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PubMed1999

Prevention of bone demineralization by calcium supplementation in precocious puberty during gonadotropin-releasing hormone agonist treatment.

We have previously demonstrated a negative impact on peak bone mass in girls with precocious puberty treated with GnRH agonist (GnRHa). Several studies have shown that a high calcium intake positively influences bone mass in prepubertal girls and leads to a higher peak bone mass. The aim of this study was to evaluate the effect of calcium supplementation in girls with precocious puberty during GnRHa treatment. Forty girls affected by true central precocious puberty and treated with the GnRHa triptorelin were studied for 2 yr. After diagnosis, the patients were randomly assigned to three groups: group A, treated only with GnRHa; group B, treated for 12 months solely with GnRHa and then supplemented with calcium gluconolactate/carbonate (1 g calcium/day in two doses) for 12 months; and group C, treated from the beginning with combined GnRHa and calcium. Bone mineral density (BMD) at the lumbar spine was measured by dual energy x-ray absorptiometry at the beginning of the study and after 12 and 24 months and was expressed as the calculated true volumetric density (BMDv) in milligrams per cm3. Group A showed a decrease in absolute BMDv levels, in SD score for chronological age (CA), and even more in SD score for bone age (BA). Group B showed the same behavior during the first year, but this trend was reversed in the second year, when calcium supplementation was added to GnRHa treatment. Group C showed an increase in absolute BMDv levels and in SD score for CA and BA. BMDv variations (expressed as absolute values, SD score for CA, and SD score for BA) became statistically significant at 24 months between groups C and A (P = 0.036, P = 0.032, and P = 0.025, respectively). The behavior of the lumbar spine BMDv in the three groups is consistent with a positive effect of calcium supplementation during GnRHa treatment. In calcium-supplemented patients, the normal process of bone mass accretion at puberty is preserved despite GnRHa treatment. Therefore, the reduction in BMD during GnRHa treatment in girls with precocious puberty is at least completely reversible and preventable if calcium supplementation is associated from the beginning.

Body Height↗
PubMed2006

Cancer-treatment-induced bone loss, part 1.

PURPOSE: The pathophysiology, frequency, sequelae, diagnosis, and treatment of cancer-treatment-induced bone loss (CTIBL) are discussed. SUMMARY: CTIBL is a long-term complication associated with cancer therapies that can directly or indirectly affect bone metabolism. Although CTIBL can occur in any patient receiving a cancer therapy known to cause bone loss, CTIBL is most common in patients with breast or prostate cancer who receive chemotherapy, hormone therapy, or surgical castration, as these can cause hypogonadism and induce bone loss. CTIBL causes bone fragility and an increased susceptibility to fractures; therefore, prevention, early diagnosis, and treatment of CTIBL are essential to decrease the risk of fracture. Bone loss occurs more rapidly and tends to be more severe in patients with CTIBL compared with those with normal age-related bone loss. Fractures of the hip, vertebra, and wrist are the fractures most commonly associated with bone loss. CTIBL is diagnosed by measuring bone mass using bone densitometry. Treatment of CTIBL consists of changing diet and lifestyle such as optimizing calcium and vitamin D intake, exercising, modifying behaviors known to increase the risk of CTIBL and pharmacologic therapy with hormone replacement therapy (HRT), selective estrogen-receptor modifiers (SERMs), calcitonin, or a bisphosphonate. CONCLUSION: Early identification and treatment of CTIBL are essential to prevent fractures. Patients should be instructed to optimize calcium and vitamin D intake, exercise regularly, and modify lifestyle behaviors known to cause bone loss. Patients with CTIBL should be treated with an oral or i.v. bisphosphonate; SERMs or HRT may be an option in some patients if contraindications do not exist.

Antineoplastic Agents↗
PubMed1997

Changes in urinary excretion of pyridinium cross-links during Spacelab-J.

