PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “BONE DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1993

[Histological classification of uremic bone disease and clinical significance of bone biopsy].

Bone biopsy was performed in 429 cases of uremic bone disease and they were classified histologically into 3 groups--high turnover 129 (30%), low turnover 102 (24%) and mixed type 198 (46%) cases. The histological features of the high turnover type were increased corrected mineralization rate (CMR) and osteoclast member and decreased mineralization lay time (MLT), while those of the low turnover type were on the contrary. In the mixed there were decrease of CMR and increase of MLT and osteoclast number. Bone aluminum positive rate was determined; it was 75% and 80% respectively in the low turnover and mixed type and 29% in high turnover. Biochemical study showed that significantly higher levels of serum PTH and alkaline phosphate in the high turnover type and low levels of serum 1,25(OH)2D3 and 25(OH)D3 in the low turnover. These results suggested that high turnover uremic bone disease is caused by secondary hyperthyroidism and low turnover mainly related to aluminum toxicity or other causes such as vitamin D deficiency.

Adolescent↗
PubMed1999

[Osteoporosis and metabolic bone diseases; clinical relationship].

Metabolic bone diseases with disturbed bone remodeling lead to loss of biomechanical quality and atraumatic fractures. Differential diagnosis, prevention and adequate treatment should already start early in the course of these disorders to prevent fractures. Thus, clinical osteology is more than the simplified connection "low bone mineral density--fractures--osteoporosis". This review summarizes physiological relations between bone tissue and calcium homoeostasis as well as the relation between structure and function. In addition, the main metabolic osteopathies "osteoporosis, primary hyperparathyroidism and osteomalacia" are presented from a clinical point of view. The importance and the diagnostic values of biochemical parameters and of the transiliacal biopsy are discussed. In this respect the quantitative measurement of the mineralization density (bone mineral density distribution = BMDD) seems to be of high value and extends the well established bone histomorphometry. This recently introduced method has the power to distinguish between small differences in the degree of mineralization of the matrix with high precision and reproducibility. The results of quantitative backscattered electron imaging in the scanning electron microscope improve the differential diagnosis of bone diseases with alterations in mineralization density, helps to detect mixed etiology (e.g. osteoporosis plus osteomalacia) and facilitate decision making for treatments. The value of biochemical, radiological, osteodensitometric and histopathological tests for diagnosis and treatment depends on the knowledge of the clinical relations and the complex interactions between calcium-, phosphate- and bone metabolism.

Age Factors↗
PubMed1994

Gorham's disease or vanishing bone disease: plain film, CT, and MRI findings of two cases.

Gorham's disease may develop in any region of the skeleton, but shows a predilection for the bones of the shoulders and pelvic girdles. Less frequently, the disease may involve the spine, and it is the proximity to the spinal cord which may worsen the patient's outcome. We report the clinical outcomes of two children with typical, yet differently localized involvement, and also review the plain film, CT and MRI findings.

Cervical Vertebrae↗
PubMed2006

Measurement of PTH fragments for assessment of renal bone disease in hemodialysis patients.

BACKGROUND: Renal bone pathology involves a spectrum from 'high-turnover' to 'low-turnover bone disease' (adynamic bone disease, classical osteomalacia). The diagnosis of the latter usually requires bone biopsy. Inhibitory parathyroid hormone (PTH) fragments may be useful for its noninvasive diagnosis. METHODS: A cross-sectional study was performed in 54 patients on chronic hemodialysis which involved measurements of intact PTH (iPTH; Nichols assay), total PTH (tPTH; Scantibodies assay), and the cyclase-activating PTH fragment (CAP). The level of cyclase-inactive PTH fragment (CIP) was calculated. At the same time, serum calcium, phosphorus, and alkaline phosphatase levels as well as the current therapy for secondary hyperparathyroidism were recorded. In selected patients, bone radiographs were evaluated for osteitis fibrosa. RESULTS: A high correlation (r = 0.94) was found between iPTH and tPTH, with the tPTH levels being lower by 30-40%. A similar association was also found for CAP (r = 0.988) and for CIP (r = 0.93). 3 out of the 54 patients had a CAP/CIP ratio of < or =1 which has been associated with adynamic bone disease. A higher CIP ratio was significantly associated with the use of aluminum-hydroxide- and calcium-containing phosphate binders. CONCLUSIONS: iPTH and tPTH assays are highly correlated. In a general hemodialysis patient population, low-turnover bone disease appears to be rare, when the CAP/CIP ratio is used as a marker. A high CIP value was associated with therapy using aluminum hydroxide, a drug known to carry a risk of adynamic bone disease.

