Osteoarthritis (OA) is the most common form of degenerative joint diseases and a major cause of disability and impaired quality of life in the elderly. OA is a complex disease involving both bone and cartilage properties, and may therefore require alternative approaches for treatment. Recent lines of evidence suggest that calcitonin acts on both osteoclasts and chondrocytes. The review summarizes emerging observations from cell biology to preliminary clinical trials, describing possible chondroprotective effects of calcitonin. This review summarizes peer-reviewed articles found using predefined search criteria and published in the PubMed database before June 2007. In addition, abstracts from the OsteoArthritis Research Society International (OARSI) conferences in the time period 2000 to 2006 were included. A range of studies, at the cellular level, in animal models, and in clinical trials, describe positive effects of calcitonin on bone health. Regarding articular cartilage, direct effects of calcitonin on chondrocytes on matrix synthesis, as well as inhibition of cartilage degradation, have been presented. In addition, clinical evidence for a chondroprotective effect of calcitonin is emerging. Several lines of evidence suggest direct anabolic effects of calcitonin on articular chondrocytes, resulting in increased proteoglycan synthesis. The anticatabolic effects of calcitonin may involve induction of cAMP, resulting in attenuation of MMP-mediated cartilage degradation. Presently there is limited availability of chondroprotective agents. Therefore, the current clinical research on calcitonin is highly anticipated, and may prove calcitonin treatment efficacious for the prevention and treatment of OA.