In SLJ-1 we proposed to study three major objectives. They were; 1. hormonal changes associated with fluid and electrolyte metabolism, 2. the effect of space flight on the circadian rhythms of endocrine and metabolic systems, 3. the changes in the indices of the bone and muscle metabolism during space flight. In this report, the changes in the bone metabolism during Spacelab-J will be presented with a special emphasis on urinary excretion of pyridinium cross-links. Timed urine samples from three Japanese payload specialists were obtained for 3 days from May 19 to 21, 1991 (one year before the launch = L-1 year). Immediately before the launch (L-3 to L-0), urine samples were obtained from a payload specialist who was on board the Space Shuttle Endeavor (PS). During the inflight period (flight from September 3 to 10 in 1992), urine samples from the PS were collected by using Urine Monitoring System (UMS). After the landing, they were obtained from the PS for three days (R+0-R+2). Various parameters related to bone metabolism such as hydroxyproline, pyridinium cross-links and calcium were determined. It was noted that excretion of hydroxyproline decreased during the preflight periods when compared with that in the control L-1 year period. The average excretory rate during control period was 846.2 +/- 198.7 milligrams/hour (mean +/- SD), while those in the preflight 474.6 +/- 171.1 milligrams/hour, suggesting the diminished collagen intake during the preflight period. Average excretion rate of pyridinium cross-links during the first 4 mission days (MD0-MD3) was similar to that of preflight and control L-1 year period. However, it was significantly increased during the last 4 mission days (MD4-MD7). It returned to the preflight level during postflight days (R+0-R+2). Increased urinary excretion of calcium during the last 4 mission days were also observed. These results suggest that increase in bone resorption could occur during relatively short stay in microgravity.

Aerospace Medicine↗
PubMed1997

Growth retardation and bone loss as determinants of axial osteopenia in juvenile chronic arthritis.

The aim of the study was to evaluate the significance of growth retardation and bone loss as determinants of axial osteopenia in children with juvenile oligo- and polyarthritis. Bone mineral density (BMD), bone size (width), and bone volumetric density (BMDvol) were determined by dual x-ray absorptiometry at the lumbar spine and femoral neck in children with juvenile oligoarthritis (n = 36), polyarthritis (n = 75), and a group of healthy children (n = 66). Comparison of measurements showed that children with juvenile polyarthritis had a significantly reduced BMDvol (p < 0.05) and bone size (p < 0.01) at the lumbar spine, resulting in a 10.5% decrease in BMD (p < 0.001). At the femoral neck, the 16% decrease in BMD (p < 0.001) was attributed only to a decrease in BMDvol (p < 0.001). In juvenile oligoarthritis, the development of osteopenia was nonsignificant except at the femur, where the 6.6% decrease of BMD was associated with significant decrease of BMDvol (p < 0.05). The bone loss associated with juvenile chronic arthritis appears to develop with concurrent growth retardation at the spine, but without detectable growth retardation at the femoral neck.

Absorptiometry, Photon↗
PubMedDate not supplied

Assessment of bone and mineral metabolism in inflammatory bowel disease: case series and review.

OBJECTIVE: To determine the prevalence of low bone mass, fractures, and vitamin D deficiency and the levels of biochemical markers of mineral metabolism in patients with inflammatory bowel disease (IBD). METHODS: Our retrospective study consisted of 30 patients with Crohn's disease (CD) and 18 patients with ulcerative colitis (UC). Dual-energy x-ray absorptiometry was performed to determine bone mineral density at the lumbar spine and hip. Serum calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D (25-OHD), and 1,25-dihydroxyvitamin D, urinary N-telopeptide cross-linked collagen type I, and 24-hour urinary calcium levels were evaluated. RESULTS: On the basis of Z-score definitions of low bone mass in the IBD group as a whole, 13 patients (27%) had low bone mass at the lumbar spine. Similarly, at the femoral neck, 13 patients (27%) had low bone mass. There was a higher prevalence of low bone mass in the UC group than in the CD group, consistent with a high prevalence of fractures in that group. Of all patients with IBD, 65% had a history of fractures, of which 23% were atraumatic. Deficiency of 25-OHD was high, with a prevalence of 55% in patients with UC and 83% in patients with CD. Secondary hyperparathyroidism, defined as a parathyroid hormone level >55 pg/mL in conjunction with a low or normal serum calcium and a low 25-OHD level, was present in 50% of patients with CD and only 7% of patients with UC. CONCLUSION: Metabolic bone disease and fractures are common in IBD. The mean bone mineral density of the spine or femoral neck did not differ significantly between patients with CD and those with UC. Patients with UC had a higher prevalence of low bone mass, as defined by a Z-score of less than -2, than did patients with CD, consistent with a high prevalence of fractures in the UC group. In contrast, hyperparathyroidism attributable to vitamin D deficiency was more prevalent in patients with CD than in those with UC. This finding suggests a different etiologic mechanism of low bone mass in patients with CD.

