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      OPG/RANKL system imbalance in a case of hepatitis C-associated osteosclerosis: the pathogenetic key?

      Clinical Rheumatology
      Absorptiometry, Photon, Aged, Biological Markers, metabolism, Biopsy, Bone Density, Bone Remodeling, physiology, Bone and Bones, pathology, radiography, radionuclide imaging, Carrier Proteins, Diagnosis, Differential, Enzyme-Linked Immunosorbent Assay, Glycoproteins, Hepacivirus, genetics, immunology, Hepatitis C Antibodies, analysis, Humans, Immunoblotting, Ligands, Male, Membrane Glycoproteins, Osteoblasts, Osteoprotegerin, Osteosclerosis, diagnosis, virology, RANK Ligand, RNA, Viral, Receptor Activator of Nuclear Factor-kappa B, Receptors, Cytoplasmic and Nuclear, Receptors, Tumor Necrosis Factor, Reverse Transcriptase Polymerase Chain Reaction

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          Hepatitis C-associated osteosclerosis (HCAO) is an impressive example of acquired diffuse osteosclerosis in adults, recently described in ten patients infected with hepatitis C virus (HCV). Its hallmark is a painful and generalized increase of bone mass. Bone biopsies show enhanced accretion rate, usually without histological abnormalities. The HCAO pathogenesis is hitherto unknown. HCV might induce a slow bone cell infection and the production of bone growth factors, such as insulin-like growth factors. Recently, receptor activator of nuclear factor-kappaB (RANK), its ligand (RANKL), and soluble decoy receptor osteoprotegerin (OPG) have been identified as a pivotal cytokine system in the bone remodeling control. We describe the 11th case of HCAO. Notably, the patient's bone biopsy showed the presence of a high number of OPG-positive osteoblasts, a slight increase of RANKL-positive stromal cells, and a dramatic reduction of the osteoclasts. Moreover, OPG serum levels were increased. These findings reported here for the first time are consistent with a pathogenetic role of the OPG/RANKL system imbalance in HCAO.

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