This review systematically summarized the core pathological mechanisms of synovial cell senescence in the onset and progression of osteoarthritis (OA) and focused on recent advances in targeted therapies for senescent synovial cells, aiming to provide a theoretical basis for precise OA interventions. Relevant literature from PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) databases in recent years was reviewed to analyze the molecular mechanisms of synovial cell senescence and its pathological effects mediated by the senescence-associated secretory phenotype (SASP). The findings indicate that senescent synovial cells release pro-inflammatory cytokines and matrix-degrading enzymes (e.g., MMP-13), which drive chronic synovial inflammation, cartilage degeneration, and loss of joint function. In recent years, emerging approaches such as senolytic drugs (e.g., dasatinib plus quercetin combination therapy), CRISPR-based gene editing, and mesenchymal stem cell transplantation have shown significant efficacy in eliminating senescent synovial cells or reversing their pathological phenotype, thereby ameliorating joint damage in OA animal models. Targeting synovial cell senescence offers a novel direction for OA treatment, and future studies are urgently needed to further elucidate the spatiotemporal dynamics of the senescent microenvironment and facilitate the clinical translation of these findings.