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

A study involving 18 patients shows that thinning of the upper cortex of the clavicle in adults under the age of 45 is most commonly due to renal osteodystrophy or coeliac disease. Cortical thinning should not therefore be regarded as synonymous with osteoporosis. Cortical thinning is usually associated with clavicular erosion in renal osteodystrophy but not in osteoporosis or osteomalacia. The radiological diagnosis of coeliac disease is suggested when thinning of the clavicular cortex is combined with air--fluid levels on abdominal radiography in a patient under the age of 45 years.
 ...
PMID:Thinning of the clavicular cortex in adults under the age of 45 in osteomalacia and hyperparathyroidism. 45 4

Two case reports from a high fluoride (10 ppm) rural community. They presented with severe degrees of dental fluorosis, hyper-sensitivity of teeth and skeletal fluorosis all arising from the ingestion of high amount of fluoride in water over a long period of time. Both cases had deformities of the upper and lower limbs. However, the deformities were more pronounced in the lower limbs than in the upper limbs, resulting in knock knee. Radiological finding showed osteosclerosis of the axial bones while the appendicular bones exhibited osteoporosis. There was marked change of bone structure observed as osteomalacia, and course trabecular bone pattern. Osteoporosis was also associated with cortical thinning. Periosteal bone apposition was observed in the bones: and genu valgum of the limbs. Biochemical tests revealed normal values for serum calcium and inorganic phosphate. However, the serum alkaline phosphatase was elevated. This may be an indication of a pathological condition where there are possible compensatory mechanisms to maintain normal levels of serum calcium and inorganic phosphate. One case which had undergone corrective surgical intervention of the lower limbs four years earlier, had continued to live in the same environment using drinking water with 10 ppmF after corrective surgery, and showed no improvement.
 ...
PMID:Skeletal and dental fluorosis: two case reports. 191 81

To study the pathophysiology of bone disorder after gastrectomy, 320 patients and 40 Wistar male rats were used. Clinically, patients who had received gastrectomy 1-15 years previously, were examined for skeletal symptoms, serum biochemistry, microdensitometry of second metacarpal bone, and 20 of them were then studied in a calcium infusion test. Using microdensitometry, abnormality of bone metabolism was observed in 38% of the patients. In severe cases, a significant decrease of serum Ca. and increase of alkaline phosphatase were observed (p less than 0.05), 65% complained of joint pain. In the calcium infusion test, severe cases showed a low urinary excretion of Ca, like osteomalacia, and unlike osteoporosis. Experimentally, body weight & amount of food intake decreased and fatty diarrhea was observed in rats after total gastrectomy. Skeletal changes including thinning of the cortex, loss of medullary trabeculation & decrease of bone ash and biochemical changes such as low serum Ca. 25(OH)D3, 24, 25(OH)2D3 and high iPTH levels were observed. Also the bone formation rate was lower than control as detected by tetracycline double labelling method. As low food intake & fatty diarrhea after gastrectomy which result in Ca. & vit. D insufficiency may be the major etiology of bone disorder.
 ...
PMID:[Bone disorder after gastrectomy--clinical & experimental studies]. 226 41

Osteopenia in the elderly is responsible for 1.3 million fractures per year in the United States. The acute care costs associated with this disorder are between $6 and $10 billion dollars annually. Although much has been learned over the last few years of the factors that predispose patients to osteoporosis and how these factors may be avoided, the precise pathophysiologic mechanisms for bone loss remain obscure. Significant technological advances have been made in the 1980s in the development of noninvasive methods for measuring bone mineral density that give indirect assessments of bone mass. However, these methods are very controversial, are not suitable for mass screening for detecting subjects potentially at risk, and have a limited place in routine clinical care. Osteoporosis is characterized by thinning and fragmentation of trabecular bone, which is probably irreversible when it is far advanced. The most reasonable therapeutic approach may be prevention, which can be achieved in many patients by estrogen therapy in the perimenopausal years and insuring an adequate dietary calcium intake, particularly in adolescents and in the elderly. Physical activity throughout life is also likely to be important in maintaining adequate bone mass. It is important to differentiate osteoporosis from other causes of osteopenia, for example, osteomalacia, primary hyperparathyroidism, and malignant diseases such as myeloma, since these bone diseases have a different natural history, pathophysiology, and treatment.
 ...
PMID:Osteopenia. 331 29

