Abstract
The prevalence of arthritic diseases is increasing in developed countries, but effective treatments are currently lacking. The injection of mesenchymal stem cells (MSCs) represents a promising approach to counteract the degenerative and inflammatory environment characterizing those pathologies, such as osteoarthritis (OA). However, the majority of clinical approaches based on MSCs are used within an autologous paradigm, with important limitations. For this reason, allogeneic MSCs isolated from cord blood (cbMSCs) and Wharton’s jelly (wjMSCs) gained increasing interest, demonstrating promising results in this field. Moreover, recent evidences shows that MSCs beneficial effects can be related to their secretome rather than to the presence of cells themselves. Among the trophic factors secreted by MSCs, extracellular vesicles (EVs) are emerging as a promising candidate for the treatment of arthritic joints. In the present review, the application of umbilical cord MSCs and their secretome as innovative therapeutic approaches in the treatment of arthritic joints will be examined. With the prospective of routine clinical applications, umbilical cord MSCs and EVs will be discussed also within an industrial and regulatory perspective.
Highlights
Arthritic diseases include different pathologies, such as rheumatoid arthritis (RA), a chronic inflammatory disorder mainly driven by autoimmune reactions
Osteoarthritis (OA), the most common arthritic disease, is a degenerative joint disease causing a progressive degradation of articular cartilage and subchondral bone [2], both leading to a significant loss of joint function, heavily affecting the patient’s quality of life
The same decrease was observed in OA chondrocytes after cocultures with wjMSCs [41]. These results suggest a protective effect of wjMSCs on damaged chondrocytes and have been confirmed in vivo, whereby the injection of wjMSCs in rat models of OA showed reduced secretions of cartilage-degrading enzymes [42], inflammatory cytokines [43], increased cartilage matrix production and decreased chondrocyte apoptosis [44]
Summary
Arthritic diseases include different pathologies, such as rheumatoid arthritis (RA), a chronic inflammatory disorder mainly driven by autoimmune reactions. Genetic predisposition is at the basis of its development, while other genetic and environmental cues contribute to its clinical onset, characterized by a proinflammatory and degenerative synovial response, inducing joint inflammation, pain and disability [1]. Osteoarthritis (OA), the most common arthritic disease, is a degenerative joint disease causing a progressive degradation of articular cartilage and subchondral bone [2], both leading to a significant loss of joint function, heavily affecting the patient’s quality of life. OA is characterized by a multifactorial etiology, including idiopathic, genetic, metabolic, inflammatory factors and joint traumas. All these predisposing factors lead to the establishment of a positive proinflammatory feedback among articular cells, associated to chondrocytes metabolic imbalance and causing.
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