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This article appears in the following Rheumatology issue: Management of Osteoporosis: A Physiological Answer for a Living Tissue. Proceedings of a satellite symposium held on the occasion of the EULAR Congress, Paris, France, June 13, 2008. The symposium and these proceedings were made possible by an unrestricted educational grant from Servier [View the issue table of contents]
Rebalancing bone turnover in favour of formation with strontium ranelate: implications for bone strength
1Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa and 2Serviço de Reumatologia e Doenças Ósseas Metabólicas, Hospital de Santa Maria, Lisbon, Portugal.
Correspondence to: J. E. Fonseca, Rheumatology Research Unit, Instituto de Medicina Molecular, Edifício Egas Moniz, Faculdade de Medicina da Universidade de Lisboa, Av. Professor Egas Moniz, 1649-028 Lisboa, Portugal. E-mail: jefonseca{at}netcabo.pt
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This review updates our current knowledge on the mechanism of action of strontium ranelate and analyses the way it rebalances bone turnover and how it influences bone biomechanics. Strontium ranelate is able to increase pre-osteoblast replication, osteoblast differentiation, collagen type I synthesis and bone matrix mineralization probably through a calcium-sensing receptor (CaR)-dependent mechanism. Paralleling this anabolic effect there is inhibition of osteoclast differentiation and activity mediated by an increase in osteoprotegerin (OPG) and a decrease in RANK ligand (RANKL). The overall effect is a rebalanced bone turnover in favour of improved bone geometry, cortical thickness, trabecular bone morphology and intrinsic bone tissue quality, which translates into enhanced bone strength.
KEY WORDS: Strontium ranelate, Osteoblast, Osteoclast, Collagen type I, Calcium-sensing receptor, RANK ligand, Osteoprotegerin, Plastic energy, Bone strength
Submitted 31 January 2008;
revised version accepted 1 April 2008.
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