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Results for “Bone Demineralization, Pathologic”

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At least 127 records · Page 7Linked to original sources

PubMed2003

[Bone metabolism in adolescent girls with short course of anorexia nervosa].

OBJECTIVE: The objective of this study was to determine the prevalence of bone mass reduction and determine its causes in young girls with short course of anorexia nervosa (AN). METHOD: Bone mineral density (BMD)of lumber spine by dual energy x-ray absorptiometry, total alkaline phosphatase (TAP), bone-Gla protein (BGP), urine deoxypyridinoline (DPYR), DPYR, urine calcium, sex hormones were measured in 24 in-patient girls with diagnosed AN and 20 healthy volunteers. RESULTS: Girls with AN had a significantly lower BMD than their age-matched controls. Osteopenia and osteoporosis were present even in the group with AN diagnosed within the previous 12 months. BMD correlated negatively with minimal BMI and positively with the duration of regular menses before AN onset. BGP and DPYR were significantly lower in AN patient than in the control group. Values of urine calcium of AN patients were comparable with control group, but showed a positive correlation with disease duration. DISCUSSION: Reduction of bone mineral density is present in girls with short course of AN. Nutritional status is the most important predictor of BMD. Bone metabolism is decreased in the early stages of the disease.

Absorptiometry, Photon↗

PubMed2003

[Changes of osteocalcin in bone and bone marrow in tail suspended rats].

OBJECTIVE: To study osteocalcin [correction of osteocakin] (OC) changes in bone and marrow and calcium deposition in bone and cartilage under simulated weightlessness. METHOD: Twenty SD rats were randomly divided into 14 d and 28 d tail suspension group and 2 corresponding control groups. Histological samples were in situ hybridized and trichrome stained. RESULT: OC expression of bone and marrow of rats were lower in tail suspended rats than that in the control (P<0.05). OC expression in 14 d tail suspended rats were higher than that in 28 d tail suspended group (P<0.05). Mineralization was inhibited, and demineralization of femur [correction of furmer] and cartilage mineralized matrix was prominent. Demineralization was more prominent in 28 d group. CONCLUSION: OC levels in bone and marrow of rats were lower after tail suspension. Calcium deposition was inhibited in bone and cartilage. Demineralization was prominent after long term hindlimb unloading.

Animals↗

PubMed2003

[Changes in bone density in hemodialysed women treated with transdermal hormone replacement therapy].

OBJECTIVES: Renal insufficiency in women can cause menstrual disturbances and changes of hormonal profile leading to the decrease of bone mass density. Drug administration during dialysis also influences the bone density and increases the risk of osteoporosis. The aim of the study is to assess the effect of transdermal hormonal replacement therapy (HRT) in hemodialysed patients with secondary amenorrhea on bone density. MATERIAL AND METHODS: 10 women aged from 22 to 45 years old were enrolled in the study. They received 17 beta-estradiol and norethisterone acetate in patches during 12 cycles. Densitometer of lumbar spine and serum estradiol concentration were measured before and after 12 cycles of therapy. RESULTS: The recurrence of regular vaginal bleeding, the increase of estradiol levels and bone mass density rate about 6% were observed. CONCLUSIONS: Transdermal hormonal replacement therapy in hemodialysed women with secondary amenorrhea revealed the efficacy of the treatment and prevention from osteoporosis.

Administration, Cutaneous↗

PubMedDate not supplied

[Assessment of physical development as a screening test for identification of children with prenosological bone mineralization disorder].

Retarded biological maturation, disharmonic and severely disharmonic morphofunctional status, the minimum thickness of fatty folds, decreased and low muscular force of the hands, delayed processes of secondary dentition concurrent with caries are shown to be prenosological criteria for osteopenia, impaired bone mineralization in children. Monitoring of children's health should include the assessment of physical development by the complex procedure supplemented by examination of somatoscopic signs.

Age Factors↗

PubMedDate not supplied

[Histomorphometry of primate's iliac bones following head-down tilting and "dry" immersion].

