Osteoporosis complicating some inborn or acquired diseases.

Osteoporosis in chronic diseases is very frequent and pathogenetically varied. It complicates the course of the underlying disease by the occurrence of fractures, which aggravate the quality of life and increase the mortality of patients from the underlying disease. The secondary deterioration of bone quality in chronic diseases, such as diabetes of type 1 and type 2 and/or other endocrine and metabolic disorders, as well as inflammatory diseases, including rheumatoid arthritis - are mostly associated with structural changes to collagen, altered bone turnover, increased cortical porosity and damage to the trabecular and cortical microarchitecture.

Involvement of bone in systemic endocrine regulation.

The skeleton shows an unconventional role in the physiology and pathophysiology of the human organism, not only as the target tissue for a number of systemic hormones, but also as endocrine tissue modulating some skeletal and extraskeletal systems. From this point of view, the principal cells in the skeleton are osteocytes. These cells primarily work as mechano-sensors and modulate bone remodeling.

Hormonal and bone parameters in pubertal girls.

Here we analyzed associations between muscles mass, total bone mineral content (BMC), lumbar spine bone density (BMD L1-L4) and serum or urine hormones in healthy peripubertal girls. Total BMC and areal BMD L1-L4, muscle mass and fat were measured by dual-energy X-ray absorptiometry (DXA). Muscle force (N) was estimated by a dynamometer.

New molecules modulating bone metabolism - new perspectives in the treatment of osteoporosis.

In this review the authors outline traditional antiresorptive pharmaceuticals, such as bisphosphonates, monoclonal antibodies against RANKL, SERMs, as well as a drug with an anabolic effect on the skeleton, parathormone. However, there is also a focus on non-traditional strategies used in therapy for osteolytic diseases. The newest antiosteoporotic pharmaceuticals increase osteoblast differentiation via BMP signaling (harmine), or stimulate osteogenic differentiation of mesenchymal stem cells through Wnt/beta-catenin (icarrin, isoflavonoid caviunin, or sulfasalazine).

Trace elements have beneficial, as well as detrimental effects on bone homeostasis.

The protective role of nutrition factors such as calcium, vitamin D and vitamin K for the integrity of the skeleton is well understood. In addition, integrity of the skeleton is positively influenced by certain trace elements (e.g.

Hypercalcemia. Pathophysiological aspects.

The metabolic pathways that contribute to maintain serum calcium concentration in narrow physiological range include the bone remodeling process, intestinal absorption and renal tubule resorption. Dysbalance in these regulations may lead to hyper- or hypocalcemia. Hypercalcemia is a potentionally life-threatening and relatively common clinical problem, which is mostly associated with hyperparathyroidism and/or malignant diseases (90 %).

Polymorphisms associated with low bone mass and high risk of atraumatic fracture.

Osteoporosis is a serious disease characterized by high morbidity and mortality due to atraumatic fractures. In the pathogenesis of osteoporosis, except environment and internal factors, such as hormonal imbalance and genetic background, are also in play. In this study candidate genes for osteoporosis were classified according to metabolic or hormonal pathways, which regulate bone mineral density and bone quality (estrogen, RANKL/RANK/OPG axis, mevalonate, the canonical circuit and genes regulating the vitamin D system).

Bone tissue as a systemic endocrine regulator.

Bone is a target tissue for hormones, such as the sex steroids, parathormon, vitamin D, calcitonin, glucocorticoids, and thyroid hormones. In the last decade, other "non-classic" hormones that modulate the bone tissue have been identified. While incretins (GIP and GLP-1) inhibit bone remodeling, angiotensin acts to promote remodeling.

[Genetics and pharmacogenetics of osteoporosis].

Osteoporosis is a serious disease characterized by high morbidity and mortality due to atraumatic fractures. In pathogenesis of osteoporosis, except environment, internal factors, such as hormonal dysbalance and genetic background, are also in play. In this review, candidate genes for osteoporosis are classified according to metabolic or hormonal pathways, which regulate bone mineral density/and or quality (estrogen, RANKL/RANK/OPG, mevalonate, Wnt circuit, genes for collagen and vitamin D).

New insights into the physiology of bone regulation: the role of neurohormones.

Bone metabolism is regulated by interaction between two skeletal cells - osteoclasts and osteoblasts. Function of these cells is controlled by a number of humoral factors, including neurohormones, which ensure equilibrium between bone resorption and bone formation. Influence of neurohormones on bone metabolism is often bimodal and depends on the tissue, in which the hormone is expressed.

[Regional migrating osteoporosis - a case report].

Regional migrating osteoporosis (RMO) was observed in young man with episodes of bone pain in bearing joints, which migrated from hip to leg and subsequently to knee on the unilateral side. Dynamic scintigraphy (SPECT) carried out during relapse of pain demonstrated increased accumulation of radioizotope in Lisfrank joint, distal epiphysis of femur and proximal epiphysis of tibia on the unilateral side due to hyperperfusion and high metabolic turnover in these regions of the skeleton. Dia-gnosis of RMO was confirmed by magnetic resonance (MRI), which showed bone marrow edema of corresponding regions.

[Drug induced osteoporosis].

Loss of bone mass resulting from the treatment of chronic diseases is not unusual. However, osteoporosis in such patients is typically diagnosed too late, usually after a fracture appears. Particular attention should be given to glucocorticoids, which are commonly used in internal medicine.

Trace elements and bone health.

The importance of nutrition factors such as calcium, vitamin D and vitamin K for the integrity of the skeleton is well known. Moreover, bone health is positively influenced by certain elements (e.g.