We examined the relationships between the changes in bone mineral deficit in the radius, determined by single-energy photon absorptiometry at standard proximal and distal sites, and in the ilium, determined by bone histomorphometry, during the treatment of osteomalacia of diverse etiology in 28 patients. In the ilium, relative osteoid volume decreased by 75-80% in both cortical bone (from 6.0% to 1.5%) and trabecular bone (from 30.1% to 6.6%) during a mean treatment duration of 2 yr. There was also a significant fall in iliac cortical porosity from 10.3% to 7.8%. As a result, mineralized bone volume increased by 7.5% in cortical and by 40.1% in trabecular bone; the cortical and trabecular increments were correlated (r = 0.69, P less than 0.001). The properly weighted increase for the entire tissue sample was 18.6%. By contrast, there was no change in bone mineral at either radial site, although there was a 2% increase at both sites when allowance was made for age-related bone loss during treatment. The proximal and distal age-adjusted increments was correlated (r = 0.76, P less than 0.001), but there was no correlation between the changes in any photon absorptiometric and any histomorphometric index. In that iliac cortical bone turnover in normal subjects was 7.2%/yr, we estimated the rate of bone turnover to be less than 2%/yr at both proximal and distal radial sites, including any trabecular bone present at the distal site. Compared to appropriate control subjects, the bone mineral deficits fell during treatment from 19.2% to 17.1% at the proximal radius (greater than 95% cortical bone) and from 20.5% to 18.5% at the distal radius (greater than 75% cortical bone). In the ilium the deficits, assuming attainment of normal values for osteoid volume and cortical porosity, fell from 41.7% to 36.1% in cortical and from 31.5% to 6.3% in trabecular bone, the properly weighted combined deficit falling from 38.6% to 27.7%. The irreversible iliac cortical deficit was entirely due to cortical thinning because of increased net endosteal resorption; the resultant expansion of the marrow cavity offset the modest loss of fractional trabecular mineralized bone. We conclude: in osteomalacia there is a large irreversible and a small reversible bone mineral deficit at both proximal and distal radial sites, in similar proportion to the iliac cortex but of smaller magnitude; the anatomic basis of the irreversible bone mineral deficit at all three sites that persists despite correction of the mineralization defect by appropriate treatment is thinning of cortical bone, most likely owing to prolonged secondary hyperparathyroidism; (c) there is no evidence that the proportion of trabecular bone in the distal radius at any site proximal to the radioulnar joint has any relevance to the interpretation of measurements made at that site; (d) there are at least three functional subdivisions of trabecular bone depending on proximity to hematopoietic marrow, fatty marrow, or synovium; and (e) single photon absorptiometry of the radius is an excellent method for measuring cortical bone mass in the appendicular skeleton, but is of little value for the assessment of changes in trabecular bone status.
 ...
PMID:Irreversible bone loss in osteomalacia. Comparison of radial photon absorptiometry with iliac bone histomorphometry during treatment. 407 86

Thinning of the upper cortex of the clavicle, measured on a standard chest radiograph, may help in the diagnosis of osteoporosis. No precise level at which osteoporosis occurs can be given, but a reading of 1.5 mm. or under is indicative of osteoporosis, while a smaller incidence is associated with readings of 2 mm. and above. There is significant correlation between thinning of the clavicular cortex and other radiological indications of osteoporosis. Thinning may occasionally point to unsuspected bone disease, in osteomalacia as well as in osteoporosis. As chest radiographs are taken in a high proportion of both outpatients and inpatients, the method has a wide applicability.
 ...
PMID:Width of clavicular cortex in osteoporosis. 576 59