Histomorphometry of the iliac bone in Macaca mulatta males was performed in experiments with 30-d head-down tilting (HDT, n = 6) and 8-10-d "dry" immersion (DI, n = 6). The iliac crest was sampled two weeks before DI or a month prior to HDT, and immediately after completion of the experiments. HDT was shown to provoke osteopenia in the bone spongy manifested by losses in the volume of spongiosa, number of trabeculae, and growth of the space in-between. Osteoids were noted to gain volume and thickness, whereas the osteoclast resorption surface was not altered The iliac spongiosa deviations following DI were qualitatively similar to those after HDT but more marked as evidenced by reduction in such integral parameter as the spongy volume. Analysis of the data and their comparison with iliac bones taken from the space-flown primates suggest that DI can be viewed as another, besides HDT, ground-based model of microgravity effects on the spongy bone. Exposure in DI was less durable and yet caused qualitatively same atrophy of the iliac spongiosa as HDT though a bit more significant.

Animals↗

PubMed2004

[A densitometric assessment of skeletal mineral levels in prostate cancer patients treated with hormones].

An assessment of the densitometry data on 76 patients established a progressively falling level of minerals in the skeleton as a result of treatment with hormones for prostate cancer. The basal mineral levels had been identified by means of dual-energy X-ray absorptiometry. While said changes were immediately caused by maximum androgen deprivation, tumor influence and medication contributed too.

Absorptiometry, Photon↗

PubMedDate not supplied

[Current views on the etiopathogenesis of idiopathic osteoporosis and osteopenia in the developmental period].

The paper presents current literature review on the clinical features and possible etiopathogenetic factors in idiopathic osteoporosis and osteopenia in children and adolescents. Genetic and environmental factors determining bone mass growth are included. The effect of cytokines and hormones in the regulation of bone remodelling has been discussed in detail. Most recent studies have demonstrated that cytokines are involved in bone formation and resorption by their direct influence on the activity of osteoclasts and osteoblasts. In this way they affect the state of dynamic balance between the process of bone formation and resorption, and thus the mineralization of the skeleton.

Bone Demineralization, Pathologic↗

PubMed2005

Exercise and pharmacological countermeasures for bone loss during long-duration space flight.

Bone loss in the lower extremities and lumbar spine is an established consequence of long-duration human space flight. Astronauts typically lose as much bone mass in the proximal femur in 1 month as postmenopausal women on Earth lose in 1 year. Pharmacological interventions have not been routinely used in space, and countermeasure programs have depended solely upon exercise. However, it is clear that the osteogenic stimulus from exercise has been inadequate to maintain bone mass, due to insufficient load or duration. Attention has therefore been focused on several pharmacological interventions that have been successful in preventing or attenuating osteoporosis on Earth. Anti-resorptives are the class of drugs most commonly used to treat osteoporosis in postmenopausal women, notably alendronate sodium, risedronate sodium, zoledronic acid, and selective estrogen receptor modulators, such as raloxifene. There has also been considerable recent interest in anabolic agents such as parathyroid hormone (PTH) and teriparatide (rhPTH [1-34]). Vitamin D and calcium supplementation have also been used. Recent studies of kindreds with abnormally high bone mineral density have provided insight into the genetic regulation of bone mass. This has led to potential therapeutic interventions based on the LRP5, Wnt and BMP2 pathways. Another target is the RANK-L/osteoprotegerin signaling pathway, which influences bone turnover by regulating osteoclast formation and maturation. Trials using such therapies in space are being planned. Among the factors to be considered are dose-response relationships, bone quality, post-use recovery, and combination therapies--all of which may have unique characteristics when the drugs are used in space.

Aerospace Medicine↗

PubMed2005

Clinical applications of bone density testing for osteoporosis.