Aged↗
PubMed1955

Distinctive diagnostic features of material aspirated from marrow in metabolic bone diseases.

In a series of cases of Paget's disease of the bone, two types of cells not previously described were observed in material aspirated from bone marrow in areas of osteitis deformans. One type was mononuclear, the other was giant, multinucleated and syncytial. They have been identified as osteoblasts and osteoclasts, respectively. The identification was based mainly on correlation with the histologic picture of osteitis deformans and of normal-growing bones as seen in section studies. Both osteoblasts and osteoclasts were recovered in aspirated bone marrow material in other instances of metabolic bone diseases associated with increased bone repair and bone resorption-in hyperparathyroidism, osteoblastic malignant lesions, rickets, hemolytic anemia in children, and in normal infants in the growth zone of bone in the tibia. They were not seen in senile and postmenopausal osteoporosis. Recognition of osteoblasts and osteoclasts in smear preparations from aspirated bone marrow material may serve as a diagnostic aid in metabolic bone diseases. The differentiation of osteoblasts from neoplastic cells is important in cases in which metastatic cancer of the bone is suspected and x-ray findings are inconclusive.

Biopsy↗
PubMed1991

Radiologic study of endosteal, intracortical, and periosteal surfaces of hand bones in metabolic bone diseases.

In metabolic bone diseases, subtle abnormalities occur on the three surfaces of bone, the recognition of which is important for diagnosis, as well as in follow-up studies, to recognize progression or regression. These resorptive and formative changes are best studied in fine-detail hand radiographs under 6 to 8 times magnification by a relatively simple radiologic method (microradioscopy). The periosteal resorption of hyperparathyroidism is thus recognized earlier than by regular radiography, and intracortical resorption, not detectable by the naked eye, can be visualized. The latter is also seen frequently in nutritional osteomalcia, renal osteodystrophy, and thyrotoxicosis, and sometimes in acromegaly. Endosteal resorption in developing involutional osteoporosis can also be recognized more efficiently by microradioscopy than by ordinary radiographs without magnification. Fine-detail hand radiographs may thus be used as an inexpensive preliminary measurement for diagnosis of osteoporosis.

Bone Diseases, Metabolic↗
PubMed2001

Bone disease after liver transplantation.

1. Bone disease is a common problem in patients with chronic liver disease and liver transplants. 2. The cause of bone disease in these patients is multifactorial. 3. Bone disease worsens initially after liver transplantation, with subsequent improvement over time. However, bone disease in liver transplant recipients is common with long-term follow-up. 4. Evaluation of these patients should include metabolic and hormonal evaluations in conjunction with dual energy x-ray absorptiometry or bone mineral density evaluation. 5. Treatment with calcium, vitamin D, and hormonal supplements should be considered when appropriate for patients awaiting and after liver transplantation. The use of bisphosphanates and calcitonin also should be considered, although published studies in these populations are few in number.

Adrenal Cortex Hormones↗
PubMed1995

Drug-induced metabolic bone disease.

Drug-induced metabolic bone disease via modification of resorption, formation, and mineralization is responsible for a spectrum of disorders classified as osteoporosis, osteomalacia, and adynamic bone disease. Bone disease and the coincident risk of fracture and disability are well-documented with use of glucocorticoids, L-thyroxine, ethanol, tobacco, anticonvulsants, neuroleptics, and chemotherapeutic agents. Physician awareness of these risks highlights the need for close monitoring of dosages and drug interactions and allows for intervention with nutritional support, antiresorptive agents, and proformation agents.

Caffeine↗
PubMedDate not supplied

Parenteral nutrition-related bone disease.

Parenteral nutrition (PN)-related bone disease remains a problem in patients of all ages. Understanding of the pathogenesis of PN-related bone disease is complicated by the effect of underlying illnesses, therapeutic interventions, and pre-existing nutrition deficiencies before the initiation of PN therapy. Interrelation of various nutrients, for example, calcium, phosphorus, and vitamin D, in their effects on bone mineralization, demands simultaneous assessment of the role of multiple nutrients and increases the difficulty in defining the role of a single nutrient in the development of bone disease. However, recent reports indicate that there exist a number of factors important in the development of PN-related bone disease and some factors such as increased mineral requirement are unique to growing infants whereas other factors such as aluminum toxicity may be common to both adult and pediatric populations. Nonnutritional factors, including chronic use of potent loop diuretics and altered acid-base status, can affect urine mineral loss, cell metabolism, and bone mineralization, particularly in small, preterm infants. Current evidence indicates that the cause of PN-related bone disease is multifactorial, and the prevention of PN-related bone disease awaits better delineation of the exact sequence of pathogenic events.

