Abstract

Osteoarthritis is a common cause of disability worldwide. Although commonly referred to as a disease of the joint cartilage, osteoarthritis affects all joint tissues equally. The pathogenesis of this degenerative process is not completely understood; however, a low-grade inflammation leading to an imbalance between anabolic and katabolic processes is a well-established factor. The complex network of cytokines regulating these processes and cell communication has a central role in the development and progression of osteoarthritis. Concentrations of both proinflammatory and anti-inflammatory cytokines were found to be altered depending on the osteoarthritis stage and activity. In this review, we analyzed individual cytokines involved in the immune processes with an emphasis on their function in osteoarthritis.

Highlights

  • Osteoarthritis (OA) is the most common musculoskeletal condition and the largest cause of disability in the world [1]

  • The aim of this review was to describe the mechanisms of action of the most important cytokines and chemokines involved in OA pathogenesis, with emphasis on knee OA

  • The pathogenesis of OA is largely determined by the imbalance of proinflammatory and anti-inflammatory mediators, leading to low-grade inflammation, which is responsible for cartilage degradation, bone remodeling and synovial proliferation [181]

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Summary

Introduction

Osteoarthritis (OA) is the most common musculoskeletal condition and the largest cause of disability in the world [1]. The most important inflammatory mediators in the pathogenesis of OA are IL-1β, TNF-α and IL-6 They are activators of a plethora of different signaling pathways that activate other cytokines and pathologic processes. Part of this unstoppable process are chemokines that, stimulated by cytokines, attract inflammatory cells to the joint that further promote the secretion of inflammatory factors and disease progression [5]. The aim of this review was to describe the mechanisms of action of the most important cytokines and chemokines involved in OA pathogenesis, with emphasis on knee OA

Proinflammatory Cytokines
Anti-Inflammatory Cytokines
Chemokines
Findings
Conclusions
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