title: Reduced proliferation and osteocalcin expression in osteoblasts of male idiopathic osteoporosis.
abstract: Osteoporosis is characterized by low bone mineral density (BMD), resulting in increasing susceptibility to bone fractures. In men, it has been related to some diseases and toxic habits, but in some instances the cause of the primary--or idiopathic--osteoporosis is not apparent. In a previous study, our group compared histomorphometric measurements in cortical and cancellous bones from male idiopathic osteoporosis (MIO) patients to those of control subjects and found reduced bone formation without major differences in bone resorption. To confirm these results, this study analyzed the etiology of this pathology, examining the osteoblast behavior in vitro. We compared two parameters of osteoblast activity in MIO patients and controls: osteoblastic proliferation and gene expression of COL1A1 and osteocalcin, in basal conditions and with vitamin D(3) added. All these experiments were performed from a first-passage osteoblastic culture, obtained from osteoblasts that had migrated from the transiliac explants to the plate. The results suggested that the MIO osteoblast has a slower proliferation rate and decreased expression of genes related to matrix formation, probably due to a lesser or slower response to some stimulus. We concluded that, contrary to female osteoporosis, in which loss of BMD is predominantly due to increased resorption, low BMD in MIO seems to be due to an osteoblastic defect.
authors.affiliation: Unitat de Recerca en Fisipatologia Ossia i Articular, Institut Municipal d'Investigació Mèdica, Hospital del Mar, Autonomous University of Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain.
authors.forename: Sílvia
authors.initials: S
authors.lastname: Ruiz-Gaspà
authors.forename: Josep
authors.initials: J
authors.lastname: Blanch-Rubió
authors.forename: Manuel
authors.initials: M
authors.lastname: Ciria-Recasens
authors.forename: Jordi
authors.initials: J
authors.lastname: Monfort
authors.forename: Laura
authors.initials: L
authors.lastname: Tío
authors.forename: Natàlia
authors.initials: N
authors.lastname: Garcia-Giralt
authors.forename: Xavier
authors.initials: X
authors.lastname: Nogués
authors.forename: Joan C
authors.initials: JC
authors.lastname: Monllau
authors.forename: Jordi
authors.initials: J
authors.lastname: Carbonell-Abelló
authors.forename: Lluis
authors.initials: L
authors.lastname: Pérez-Edo
mesh_terms: D000328:Adult; D000368:Aged; D001842:Bone and Bones / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002762:Cholecalciferol / Q000378:metabolism / Q000494:pharmacology; D024042:Collagen Type I / Q000235:genetics; D000090602:Collagen Type I, alpha 1 Chain; D015536:Down-Regulation / Q000235:genetics; D005109:Extracellular Matrix / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology; D005819:Genetic Markers / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D010006:Osteoblasts / Q000187:drug effects / Q000378:metabolism*; D015675:Osteocalcin / Q000235:genetics*; D010012:Osteogenesis / Q000235:genetics; D010024:Osteoporosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D012727:Sex Characteristics
chemical_list: D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D005819:Genetic Markers; D012333:RNA, Messenger; D015675:Osteocalcin; D002762:Cholecalciferol