Aluminum↗
PubMed1996

Metabolic bone disease of prematurity.

Metabolic bone disease is recognized with increasing frequency in very-low-birth-weight infants. Radiological changes characteristic of rickets have been found in 55% of infants with a birth weight of less than 1000 g and in 23% of infants weighing less than 1500 g at birth. Twenty-four per cent of infants with a birth weight of less than 1500 g have fractures. The main aetiological factor is insufficient phosphorus supplementation. The aetiology is, however, multifactorial and also includes calcium deficiency, vitamin D deficiency, certain drugs, aluminium loading and immobilisation. The method of choice in detecting subclinical mineral bone disease of prematurity is measurement of bone mineral density, but there is as yet no single good diagnostic method available for premature infants. The optimal mineral and vitamin D requirement of the premature infant must be established so that proper recommendations can be given. The current recommended vitamin D dose in Europe (ESPGAN 800-1000 IU/day) is probably too high when extra minerals are supplied. Moreover, the duration of mineral supplementation may need to be continued until the infant has reached a body weight of 3.5 kg. This article deals with the aetiology, pathogenesis, diagnosis and future prospects of metabolic bone disease of prematurity.

Bone Diseases, Metabolic↗
PubMed1996

Low serum levels of alkaline phosphatase of bone origin: a good marker of adynamic bone disease in haemodialysis patients.

BACKGROUND: Adynamic bone disease was recently described to be increasingly prevalent in the dialysis population. At present the diagnosis of this type of renal osteodystrophy can only be made by bone histomorphometry. We assessed the value of different biochemical serum markers in the diagnosis of adynamic bone disease. METHODS: In 103 haemodialysis patients a bone biopsy was performed after double tetracycline labelling, and the serum levels of intact PTH, osteocalcin, and the bone isoenzyme of alkaline phosphatase were determined. Bone alkaline phosphatase was measured by an optimized agarose gel electrophoretic method, recently shown to have a high accuracy, precision and reproducibility, also in the lower range. RESULTS: In 38 (37%) of the patients the diagnosis of adynamic bone disease was histologically established. Constructing receiver operator curves optimal cut-off levels for the diagnosis of adynamic bone disease were determined, being <=27 U/litre for the bone isoenzyme of alkaline phosphatase, <=14 microg/litre for osteocalcin and <=150 pg/ml for intact PTH. Concentrations of bone alkaline phosphatase or intact PTH below these cut-off levels, were shown to be the best performing tests in the detection of adynamic bone disease as indicated by a sensitivity of 78.1 and 80.6% and a specificity of 86.4 and 76.2% respectively. Applying Bayes' theorema, it was calculated that in the current haemodialysis population in which a prevalence of adynamic bone disease up to 35% has been described, the positive predictive values for the proposed cut-off values are 75% for bone alkaline phosphatase, 65% for intact PTH and 55% for osteocalcin. Moreover, in this population, levels of bone alkaline phosphatase and intact PTH below the optimal cut-off excluded hyperparathyroid bone disease. CONCLUSION: In view of the relative easy and accurate methodology for bone alkaline phosphatase determination, the closer physiological link with osteoblast function and the lesser expense for its determination we suggest that this marker is a useful tool in the non-invasive diagnosis of the adynamic type of bone disease in the individual patient.

Alkaline Phosphatase↗
PubMed2003

The pathophysiology of bone disease in gastrointestinal disease.

Reduced bone mass and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Undoubtedly, genetics play an important role, but other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in inflammatory bowel disease (IBD) and other lifestyle factors, such as smoking or being sedentary, may contribute to reduced bone mass. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD and probably also in coeliac disease are also known to enhance bone resorption. The discovery of the role of the receptor to activated NFkappaB (RANK) interaction with its ligand RANKL in orchestrating the balance between bone resorption and formation may link mucosal and systemic inflammation with bone remodelling, since RANK-RANKL are also involved in lymphopoiesis and T-cell apoptosis. Low circulating leptin in response to weight loss in any gastrointestinal disease may be an important factor in reducing bone mass. This report will summarize current concepts regarding gastrointestinal diseases (primarily IBD, coeliac disease and postgastrectomy states) and low bone mass and fracture.

Bone Density↗
PubMed1992

Early kidney transplantation may prevent aluminium-related bone disease.

