Bone Abstracts

Aim of the study: Animal studies have also been reported demonstrating enhanced development of osteomalacia and increased osteoids following long-term high-dose administration of Al compound in rats, especially in those with renal failure rats (Robertson et al.).For histologic detection of Al. aluminon and other staining reagents have usually been used but are not adequately sensitive and lack in specificity. We have recently developed a method ...

Vertebral fractures (VF) in adults are the most common osteoporotic fracture, are powerful predictors of future fracture risk (hip X2; spine X5) and their prevalence increases as bone mineral density (BMD) declines. The most common imaging method for diagnosis is spinal radiography, but they can be identified fortuitously also on other imaging techniques performed for various clinical indications.1 Midline reformations of multi-detector CT (MDCT) scans of thorax and...

Elevated levels of circulating serotonin have been reported to decrease bone mineral density1. Conversely, reduced serotonin (5HT) in mice lacking TPH1, the rate limiting enzyme for 5HT synthesis, was reported to be anabolic to the skeleton with high osteoblastic activity2. However, in other studies TPH1 deletion led to either an initial increase in BMD due to inhibition of osteoclastic bone resorption3, or had no bone effect4</su...

One growth factor that potentially plays a role in fracture healing is midkine (Mdk). Mdk is expressed in chondrocytes during bone repair (Ohta et al. 1999) and has been shown to influence bone mass and mechanotransduction (Neunaber et al. 2010, Liedert et al. 2011). The aim of the present study was to evaluate the effects of Mdk-deficiency on bone repair in a standardized mouse femur osteotomy model.Mdk-deficient and wildtype ...

Postmenopausal women with forearm fracture have higher cortical porosity and lower trabecular density perhaps due to excessive age-related bone loss1. Remodelling becomes unbalanced and rapid only after ~45 years of age. We therefore proposed that bone fragility in premenopausal women with a forearm fracture originates during growth. At metaphyses, trabeculae emerging from the periphery of the growth plate form cortex by ‘corticalization’)2. We ...

Interleukin-6 (IL-6) plays an important role in bone metabolism and regulates fracture healing in a presently unknown process. In the fracture callus IL-6 expression is biphasic; it peaks during the inflammatory phase and again during intramembranous and endochondral ossification (Ai-Aql et al. 2008). Few studies using IL-6 knockout mice indicate that IL-6 might be crucial for bone healing (Yang et al. 2007). However, a generalized IL-6 knockout induces multi...

Bones’ fracture resistance is achieved in vivo by adaptation to habitual loading. Aged bone can adapt to exercise1 but in female rodents ageing impairs the adaptive response to artificial loading2,3. This inconsistency led us to investigate whether treadmill exercise, sufficiently mild to not itself stimulate new bone formation, could rescue aged bone’s diminished response to artificial loading.Young adult 17-week...

In rural Gambian prepubertal children with low calcium intakes (mean 300 mg/day) we reported positive effects, sustained for at least a year (y), on bone mineral content (BMC) after 12 months supplementation with calcium carbonate to international levels1,2. The group was followed up regularly until the end of height growth, and supplementation did not affect height growth in the girls3. Our aim was to determine whether the supplementation altered the tim...

Metatropic dysplasia (MD) was first described by Maroteaux et al. in 1966. Its name was derived from the Greek word metatropos which means ‘changing pattern’ because individuals with this diagnosis begin life with a short-limbed dysplasia and a long trunk with narrow chest, and over time their dysplasia becomes short-trunked due to progressive kyphoscoliosis1. It is now recognized that MD is caused by gain-of-function mutations in transie...

Objective: The physis, or growth plate, is comprised of precisely organized chondrocytes that confer longitudinal growth of the bone. Multiple signaling pathways cooperate to regulate growth through their control of chondrocyte shape, polarity, proliferation, and differentiation.1,2 Disruption of these cellular events result in physeal defects, skeletal deformities, and abnormal limb growth. Loss of function mutations in Smad4, a common intracellular effector of all...