Adolescent↗
PubMed1995

Comparative study of a biochemical index for the estimation of bone demineralization and dual photon absorptiometry.

Multivariate classification methods were used to create an early detection technique for determining bone density. This biochemical index (QuiOs) is clinically useful as a potential adjunct in identifying the presence of biochemical deficiencies known to cause osteopenia and the devastating effects of osteoporosis. The test uses the following serum concentrations of a predetermined set of blood constituents: calcium, phosphorus, alkaline phosphatase (ALP), two alkaline phosphatase isoenzymes (liver and intestine), estradiol, and progesterone. Using the results of these six biochemical and hormonal tests, a correlation equation was developed that demonstrates a nonlinear relationship between QuiOs and Ward's triangle of DPA. A sensitivity of 86% and a specificity of 80% was demonstrated for this biochemical index against DPA in this clinical trial.

Absorptiometry, Photon↗
PubMed1999

[Effect of gravitation loading and retabolil on development of atrophy in muscles and bones of rats due to suspension].

In a 3-wk experiment with tail-suspended rats histological and histomorphometric methods were used to determine the effects of graded gravitational loading (GGL) and anabolic steroid retabolil (nortestosterone decanoate) on the course of atrophy in soleus m. (SM), gastrocnemius m. (GM), tibia and humerus, and functioning of somatotrophic hormones (STH) of the pituitary and thyrocytes of the thyroid. Suspension was found to produce atrophy in SM and, to a less degree, in GM, partial transformation of SM slow fibers into the fast ones, suppression of the tibial longitudinal growth, demineralization of the tibial and humeral spongious metaphyses; besides, functional activities of STH-cells and thyrocytes were inhibited. Graded gravitational loading of rats by intermittence of suspension for 2 hrs slowed down atrophy in both muscles and osteopenia in tibia, stimulated the synthetic and secretory functions of STH-cells without any marked effect on thyrocytes or humeral osteopenia. GGL failed to influence the slow-to-fast transformation of SM fibers. Two injections of retabolil at the total dose of 3 mg/kg of the body mass somewhat interfered with the SM atrophy and humoral osteopenia, and were favorable to the synthetic but not secretory activity of STH-cells. Neither SM and tibial atrophies nor thyroid activity of the gland were improved. The prophylactic action of GGL upon the SM and humeral atrophies was significantly higher when combined with retabolil, whereas GM and tibia were not noticeably cured by retabolil. Inhibition of the SM atrophy and humeral osteopenia in rats treated with GGL and retabolil concurred with elevated activities of STH-cells and thyrocytes indirectly suggesting their more intensive production of the growth hormone and thyroid hormones, respectively.

Anabolic Agents↗
PubMed2000

Changes in calcium metabolism and bone demineralization after orthotopic intestinal neobladder creation.