Bone mineral density (BMD) testing is a clinical tool to diagnose osteoporosis or low bone density, predict fracture risk, and monitor changes in bone density over time. Non-invasive measurement of BMD is done with a variety of technologies for many different skeletal sites. Dual-energy X-ray absorptiometry (DXA) is the gold-standard for diagnosing osteoporosis and monitoring changes in BMD over time. Optimal use of DXA requires staff training and standard operating procedures that include quality controls for instrument maintenance, patient education, indications and contraindications for testing, precision assessment, scan acquisition, analysis, interpretation, and reporting. Other technologies, as well as DXA, are used to estimate the risk of fracture. BMD is commonly expressed as a T-score, the standard deviation variance of the patient's BMD compared to a young-normal reference population. In untreated postmenopausal women, there is a strong correlation between T-score and fracture risk, with fracture risk increasing about two-fold for every standard deviation decrease in bone density. BMD in postmenopausal women is classified as normal, osteopenia, or osteoporosis according to criteria established by the World Health Organization. BMD testing, combined with assessment of clinical risk factors for fracture, allows healthcare providers to identify patients who may benefit from pharmacologic therapy to reduce the risk of future fractures. Clinical applications of BMD testing are presented in this review.

Absorptiometry, Photon↗

PubMed2004

Modern analysis of bone loss mechanisms in microgravity.

A summary of results of investigations by the author and a brief review of some literature data on human bone tissue deprived of mechanical loading (spaceflight, hypokinesia) is given. The direction and markedness of changes in bone mass--the bone mineral density and the bone mineral content--in different skeletal segments depend on their position relative to the gravity vector. A theoretically expected bone mass reduction was revealed in the trabecular structures of the bones of the lower part of the skeleton (local osteopenia). In the upper part of the skeleton, an increase in the bone mineral content is observed, which is considered as a secondary response and is due to redistribution of body fluids cephalad. The main cause of osteopenia is mechanical unloading. Arguments are presented that osteocyte osteolysis, delayed osteoblast histogenesis, and osteoclast resorption provoked by rearrangement in the hierarchy of the systems of fluid volume and ion regulation, and the endocrine control of calcium homeostasis are the main mechanisms of osteopenia.

Absorptiometry, Photon↗

PubMed2004

Bone demineralization mechanisms at level of free radicals and nanoscale subsystems of bone tissue.

Influence of simulated microgravity on characteristics of rat bones was investigated by electron paramagnetic resonance (EPR). For simulation of microgravity condition the hanging of animal by tail was used. The main measurements were performed for diaphysis of femoral bones. The quantity of native radicals Rn, localized in an organic matrix, and carbonate radicals CO2-, localized on a surface of bioapatite nanocrystals, were determined. The decrease of CO2- radical quantity in bones of experimental animals have shown, that due to simulation of microgravity the decrease of "collagen-nanocrystals" interaction takes place. It is shown that the EPR method open possibilities to receive the unique information about bone demineralization processes at level of free radicals and nanoscale subsystems of bone tissue.

Animals↗

PubMed1994

[Peri-tumor mandibular demineralization].

This study describes hitherto unpublished observations suggesting mechanism by which a tumor can cause massive resorption of the mandible. Microradiographic analysis of the cancerous areas has shown a mobilization of minerals from compact and spongious bone tissue accompanied by incomplete degradation of collagen fibres. The minerals are deposited in the lumen of the Haversian canals, the medullar cavity and the perimandibular soft tissue, areas which are not normally mineralized. Electronic microprobe and X-ray diffraction analysis revealed that in the mineralized zones undergoing demineralization, and in the heterotropic regions, a transformation of the crystal structure of the calcium phosphate salts had occurred. These zones, composed of hydroxylapatite in normal bone and dental tissue, had changed instead to brushite (known to be stable in acidic conditions). Our observations add a new dimension to the bone marrow demineralization process.

Aged↗

PubMed1996

Is continuous intranasal salmon calcitonin effective in treating axial bone loss in patients with active rheumatoid arthritis receiving low dose glucocorticoid therapy?

OBJECTIVE: To investigate the efficacy of intranasal salmon calcitonin (sCT) in treating axial bone loss in patients with rheumatoid arthritis (RA) taking low dose glucocorticoids. METHODS: In this open, multicenter study 32 women with RA were treated one year with sCT 100 IU/day and calcium (Ca) 500 mg/day; 31 women were treated with Ca alone. Bone mineral density (BMD) was measured at the lumbar spine and proximal femur (femoral neck, Ward's triangle, trochanter) before sCT therapy and again after 6 and 12 months. RESULTS: Among valid completers treated with sCT and Ca (n = 26), the mean BMD increased at the lumbar spine (L1-L4), femoral neck, and Ward's triangle. In contrast, valid completers treated with Ca (n = 23) showed bone loss at the spine (L1-L4), femoral neck, Ward's triangle, and trochanter area. The differences of the changes in BMD were statistically significant between these groups at the femoral neck, Ward's triangle, and trochanter. There were no significant differences between groups in bone loss over 12 months at the lumbar spine (L1-L4), although analysis of the upper segment (L1-L2) suggested some possible benefit of sCT. CONCLUSION: Intranasal sCT (100 IU/day) appears to have beneficial effects on bone loss at the proximal femur in patients with active RA treated with low dose glucocorticoids for 12 months; longer studies are needed to exclude transient bone remodelling effects.

