Active clinical trials for "Bone Diseases"

In this study researchers would like to learn more about the low levels of bone mineral density seen in approximately half of women in their forties diagnosed as currently having or previously had depression. Bones are always undergoing a process of building (formation) and breakdown (resorption). This process is referred to as bone remodeling. When more bone is formed than resorbed, the density (level of calcium) in bone increases and the bones become stronger. However, if more bone is resorbed than formed the density of bone decreases and the bones become weak. This condition is called osteoporosis. It is unknown if women with depression have decreased bone mineral density as a result of too much breakdown of bone or not enough building. It is important to know the cause of low bone mineral density because it will influence the way a patient is treated. Medications like bisphosphonates are used when there is too much bone breakdown. Growth hormone replacement can be given in cases where there is not enough bone production. Presently, bone biopsy and a procedure known as histomorphometry can determine what processes are going on in bones. Researchers have decided to use a sample of bone (biopsy) from part of the hip bone (iliac crest). In addition, researchers will collect a sample of bone marrow (the soft tissue found in the center of bones) to tell them more about the biochemical, cellular, and molecular processes that may be contributing to the problem of decreased bone density in depressed premenopausal women.

COD lesions effect a wide range of different anatomical areas, show different volume and morphometric characteristics.

Treatment of bone and joint infections remains difficult and variable according to centres and countries. Clindamycin given intravenously and followed by an oral route is recommended for the treatment of staphylococcal, streptococcal and anaerobes bone and joint infections by the French Society for Infectious Diseases. For staphylococcal bone and implant infections, rifampin is a major drug, as it remains active in bacterial biofilm and on quiescent staphylococci. For that reasons, clindamycin-rifampin combination therapy is frequently used in these infections.Clindamycin is metabolized by the P450 3A4 cytochrome, an enzyme strongly inducible by rifampin. A retrospective study published in 2010 on 70 patients treated for bone and joint infections showed that clindamycin serum concentrations were significantly lower when clindamycin was combined with rifampin (5.3 mg/liter vs 8.9 mg/liter; p<0.02). This drug interaction could even be stronger with the oral route, because of hepatic first-past effect, ending up with very low clindamycin serum concentration, a risk of selecting resistant microorganisms and treatment failure. This latter point is an important issue, because clindamycin has an excellent oral bioavailability and is frequently used in oral regimens. In the above study, a wide variability of clindamycin serum concentration was observed in the group of patients treated with combination therapy (1-12mg/l) suggesting interindividual variability. Rifampin induction of CYP 450 3A4/A5 depends on different receptor (PXR, RXR, LXRalpha) submitted to genetic polymorphism. Hypothesis: Plasma clearance of clindamycin (CLclin) combined with rifampicin (CLclinrif) is higher when clindamycin is administered by the oral route (CLclinrif OR) compared with IV administration (CLclinrif IV).

This study is part of a research project for a University MD Program. This is an observational study aimed at comparing the differences in bone metabolism and microcirculation in patients with type 2 diabetes mellitus (with and without diabetic neuropathy and Charcot foot) with healthy subjects. Diabetes is gradually becoming a global epidemic along with its associated complications. Diabetes can affect several systems in our body particularly the eyes, nerves and the kidneys. The damaging effects occur at the level of the small blood vessels (microcirculation) that supply these vital structures. Normally, the inner lining of these blood vessels (endothelium) plays a very important role in maintaining adequate blood flow. The endothelium releases a chemical substance called nitric oxide, which relaxes these small blood vessels thereby ensuring sufficient blood supply to these key structures. Nitric oxide also prevents blockage of these vessels. Any form of metabolic stress like hyperglycaemia (raised blood sugar as seen in diabetes) can cause abnormal changes in the normal behaviour of the endothelium (endothelial dysfunction). Therefore hyperglycaemia promotes endothelial dysfunction by lowering nitric oxide levels, which may lead to diabetic complications like diabetic retinopathy (eye damage), nephropathy (kidney damage) or neuropathy (nerve damage). In addition, patients with diabetes also suffer from osteoporosis (thinning of bones). Osteoporosis is a bone disorder characterised by a reduction in bone mineral content leading to an increased risk of developing fractures. The increased risk of fractures in patients with type 2 diabetes is attributed to poor bone quality resulting from the harmful effects of high blood glucose. Studies have also shown that nitric oxide has a bone protective effect as demonstrated by its ability to prevent bone fragmentation and improve bone strength. Study of markers of endothelial function and bone metabolism will facilitate a better understanding about the origin of diabetic complications. This will aid in the development of novel therapeutic agents that target the harmful triggers in diabetes and eventually may prevent and retard the onset of the debilitating diabetic complications.

