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Smith, M.D., Barg, E., Weedon, H., Papengelis, V., Smeets, T., Tak, P.P., et al. (2003) Microarchitecture and Protective Mechanisms in Synovial Tissue from Clinically and Arthroscopically Normal Knee Joints. Annals of the Rheumatic Diseases, 62, 303-307.
https://doi.org/10.1136/ard.62.4.303

has been cited by the following article:

• TITLE: The Role of Macrophage Polarization in OA: Insights for a Successful Strategy

  AUTHORS: Molly Milano, Daniel Grande

  KEYWORDS: Osteoarthritis, Macrophage Transition, Joint, Orthopaedics

  JOURNAL NAME: Open Journal of Regenerative Medicine, Vol.15 No.1, March 31, 2026

  ABSTRACT: Introduction: Osteoarthritis (OA) is the most prevalent joint pathology worldwide. OA is the leading cause of disability among older individuals. The medical and societal burden of OA makes the understanding of its pathogenesis and potential treatments paramount. Objectives: This narrative review seeks to explore the most up-to-date literature regarding the M1 - M2 macrophage transition that has been proposed as the possible solution for the pathogenesis of OA. Methods: PubMed was queried for “macrophages and the pathogenesis of OA”, as well as “M1 to M2 transition in OA”. Articles were included in our review if they focused primarily on the role of macrophages in OA pathogenesis and the specific role the M1 to M2 macrophage transition has in the development and resolution of osteoarthritis. We focused on key examples where the M1 - M2 transition could be exploited in the resolution of OA. Results: Aberrances in the physiologic M1 - M2 macrophage transition can promote the pathogenesis of osteoarthritis and a degenerative state. When there is a predilection for M1 proinflammatory macrophages in the joint, progression to OA may result. Conversely, when there is a predilection for M2 macrophages in the joint, OA is typically absent, and the induction of an M2 predominant state may alleviate symptoms and further joint destruction of OA. Conclusion: The M1 - M2 macrophage transition plays a key role in the pathogenesis and severity of OA. Exploiting biochemical pathways involved in this transition may prove to be a suitable treatment for patients with OA.