El calcitonin está implicado en la homeostasis del cartílago. (I)

M.A. Karsdal Ph.D.†, , , L.B. Tanko M.D.‡, B.J. Riis M.D., Ph.D.‡, B.C. Sondergard M.Sc.†, K. Henriksen M.Sc.†, R.D. Altman M.D.§, Professor of Medicine, Rheumatology and Immunology, P. Qvist Ph.D.† and C. Christiansen M.D., Ph.D.‡

§University of California at Los Angeles, Los Angeles, USA †Nordic Bioscience Diagnostics, Herlev, Denmark ‡Center for Clinical and Basic Research (CCBR), Ballerup, Denmark

Summary

Objective 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. Recent observations suggest that calcitonin may act on both osteoclasts and chondrocytes. The present review was sought to summarize emerging observations from the molecular level to the preliminary clinical findings of possible chondroprotective effects of calcitonin.

Method This review summarizes peer-reviewed articles found using pre-defined search criteria and published in the PubMed database before January 2006. In addition, abstracts from the OsteoArthritis Research Society International (OARSI) conferences in the time period 2000–2005 have been included in the search.

Results Ample evidence for the effect of calcitonin on bone resorption was found. Support for direct effects of calcitonin on chondrocytes on matrix synthesis and inhibition of cartilage degradation have been published. In addition, clinical evidence for the effect of calcitonin on cartilage degradation is emerging.

Conclusion Several independent lines of evidence suggest a direct chondroprotective effect of calcitonin in addition to the well-established effect on bone resorption. Given the currently limited availability of chondroprotective agents, much expectation regards the ongoing clinical assessment of calcitonin therapy for the prevention and treatment of OA.