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dc.contributor.authorShigdel, Rajesh-
dc.contributor.authorOsima, Marit-
dc.contributor.authorAhmed, Luai A-
dc.contributor.authorJoakimsen, Ragnar M-
dc.contributor.authorEriksen, Erik F-
dc.contributor.authorZebaze, Roger MD-
dc.contributor.authorBjørnerem, Åshild-
dc.identifier.citationBone 2015; 81: 1-6en_US
dc.description.abstractBone turnover markers (BTM) predict bone loss and fragility fracture. Although cortical porosity and cortical thinning are important determinants of bone strength, the relationship between BTM and cortical porosity has, however, remained elusive. We therefore wanted to examine the relationship of BTM with cortical porosity and risk of non-vertebral fracture. In 211 postmenopausal women aged 54-94 years with non-vertebral fractures and 232 age-matched fracture-free controls from the Tromsø Study, Norway, we quantified femoral neck areal bone mineral density (FN aBMD), femoral subtrochanteric bone architecture, and assessed serum levels of procollagen type I N-terminal propeptide (PINP) and C-terminal cross-linking telopeptide of type I collagen (CTX). Fracture cases exhibited higher PINP and CTX levels, lower FN aBMD, larger total and medullary cross-sectional area (CSA), thinner cortices, and higher cortical porosity of the femoral subtrochanter than controls (p≤0.01). Each SD increment in PINP and CTX was associated with 0.21-0.26 SD lower total volumetric BMD, 0.10-0.14 SD larger total CSA, 0.14-0.18 SD larger medullary CSA, 0.13-0.18 SD thinner cortices, and 0.27-0.33 SD higher porosity of the total cortex, compact cortex, and transitional zone (all p≤0.01). Moreover, each SD of higher PINP and CTX was associated with increased odds for fracture after adjustment for age, height, and weight (ORs 1.49; 95% CI, 1.20-1.85 and OR 1.22; 95% CI, 1.00-1.49, both p<0.05). PINP, but not CTX, remained associated with fracture after accounting for FN aBMD, cortical porosity or cortical thickness (OR ranging from 1.31 to 1.39, p ranging from 0.005 to 0.028). In summary, increased BTM levels are associated with higher cortical porosity, thinner cortices, larger bone size and higher odds for fracture. We infer that this is produced by increased periosteal apposition, intracortical and endocortical remodeling; and that these changes in bone architecture are predisposing to fracture.en_US
dc.subjectBone mineral densityen_US
dc.subjectBone turnover markersen_US
dc.subjectCortical porosityen_US
dc.subjectNon-vertebral fractureen_US
dc.titleBone turnover markers are associated with higher cortical porosity, thinner cortices, and larger size of the proximal femur and non-vertebral fracturesen_US
dc.typeJournal Articleen_US
dc.identifier.affiliationAustin Health, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Health and Care Sciences, UiT-The Arctic University of Norway, Tromsø, Norwayen_US
dc.identifier.affiliationDepartment of Community Medicine, UiT-The Arctic University of Norway, Tromsø, Norwayen_US
dc.identifier.affiliationInstitute of Public Health, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emiratesen_US
dc.identifier.affiliationDepartment of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norwayen_US
dc.identifier.affiliationDepartment of Internal Medicine, University Hospital of North Norway, Tromsø, Norwayen_US
dc.identifier.affiliationDepartment of Clinical Endocrinology, Oslo University Hospital, Oslo, Norwayen_US
dc.identifier.affiliationEndocrine Centre, Austin Health, University of Melbourne, Heidelberg, Victoria, Australiaen_US
dc.type.austinJournal Articleen_US
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
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