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PubMed1999

Primary hyperparathyroidism: short-term changes in bone remodeling and bone mineral density following parathyroidectomy.

Changes in bone remodeling and bone mineral density were observed during a period of 6 months after surgery in 24 patients with primary hyperparathyroidism (20 women and 4 men; age 54+/-12 years, range 26-69 years). All bone markers declined significantly within the 6 month follow-up period, but the time course for changes in renal N-terminal telopeptide of type 1 collagen (NTx) excretion differed from those of the other markers by a steep and significant reduction (p < 0.05) after less than 1 month. During the 6 month period, bone mineral density (BMD) increased significantly at all sites measured (p < 0.05) apart from the femoral neck and the proximal and midforearm. The greatest increase of 4.2% was observed in the trochanteric region (p < 0.001). The increase in BMD in spine, trochanteric, and intertrochanteric regions of the hip correlated inversely with baseline forearm BMD values (p < 0.05). Baseline bone markers (serum alkaline phosphatase [AP], serum bone AP, serum pyridinoline crosslinked telopeptide of type 1 collagen, urinary hydroxyproline, urinary osteocalcin), as well as baseline histomorphometric indices of bone turnover (eroded and labeled surface, bone formation rate, activation frequency, and cortical porosity) were positively correlated with changes in spinal BMD over 6 months (p < 0.05). It was concluded that, within 6 months after parathyroidectomy, patients with primary hyperparathyroidism obtain normalization of bone remodeling and a substantial increase in bone mineral density in regions rich in cancellous bone but no significant changes in regions with predominantly cortical bone.

Aged↗
PubMedDate not supplied

[Apoptosis--basic regulatory mechanism of bone remodeling].

Bone remodeling and regeneration take place permanently and are the result of a perfect balance between osteoclastic bone resorption and osteoblastic bone synthesis performed in the bone multicellular unit. Osteoblasts and osteoclasts differentiate from precursors under the influence of cytokines, growth factors mand cellular interactions controlled by adhesion molecules. The same growth factors and cytokines that promote bone cell differentiation have an important role in the prevention of cell death that is usually produced by apoptosis. The molecular mechanism of cytokines' and growth factors' actions is the activation of the pathway glicoprotein 130/Janus kinases/signal transductors and activators of transcription. The final step is the inhibition of cycline-dependent kinases, resulting in the inhibition of cell cycle and transition from G1 phase to S phase. Osteoblastogenesis and osteoclastogenesis are strongly bound together. Osteocytes are the most numerous bone cells, they have a long life, but ultimately die by apoptosis.

Apoptosis↗
PubMed2002

Relationships between trabecular bone remodeling and bone vascularization: a quantitative study.

Beside its well-known role in bone development, vascularization plays a major role in bone cell migration for bone remodeling and metastatic tumor invasion. However, the various techniques used to identify vessels in bone have never been tested for trabecular bone vessel quantification, whereas bone remodeling quantitative parameters are commonly assessed. In this context, we developed and compared various histological techniques used to visualize blood vessels in rat bone in order to quantify them. First, several products were tested by intracardiac infusion to opacify the bone vascular network. The best results were obtained using either an India ink-1% agarose solution or an India ink-saturated barium sulfate solution followed by X-ray microradiography. Second, to identify the types of vessels, we also performed histoenzymology and immunohistochemistry stainings. Neither alkaline phosphatase (for endothelial cells) nor adenosine triphosphatase (ATPase) stainings (for smooth muscle cells) provided a low enough background to allow for vessel identification and quantification. For immunohistochemistry, various specific vessel constituents were analyzed: laminin, smooth muscle cell alpha-actin, factor VIII, and lectin Griffonia simplifolia. Anti-laminin and anti-smooth muscle cell alpha-actin antibodies gave the best results for quantification. Third, after optimization of these techniques, we performed quantitative bone and vessel histomorphometry on two groups of 12 rats each, for which bone remodeling and vessel number and area parameters were measured. No statistical differences were observed between the two groups, confirming the reproducibility of our measurements. A significant relationship was found between vessel number and histodynamic parameters; that is, bone formation rate correlated positively with India ink-positive vessel area (p < 0.009, r2 = 0.54) and alpha-actin-positive vessel number (p < 0.05, r2 = 0.66). Furthermore, we report reproducible techniques for visualization and quantification of vessels in bone that also allowed for simultaneous conventional bone histomorphometry. This methodology should help researchers to better understand the functional and anatomical relationship between trabecular bone and its vascularization during normal or pathological processes.