[Neuro-skeletal biology and its importance for clinical osteology].

Bone remodeling is determined by function of two basic cell forms--bone resorbing osteoclasts and bone formation activating osteoblasts. Both cells are under control of a variety of endogenic and environmental factors, which ensure balance between bone resorption and bone formation. This article reviews the neuro-hormonal factors with osteoanabolic (central isoform of serotonin, melatonin, cannabinoids, beta 1 adrenergic system, oxytocin, ACTH and TSH) or osteocatabolic effects (neuropeptide Y, neuromedin U, beta2 adrenergic system).

[Soft tissues, hormones and the skeleton].

Mechanical load activates bone modeling and increases bone strength. Thus physical activity is extremely important for overall bone health. Muscle volume and muscle contraction are closely related to bone mineral density in men and women, although these relationships are more significat in men.

[Role of genetics in prediction of osteoporosis risk].

Osteoporosis is in 60-80% a hereditary disease with a characteristic multifactorial pathogenesis during which the effects of many "weak" genes interact with external factors. To date, most information relating to the correlations between genes and bone parameter variability (density, quality and metabolism) has been provided by association studies of candidate genes for osteoporosis. The best known genes related to bone density have been identified as the genes for the vitamin D, estrogen and calcitonin receptor, LRP5 and LRP6.

[Familial hypercalcemia and hypophosphatemia: importance in differential diagnosis of disorders in calcium-phosphate metabolism].

Hypercalcemia and hypophosphatemia are symptoms of two relatively rare hereditary diseases and are extraordinarily important from the standpoint of the differential diagnosis. Mutation in calcium sensing receptor gene (CaSR) clinically manifests as familial hypocalciuric hypercalcemia (FHH) or as the much more serious neonatal hyperparathyreosis. Hypercalciuric hypocalcemia is extremely rare.

[Relationships of hormones of adipose tissue and ghrelin to bone metabolism].

Body adipose tissue influences bone metabolism through mechanical load, as well as via hormones released into circulation. Such hormones are adipocytokines--leptin, adiponectin, TNF-alpha, IL-6, resistin and visfatin. Some of them exert an osteoanabolic effect, while the others activate bone resorption.

[Celiac disease and its relation to bone metabolism].

Celiac disease (nontropical sprue) is autoimmune disorder of the intestinal mucose, which usually develops in humans hypersensitive to gluten. The disease can occur at any age, with the greatest occurrence in early adulthood. Besides intestinal symptomatology--abdominal pain, diarrhoea and weight loss--celiac disease is often accompanied by extra-intestinal complications including osteopenia or osteoporosis and osteomalacia.

[Pathogenetically complicated case of osteoporosis in a young man].

Osteoporosis, is a serious disease both in women and men, with a high risk of fractures. However, its pathogenesis differs markedly, with the secondary form being more common in men. The aim of this case study is to demonstrate the complex pathogenesis of a severe osteoporosis in a 23-year-old heavy smoker with histiocytosis X, diabetes insipidus (DI), subclinical hypogonadism and low serum levels of IGF-I.

Biochemical markers of bone remodeling correlate negatively with circulating TSH in postmenopausal women.

Objective: To evaluate the interrelations between circulating TSH and bone metabolism in postmenopausal women.

Patients And Methods: In a total of 60 postmenopausal women serum level of several hormones (thyrotropin [TSH], free thyroxine [FT4], dehydroepiandrosterone sulfate [DHEAS], parathyroid hormone [PTH]), bone turnover markers (carboxyterminal propeptide of type I procollagen [PICP] and cross-linked telopeptide of type I collagen [ICTP]) as well as of other compounds such as IGF-I, sex hormone binding globulin (SHBG), 25-OH vitamin D3 (25-OHD3) and urinary free deoxypyridinoline (Dpd (2h)) concentrations were estimated. Bone mineral density (BMD) at the spine and BMD at the hip were measured by DXA method.

Is A163G polymorphism in the osteoprotegerin gene associated with heel velocity of sound in postmenopausal women?

Osteoprotegerin (OPG) plays an important inhibitory role in osteoclastogenesis. Polymorphisms in the OPG gene recently have been associated with various bone phenotypes including fractures. The aim of the present study was to investigate the association between three informative OPG polymorphisms and quantitative ultrasound variables of the heel.

Hormonal aspects of the muscle-bone unit.

Osteoporotic fractures are the result of low density and especially inferior bone quality (microarchitecture) caused by both internal (genes, hormones) and external (life style) influences. Bone mechanosensors are extremely important for the overall integrity of the skeleton, because in response to mechanical load they activate its modeling, resulting in an increase in bone density and strength. The largest physiological loads are caused by muscle contractions.

Increase of nocturnal melatonin levels in hemodialyzed patients after parathyroidectomy: a pilot study.

In hemodialyzed patients hormonal disturbances are known to occur. However, melatonin levels have not been completely studied. The aim of the study was to find whether changes in calcaemia affect melatonin secretion.

Long-term 1,25(OH)2 vitamin D therapy increases bone mineral density in osteopenic women. Comparison with the effect of plain vitamin D.

Background And Aims: Although the bone protective effect of vitamin D has been studied intensively, the usefulness of 1,25(OH)2D3 in treating osteoporosis is still questionable. The aim of the present prospective study was to evaluate the effect of a standard pharmacological dose of 1,25(OH)2D3 in postmenopausal unsubstituted women.

Methods: Our study group comprised 52 post-menopausal women with low normal or osteopenic values of bone mineral density (BMD).