral bone changes, and synovium inflammation. The difficulty in discovering new efficient treatments for OA patients up to now comes from the adoption of monotherapy approaches targeting either joint tissue repair/catabolism or inflammation to address the diverse components of OA. When satisfactory, these approaches only provide short-term beneficial effects, since they only result in the repair and not the full structural and functional reconstitution of the damaged tissues. In the present review, we will briefly discuss the current therapeutic approaches used to repair the damaged OA cartilage. We will highlight the results obtained with cell-based products in clinical trials and demonstrate how the current strategies result in articular cartilage repair showing restricted early-stage clinical improvements. In order to identify novel therapeutic targets and provide to OA patients long-term clinical benefits, herein, we will review the basis of the regenerative process. We will focus on macrophages and their ambivalent roles in OA development and tissue regeneration, and review the therapeutic strategies to target the macrophage response and favor regeneration in OA.
Highlights
Osteoarthritis (OA) is the most common degenerative and inflammatory joint disorder
Cartilage homeostasis is insured by articular chondrocytes, which are quiescent and differentiated cells that maintain the balance between the catabolic and anabolic functions in healthy cartilage
Based on their biological properties and results obtained after intra-articular (IA) injection of murine mesenchymal stem/stromal cell (MSC) in experimental OA showing a reduced synovial thickening, osteophyte formation, and cartilage destruction, IA injection of MSC from various sources in OA patients was contemplated
Summary
Osteoarthritis (OA) is the most common degenerative and inflammatory joint disorder. The prevalence of OA is continuously increasing, so far no biological or pharmacological therapy exists to both control inflammation and restore joint tissue integrity. The main OA alterations appear progressively over time without a particular defined chronological order and include cartilage damage, osteophyte formation, subchondral bone remodeling, and a chronic low-grade inflammation (Chen et al, 2017). Cartilage homeostasis is insured by articular chondrocytes, which are quiescent and differentiated cells that maintain the balance between the catabolic and anabolic functions in healthy cartilage. In OA, chondrocytes respond to deleterious stresses by undergoing intrinsic modifications such as an abnormal production of the extracellular matrix (ECM) and an increased activity of proteolytic enzymes
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