title: Bone remodelling does not decline after menopause in vertebral fracture osteoporosis.
abstract: There is considerable current interest in whether activators of bone remodelling, such as IL-1 and other cytokines, are involved in the pathogenesis of osteoporosis. We have therefore studied indices relating to remodelling activation in 50 patients with postmenopausal vertebral osteoporosis and 12 with hip fracture osteoporosis in comparison with 25 age- and sex-matched controls. Because of uncertainty regarding the accuracy of current biochemical markers of bone formation with respect to the estimation of whole body rates of bone formation, a 85Sr-based radioisotopic method was used. This method was previously validated by comparison with data obtained after double in vivo labelling of transiliac biopsies taken nearly simultaneously. Bone resorption was estimated from urinary hydroxyproline data. Controls selected for their continued good health showed a progressive and statistically highly significant decline in indices of bone formation with time after menopause. No such decline was seen in the vertebral fracture patients (P less than 0.005). There were no hip fracture patients within 10 years of menopause so this statistical test could not be applied appropriately to them. The hydroxyproline data were consistent with the suggestion arising from the bone formation data that remodelling declines progressively after menopause in the controls but not in the vertebral fracture patients. The data also suggested that these two fracture groups were in more negative calcium balance than the controls, this being particularly marked in the hip fracture cases. Plasma osteocalcin data correlated moderately well with the kinetic measurements of bone formation. It is concluded that vertebral fracture osteoporosis is associated with prolongation of menopausal levels of bone remodelling which is inappropriate by comparison with healthy controls.
authors.affiliation: MRC Clinical Research Centre, Harrow, UK.
authors.forename: J S
authors.initials: JS
authors.lastname: Wand
authors.forename: J R
authors.initials: JR
authors.lastname: Green
authors.forename: R
authors.initials: R
authors.lastname: Hesp
authors.forename: J N
authors.initials: JN
authors.lastname: Bradbeer
authors.forename: P N
authors.initials: PN
authors.lastname: Sambrook
authors.forename: T
authors.initials: T
authors.lastname: Smith
authors.forename: L
authors.initials: L
authors.lastname: Hampton
authors.forename: J M
authors.initials: JM
authors.lastname: Zanelli
authors.forename: J
authors.initials: J
authors.lastname: Reeve
mesh_terms: D000367:Age Factors; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000378:metabolism; D003404:Creatinine / Q000378:metabolism; D005260:Female; D050723:Fractures, Bone / Q000503:physiopathology*; D006801:Humans; D006909:Hydroxyproline / Q000378:metabolism; D007700:Kinetics; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D015663:Osteoporosis, Postmenopausal / Q000503:physiopathology*; D016103:Spinal Fractures / Q000503:physiopathology
chemical_list: D015675:Osteocalcin; D003404:Creatinine; D000469:Alkaline Phosphatase; D006909:Hydroxyproline