PURPOSE: We evaluated calcium metabolism and bone demineralization by measuring specific markers for bone reabsorption and bone mineral density in patients with an intestinal neobladder. MATERIALS AND METHODS: We studied 33 men 55 to 72 years old who underwent creation of an orthotopic sigmoid (23), ileocolic (8) or ascending colon (2) neobladder after cystectomy. Mean followup plus or minus standard deviation (SD) was 28.4+/-30.1 months (range 4 to 114). Serum electrolytes and arterial blood gases were measured. As markers of bone absorption we assayed urinary pyridinoline, deoxypyridinoline and N-terminal pyridinoline cross-linked telopeptides, and serum pyridinoline cross-linked C-terminal telopeptide of type I collagen. Bone mineral density of the spine and femur was determined by dual x-ray absorptiometry. RESULTS: Mean blood pH plus or minus SD was 7.38+/-0.04 (range 7.29 to 7.43). Mean plasma bicarbonate was 22.9+/-3.4 mmol./l. and mean base excess was -1.63+/-3.61 mmol./l. Serum sodium, potassium, calcium, alkaline phosphatase and phosphate were normal in most patients. Mean serum chloride was 108.0+/-3.5 mEq./l., and was elevated in 9 of the 33 patients (27.3%). Serum intact parathyroid hormone was normal in all patients, osteocalcin was increased in 2 and 1alpha, 25-dihydroxyvitamin D3 was decreased in 2. Pyridinoline cross-linked C-terminal telopeptide of type I collagen was higher in 19 of 33 cases (57.6%) and N-terminal pyridinoline cross-linked telopeptides were elevated in 6 (18.2%). Pyridinoline and deoxypyridinoline were higher than normal in 19 (57.6%) and 7 (21.2%) patients, respectively. C-terminal telopeptide of type I collagen and deoxypyridinoline significantly correlated with serum pH (p = 0.017 and 0.0418, respectively). Z score for the bone mineral density of L2 to L4, the femoral neck and Ward's triangle was -0.350+/-1.031, -0.82+/-0.99 and -0.94+/-1.01, respectively. CONCLUSIONS: In patients with a neobladder of intestinal segments metabolic acidosis results in increased bone absorption and decreased bone mass. Thus, attention should be given to bone metabolism in patients with even mild acidosis after orthotopic neobladder creation.

Aged↗
PubMed1999

[The prevention of bone mineral loss with hormonal replacement therapy in premenopausal women on dialysis with estrogen deficiency].

In 25-30% of premenopausal dialysis women low serum estrogen concentrations are observed. This "premature menopause" can significantly contribute to accelerated bone loss. The aim of the study was to evaluate the effect of estrogen-gestagen replacement therapy on bone mineral density (BMD) in hemodialysis women with secondary to uremia estrogen deficiency. Among 20 hemodialysis women, aged 18-45 years, with serum 17 beta-estradiol < 30 pg/ml, ten (group I) received transdermal estradiol with cyclic addition of noretisterone acetate (Estracomb TTS 50/0.25), and another ten formed the control group (group II). BMD was evaluated by dual photon x-ray absorptiometry (DEXA, Lunar) in: lumbar spine (L2-L4), 1/3 distal radius and femoral neck, before and after the study. Serum 17 beta-estradiol concentrations were measured before, and after 1, 3, 6 and 12 months of the study. After one year, in group I, in which serum 17 beta-estradiol normalized already during the first month (p < 0.001), an increase of in BMD was noted, although significant only in L2-L4 (p < 0.05). In group II, no change in serum 17 beta-estradiol and mild but insignificant decrease in BMD were observed. However, a comparison of BMD values after 12 months in both groups revealed the marked differences in all studied sites (p < 0.01, p < 0.02, p < 0.05 in L4-L2, distal radius and femoral neck, respectively). The mean serum calcium, phosphate, PTH and alkaline phosphatase activity were similar in both groups and did not change during the study. In premenopausal hemodialysis women with estrogen deficiency, hormonal replacement therapy inhibits bone demineralization and can be useful in prevention of early osteoporosis.

Adolescent↗
PubMedDate not supplied

[The effect of smoking tobacco and drinking of alcohol and coffee on bone mineral density of healthy men 40 years of age].

