View clinical trials related to Bone Loss.
Filter by:The objective of this study is to determine whether patient follow up for osteoporosis is aided using a quantitative ultrasound (QUS) measurement. Using the QUS measurement could potentially improve osteoporosis follow-up rates, and in-office patient measurements have been previously shown to increase compliance with treatment in other conditions. Increased compliance with follow-ups and medication recommendations have been shown to decrease fracture rates in patients with osteoporosis.
Exercise is an important factor in bone health. Sclerostin is one of the key molecules involved in bone response to mechanical loading. In particular, sclerostin decreases bone formation directly through the inhibition of Wnt/ β-catenin signaling and increases bone resorption indirectly via upregulation of the RANK/RANKL. The Wnt pathway is an anabolic signaling pathway, which leads to the activation of osteoblasts. OPG is another osteokine secreted by osteoblasts and osteogenic stomal cells that has a protective osteogenic role in humans by inhibiting the binding of RANKL to its receptor RANK. The RANK/RANKL pathway is a catabolic signaling pathway controlling osteoclast differentiation. Only a few studies have examined the effects of one single bout of high impact exercise on serum sclerostin levels in adults, most of which are from the investigators' lab. However, not many studies have examined the acute effects of moderate intensity, low-impact exercise on osteokines of the Wnt signaling. Previous studies have only investigated the impact of high intensity cycling on sclerostin, OPG and RANKL, however, no research has been done to investigate the response of osteokines to moderate intensity continuous cycling. This study aims to investigate differences in osteokines and markers of bone turnover following three moderate intensity cycling trials of different duration (30, 60 and 120 min) in an energy replete state. The question we aim to answer is whether there is a threshold of time where continued stimulus from moderate strain on the bone fails to elicit an additional metabolic response in bone or even becomes osteocatabolic, when athletes are in an energy replete state. Additional biochemical responses to the exercise will also be examined including inflammatory markers, glucose, anabolic/hormonal markers and oxidative stress.
The adolescent and young adult years are a critical window in time for bone mineral accrual. More than 90% of peak bone mass is achieved by 18 years, and data indicate that insults sustained during adolescence and young adulthood may result in permanent deficits in bone accrual. Adult athletes with amenorrhea (AA) have low bone mineral density (BMD) secondary to hypogonadism, associated with increased fracture risk and associated co-morbidities. We will examine whether estrogen replacement will increase BMD and improve measures of bone microarchitecture in adolescents and young women with AA, thus optimizing peak bone mass.