Abstract

Degenerative disorders of joints, especially osteoarthritis (OA), result in persistent pain and disability and high costs to society. Nevertheless, the molecular mechanisms of OA have not yet been fully explained. OA is characterized by destruction of cartilage and loss of extracellular matrix (ECM). It is generally agreed that there is an association between pro-inflammatory cytokines and the development of OA. There is increased expression of matrix metalloproteinase (MMP) and “a disintegrin and metalloproteinase with thrombospondin motifs” (ADAMTS). Mesenchymal stem cells (MSCs) have been explored as a new treatment for OA during the last decade. It has been suggested that paracrine secretion of trophic factors, in which exosomes have a crucial role, contributes to the mechanism of MSC-based treatment of OA. The paracrine secretion of exosomes may play a role in the repair of joint tissue as well as MSC-based treatments for other disorders. Exosomes isolated from various stem cells may contribute to tissue regeneration in the heart, limbs, skin, and other tissues. Recent studies have indicated that exosomes (or similar particles) derived from MSCs may suppress OA development. Herein, for first time, we summarize the recent findings of studies on various exosomes derived from MSCs and their effectiveness in the treatment of OA. Moreover, we highlight the likely mechanisms of actions of exosomes in OA.

Highlights

  • Osteoarthritis (OA), one of the most common musculoskeletal diseases, is characterized by sub-chondral bone sclerosis, synovial inflammation, cartilage degradation, ligament calcification, and osteophyte formation [1, 2]

  • Exosomes carry out many different functions in organisms that include repair of tissue injuries, regulation of immune response, and inhibition of inflammation

  • Different disease models have been studied in Mesenchymal stem cells (MSCs)-derived exosome experiments

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Summary

Introduction

Osteoarthritis (OA), one of the most common musculoskeletal diseases, is characterized by sub-chondral bone sclerosis, synovial inflammation, cartilage degradation, ligament calcification, and osteophyte formation [1, 2].

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