Bone histology, bone mineral content, and calcium absorption were evaluated in 10 patients with primary biliary cirrhosis and osteopenia, before and after 1 yr of treatment with oral 25-hydroxycholecalciferol. Before treatment, quantitative histomorphometric analysis of full-thickness iliac crest bone biopsy specimens with double-tetracycline labeling demonstrated that 9 of 10 patients had osteoporosis. None had osteomalacia. Fasting intestinal calcium absorption correlated well with trabecular bone volume (r = 0.85). Bone mineral content measured by 125I-photon absorption was low in 6 of 10 patients, and it correlated poorly with iliac crest trabecular bone volume. After 1 yr of treatment with oral 25-hydroxyvitamin D3, bone mineral content fell in all 8 patients who were restudied. Iliac crest trabecular bone volume increased in 3 patients, 2 of whom had the greatest pretreatment impairment in calcium absorption, but fell in 5. Bone fractures continued to occur in 3 of 5 patients who were alive after 1 yr and developed for the first time in a sixth patient. We conclude that 25-hydroxyvitamin D3 is ineffective in reversing the bone thinning in the majority of primary biliary cirrhosis patients, but it may be helpful in a few selected patients.
 ...
PMID:Osteoporosis in primary biliary cirrhosis: effects of 25-hydroxyvitamin D3 treatment. 707 48

Three-w-old male Sprague-Dawley rats were given a zinc (Zn)-deficient (0 ppm Zn) or a Zn-adequate diet (30 ppm Zn) supplemented with 0, 0.5 or 100 ppm cadmium (Cd) for up to 5 mo. The proximal convoluted tubules of the kidneys had degenerative changes in the rats fed the Zn-deficient diet containing 100 ppm Cd [Zn 0, Cd 100], but there were no lesions in other groups. Electron microscopy showed cytoplasmic vacuolation of the proximal tubules, mitochondrial swelling and coagulative necrosis in Zn 0:Cd 100 rats. The present study revealed diminished bone growth and cortical thinning of the femur, but there was no osteomalacia seen in Itai-Itai disease patients. The results indicate that Zn deficiency may enhance the renal toxicity of Cd, but that dietary Cd did not cause osteomalacia even under severe Zn-deficient conditions.
 ...
PMID:Effect of cadmium in the zinc deficient rat. 757 44

To characterize the magnitude and location of mineralized bone loss, 40 patients (20 men, 20 women, 29 white, 11 black) with clinically significant renal osteodystrophy who could be unambiguously classified based on histologic criteria as having osteitis fibrosa (OF; 20 cases) or osteomalacia (OM; 20 cases) were studied; they had been on maintenance hemodialysis for 4.6 +/- 3.0 yr. One hundred forty-two healthy women of similar age and ethnic composition served as control subjects. In all subjects, the proportions of mineralized bone, osteoid, and porosity (nonbone soft tissue) were measured separately in cortical and cancellous bone tissue, from intact full-thickness biopsies of the ilium, representative of the axial skeleton. The results were related to the volumes of cortical and cancellous bone tissue separately and to the volume of the entire biopsy core. Approximately three-quarters of the patients had measurements in the appendicular skeleton by single photon absorptiometry of the radius and morphometry of the metacarpal. Disease effects did not differ significantly between ethnic groups. Mineralized cortical bone volume (per unit of core volume) was reduced by approximately 45% in both patient groups. Mineralized cancellous bone volume was significantly increased by 36% in the patients with OF and nonsignificantly reduced by 9% in the patients with OM; however, the reduction in the latter patients was significant in relation to tissue volume. The combined total deficit for both types of iliac bone was approximately 20% in the patients with OF and approximately 40% in the patients with OM. Significant reductions in appendicular cortical bone were demonstrated in both patient groups at both measurement sites. Regardless of the current histologic classification, the major structural abnormality in the skeleton is generalized thinning of cortical bone due to increased net endocortical resorption, the most characteristic effect on bone of hyperparathyroidism. Protection of the skeleton from the adverse consequences of renal failure will require therapeutic intervention in patients with no symptoms of either renal or bone disease.
 ...
PMID:Mineralized bone loss at different sites in dialysis patients: implications for prevention. 964 32

