Osteoarthritis (OA) has long been described as a “wear and tear” degenerative joint disorder, yet this definition fails to capture the complexity of the disease. Emerging evidence suggests that OA is more accurately characterized as a whole-joint disorder involving coordinated changes in cartilage, synovium, subchondral bone, and the local microenvironment. At the subcellular level, OA progression appears to involve not a single failing organelle, but disrupted communication among mitochondria, the endoplasmic reticulum, the Golgi apparatus, lysosomes, and intracellular trafficking systems in joint cells. In chondrocytes, disrupted organelle crosstalk promotes oxidative stress, unfolded protein response, lysosomal dysfunction and senescence, thereby amplifying cartilage degeneration. This review reexamines OA pathogenesis from the perspective of inter-organelle communication. We summarize major forms of organelle interaction in chondrocytes, including membrane contact sites (MCSs), vesicular trafficking, and autophagosome-lysosome fusion. We further discuss mitochondria-related crosstalk, endoplasmic reticulum stress regulation, and the lysosome-mTOR-autophagy network in OA progression. Furthermore, we address the preliminary evidence for migrasomes as an emerging research direction and compare the heterogeneous patterns of organelle crosstalk across chondrocytes, synovial cells, macrophages, and subchondral bone-related cells. By bridging subcellular dysfunction with whole-joint pathological changes, this review offers fresh insights and provides a new entry point for developing therapeutic strategies.