Administration, Intranasal↗

PubMed1997

Cyclical etidronate increases lumbar spine bone density in patients on long-term glucocorticosteroid therapy.

To determine whether cyclical etidronate modifies bone density in patients on chronic glucocorticosteroid therapy, annual bone density measurements were performed on 55 patients receiving glucocorticosteroids who were randomised to either continuous calcium supplementation or cyclical etidronate plus calcium supplementation in this secondary prevention study. Median L1-L4 lumbar spine bone density decreased by 0.7% in the calcium treated group after one year but increased by 3.1% in the group treated by calcium and etidronate (p = 0.00116). Median L1-L4 bone density decreased by 2.8% from baseline after two years in the calcium treated group but increased by 4.7% from baseline in the group treated by calcium and etidronate (p = 0.04). There were no significant effects of treatment on femoral neck density. Cyclical etidronate and calcium increased lumbar spine bone density in patients established on prednisolone treatment over a two-year period but had no effect on femoral density.

Adult↗

PubMed1998

Turner syndrome and osteoporosis: mechanisms and prognosis.

Despite only limited reports of a greater number of fractures during childhood or adulthood, osteoporosis historically has been described as a feature in Turner syndrome, because of the frequent observation of radiographic osteopenia and the coarse trabecular pattern of the carpal bones on radiographs. The pathogenesis of the skeletal demineralization remains unclear, but the data support the concept of an intrinsic bone defect that is then exacerbated by a number of hormonal factors, including the growth-regulating hormones, the gonadal steroids, and possibly the calcium-regulating hormones. The advent of more refined methods, such as single- and dual-photon absorptiometry and dual energy x-ray absorptiometry, has led to improved insights into bone mineral density (BMD) status in Turner syndrome (TS). A major limitation of these projection methods is that they report areal and not true volumetric BMD, resulting in an underestimation of the true BMD in smaller subjects. In assessing BMD in TS, various methods have been used to eliminate the confounding effect of bone size. Some consistent patterns do emerge in persons with TS who are not treated with long-term growth hormone (GH) or estrogen therapy. A significant deficit in cortical bone commonly appears in childhood and usually is associated with a low bone-turnover state. Significant osteopenia at predominantly trabecular sites develops during mid- to late adolescence and persists into adulthood, when it is associated with increased bone turnover. Preliminary BMD data on patients after long-term GH therapy show an absence of osteopenia. With respect to the impact of long-term estrogen therapy, the BMD deficit in adults with TS who have been treated adequately with estrogen, but who have not been treated with GH, is less than it is in those who have been insufficiently treated or not treated at all with estrogen. The available data indicate that long-term GH treatment during the prepubertal and early to midpubertal years optimizes BMD and improves the prognosis for adequate peak bone mass being achieved after a puberty that, most often, has been induced with exogenous estrogen. Long-term treatment with estrogen and progestin that is initiated during mid- to late adolescence and is continued throughout adulthood appears necessary for a normal peak bone mass to be achieved and the BMD to be preserved well beyond the time of peak bone mass. Additional measures to prevent osteoporosis must be used, such as ensuring adequate calcium intake and ample weight-bearing activities, focusing on preventing injuries and avoiding overtreatment with thyroid hormones. Long-term surveillance with measurement of BMD and of bone turnover in a large TS population into their later adult years is necessary before it can be concluded that the osteopenia observed in TS is a nonprogressive asymptomatic bone defect of no clinical consequences.

