Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gaucher's disease is characterized by hepatosplenomegaly, bone-marrow infiltration, osteonecrosis and bone thinning, associated with the presence of pathological macrophages that contain undegraded glycosphingolipids. To investigate the possible role of cytokines in the systemic and local manifestations of established Gaucher's disease, interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF alpha) and interleukin-10 (IL-10) were measured in freshly-separated serum. Samples from eight male and 14 female patients with type 1 Gaucher's disease were compared with sera from 22 healthy age- and sex-matched controls. Concentrations of IL-6 and IL-10 were significantly elevated in sera from patients with Gaucher's disease (11.9 +/- 1.8 (SEM) pg/ml and 5.4 +/- 0.5 (SEM) pg/ml, respectively) compared with those of controls (4.1 +/- 0.9 (SEM) and 0.8 +/- 0.3 (SEM) pg/ml, p < 0.0001). No significant differences in concentrations of TNF alpha or IL-1 beta were identified. IL-6 has been implicated in the development of localized osteolysis in multiple myeloma and in the development of post-menopausal osteoporosis. High concentrations of IL-6 in the serum of patients with Gaucher's disease may thus reflect the development of the bone lesions commonly associated with this disorder. Since IL-6 and IL-10 are important regulators of lymphocyte growth and differentiation, and IL-6 concentrations were significantly raised in patients with oligo- or polyclonal increases in serum immunoglobulins, enhanced release of these cytokines from pathological macrophages provides a pathological link between Gaucher's disease and associated lympho-proliferative disorders.
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PMID:Pro-inflammatory cytokines and the pathogenesis of Gaucher's disease: increased release of interleukin-6 and interleukin-10. 909 85

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

A novel method for the development of a user-defined structural model simulating cancellous bone of the human calcaneus is described using stereolithography (SL). The digital image of a cancellous bone section was modified by skeletonisation and dilation to produce a structural model of uniform wall thickness, determined by the resolution of the stereolithography system. Six SL models were produced using the same data file. The SL models were assessed using the McCue CUBAclinical ultrasound bone densitometer. The broadband ultrasound attenuation (BUA) and velocity (VOS) values obtained were commensurate with the commercial phantom provided with the CUBAclinical system. The intra- and inter-sample variability for the six SL models were similar at 5% for BUA and 2.5% for VOS. Stereolithography offers the potential to firstly, simulate perforation and thinning of cancellous bone associated with osteoporosis, and secondly, to evaluate the dependence of ultrasonic and mechanical parameters upon cancellous bone structure.
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PMID:Development of a cancellous bone structural model by stereolithography for ultrasound characterisation of the calcaneus. 945 93

The architecture of trabecular bone is thought to be controlled by mechanosensitive bone cells, where hormones provide a background for their responses to mechanical signals. It has been suggested that, in osteoporosis, this response is hampered by changed hormonal levels, thereby increasing the mechanical set point of the cells, which would lead to bone loss. We have investigated if a temporary increase of the mechanical set point causes deterioration of trabecular bone architecture, such as seen in osteoporosis. Furthermore, the effects of a changed loading pattern were investigated for the same reason. For this purpose, we used a computer simulation model, which was based on the regulation of bone architecture by mechanosensitive osteocytes. It was found that a temporary shift of the mechanical set point causes no lasting changes in architecture. Although an increase of the mechanical set point induces bone loss, the mechanism of bone loss (trabecular thinning) differs from what is observed in osteoporosis (loss of whole trabeculae). Hence, a change of the mechanical set point alone cannot explain bone loss as seen in osteoporosis. On the other hand, the removal of load components in a particular direction resulted in irreversible loss of whole trabeculae. These results indicate that such temporary changes in loading patterns could be important risk factors for osteoporosis.
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PMID:Effect of mechanical set point of bone cells on mechanical control of trabecular bone architecture. 947 35

The decline in skin thickness that occurs with aging interests many different groups. Among these are pharmaceutical, cosmeceutical, and cosmetic companies promoting antiaging or antiwrinkling products, geriatricians and rheumatologists treating elderly and steroid-dependent patients who are "outliving" their skin, cosmetic surgeons, and dermatologists. Dermatologists are frequently asked how to prevent or slow aging of the skin. The answer regarding "photoaging" of sun-exposed skin is obvious; the answer regarding aging of photoprotected skin is not. Although the bulk of epidemiologic literature about aging and thinning of photoprotected skin is from the 1970s, literature regarding risk factors for and treatment of aging and thinning of the bony skeleton is more recent. Because both skin and bone are composed of more than 70% type I collagen, it may be hypothesized that the pathophysiologic processes involved in chronological atrophy of both tissues may overlap, thereby providing a foundation for further investigation of the skin. A better understanding of skin and bone loss may motivate the "appearance-conscious" public to modify risk factors (e.g., begin exercising) or select hormonal therapies (e.g., postmenopausal hormone replacement) to reduce aging of the skin. These measures may provide additional benefits, such as decreasing the risk of osteoporosis.
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PMID:Risk factors for reduced skin thickness and bone density: possible clues regarding pathophysiology, prevention, and treatment. 948 82

Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.
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PMID:osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. 957 43

Bone thinning causing both fractures and severe pain not associated with fractures has been recognized in patients with chronic liver diseases. The patients most commonly affected are those with primary or secondary biliary cirrhosis, but those with alcoholic liver disease and cirrhosis after active chronic hepatitis may also be involved. Chronic liver disease has also been recognized as an important cause of osteoporosis in both sexes, with the mechanism thought to be a combination of calcium and/or vitamin D. The 9.1% patients with chronic active hepatitis accompanied with osteodystrophy. But 50% cirrhotic patients accompanied with osteodystrophy. Bone densitometry was determined by Digital Image Processing Method (Osteodystrophy < mean-2SD: age- and sex-matched normal value). Serum levels of osteocalcin (BGP) and parathyroid hormone (PTH) in patients of hepatic cirrhosis without osteodystrophy were lower than those with osteodystrophy. These results were suggested that hepatic osteodystrophy was rapidly turnover osteodystrophy. To function physiologically, vitamin D must be hydroxylation in liver to 25-(OH)-D and subsequently by the kidney to 1 alfa, 25-(OH)2-D. Osteodystrophy associated with hepatic cirrhosis is due to a defect in the 1 alfa-hydroxylation by the kidney rather than a hepatic hydroxylation defect. 1 alfa OH-D3 is very useful for treatment for hepatic osteodystrophy.
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PMID:[Hepatic osteodystrophy]. 964 89

Senescence is the effect of the immune system incapacity to see "self" and "non-self"; timo-involution induced down-regulation of immunoregulatory -T and B-lymphocytes. Immunosenescence mutations in oral cavity are examined. Even the oral ecosystem presents disorders in quality and quantity of the bacterial plaque and a different immune response. Age senescence is particularly evident in the masticatory apparatus, in fact the dental tissues have remarkable morpho-structural physiological changes; the epithelial, connective and osseous tissues of the periodontium have structural age changes related to the collagen synthesis and physical properties, with an increase of the stroma and a decrease of cell population. The osseous tissue presents cellular atrophy, sclerosis, osteoporosis and is undergoing a continuous structural remodelling; the oral mucous membranes show a thinning of epithelium and an increase of the stroma related to the parenchyma. Specific individual changes could be appraised in the involution of stomatognathic apparatus, more than an indefinite reduction of the performances.
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PMID:[Changes in the biological and immunologic parameters in the oral cavity of the aged. Review]. 979 66

Twenty-seven thalassaemic patients (13 F, 14 M, aged 8.1-14.9 yr), regularly transfused and chelated with desferrioxamine (30-40 mg/kg/day) were studied. Every patient was submitted to auxological evaluations, dual X-ray absorptiometry to measure bone mineral density (BMD), and to the determination of bone metabolic markers of osteoclastic activity (total urinary hydroxylysylpyridinoline crosslinks, carboxyterminal pyridinoline crosslinked telopeptide of type I collagen [ICTP]) and of osteoblastic activity (bone Gla protein [BGP] and carboxyterminal propeptide of type I procollagen [PIPC]). The evaluations were repeated after 1 year, during which 13 patients continued desferrioxamine chelation while 14 underwent deferiprone chelation (75 mg/kg/day in 3 doses). The data demonstrate widespread bone alterations consisting of osteoporosis, growth failure and bone age delay. Lumber spine (L2-L4) BMD areal values (Z score) inversely correlated with age, as did height SDS of both male and female patients, indicating osteoporosis progressing with age in parallel with growth insufficiency. No clear-cut alterations in bone mineral metabolism were found in basal state and after 1 year. Extensive MR imaging studies are needed to define the contribution of residual bone marrow hyperplasia to thalassaemic osteopathy suggested by subtle radiological signs as enlargement of bone marrow cavities with thinning of the cortical bone and abnormalities of the trabecules of spongy bone.
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PMID:Bone density and metabolism in thalassaemia. 1009 Nov 47

Using histopatholoical method, we investigated the bone histomorphometric changes in ovariectomied goats at different time courses. Eight goats, female, aged one and a half years, were randomly divided into two groups, the control and the ovariectomy (OVX). Iliac crest biopsies were separately processed before ovariectomy and at 60 days, 120 days and 180 days after ovariectomy. The histomorphometric changes were observed. It was found that the bone structure in trabecular bone remained relatively constant in the control group throughout the whole study. In contrast, the trabecular quantity was slightly decreased and the trabeculae were disconnected in OVX at 60 days after ovariectomy. The bone structure was characterized by the thinning of the trabeculae, the further discontinuance and quantity loss of trabeculae, and the anlargement of marrow cavity at 120 days to 180 days after ovariectomy. Apparently, these bone structural changes manifested with typical osteopenia pathological changes. Our results may serve as a basis for the design of further studies using OVX goat as an animal model for postmenopausal osteoporosis.
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PMID:[Bone histomorphometric changes in ovariectomized goat at different time courses]. 1068 56


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