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)

Three of seven Arctic fox kits, Alopex lagopus, trapped on St. Paul Island, Alaska, had evidence of rickets and hyperparathyroidism. Radiographic, morphologic and histologic examination confirmed the diagnosis. The disease was presumed to be a juvenile-onset disease due to calcium-deficient intake following weaning. The possibility of insufficient exposure to sunlight could not be determined. No other abnormalities (e.g., genitourinary) were found. Skeletal involvement was quite varied. All growth plates exhibited columnar hyperplasia compatible with rickets, while the metaphyses showed decreased trabeculation and cortical thinning compatible with osteodystrophia fibrosa. One fox had bilateral metaphyseal fractures through this osteodystrophic bone.
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PMID:Juvenile rickets and hyperparathyroidism in the Arctic fox. 52 28

The assumption that a change in interstitial bone thickness reflects a converse change in resorption depth was recently found to be incorrect. Accordingly, we re-examined previously published data concerning trabecular thickness and wall thickness in 15 patients with nonosteomalacic osteopenia following intestinal bypass surgery for obesity. The average number of remodeling cycles completed since the operation was calculated according to two assumptions: First, that the measured activation frequency had been present since the operation; second, that activation frequency had increased in the first two years after operation because of secondary hyperparathyroidism. In comparison with mean wall thickness in 40 normal subjects (38.6 microns), resorption depth calculated in accordance with the first assumption was significantly increased (54.1 microns; p less than 0.001), but calculated in accordance with the second assumption was unchanged (42.1 microns; NS). Reasons are given for believing that the second assumption is more likely to be correct than the first. Mean trabecular thickness and mean wall thickness were significantly correlated (r = 0.68; p less than 0.005). We conclude: 1) Mean resorption depth cannot be inferred from interstitial bone thickness, but can be calculated if the number of remodeling cycles corresponding to the observed structural changes is known. 2) Even though interstitial bone thickness is reduced, trabecular thinning following intestinal bypass surgery is mainly due to decreased wall thickness, as the result of defects in the recruitment and/or function of osteoblasts. The same probably applies to cancellous osteopenia in various other gastrointestinal and hepatobiliary disorders. 3) The study of intestinal bone disease may shed light on the pathogenesis of other, more common, forms of osteoporosis.
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PMID:The ambiguity of interstitial bone thickness: a new approach to the mechanism of trabecular thinning. 206 39

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.
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PMID:Irreversible bone loss in osteomalacia. Comparison of radial photon absorptiometry with iliac bone histomorphometry during treatment. 407 86

X-ray images of the second metacarpals of 153 hyperparathyroid subjects were measured and an index of cortical bone was derived. Compared with normal standards, the cortical index was above the 50th percentile in only 17.8% of women and 13.6% of men. Comparing the mean index of hyperparathyroid subjects with the normal indices of each 10-year age group, it was found that the differences were highly significant and were the same for all age groups in each sex. In particular, the difference was not greater between older female hyperparathyroid and normal subjects than it was between younger female hyperparathyroid and normal subjects. It appears that bone involvement in the form of excessive cortical thinning is extremely common in hyperparathyroidism and that sex and age do not further influence its incidence or severity.
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PMID:Bone loss in primary hyperparathyroidism. 474 15

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.
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PMID:Bone lesions in growing swine fed 3% cement kiln dust as a source of calcium. 708 4

Aging and menopause are the two main determinants of osteoporosis, a rarifying osteopathy due to bone loss. Type I osteoporosis observed in post-menopausal women is characterized mainly by trabecular bone loss results from an unbalanced coupling between resorption and formation inducing a thinning of trabeculae and from an increased osteoclast activation resulting in irreversible trabecular perforation. Anti-osteoclastic drugs prevent trabecular and cortical bone loss. Drugs that stimulate osteoblastic proliferation thicken trabecular plates but do not restore the normal trabecular microarchitecture after complete destruction of a large number of trabeculae. In type II osteoporosis, cortical bone loss is favoured by secondary hyperparathyroidism and is responsible for hip fracture. Calcium and vitamin D supplementations decrease the risk of hip fractures by reducing the secondary hyperparathyroidism.
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PMID:[Mechanisms of bone loss in osteoporosis]. 779 29

The aims of this review on the use of skeletal surveys in the radiological assessment of renal osteodystrophy were threefold: to describe the radiological pattern of renal osteodystrophy in a local cohort of patients with chronic renal failure, to assess whether serial radiographs of the hands may effectively replace full radiological skeletal surveys in the long-term follow-up assessment of renal bone disease, and to formulate a grading system for bone resorption due to hyperparathyroidism. A radiological study of 61 patients with chronic renal failure revealed 20 (32.8%) patients with unequivocal radiological signs of renal osteodystrophy. The main abnormal radiological features observed in descending order of frequency were: osteopenia with associated cortical thinning and coarsened bone trabecular pattern (75%), subperiosteal resorption (60%), osteosclerosis (50%), extraosseous calcification (30%) and periosteal new bone formation (15%). A five-grade method of assessing the severity and extent of bone resorption was formulated. The study showed that 40% of the patients with a radiological diagnosis of renal osteodystrophy did not show changes in the hand radiographs. This finding precluded a recommendation of hand radiographs being used alone in the long-term radiological follow-up of patients with renal bone disease. An alternative was proposed and this was a limited radiological skeletal survey of three projections: radiographs of both hands, chest including the clavicles and the pelvis. This limited study would result in a cost saving of 62% as compared to a full study.
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PMID:Use of skeletal surveys in the radiological assessment of renal osteodystrophy--a study in the Singapore General Hospital. 826 51

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.
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PMID:Mineralized bone loss at different sites in dialysis patients: implications for prevention. 964 32

There is no one cause of bone fragility; genetic and environmental factors play a part in development of smaller bones, fewer or thinner trabeculae, and thin cortices, all of which result in low peak bone density. Material and structural strength is maintained in early adulthood by remodelling; the focal replacement of old with new bone. However, as age advances less new bone is formed than resorbed in each site remodelled, producing bone loss and structural damage. In women, menopause-related oestrogen deficiency increases remodelling, and at each remodelled site more bone is resorbed and less is formed, accelerating bone loss and causing trabecular thinning and disconnection, cortical thinning and porosity. There is no equivalent midlife event in men, though reduced bone formation and subsequent trabecular and cortical thinning do result in bone loss. Hypogonadism contributes to bone loss in 20-30% of elderly men, and in both sexes hyperparathyroidism secondary to calcium malabsorption increases remodelling, worsening the cortical thinning and porosity and predisposing to hip fractures. Concurrent bone formation on the outer (periosteal) cortical bone surface during ageing partly compensates for bone loss and is greater in men than in women, so internal bone loss is better offset in men. More women than men sustain fractures because their smaller skeleton incurs greater architectural damage and adapts less effectively by periosteal bone formation. The structural basis of bone fragility is determined before birth, takes root during growth, and gains full expression during ageing in both sexes.
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PMID:Pathogenesis of bone fragility in women and men. 1204 92

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.
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PMID:Renal bone disease: a new conceptual framework for the interpretation of bone histomorphometry. 1281 35


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