Adenosine Triphosphatases↗
PubMed2002

Cyclical behavior of bone remodeling and bone loss in healthy women after menopause: results of a prospective study.

Annual changes in lumbar bone mineral density (LBMD) and bone remodeling markers were measured in 238 healthy pre- and postmenopausal women, aged 45-74 years. The subjects were divided into groups according to their menstrual status and years since menopause. The results obtained indicate that bone loss is not a constant process over time but rather exhibits cyclical damping oscillations. When the log-linear trend of LBMD decrement was transformed into a constant by considering annual percentage changes, the presence of a cyclical component of 7 years was evident. By employing a harmonic regression model, the cyclical component was also statistically significant on baseline data. The cyclical behavior of LBMD decrement corresponded to an analogous behavior of the bone remodeling markers. These results suggest that a lack of estrogen acts as a synchronizer on bone remodeling by triggering a latent cyclical rhythm of bone loss that persists throughout life after menopause. The existence of a chronobiological rhythm of bone loss starting after menopause, if confirmed, could have important clinical implications.

Aged↗
PubMed2003

Bone remodeling and bone mineral density during pregnancy.

INTRODUCTION: The effect of pregnancy upon the maternal skeleton is not fully understood. The information that has been gathered by recent studies is conflicting with regard to overall loss or gain of bone during pregnancy. The aim of the present longitudinal, controlled study, therefore, was to investigate the effect of pregnancy on lumbar spine, wrist, and hip bone mineral density, and to describe bone remodeling during pregnancy as indicated by biochemical markers of both bone resorption and formation. MATERIALS AND METHODS: Thirty healthy women (15 subjects seeking pregnancy and 15 non-pregnant controls) were studied. Bone mineral density (BMD) was measured by dual-energy x-ray absorptiometry before conception and within 2 weeks after parturition. Markers of bone resorption (urinary cross-linked type I collagen N-telopeptides, serum type I collagen C-telopeptides) and bone formation (total and bone specific alkaline phosphatase, osteocalcin), and total serum calcium were analyzed before, during (once in each trimester), and after pregnancy. RESULTS: During pregnancy, BMD decreased significantly by 3.4+/-4.1% at the lumbar spine and 4.3+/-3.9% at the trochanter, while there was a slight but significant increase in BMD at the proximal 1/3 of the forearm (1.3+/-1.9%). Total hip and femoral neck BMD did not change significantly, nor did total and ultradistal forearm BMD. Bone resorption increased during pregnancy with peak levels in the third trimester (N-telopeptides) or post partum (C-telopeptides), respectively. The increase in bone resorption was accompanied by a significant decrease in serum calcium in the third trimester. Markers of bone formation showed a biphasic pattern with decreases from baseline to the first (total and bone specific alkaline phosphatase) or second trimester (osteocalcin), respectively, followed by a significant increase in the third trimester and post partum. There was no change in any parameter in the control group throughout the study. CONCLUSION: In conclusion, pregnancy is characterized by high bone turnover with resorption preceding formation. During the first and second trimester bone remodeling is uncoupled. Serum calcium decreases as bone resorption peaks in late pregnancy. There are significant decreases in bone mineral density at sites rich in trabecular bone, such as the lumbar spine and the trochanter.

Adult↗
PubMed1997

The effects of androgen deficiency on murine bone remodeling and bone mineral density are mediated via cells of the osteoblastic lineage.

Both estrogens and androgens act on bone marrow stromal/osteoblastic cells to inhibit the production of local factors that promote osteoclast development. Based on this and the evidence that loss of sex steroids up-regulates not only osteoclastogenesis but also osteoblastogenesis, we have hypothesized that cells of the osteoblastic lineage are the mediators of the adverse effects of sex steroid deficiency on bone. To test this hypothesis, we used the senescence-accelerated mouse (SAMP6), a model of defective osteoblast development, and examined the effects of orchidectomy on static and dynamic histological features of bone remodeling and on bone mineral density. After orchidectomy in SAMP6 mice, the expected increases in osteoblast precursors, cancellous osteoclasts and osteoblasts, frequency of remodeling events, trabecular spacing, and rate of bone formation were absent or greatly attenuated. Moreover, whereas bone mineral density decreased in orchidectomized controls, it did not change in SAMP6. Our data indicate that when osteoblast development is defective, orchidectomy fails to result in bone loss. This evidence suggests that cells of the osteoblastic lineage are essential mediators of the changes in the rate of bone remodeling and loss of bone mass that ensue following loss of androgens.

