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Andersen S.,University of Southern Denmark | Frederiksen K.D.,University of Southern Denmark | Hansen S.,University of Southern Denmark | Brixen K.,University of Southern Denmark | And 3 more authors.
Calcified Tissue International | Year: 2014

Obesity is associated with high bone mineral density (BMD), but whether obesity-related higher bone mass increases bone strength and thereby protect against fractures is uncertain. We estimated effects of obesity on bone microarchitecture and estimated strength in 36 patients (12 males and 24 females, age 25-56 years and BMI 33.2-57.6 kg/m2) matched with healthy controls (age 25-54 years and BMI 19.5-24.8 kg/m2) in regard to gender, menopausal status, age (±6 years) and height (±6 cm) using high resolution peripheral quantitative computed tomography and dual energy X-ray absorptiometry. In radius, total bone area and trabecular area were significantly higher in obese patients (both p < 0.04). In tibia, cortical area was larger in obese patients (p < 0.001) compared with controls. Total BMD was higher in tibia (p = 0.03) but not in radius. Trabecular integrity was strengthened in obese patients compared with controls in radius and tibia with higher trabecular number (p = 0.002 and p < 0.001) and lower trabecular spacing (p = 0.01 and p < 0.001). Finite element analysis estimated failure load (FL) was higher in tibia (p < 0.001), but not in radius in obese patients. FL was significantly lower per kg body weight in radius and tibia in obese patients compared with controls (p = 0.007 and p < 0.001). Furthermore, the ratios of FLs between groups were comparable in both sites. These findings suggest that mechanical loading is not the primary mediator of the effects of obesity on estimated FL, and suggest that bone strength adaptations in morbid obesity may be inadequate with respect to the increased mechanical demands. © 2014 Springer Science+Business Media.

Beck-Nielsen S.S.,Hospital of Southwest Denmark
Danish medical journal | Year: 2012

Rickets is a heterogeneous group of diseases of the growing child caused by defect mineralization of bone. Nutritional rickets is caused by deficiency of vitamin D, calcium or both. Several hereditary forms of rickets exist where the disease proceeds into adulthood. Nutritional rickets was common in the past, but by introduction of preventative administration of cod liver oil and vitamin D supplementation, nutritional rickets became a rarity. During the last decades, case reports of nutritional rickets reappear in the industrialized countries. It is the general conception that in the industrialized countries, hereditary rickets is the most prevalent cause of rickets today. However, the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown. The most common form of hereditary rickets is hypophosphatemic rickets (HR). The geno- and phenotype among Scandinavian patients have not been characterized. Especially, the disease in adult patients is not well described. Moreover, there are conflicting reports of the benefits of medical treatment throughout childhood, and in addition on gender differences in disease severity.

Folkestad L.,University of Southern Denmark | Hald J.D.,Aarhus University Hospital | Hansen S.,University of Southern Denmark | Gram J.,Hospital of Southwest Denmark | And 3 more authors.
Journal of Bone and Mineral Research | Year: 2012

Osteogenesis imperfecta (OI) is a hereditary disorder characterized by decreased biosynthesis or impaired morphology of type I collagen that leads to decreased bone mass and increased bone fragility. We hypothesized that patients with OI have altered bone microstructure and bone geometry. In this cross-sectional study we compared patients with type I OI to age- and gender-matched healthy controls. A total of 39 (13 men and 26 women) patients with OI, aged 53 (range, 21-77) years, and 39 controls, aged 53 (range, 21-77) years, were included in the study. Twenty-seven of the patients had been treated with bisphosphonates. High-resolution peripheral quantitative computed tomography (HR-pQCT) at the distal radius and distal tibia and dual-energy X-ray absorptiometry of total hip, femoral neck, trochanteric region, and the lumbar spine (L1-L4) were performed. The patients were shorter than the controls (159 ± 10 cm versus 170 ± 9 cm, p < 0.001), but had similar body weight. In OI, areal bone mineral density (aBMD) was 8% lower at the hip (p < 0.05) and 13% lower at the spine (p < 0.001) compared with controls. The trabecular volumetric bone mineral density (vBMD) was 28% lower in radius (p < 0.001) and 38% lower in tibia (p < 0.001) in OI compared with controls. At radius, total bone area was 5% lower in OI than in controls (p < 0.05). In the tibia, cortical bone area was 18% lower in OI (p < 0.001). In both radius and tibia the number of trabeculae was lower in patients compared to the controls (35% and 38%, respectively, p < 0.001 at both sites). Furthermore, trabecular spacing was 55% higher in OI in both tibia and radius (p < 0.001 at both sites) when compared with controls. We conclude that patients with type I OI have lower aBMD, vBMD, bone area, and trabecular number when compared with healthy age- and gender-matched controls. Copyright © 2012 American Society for Bone and Mineral Research.