Bone Demineralization, Pathologic↗

PubMed1999

Three year followup of bone mineral density change in premenopausal women with systemic lupus erythematosus.

OBJECTIVE: To measure the change in bone mineral density (BMD, g/cm2) in a female population with systemic lupus erythematosus (SLE) over 3 years, to identify factors predictive of bone loss, including the role of corticosteroid and disease related variables, and to determine the predictive value of urinary collagen crosslinks for bone loss. METHODS: All premenopausal women with SLE who participated in a cross sectional study of BMD in 1994 were invited to undergo a standardized interview, examination, medical record review, and BMD measurement of the lumbar spine and femoral neck by dual energy x-ray absorptiometry. RESULTS: Thirty-two women participated with a mean (SEM) age of 35.2 (1.5) years, duration of SLE of 7.0 (0.8) years, and mean (range) time to followup of 3.2 (2.9-3.4) years. Twenty-one subjects were exposed to corticosteroids during the study period with a mean (range) daily dose of prednisolone of 11.1 (2.8-22.9) mg. There was no significant change over the 3 years in BMD at the lumbar spine (1.161+/-0.122 vs. 1.169+/-0.022; p = 0.39) or femoral neck (0.944+/-0.023 vs. 0.955+/-0.020; p = 0.47) for the group as a whole, or when subjects were divided according to corticosteroid exposure. However, in the corticosteroid exposed subgroup, patients treated with > or = 7.5 mg/day (n = 14) lost lumbar spine BMD (-0.50%/yr) in contrast to those receiving <7.5 mg/day, who gained 1.06%/yr (p = 0.02). Furthermore, no participant receiving <7.5 mg/day lost lumbar spine BMD, while 57% of patients receiving > or =7.5 mg/day lost lumbar spine BMD (p = 0.01). In the corticosteroid exposed subgroup only, subjects who did not exercise regularly lost femoral neck BMD, while those who did gained femoral neck BMD (-0.54%/yr vs. 1.39%/yr; p = 0.02). Disease related variables (disease severity, activity, duration, functional capacity) and baseline urinary collagen crosslink levels were not predictive of BMD change. CONCLUSION: Loss of lumbar spine and femoral neck BMD in this premenopausal female SLE population was minimal for the group as a whole; however, a daily dose of prednisolone of > or =7.5 mg was associated with loss of lumbar spine BMD. In corticosteroid exposed patients, regular exercise was protective of femoral neck BMD loss. A single baseline measurement of urinary collagen crosslinks was not predictive of bone loss.

Absorptiometry, Photon↗

PubMedDate not supplied

[Radiation therapy in treatment of the sclerotic form of pathological rearrangement of bone tissue of the lower extremities].

An analysis was done of treatment of 77 servicemen with a sclerotic form of pathological rearrangement of bones of the inferior limbs. Used in the above subjects was oteoscintillography that promoted the accuracy of diagnosis and allowed the study of the time-related course of the process in bones, which measure permitted correcting the therapeutic regimen designed to deal with the pathology under consideration. The complex of conservative treatment was supplemented by a course of gamma-radiation therapy in a cumulative dose of 1.6 Gy, which measure has been shown to yield better results as compared with the control group of patients.

Adolescent↗

PubMed2006

Skeletal demineralization and fractures caused by fetal magnesium toxicity.

Two surviving female infants, born from a triplet pregnancy at 30 weeks gestation, were noted to have severe osteopenia and multiple fractures diagnosed at 20 days of age. Their mother had been treated for preterm labor with intravenous magnesium sulfate from week 22 until their birth at 30 weeks gestation. At birth, the triplets exhibited craniotabes with enlarged fontanelles and sutures. All developed Respiratory Distress Syndrome (RDS) and the two surviving infants required prolonged respiratory support. Serum calcium and phosphate levels were normal and alkaline phosphatase levels were increased. The infants were treated with supplements of calcium and phosphorous, with resultant healing of the multiple fractures without deformity. Fetal magnesium toxicity impairs bone mineralization and can lead to serious bone demineralization that may cause fractures in the newborn period that complicate recovery from respiratory disease. Early recognition and treatment may minimize complications related to osteopenia caused by fetal magnesium toxicity.

Adult↗