The aim of the study was to evaluate the effects of smoking, alcohol and coffee drinking on bone mineral content (BMC) in a group of 258 healthy men, aged 40-63, occupationally active inhabitants of Wroclaw. Trabecular, cortical and total BMC at the distal radius of the non-dominant hand were measured by pQCT method using the Stratec apparatus. The data concerning smoking, alcohol and coffee intake were obtained through a questionnaire. The significance of BMC differences between groups were tested using a one-way analysis of variance ANOVA. The extent of alcohol intake did not differentiate BMC values at the distal radius, whereas the significant detrimental effects of both smoking and coffee drinking on trabecular (but not cortical and total) BMC were revealed. Among healthy Polish males coffee drinking was associated with a significant reduction of trabecular BMC. Simultaneously, smokers and ex-smokers (when compared to never-smokers) had lower trabecular BMC.

Adult↗
PubMed1995

Transduction of mechanical strain in bone.

One physiologic consequence of extended periods of weightlessness is the rapid loss of bone mass associated with skeletal unloading. Conversely, mechanical loading has been shown to increase bone formation and stimulate osteoblastic function. The mechanisms underlying mechanotransduction, or how the osteoblast senses and converts biophysical stimuli into cellular responses has yet to be determined. For non-innervated mechanosensitive cells like the osteoblast, mechanotransduction can be divided into four distinct phases: 1) mechanocoupling, or the characteristics of the mechanical force applied to the osteoblast, 2) biochemical coupling, or the mechanism through which mechanical strain is transduced into a cellular biochemical signal, 3) transmission of signal from sensor to effector cell and 4) the effector cell response. This review examines the characteristics of the mechanical strain encountered by osteoblasts, possible biochemical coupling mechanisms, and how the osteoblast responds to mechanical strain. Differences in osteoblastic responses to mechanical strain are discussed in relation to the types of strain encountered and the possible transduction pathways involved.

Animals↗
PubMed1993

Predicting skeletal adaptation in altered gravity environments.

It is generally agreed that the single factor that most limits human survivability in non-Earth environments is the phenomenon of bone demineralization and the medical problems induced by the subsequent imbalance in the calcium metabolism. Alterations of skeletal properties occur as a result of disturbances in the normal mechanical loading environment of bone. These alterations or "adaptations" obey physical laws, but the precise mathematical relationships remain to be determined. Principles governing unloading and overloading of bone are gaining more attention as a consequence of the planning of manned space stations, moon and Mars bases and spaceflights of long duration. This paper reviews the subject of bone remodeling and presents a mathematical framework which allows for the prediction of skeletal adaptation on Earth and in non-Earth gravity environments by power law relationships.

Adaptation, Physiological↗
PubMed1993

The effects of prolonged weightlessness and reduced gravity environments on human survival.

The manned exploration of the solar system and the surfaces of some of the smaller planets and larger satellites requires that we are able to keep the adverse human physiological response to long term exposure to near zero and greatly reduced gravity environments within acceptable limits consistent with metabolic function. This paper examines the physiological changes associated with microgravity conditions with particular reference to the weightless demineralizatoin of bone (WDB). It is suggested that many of these changes are the result of physical/mechanical processes and are not primarily a medical problem. There are thus two immediately obvious and workable, if relatively costly, solutions to the problem of weightlessness. The provision of a near 1 g field during prolonged space flights, and/or the development of rapid transit spacecraft capable of significant acceleration and short flight times. Although these developments could remove or greatly ameliorate the effects of weightlessness during long-distance space flights there remains a problem relating to the long term colonization of the surfaces of Mars, the Moon, and other small solar system bodies. It is not yet known whether or not there is a critical threshold value of 'g' below which viable human physiological function cannot be sustained. If such a threshold exists permanent colonization may only be possible if the threshold value of 'g' is less than that at the surface of the planet on which we wish to settle.

Adaptation, Physiological↗
PubMed1989

Calcium metabolism and the osteopenia of space flight.

This paper briefly reviews the subject of bone remodelling and calcium homeostasis and considers the changes that occur in the microgravity environment of space. The effectiveness of exercise as a countermeasure to bone demineralisation is discussed.

Bone Demineralization, Pathologic↗