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[Osteoporosis and vascular calcification in rheumatoid arthritis - the role of osteoprotegerin and sclerostin].
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2017
Year
SclerostinOsteogenesisBone TissueOsteoporosisOrthopaedic SurgeryBone DiseaseBone Tissue MetabolismBone HomeostasisCell SignalingRheumatoid ArthritisHealth SciencesMolecular SignalingRheumatologySkeletal BiologyVascular BiologyCell BiologyBone MetabolismOsteocalcinPhysiologyMedicineVascular Calcification
Disorders of bone tissue metabolism and increased frequency of cardiovascular diseases are among the well-known, extra-articular complications of rheumatoid arthritis (ra). The mechanisms leading to local and generalized loss of bone tissue as well as those promoting calcification of vessels are similar. Recently, a great interest has aroused among the studies related to the meaning of the RANKL/RANK/OPG system and the Wnt/β-catenin signaling pathway, as biological links between the bone and vascular systems. In the course of ra, lowering of the mineral density of bones and intensification of vascular calcification seem to be associated with the increase of plasma concentration of osteoprotegerin (OPG) and sclerostin - the regulatory proteins of the RANKL/RANK/OPG system and the Wnt/β-catenin pathway. Molecular mechanisms associated with the osteoblasts' activation and repression of bone resorption in the future can become the target of a precise, combination therapy in osteoporosis and calcification changes. The article presents the role of the RANKL/RANK/ OPG system and the Wnt/β-catenin pathway in the pathogenesis of disorders of bone tissue metabolism and calcification of vessels in ra, with particular emphasis on the role of OPG and sclerostin.