Bouteldja N.,Hospital of Southwest Denmark | Andersen L.T.,Aarhus University Hospital | Moller N.,Aarhus University Hospital | Gormsen L.C.,Aarhus University Hospital
Metabolism: Clinical and Experimental | Year: 2014

Ketone bodies - 3-hydroxybutyrate and acetoacetate - are important fuel substrates, which can be oxidized by most tissues in the body. They are synthesized in the liver and are derived from fatty acids released from adipose tissue. Intriguingly, under conditions of stress such as fasting, arterio-venous catheterization studies have shown that the brain switches from the use of almost 100% glucose to the use of > 50-60% ketone bodies. A similar adaptive mechanism is observed in the heart, where fasting induces a shift toward ketone body uptake that provides the myocardium with an alternate fuel source and also favorably affects myocardial contractility. Within the past years there has been a renewed interest in ketone bodies and the possible beneficial effects of fasting/semi-fasting/exercising and other "ketogenic" regimens have received much attention. In this perspective, it is promising that positron emission tomography (PET) techniques with isotopically labeled ketone bodies, fatty acids and glucose offer an opportunity to study interactions between ketone body, fatty acid and glucose metabolism in tissues such as the brain and heart. PET scans are non-invasive and thus eliminates the need to place catheters in vascular territories not easily accessible. The short half-life of e.g. 11C-labeled PET tracers even allows multiple scans on the same study day and reduces the total radiation burden associated with the procedure. This short review aims to give an overview of current knowledge on ketone body metabolism obtained by PET studies and discusses the methodological challenges and perspectives involved in PET ketone body research. © 2014 Elsevier Inc.

Beck-Nielsen S.S.,University of Southern Denmark | Brixen K.,University of Southern Denmark | Gram J.,Hospital of Southwest Denmark | Molgaard C.,University of Southern Denmark | Molgaard C.,Copenhagen University
Osteoporosis International | Year: 2013

Bone mineral apparent density (BMAD) in children with X-linked hypophosphatemia (XLH) was evaluated, as they are unlikely to have extra-skeletal ossifications contributing to the elevated bone mineral density of the spine in adult patients. Children with XLH also had significantly higher BMAD of the spine compared to femoral neck. Introduction: BMAD obtained by dual-energy X-ray absorptiometry scans in children with XLH was evaluated, as they are unlikely to have the extra-skeletal ossifications contributing to the elevated bone mineral density of the spine in adult patients. Methods: A total of 15 children with biochemically and genetically verified XLH were recruited. Anthropometric measurements were performed, and to correct for the short stature (small bones), the BMAD of the spine and the femoral neck was evaluated. Results: Z-scores of BMAD of the spine (mean (95 % CI); 2.0 (1.3-2.7); p < 0.001) were significantly elevated compared to reference children. Z-scores of the femoral neck (1.0 (-0.0 to 2.1); p = 0.059) tended to be elevated. Spine Z-scores were significantly higher than the Z-scores of the femoral neck, (paired t test, p = 0.02). BMAD of the spine was evaluated according to the Molgaard's approach; XLH children had normal bone size of the spine for age due to a normal sitting height Z-score of -0.4 (-1.0 to 0.1); p = 0.1. Z-scores of bone mineral content (BMC) of the spine for bone area were elevated (1.4 (0.8-2.1); p < 0.001). No reference data were available to allow evaluation of the BMAD of the femoral neck by the Molgaard's approach. Conclusions: Children with XLH have an increased BMAD and a high BMC for bone area at the lumbar spine, and this was due to causes other than extra-skeletal ossifications and corrected for bone size. The BMAD of the spine was significantly higher compared to the femoral neck. © 2013 International Osteoporosis Foundation and National Osteoporosis Foundation.

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