In uraemia patients aluminium (Al) accumulation in bone leads to low turn-over bone disease. Al-related bone disease causes bone pain, non-traumatic fractures and hypercalcaemia, and does not respond to treatment with vitamin D compounds. Al-contaminated dialysate and ingestion of Al-containing phosphate binding agents are the main risk factors for bone Al accumulation. Studies of selected patients have indicated that Al-related bone disease ameliorates after successful kidney transplantation, but systematic studies of bone Al have not been reported. In a prospective study we investigated the effect of successful kidney transplantation on bone Al and clinical bone disease.

Adrenal Cortex Hormones↗
PubMed2001

Posttransplant bone disease: a case illustrating dramatic improvements in bone density with vitamin D replacement therapy.

Although bisphosponates are proposed as first-line treatment for posttransplant bone disease they are not optimal in all situations. A kidney transplant recipient developed hypercalcemia from mobilization of extraskeletal calcium. He had low serum parathyroid hormone and vitamin D; high calcium excretion; and normal calcium intake. Bone biopsy revealed severe osteomalacia. Bisphosphonates, used in the early treatment of acute hypercalcemia, were not indicated to treat osteomalacia. However, over several months serum calcium declined sufficiently to allow treatment of the bone disease with oral calcitriol. Dual-energy radiographic absorptiometry over the next 2 years documented dramatic improvements in bone density (percent of young-normal controls) : from 63 to 85%, at the lumbar spine; from 38 to 67%, at the femoral neck. This response to treatment could not have been achieved with an antiresorptive strategy. Optimal management of posttransplant bone disease requires a diagnostic approach, which considers all plausible contributing factors.

Absorptiometry, Photon↗
PubMed1993

Uremic mixed bone disease. A case report.

Renal osteodystrophy (ROD) is a complex disease of bone caused by renal failure. A case of uremic mixed bone disease with severe maxillofacial involvement is reported. The pathogenesis and various pathologic features of ROD are discussed.

Adult↗
PubMed1980

An evaluation of 1 alpha-hydroxy-and 1,25-dihydroxyvitamin D3 in the treatment of renal bone disease.

40 patients with bone disease due to chronic renal failure have been treated with 1 alpha-hydroxyvitamin D3 or 1,25-dihydroxyvitamin D3 for a total of 750 patient-months. Both compounds were very effective in relieving bone pain and muscle weakness, and in reversing the radiographic and biochemical indices of disturbed skeletal metabolism. Their effects as judged from bone biopsies were, however, less complete, and histological improvement occurred only in a few patients. Patients with the combination of osteitis fibrosa and osteomalacia responded better than patients with either abnormality alone. Factors of importance in adversely influencing the outcome of treatment included a high pre-treatment level of calcium or immunoreactive parathyroid hormone, and a failure to augment secretion of calcitonin during treatment. It is concluded that a major therapeutic advantage of 1 alpha-OHD3 and 1,25(OH)2D3 over previously available forms of vitamin D is their rapid onset and reversal of action. These drugs do not invariably reverse bone disease and may give rise to unwanted effects. They should therefore only be used with adequate clinical, biochemical and radiographic supervision. They should not be used indiscriminately in all renal patients.

Adolescent↗
PubMedDate not supplied

Bone disease in primary biliary cirrhosis: increased bone resorption and turnover in the absence of osteoporosis or osteomalacia.

The role of vitamin D in hepatic osteodystrophy was examined. Eleven unselected patients with primary biliary cirrhosis (PBC) were assessed for disorders of mineral and vitamin D metabolism. Six were not receiving supplementary vitamin D, and five were being treated with oral vitamin D (50,000 IU daily). Serum levels of 25-hydroxyvitamin D were normal in all patients receiving oral therapy and in 4 of 6 untreated patients. Levels of serum 1,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D were normal or near normal in all patients. Studies were repeated after 6 months of therapy with parenteral vitamin D2 (100,000 IU i.m. monthly) in 7 patients. Initial bone histomorphometry revealed no evidence of osteomalacia or osteoporosis. However, the bone resorption surface of trabecular bone was increased. This abnormality was no longer present on repeat bone biopsies obtained after parenteral vitamin D therapy, and bone formation had decreased. In addition, trabecular bone volume remained normal in the face of the lower rate of bone formation. Increased bone resorption surface in the absence of osteoporosis or osteomalacia has not been previously described in PBC. Improvement in this bone parameter, associated with the finding of a decrease in the formation of bone and in hydroxyproline excretion in urine after parenteral vitamin D, suggests that increased turnover may be an early feature of the bone disease which complicates PBC and that parenteral vitamin D may retard the rate at which hepatic osteodystrophy develops in chronic cholestatic liver disease.

Adult↗