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Previous reviews on osteoarthritis have primarily focused on inflammation caused by cartilage destruction, often overlooking the role of synovitis in the progression of osteoarthritis (OA). Macrophages, T cells, and neutrophils play critical roles in the advancement of synovitis. Therefore, this article emphasizes the functions of macrophages, T cells, and neutrophils in OA-related synovitis, aiming to provide a deeper understanding of the interactions among damage-associated molecular patterns, immune cell activation, and signaling pathways (such as NF-κB and mTOR) in OA, thereby offering new therapeutic targets. In OA, the accumulation of macrophages within inflamed synovial fluid, along with elevated levels of RANKL, tumor necrosis factor-alpha, and interleukin-1, enhances the capacity of synovial macrophages to differentiate into osteoclasts. Furthermore, synovial macrophages can polarize into either pro-inflammatory M1 or anti-inflammatory M2 phenotypes, with a predominance of the M1 phenotype promoting cartilage destruction. T cells-particularly Th17 and regulatory T cells-disrupt immune homeostasis and exacerbate inflammation. Neutrophils contribute to tissue damage by releasing elastase and reactive oxygen species, which directly injure cartilage and bone. Current OA management primarily focuses on symptomatic relief through agents such as non-steroidal anti-inflammatory drugs and corticosteroids. In contrast, emerging therapeutic strategies aim to modulate immune pathways. Promising approaches include platelet-rich plasma, mesenchymal stem cell therapy, and photobiomodulation, which have shown potential in regulating inflammation and promoting cartilage repair. A deeper understanding of the interactions among damage-associated molecular patterns, immune cell activation, and signaling pathways-such as NF-κB and mTOR-offers new therapeutic targets. Ultimately, OA management may evolve toward a precision medicine approach that integrates immune modulation with regenerative strategies to restore joint homeostasis.
Wen et al. (Sat,) studied this question.