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At least 19 recordsLinked to original sources
PubMed1981

Bone scintigraphy and densitometry in symptomatic haemodialysis bone disease.

Bone scintigraphy and densitometry (iodine-125 photon absorptiometry) were performed in eight patients with symptomatic haemodialysis bone disease. The bone scintiscan showed either hot spots or hyperactivity as a feature of metabolic bone disease. The bone density (BMC/W) was reduced, but could not be distinguished from the degree of demineralisation found in asymptomatic patients on long-term haemodialysis. Therefore, bone density measurements require critical interpretation. Complementary bone scintigraphy should be used in symptomatic haemodialysis bone disease for assessing the extent of the disease.

Adult↗
PubMed2001

Myeloma bone disease.

Bone destruction is a hallmark of myeloma, with 70% to 80% of patients manifesting bone involvement. Destruction is mediated through normal osteoclasts (OCLs), which respond to local osteoclast-activating factors (OAFs) produced by myeloma cells or by other cells in the local microenvironment. OAFs implicated in myeloma bone disease include tumor necrosis factor-beta (TNFbeta), RANK ligand (RANKL), interleukin-1 (IL-1), parathyroid hormone-related protein (PTHrP), hepatocyte growth factor (HGH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFalpha), and macrophage inflammatory protein-1-alpha (MIP-1alpha). To date, the leading candidates for OAFs are MIP-1alpha and RANKL. Adhesive interactions between marrow stromal cells and myeloma cells induce marrow stromal cells to secrete IL-6, a potent myeloma growth/survival factor that may contribute to the bone disease. Evaluation of myeloma bone disease includes plain radiographs, and newer methods, such as magnetic resonance imaging (MRI), positron emission tomography (PET) scans, technetium-99m-sestamibi (Mibi) scanning, and dual-energy x-ray absorptiometry (DEXA) scanning, may provide more complete information. In addition, biochemical markers of bone resorption are being evaluated, although the limited availability of these assays and lack of extensive testing in patients make their routine use premature. Treatment of myeloma bone disease includes radiation therapy, vertebroplasty, surgery, and bisphosphonates. New developments on the pathogenesis and treatment of myeloma bone disease present great opportunities to combat bone disease.

Animals↗
PubMedDate not supplied

Disturbances of acid-base balance and bone disease in end-stage renal disease.

Bone disease in patients with chronic renal failure (CRF) is thought to be the consequence primarily of the interplay of several factors, including the serum levels of parathyroid hormone (PTH), vitamin D, calcium, and phosphorus, and exposure to bone toxins such as aluminum or amyloid. Recently the metabolic acidosis noted with CRF has been implicated as an additional factor contributing to the genesis of bone disease. Although metabolic acidosis might be the dominant factor in the cause of bone disease in some instances, more commonly this acid-base disturbance interacts with other factors contributing to the development of bone disease. The following article summarizes the data in support of an important role for metabolic acidosis in the genesis of bone disease in patients with CRF and presents our recommendations for treatment of uremic acidosis to prevent or treat the bone disease.

Acid-Base Imbalance↗
PubMed1992

[Bone histology and clinical diagnostic criteria in aluminum-induced bone disease].

Bone remodeling and aluminum (Al) staining were carried out in 429 bone biopsies from patients with uremic bone disease, 273 cases were Al positive (64%). In high-turnover, low-turnover and mixed type of renal osteodystrophy the Al-positive rate was 29%, 75% and 80%, and Al deposition on bone surfaces was 44 +/- 33%, 80 +/- 30% and 62 +/- 35% respectively. Thus the low-turnover and mixed type have a higher Al-positive rate and more Al deposition than the high-turnover type. Animal experiments using decalcified bone matrix implants showed that Al inhibited all bone remodeling processes except cartilage formation. These and other data indicate that Al induces low-turnover bone disease, i.e., osteomalacia or aplastic bone disease. Osteomalacia in our series showed increased osteoid area and mineralization lag time, and decreased calcified bone area, bone mineralization rate and cells number. Aplastic bone disease was similar with that but had reduced osteoid and a normal ratio of steroid to calcified bone. The relationship of these studies to clinical diagnostic criteria of Al-induced bone disease is discussed.

Adolescent↗
PubMed2001

An update on the nonoperative treatment of patients with metastatic bone disease.

Bone metastases constitute a major problem in oncology because of their frequency and the therapeutic problems they present. Treatment indications depend on accurate diagnosis including histologic type, number, location, and sensitivity to treatment. New findings in the pathophysiology of bone metastases, new staging procedures, new treatment modalities, and better guidelines improve therapeutic effectiveness and the quality of life of patients. There are biologic and biomechanical indications for treatment. The goals of treatment are pain relief, restoration and maintenance of function, and the prevention of complications. The nonsurgical treatment of patients with metastatic bone disease includes analgesics, hormones, radiation therapy, cytotoxic drugs, radiopharmaceuticals, chemoablation, vertebroplasty, and bisphosphonates. The future of the treatment of patients with metastatic bone disease may involve the identification of biochemical markers. The author presents an overview of the current scientific concepts of metastatic bone disease and indications and specific strategies for nonoperative treatment of patients with tumor-induced osteolysis from metastatic bone disease.