Androgens↗
PubMed2005

Comparative effects of bicalutamide (Casodex) versus orchidectomy on bone mineral density, bone remodelling, and bone biomechanics in healthy rats.

INTRODUCTION: The aim of this work was to analyze the effects produced on bone mineral density (BMD) by the administration of bicalutamide and to compare them with those produced by orchidectomy. Bone formation rate (serum osteocalcin), bone resorption (serum carboxyterminal telopeptide of collagen I; CTX), and biomechanical properties of bone were also studied. METHODS: Thirty-eight male Wistar rats were used: (1) Sham group, rats sham operated at 16 weeks of age; (2) OQX group, rats orchidectomized at 16 weeks of age, and (3) Bic group, rats sham operated at 16 weeks of age and treated during 6 weeks with bicalutamide. The rats were sacrificed at 22 weeks of age, and the BMD in femur and lumbar spine was determined. Serum osteocalcin and serum CTX were also analyzed. Biomechanical parameters related to torsion assay were also studied. RESULTS: The OQX group showed a significant decrease in femoral BMD with respect to Sham rats, whereas bicalutamide treatment did not produce any significant change in BMD. Both Sham and Bic groups showed similar serum osteocalcin and CTX values, whereas OQX rats presented higher osteocalcin and CTX levels than the Sham group. The OQX group showed a significant decrease in femoral thickness. No significant differences were observed in the rest of the biomechanical parameters between groups. CONCLUSION: These results indicate that bicalutamide treatment, in spite of its anti-androgenic properties, does not affect bone remodelling nor BMD in male healthy rats, suggesting that this compound may function as a selective androgen receptor modulator for effects on bone remodelling in the osteoblasts.

Androgen Antagonists↗
PubMed1999

Biochemical markers of bone remodeling and bone sialoprotein in ankylosing spondylitis.

The aim of this work was to determine bone mineral density (BMD) in a group of patients with ankylosing spondylitis (AS) and to study alterations in bone remodeling in these patients. Eighteen patients (16 males and two females) with AS, mean age 44.7, range 21-75, and 18 age- and sex-matched healthy controls were studied. BMD was evaluated by dual energy X-ray absorptiometry. The following biochemical markers of bone remodeling were studied: formation - serum amino and carboxyterminal propeptides of procollagen I (PINP and PICP); resorption - urinary total and free deoxypyridinoline and pyridinoline (TDpyr, FDpyr, TPyr and FPyr), crosslinked aminoterminal telopeptides of collagen I (NTX), carboxyterminal telopeptide of collagen I (CTX) and serum bone sialoprotein (BSP). Receiver operating characteristic (ROC) curves of markers were also performed. We found a decrease of bone mass and an increase in TPyr, FPyr, TDpyr, FDpyr, NTX and BSP in AS, but no significant differences were found in PICP, PINP and CTX. FDpyr, FPyr and TPyr showed the highest discrimination between patients and controls according to the results of the ROC curves. TPyr/TDpyr was higher in AS than in controls. We found osteopenia, with a normal formation and a significant increase in bone resorption in AS. FDpyr, FPyr and TPyr seem to present the best sensitivity for the study of alterations of bone resorption in this pathology, although NTX, TDpyr and BSP also show significant differences. The elevation in the ratio TPyr/TDpyr in AS compared to controls indicates that in AS there is a type I-collagen degradation in tissues different from bone.

Adult↗
PubMed1978

Menopausal changes in bone remodeling.

Bone remodeling was measured by a calcium-kinetic method in 151 normal perimenopausal women, and the effect of estrogen status on remodeling level and skeletal balance was determined. Premenopausal women exhibited remodeling rates of 0.337 gm/day Ca for mineral accretion and 0.358 gm/day Ca for mineral resorption. The difference between the two rates (computed skeletal balance) was -0.021 gm/day Ca. Postmenopausal women treated with estrogen in a mean dose of 0.0188 mg equivalents of ethinyl estradiol exhibited values for accretion and resorption (0.332 and 0.351 gm/day Ca), essentially identical with those of the premenopausal group. However, untreated postmenopausal women exhibited remodeling rates of 0.387 gm/day Ca for accretion and 0.425 gm/day Ca for resorption, with a computed skeletal balance of -0.038 gm/day Ca. These values were significantly higher than those of either the premenopausal or treated postmenopausal groups. Paired studies across menopause in 15 of the women demonstrated a rise in remodeling rates virtually identical to that estimated from the differences between groups. Estrogen loss at menopause is thus associated with an apparent partial release from an inhibition of skeletal resorption, and this release is, in whole or part, responsible for the negative skeletal balance shift associated with the postmenopausal years.