My purpose in this article is to restore the histologic appraisal of renal bone disease to the mainstream of bone and mineral metabolism from which it has been separated for many years. Historically, both the two major components were found in varying degrees in most patients, although one or other of them often predominated. For more than 15 years bone biopsy has been used almost exclusively to classify individual patients into hyperparathyroid, osteomalacic, mixed and adynamic categories according to rigid non-overlapping criteria, and remarkably few histologic data have been reported. All metabolic bone diseases result from disordered bone remodeling, the physiologic mechanism for replacing bone that has become too old to carry out its mechanical or metabolic functions. Bone remodeling is not directly concerned with the regulation of plasma calcium, which reflects the level of equilibration at quiescent bone surfaces between systemic and bone extracellular fluid set by parathyroid hormone. The separation of remodeling from homeostasis explains the concurrence of increased turnover and decreased plasma calcium in chronic renal failure; it is the homeostatic system, rather than the remodeling system, which is resistant to parathyroid hormone. The effect of mild hyperparathyroidism is a nonspecific increase in bone turnover, of which the best index is the bone formation rate measured by double tetracycline labeling expressed per unit of bone surface. Increased turnover is always accompanied by increased reversible mineral deficit. In prolonged hyperparathyroidism there is also accelerated irreversible bone loss manifested mainly as thinning of cortical bone, detectable in chronic renal failure before any symptoms, due to increased resorption depth on the endocortical surface. In severe hyperparathyroidism resorbed bone is replaced, not by a lesser quantity of normal bone, but by a mixture of vascular fibrous tissue and woven bone, referred to as osteitis fibrosa. In osteomalacia there is increased accumulation of osteoid, due not to increased turnover, but to prolongation of mineralization lag time, which in conjunction with increased thickness, surface and volume of osteoid is diagnostic. Converting histomorphometric data into category assignment discards most of the useful information, which can be retained by two-dimensional representation of severity. For the hyperparathyroid dimension, bone formation rate measured by double tetracycline labeling expressed per unit of bone surface is the most useful although not ideal. For the osteomalacic dimension a mineralization index was constructed that is unaffected by age or race. In patients with osteitis fibrosa, bone formation rate per unit of bone surface and mineralization index were inversely correlated. For the third dimension a structure/formation index was constructed which increases with age in healthy women and shows weak inverse correlation with bone formation rate. The structure/formation index is lower than normal in patients with osteitis fibrosa, and should be useful in the study of osteopenia in chronic renal failure. Bone formation rate is low in osteomalacia, but some patients have subnormal rates through quite a different mechanism. The frequency of this finding has been overestimated for several reasons: failure to exclude atypical osteomalacia (increased surface and volume but not thickness of osteoid), use of inappropriate reference values, and failure to measure the bone formation rate on endocortical and intracortical surfaces. In healthy women bone formation rate can be zero on the cancellous surface alone. Low bone formation rate is sometimes due to diabetes but most often is the expected response to subnormal parathyroid hormone secretion accompanying an excess of calcium, a situation recognized only recently because of improvement in parathyroid hormone assay methodology. Low cancellous bone formation rate should not increase fracture risk because turnover is much lower in the peripheral than in the central skeleton, and all reports of increased fracture risk are flawed or open to different interpretation. Low bone formation rate is associated with reduced skeletal buffering of calcium and increased soft tissue calcification. This is not a new disease needing its own treatment, however, but represents the final stage of skeletal adaptation to a surfeit of calcium. The concept of adynamic bone disease has been harmful by directing attention away from the most important consequence of over-treatment of hyperparathyroidism.
 ...
PMID:Renal bone disease: a new conceptual framework for the interpretation of bone histomorphometry. 1281 35


1 2 Next >>