Biology↗
PubMed1988

Uses and limitations of bone biopsy in management of metabolic bone disease.

Bone biopsy is now an established diagnostic and investigative procedure which is widely used in the management of metabolic bone diseases. Its unique feature is that it facilitates direct visualization of bone cells and bone structure and, through double tetracycline labelling, allows the indirect measurement of bone turnover. Its main diagnostic contribution has been in unravelling the complexities of renal osteodystrophy, which consequently is now much better understood. However, it has also uncovered a variety of mineralization defects caused by agents such as fluoride, diphosphonates and aluminum that might otherwise have bone unsuspected clinically. Its main investigative roles have been to provide unique insight into the mechanisms of bone loss with age and in osteoporosis, and to assess the effects on bone and bone cells of potential therapeutic agents in established osteoporosis. This has been possible through the use of histomorphometry, which is used to quantify changes in bone volume and turnover as well as alterations in the microanatomical structure of bone that can reduce bone strength and increase the risk of fracture. Although most biopsies will continue to be taken for histomorphometry, recent studies have shown that specimens may be used to provide additional information such as quantitation and localization of elements within bone, and to provide bone cells for in vitro culture. It is likely that, in future, specimens will be taken from patients with various disorders so that the techniques of cell and molecular biology can be applied to harvested bone cells and thus provide a new dimension to our understanding of metabolic bone disease.

Biopsy, Needle↗
PubMed1982

Changes in plasma bone GLA protein during treatment of bone disease.

Bone Gla protein (BGP) was measured in the plasma by radioimmunoassay (RIA) during treatment of 59 patients with bone diseases including Paget's disease (N = 9), primary hyperparathyroidism (N = 25), chronic renal failure (N = 20), and cancer involving bone (N = 5). Plasma BGP was increased above normal in all patients. BGP decreased in the patients with Paget's disease following the acute and chronic administration of salmon calcitonin. Plasma BGP was higher in women then in men with primary hyperparathyroidism. Following parathyroidectomy, BGP decreased in both sexes but the decrease was significant in women only. Plasma BGP was increased in patients with renal osteodystrophy and did not change after hemodialysis. In the patients with bone cancer, plasma BGP decreased during treatment of the attendant hypercalcemia with salmon calcitonin. Although plasma BGP and serum alkaline phosphatase (AP) levels were generally correlated in these studies, there were examples of dissociation between the two. The measurement of plasma BGP appears to provide a specific index of bone metabolism that may in some circumstances be more sensitive than serum alkaline phosphatase measurement. However, further studies are necessary to establish the clinical value of plasma BGP measurement by RIA in the management of patients with bone diseases.

Alkaline Phosphatase↗
PubMed1976

[Recent progress in morphology and diagnosis of bone diseases and bone tumors (author's transl)].

1. Bone structure is shaped by a specialized bone cell system comprising osteoblasts, osteocytes and osteoclasts. --2. The function of this bone cell system is impaired by metabolic bone disease altering bone structure, bone mass and mineral content. --3. In metabolic bone disease a striking improvement in morphologic diagnosis could be obtained recently using undecalcified preparations of bone tissue as well as histomorphometric methods. --4. For exact diagnosis and successful therapy of bone tumors interdisciplinary cooperation is mandatory. The advantages of modern morphologic methods are proven helpful in diagnosing benign and malignant bone tumors.

Age Factors↗
PubMed1999

Recent advances in bone biology provide insight into the pathogenesis of bone diseases.

Bone is modeled during embryonic development by endochondral and membranous ossification and is continuously remodeled thereafter under the influence of local and systemic factors to provide structural support and assist in calcium homeostasis. Recent studies of knockout and transgenic mice have increased understanding of the regulation of bone modeling during development and of remodeling of mature bone and have shed new light on the pathogenesis of a number of bone disorders. For example, fibroblast growth factor receptor-3, parathyroid hormone-related protein, and tartrate-resistant acid phosphatase affect the function of chondrocytes during endochondral ossification (the latter two by regulating their life spans and thus growth plate thickness and bone length). Some ubiquitously expressed genes seem unexpectedly to have unique functions that are largely confined to bone cells: M-CSF, C-Fos, PU.1, and NF-kappaB are required for osteoclast formation, whereas c-Src and Mitf (microphthalmia transcription factor) are required for osteoclast activity after the cells have formed. Knockout of these genes results in osteopetrosis, a disorder characterized by persistence in marrow cavities of unresorbed osteocartilaginous matrix and, as in some affected humans, by increased mortality. Some proteins seem to act as negative regulators of bone cell function, for example osteoprotegerin (a soluble TNF receptor) in osteoclasts; osteocalcin, bone sialoprotein, and 5-lipoxygenase in osteoblasts. Regulation of osteoclast life span may be an important mechanism by which estrogen and bisphosphonates prevent bone loss in conditions characterized by increased bone resorption, such as postmenopausal osteoporosis. The unique requirement of bone cells for certain gene products raises the possibility that these cells may have specific responses to inhibitory or stimulatory agents, and that signaling molecules in these response pathways could be specific targets for novel therapies to treat or prevent common bone diseases.