Adult↗
PubMed2005

[Biochemical markers of bone remodeling].

Bone markers are aimed to assess bone cells activity. Some are specific of bone formation (osteocalcin, bone alkaline phosphatase, extension peptides of type I procollagen); others are specific of bone resorption (deoxypyridinoline and peptidebound forms.). Their main applications are: evaluation of fracture risk and follow-up of antiosteoporotic treatments. Their use in clinical practice is difficult: choice of the most appropriate bone marker, relevance of changes, and may require the specialist's opinion.

Acid Phosphatase↗
PubMed1992

Bone remodelling.

Bone is a specialised connective tissue that, together with cartilage, makes up the skeleton. These tissues serve three functions: (a) mechanical support and site of muscle attachment for locomotion; (b) protection for vital organs and bone marrow and (c) a metabolic reserve of ions for the entire organism, especially calcium and phosphate. The fundamental constituents are the cells and a calcified extracellular matrix. The latter is particularly abundant and is composed of collagen fibres and a ground substance rich in glycosaminoglycans. The osteoclasts and osteoblasts have evolved to regulate the growth and turnover of bone and mediate ion fluxes between the bone and blood. The osteoclasts solubilise the mineralised organic matrix, and the osteoblasts are capable of forming bone and synthesising the various structural proteins and growth factors. Except during growth, a balance between bone resorption and formation is maintained. The activities of the bone formation and resorbing cells are regulated by local and systemic humoral factors, such as parathyroid hormone, cytokines, 1,25,dihydroxy vitamin D3 and the eicosanoids. Any dysfunction of either the local or systemic regulatory systems will lead to pathological changes in the rate of bone formation or resorption and ultimately a clinical disease of the skeleton.

Bone Remodeling↗
PubMed1996

Biochemical markers of bone remodeling.

Bone formation and resorption (or bone turnover) are reflected by levels in blood and urine of various enzymes from bone cells, byproducts of bone matrix synthesis, or breakdown products of bone. These biochemical markers provide information about projected rates of bone loss and can be useful in assessing the effectiveness of antiresorptive therapy for osteoporosis. Biochemical markers provide adjunctive information to bone density measurements, and may be independent predictors of fracture risk. For clinical use, combining markers of resorption and formation should give better information than a single marker.

Biomarkers↗
PubMed2001

Extracellular nucleotide signaling: a mechanism for integrating local and systemic responses in the activation of bone remodeling.

Bone turnover occurs at discreet sites in the remodeling skeleton. The focal nature of this process indicates that local cues may facilitate the activation of bone cells by systemic factors. Nucleotides such as adenosine triphosphate (ATP) are locally released, short-lived, yet potent extracellular signaling molecules. These ligands act at a large family of receptors-the P2 receptors, which are subdivided into P2Y and P2X subtypes based on mechanism of signal transduction. Nucleotides enter the extracellular milieu via non-lytic and lytic mechanisms where they activate multiple P2 receptor types expressed by both osteoblasts and osteoclasts. In this review the release of ATP by bone cells is discussed in the context of activation of bone remodeling. We provide compelling evidence that nucleotides, acting via P2Y receptors, are potent potentiators of parathyroid hormone-induced signaling and transcriptional activation in osteoblasts. The provision of a mechanism to induce activation of osteoblasts above a threshold attained by systemic factors alone may facilitate focal remodeling and address the paradox of why systemic regulators like PTH exert effects at discreet sites.

Adenosine Triphosphate↗
PubMed1998

Recombinant human interleukin-11 does not modify biochemical parameters of bone remodeling and bone mineral density in adult ovariectomized rats.

