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Review
. 2023 Oct;31(10):1303-1311.
doi: 10.1016/j.joca.2023.06.005. Epub 2023 Jun 21.

Fundamentals of osteoarthritis: Inflammatory mediators in osteoarthritis

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Free article
Review

Fundamentals of osteoarthritis: Inflammatory mediators in osteoarthritis

Astrid De Roover et al. Osteoarthritis Cartilage. 2023 Oct.
Free article

Abstract

Objectives: As more has become known of the pathophysiology of osteoarthritis (OA), evidence that inflammation plays a critical role in its development and progression has accumulated. Here, we aim to review current knowledge of the complex inflammatory network in the OA joint.

Design: This narrative review is presented in three main sections: local inflammation, systemic inflammation, and therapeutic implications. We focused on inflammatory mediators and their link to OA structural changes in the joint.

Results: OA is characterized by chronic and low-grade inflammation mediated mostly by the innate immune system, which results in cartilage degradation, bone remodeling and synovial changes. Synovitis is regarded as an OA characteristic and associated with increased severity of symptoms and joint dysfunction. However, the articular cartilage and the subchondral bone also produce several pro-inflammatory mediators thus establishing a complex interplay between the different tissues of the joint. In addition, systemic low-grade inflammation induced by aging, obesity and metabolic syndrome can contribute to OA development and progression. The main inflammatory mediators associated with OA include cytokines, chemokines, growth factors, adipokines, and neuropeptides.

Conclusions: Future research is needed to deeper understand the molecular pathways mediating the inflammation in OA to provide new therapeutics that target these pathways, or to repurpose existing drugs.

Keywords: Adipokines; Cartilage; Cytokines; Inflammation; Osteoarthritis; Synovium.

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Conflict of interest statement

Conflict of interest Leuven Research and Development, the technology transfer office of KU Leuven, has received consultancy and speaker fees and research grants on behalf of R.J.L. from Abbvie, Boehringer-Ingelheim, Amgen (formerly Celgene), Eli-Lilly, Galapagos, Janssen, Fresenius Kabi, MSD, Novartis, Pfizer, Biosplice Therapeutics (formerly Samumed) and UCB. The other authors declare that they have no competing financial interests.

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