Animals↗
PubMed1980

A comparison of bone scanning and radiology in the evaluation of patients with metabolic bone disease.

Bone scans and radiographs were evaluated in 80 patients with metabolic bone disease (27 with osteoporosis, 14 with primary hyperparathyroidism, 24 with renal osteodystrophy and 15 with osteomalacia). The bone scan did not suggest a metabolic bone disorder in any of 27 patients with histologically proven osteoporosis. In 22 (81%) patients radiographs were reported as showing osteoporosis. In 10 (70%) vertebral fractures were seen on X-ray while these were noted in 11 (41%) patients on the bone scan. Vertebral fractures were usually visualised on the bone scan when these had occurred less than one year previously. In primary hyperparathyroidism the bone scan was suggestive of a metabolic bone disorder in 7 of 14 (50%) patients, while radiographs were reported as showing evidence of hyperparathyroidism in three (21%) cases. The bone scan suggested the presence of a metabolic bone disorder in all 24 patients with renal osteodystrophy and 15 patients with osteomalacia while the correct diagnosis was obtained in 14 (58%) and nine (60%) of these patients on X-ray. It is concluded that the bone scan is the more sensitive investigation in patients with osteomalacia, primary hyperparathyroidism and renal osteodystrophy. For osteoporosis radiology is the investigation of choice but the bone scan may be of value in assessing the duration of vertebral collapse.

Animals↗
PubMedDate not supplied

Vitamin D deficiency: a culprit in metabolic bone disease.

Bone formation and bone remodeling are complicated processes regulated by systemic hormones and paracrine factors which regulate calcium and phosphate fluxes and cellular differentiation. The many actions of vitamin D reinforces its importance in the process of growth, maturation and aging of bone. An understanding of these important regulators of bone metabolism is important to understanding the clinical disorders as they are related to alterations in vitamin D metabolism and metabolic bone disease. Specific disorders of vitamin D metabolism can be related to clinical disease states of aging, altered lifestyles, gastrointestinal, renal and hepatic disease. A classification of altered vitamin D metabolism as related to its clinical states is presented. The scope of vitamin D deficiency from childhood rickets to adult osteomalacia and osteoporosis is presented, Intermediate syndromes of high turnover osteoporosis, subclinical vitamin D-deficiency states, role of vitamin D analogues in treating type I and type II osteoporosis is discussed. Treatment guidelines for managing this scope of clinical vitamin D disorders are provided.

Aging↗
PubMed2001

The clinical impact of metabolic bone disease in coeliac disease.

Bone mineral density was measured by dual energy x ray absorptiometry (DEXA) at the lumbar spine and femoral neck in 15 adults who had metabolic bone disease in association with coeliac disease (mean age at diagnosis 53.5 years, range 37 to 66). Results were expressed as a T score (the number of standard deviations by which patient's bone density differed from the sex matched young adult mean). Three patients had no skeletal symptoms and normal routine calcium biochemistry but severely reduced axial bone mineral density on DEXA. Eleven patients had symptomatic skeletal fractures, including fractures of proximal femur (3), vertebrae (4), and radius (6). Three patients had osteomalacia confirmed on bone biopsy, two of whom had characteristic biochemistry. Secondary and tertiary hyperparathyroidism were seen. Seventy five further patients (60 female) with coeliac disease (mean age 52.0 years, median duration of gluten-free diet 3.4 years) and 75 paired healthy age and sex matched controls were questioned on past fracture history. Patients with coeliac disease underwent detailed studies of calcium biochemistry, dietary intake, and bone mineral density. Sixteen had a past history of fractures (chi(2) = 10.7, p = 0.0004, v controls), which were of typical osteoporotic type. Ten patients had fracture before diagnosis of coeliac disease and six after diagnosis. Patients who had a fracture were older (56.3 v 50.3 years, p < 0.02, Wilcoxon rank sum test) than those with no fracture. There was no significant difference in bone mineral density (z score -0.31 v -0. 77), serum calcium (2.30 v 2.26 mmol/l), 25-hydroxyvitamin D (19.7 v 23.7 nmol/l), parathyroid hormone (2.6 v 3.1 pmol/l), or dietary calcium intake (1021.0 v 1033.0 mg/day) in patients with fracture compared with those without fracture. Metabolic bone disease is common in coeliac disease and is associated with premature osteoporotic fractures.

Absorptiometry, Photon↗