The purpose of this study is to define the prevalence of low bone density (osteopenia/osteoporosis) in patients with chronic pancreatitis. Secondary aims include investigating the prevalence of hypogonadism (low sex hormones) in patients with chronic pancreatitis and determining if hypogonadism and/or use of narcotic pain medications are risk factors for low bone density in this patient population. Hypothesis: Patients with chronic pancreatitis are at increased risk of low bone density (osteopenia/osteoporosis), and hypogonadism (low sex hormone levels) and narcotic pain medication use are independent risk factors for the development of low bone density in this patient population. The outcome measures include: i) Prevalence of low bone density (osteopenia/osteoporosis) in patients with chronic pancreatitis (as determined by DXA scan and fracture history). ii) Prevalence of hypogonadism (low sex hormones) in patients with chronic pancreatitis (as determined by sex hormone levels and clinical history). iii) Identification of hypogonadism and/or opioid use as risk factors for low bone density in patients with chronic pancreatitis (as determined by univariate and multivariate analysis of multiple risk factors). After obtaining written consent from potential subjects, a questionnaire will be performed outlining risk factors for low bone density. Dual X-ray absorptiometry (DXA scan) will be performed to evaluate for low bone density and a blood test will be performed to evaluate for low sex hormones, low levels of vitamin D, and other risk factors for low bone density.

The purpose of this study is to expand and continue a cohort of HIV-infected adults to establish the longitudinal Boston ARCH Cohort of 250 HIV-infected men and women with current substance dependence or ever injection drug use that have a spectrum of alcohol use; and to determine the effect of alcohol consumption on changes in bone health prospectively in the Cohort.

The aims of the present study are to investigate the effect of vitamin K2 on bone turnover, bone mass, bone structure, glucose metabolism, and arteriosclerosis. Osteoporosis, diabetes, metabolic syndrome and cardiovascular disease are common diseases that affect large groups of people in the Western world. Our hypotheses is that vitamin K2 (MK-7) reduces undercarboxylated osteocalcin in postmenopausal women and reduces bone turnover and increases bone mineral density; increases insulin sensitivity and decreases indices of arterial calcification.

The primary aim of the study is to measure bone formation in both lactating and non-lactating post-partum women and compare these to those in healthy non-pregnant controls. The secondary aim is to obtain measurements of Parathyroid Hormone-related Protein (PTHrP), markers of bone resorption, and calcium and vitamin D metabolism in these subjects. The investigators believe that lactating women will have an increase in bone resorption but no increase in bone formation when compared to non-lactating post-partum women and normal controls.

The primary aim of this study is to obtain measures of amino-terminal telopeptides of procollagen 1 (P1NP), a marker of bone formation, in lactating and non-lactating post-partum African-American women both at 6-8 and at 12-14 weeks post-partum, and to compare these values to those of normal controls. The secondary aim is to obtain at the same time points, measurements of Parathyroid Hormone-related Protein (PTHrP), additional markers of bone turnover [e.g. N-telopeptide of collagen cross-links (NTx), C-telopeptide of collagen cross-links (Ctx),bone specific alkaline phosphatase (BSAP) and osteocalcin (OC)], calcium and vitamin D metabolism in these subjects. These results will be compared with a non-African-American cohort of post-partum women and normal controls. The investigators hypothesize that African-American lactating women will have increased bone turnover when compared to non-lactating postpartum women and normal controls. The investigators further hypothesize that bone turnover is increased in lactating women independent of race.

Progress in the treatment of myeloma and myeloma bone disease has substantially increased overall survival, but relapse is inevitable and better treatment is needed. The bone microenvironment is tremendously complex, so that targeting single interactions between tumor and bone is unlikely to be effective. Treatments need to block centrally important, multifunctional pathways. The investigators data point to a central role of the osteocyte to induce heparanase, a multifunctional mediator of myeloma bone disease. Increased heparanase due to FGF23 may make systemic inhibitors of heparanase less effective in bone than elsewhere. FGF23 neutralizing antibodies have been developed for non-cancer conditions of FGF23 excess, such as chronic kidney disease (Shimada & Fukamoto, 2012), and could be used in MM alone or in combination with heparanase inhibitors. Complete neutralization of FGF23 has adverse effects, but neutralization of FGF23 excess may be practical, or in the future, suppression of excess FGF23 biosynthesis by osteocytes. The investigators hope to determine serum FGF23 and heparanase, Dkk1 and plasma klotho levels in patients with newly diagnosed and relapsed myeloma compared to healthy controls with this exploratory study.