Interleukin (IL)-11 stimulates osteoclast formation and inhibits osteoblast function in vitro and has been implicated in estrogen deficiency-induced bone loss. Herein we report the in vivo effect of recombinant human IL-11 (rHU-IL-11), administered s.c. in doses between 10 and 200 microg/kg/day for 6 weeks into 6-month-old rats after ovariectomy. There was no difference between vehicle-treated and rHu-IL-11 treated rats in the ovariectomy-induced increase in the urinary excretion of pyridinoline and deoxypyridinoline. Neither was there a significant effect of rHu-IL-11 on the plasma concentrations of osteocalcin and on bone mineral density (BMD) measured at a metaphyseal area of the distal femur after 6 weeks. At all dosages tested, rHu-IL-11 increased the femoral diaphyseal area. In conclusion, IL-11 has no deleterious in vivo effect on biochemical parameters of bone remodeling and BMD in estrogen-deficient rats.

Amino Acids↗
PubMed1982

The relationship between in vivo strains and cortical bone remodeling.

Bone has the capacity to remodel in response to the mechanical demands which are made on it during in vivo activities. It has long been assumed that mathematical laws exist which can describe the relationship between bone stress or strain histories and the remodeling activity of the bone tissue. Despite extensive research into bone stress/remodeling relationships, these mathematical laws have not yet been formulated. Research into this important area of bone physiology will be reviewed and the current state of knowledge assessed. Promising new directions in this research area will be discussed.

Animals↗
PubMed1996

Effect of nasal salmon calcitonin on bone remodeling and bone mass in postmenopausal osteoporosis.

The effect of nasal salmon calcitonin (SCT) on bone has been investigated by densitometry, biochemical markers of bone turnover, and histomorphometry. 62 women (mean age 65 years) who had experienced Colles' fracture after menopause were randomized to receive either nasal salmon calcitonin (SCT) 200 IU or nasal placebo daily for 24 months. All received a daily supplement of 0.5 g calcium. There was a significant increase above baseline in the bone mineral density of the lumbar spine in the SCT group (2.5%; 95% confidence interval 0.9--4.2%) and in the placebo group (1.7%; 95% confidence interval 0.3--3.1%) after 24 months, but the difference between the groups was not significant (0.8%; 95% confidence interval -1.2-3.0%). Serum levels of osteocalcin decreased significantly below baseline in the SCT group, whereas they were unchanged in the placebo group. At months 12 and 24, serum levels of osteocalcin were significantly lower in the SCT group than in the placebo group (p < 0.03). Urinary levels of deoxypyridinoline/creatinine decreased significantly below baseline in the SCT group, whereas only a transient decrease was observed in the placebo group. The differences between the groups were, however, not significant. The erosion depth was significantly lower in the SCT group than in the placebo group after 12 months (median [interquartile range]; 46.9 mu m [10.4] vs. 50.5 mu m [10.7]; p = 0.03), whereas bone volume and activation frequency did not differ between the groups. This study indicates that nasal SCT in a dose of 200 IU daily induces only a minor inhibition of bone resorption and therefore produces only a minor increase in bone mass. Furthermore, it seems that nasal SCT in a dose of 200 IU does not interfere with the recruitment of new bone multicellular units, but preferably decreases ongoing osteoclastic bone resorption.

Administration, Intranasal↗
PubMed1993

[Biochemical markers of bone remodeling and bone density in healthy postmenopausal women].

The aim of this study was to study bone turnover and density in postmenopausal women. One hundred healthy postmenopausal women aged 45 to 86 years, in whom menopause occurred between 3 months and 33 years before and were not receiving medications that could alter bone metabolism, were studied. Measurements performed were serum alkaline phosphatases, urine hydroxyproline/creatinine and calcium/creatinine excretion ratios and lumbar spine and femoral bone densities. Mean urinary hydroxyproline/creatinine excretion ratio was 39.5 +/- 11.9 (over 45 in 26% of women) and calcium/creatinine ratio was 0.11 +/- 0.08 (over 0.12 in 29% of women). At least one of these measurements were increased in 39% of women and no relationship of these values with age or length of postmenopausal period was found. Alkaline phosphatases were elevated in 9.6% of women. Twenty six percent of women had lumbar spine osteopenia and 10% femoral neck osteopenia. There was an inverse relationship between the length of hypoestrogenism and bone density. It is concluded that more than one third of studied women had biochemical evidences of bone resorption and that these women had a higher frequency of osteopenia than the general population. A decrease in bone density and an increase in bone resorption indices identify women with higher risk of osteoporosis that could be benefitted with an opportune treatment.

Absorptiometry, Photon↗