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PubMedDate not supplied

[Histologic diagnosis of metabolic bone diseases: bone histomorphometry].

Histomorphometry or quantitative histology is the analysis on histologic sections of bone resorption parameters, formation and structure. It is the only technique that allows a dynamic evaluation of the activity of bone modelling after labelling with tetracycline. Moreover, the new measurement procedures through the use of the computer allow an assessment of bone microarchitecture too. Histomorphometric bone biopsy is a reliable and well-tolerated procedure. Complications are reported only in 1% of the subjects (hematoma, pain, transient neuralgia). Histomorphometry is used to exclude or confirm the diagnosis of osteomalacia. It is employed in the evaluation of bone damage associated with particular treatments (for example, anticonvulsants) or in case of rare bone diseases (osteogenesis imperfecta, systemic mastocytosis). It is also an essential approach when clinical, biochemical and other diagnostic data are not consistent. Finally, it is a useful method to understand the pathophysiologic mechanisms of drugs. The bone sample is taken at the level of iliac crest under local anesthesia. It is then put into methyl-metacrilate resin where the sections are prepared for the microscopic analysis of the various histomorphometric parameters.

Biopsy↗
PubMed2004

[Bone scintigraphy for the diagnosis of metabolic bone diseases].

Bone scintigraphy may show well recognized changes in metabolic bone diseases. Diffuse scintigraphic changes are generally of little diagnostic value. However, focal changes are often helpful in the complex diagnostic work-up of metabolic diseases; in some disorders such as Paget's disease bone scintigraphy may even give the major input regarding diagnostic imaging. The article presents the different scintigraphic patterns seen in metabolic bone diseases and discusses the use of bone scintigraphy in clinical practice.

Bone Diseases, Metabolic↗
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↗
PubMed2005

Myeloma bone disease.

Bone destruction is a hallmark of multiple myeloma, and recent studies demonstrated a strong interdependence between tumor progression and bone resorption. Increased bone resorption as a major characteristic of multiple myeloma is caused by osteoclast activation and osteoblast inhibition (uncoupling). Myeloma cells alter the local regulation of bone metabolism by increasing the receptor activator of NF-kappaB ligand (RANKL) and decreasing osteoprotegerin (OPG) expression within the bone marrow microenvironment, thereby stimulating the central pathway for osteoclast formation and activation. In addition, they produce the chemokines MIP-1alpha, MIP-1beta and SDF-1alpha, which also increase osteoclast activity. Furthermore, myeloma cells suppress osteoblast function by the secretion of osteoblast inhibiting factors, e.g. Dickkopf (DKK)-1. The resulting bone destruction releases several cytokines, which in turn promote myeloma cell growth. Therefore, the inhibition of bone resorption could stop this vicious circle and not only decrease myeloma bone disease, but also the tumor progression. Preclinical studies provided strong evidence that the suppression of the osteoclast activity using bisphosphonates, RANKL blockade or inhibition of MIP-1alpha or MIP-1beta is effective both in reducing myeloma bone disease and tumor growth and therefore may offer an important treatment strategy in multiple myeloma.

Bone Diseases↗
PubMed2005

Involvement of ICAM-1 in bone metabolism: a potential target in the treatment of bone diseases?

Bone diseases such as osteoporosis, osteoarthritis and rheumatoid arthritis (RA) affect a great proportion of individuals, with debilitating consequences in terms of pain and progressive limitation of function. Existing treatment of these pathologies has been unable to alter the natural evolution of the disease and, as such, a clearer understanding of the pathophysiology is necessary in order to generate new treatment alternatives. One therapeutic strategy could involve the targeting of intercellular adhesion molecule-1 (ICAM-1; CD54). In bone, ICAM-1 is expressed at the surface of osteoblasts (Obs) and its counter-receptor, leukocyte function-associated antigen-1 (LFA-1; CD11a), at the surface of osteoclast (Oc) precursors. ICAM-1 blockade between the Ob and the pre-Oc results in an inhibition of Oc recruitment and a modulation of inflammation, which could potentially help in controlling disease activity in bone pathologies. So far, clinical studies on ICAM-1 blockade in bone diseases have been limited to RA. A better understanding of the implication of this adhesion molecule in Ob/Oc interactions and inflammatory mediation in the bone pathological state, however, is needed. As new discoveries on the role of this adhesion molecule are being reported, ICAM-1 could become a potential target for other bone diseases as well.

Animals↗
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↗