Osteoarthritis (OA) is a highly prevalent joint disorder traditionally considered a consequence of mechanical cartilage wear; however, it is now recognized as a complex, multifactorial disease driven by interconnected molecular and cellular mechanisms. This narrative review synthesizes current knowledge on key pathogenic pathways underlying OA progression, with a focus on inflammatory signaling, subchondral bone remodeling, and dysregulation of mineral metabolism. Chronic low-grade inflammation promotes catabolic responses in chondrocytes and contributes to cartilage degradation. In addition, obesity influences OA pathogenesis through both biomechanical loading and adipokine-mediated inflammatory mechanisms. Alterations in the receptor activator of nuclear factor kappa-B/receptor activator of nuclear factor kappa-B ligand/osteoprotegerin (RANK/RANKL/OPG) axis disrupt bone homeostasis and promote pathological subchondral remodeling, while imbalances in inorganic phosphate metabolism contribute to crystal deposition and further joint damage. These processes interact synergistically, driving disease progression. Current therapeutic strategies remain largely symptomatic and do not adequately target underlying molecular drivers. A deeper understanding of these mechanisms may facilitate the development of disease-modifying therapies.