Osteoarthritis (OA) is a chronic degenerative disease characterized by cartilage degeneration, synovial inflammation, and abnormal bone remodeling. Emerging evidence indicates that helper T (Th) cells play a pivotal role in OA pathogenesis. In the OA joint microenvironment, a marked imbalance among Th cell subsets is observed, manifested as overactivation of Th1 and Th17 cells alongside impaired function of Th2 and regulatory T cells. This imbalance leads to elevated levels of pro-inflammatory cytokines, such as interleukin (IL)-17, interferon-gamma, and tumor necrosis factor-alpha, whereas anti-inflammatory cytokines, including IL-4 and IL-10, are relatively deficient, resulting in chondrocyte apoptosis, extracellular matrix degradation, and synovial inflammation. This article systematically summarizes the molecular mechanisms of different Th cell subsets in OA development and elucidate their synergistic interactions with macrophages, providing a theoretical basis for Th cell-targeted immunomodulatory strategies in OA therapy.