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Clin Exp Rheumatol. 2019 Sep-Oct;37 Suppl 120(5):57-63. Epub 2019 Oct 15.

Innate inflammation and synovial macrophages in osteoarthritis pathophysiology.

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Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, and Reynolds Oklahoma Center on Aging, Department of Biochemistry and Molecular Biology, Dept.of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Translational Musculoskeletal Research Center & Dept. of Medicine, Corporal Michael J. Crescenz Department of Veterans Affairs Medical Center, Philadelphia, and Div. of Rheumatology, Univ. of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.


Although osteoarthritis (OA) was historically referred to as the non-inflammatory arthritis, it is now considered a condition involving persistent low-grade inflammation and activation of innate inflammatory pathways. Synovitis increases the risk of OA onset and progression and involves the recruitment of monocytes, lymphocytes, and other leukocytes. In particular, macrophages are important mediators of synovial inflammatory activity and pathologic cartilage and bone responses that are characteristic of OA. Advances in understanding how damage-associated molecular patterns (DAMPs) trigger monocyte/macrophage recruitment and activation in joints provide opportunities for disease-modifying therapies. However, the complexity and plasticity of macrophage phenotypes that exist in vivo have thus far prevented the successful development of macrophage-targeted treatments. Current studies show that synovial macrophages are derived from distinct cellular lineages, which correspond to unique functional roles for maintaining joint homeostasis. An improved understanding of the aetiology of synovial inflammation in specific OA-subtypes, such as with obesity or genetic risk, is a potential strategy for developing patient selection criteria for future precision therapies.

[Available on 2020-10-15]
[Indexed for MEDLINE]
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