Journalartikel
Autorenliste: Lange, U; Schulz, A
Jahr der Veröffentlichung: 2005
Seiten: 354-362
Zeitschrift: Aktuelle Rheumatologie
Bandnummer: 30
Heftnummer: 6
ISSN: 0341-051X
eISSN: 1438-9940
DOI Link: https://doi.org/10.1055/s-2005-858833
Verlag: Georg Thieme Verlag
Abstract:
Osteoporosis is a systemic skeletal disorder affecting bone mass and bone structure, with increased bone fragility and fracture risk. The clinical state of manifest osteoporosis is the final outcome of an initially inapparent, yet progressive reduction of bone mineral density and bone mass, osteopenia. To date, existing diagnostic methods reflect only the current state of the disease. Future predictive parameters, would however be of great clinical value. Osteoporosis exhibits a substantial genetic component as revealed by prevalence studies in families and twins. Genetic research on osteoporosis and bone metabolism, has been well established in recent years. So far however, research on potential genes and polymorphisms is chiefly of scientific interest without clinical relevance. The Vitamin D receptor gene has been shown to be a molecular marker, correlating with the development of osteoporosis. Other candidate gene polymorphisms such as hormone receptor, cytokine and collagen genes are currently being analysed regarding complex gene-gene and gene-environment interactions. Research on genetic factors for bone metabolism disorders in osteoporosis is still at its beginning, but we are looking forward to important new insights into skeletal pathophysiology that will contribute to new terms of prevention (predictive risk factors), diagnosis and treatment (biochemical and molecular gene function) of osteoporosis.
Zitierstile
Harvard-Zitierstil: Lange, U. and Schulz, A. (2005) Osteoporosis and genetics of bone metabolism, Aktuelle Rheumatologie, 30(6), pp. 354-362. https://doi.org/10.1055/s-2005-858833
APA-Zitierstil: Lange, U., & Schulz, A. (2005). Osteoporosis and genetics of bone metabolism. Aktuelle Rheumatologie. 30(6), 354-362. https://doi.org/10.1055/s-2005-858833
Schlagwörter
ANKYLOSING-SPONDYLITIS; bone density; D-RECEPTOR GENOTYPES; Hormone replacement therapy; molecular medicine; OSTEOCALCIN GENE; OSTEOPROTEGERIN GENE; POSTMENOPAUSAL JAPANESE WOMEN; PREMENOPAUSAL WOMEN; SP1 BINDING-SITE; TRANSFORMING GROWTH-FACTOR-BETA-1 GENE