Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bone Remodeling”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMedDate not supplied

Regulation of bone remodeling: impact of novel therapies.

The kidneys serve as both an endocrine organ and as a target of endocrine action, with the aim of controlling mineral and water balance. Hormones and other key metabolites regulate mineral homeostasis by altering gene function directly or by initiating a sequence of events, leading ultimately to a change in enzyme function. Two of these hormones, parathyroid hormone (PTH) and calcitriol (the active form of vitamin D), interact in multiple tissues in the body to regulate the flux of calcium and phosphorus between extra- and intracellular compartments. Changes in the concentration of PTH and vitamin D, or the interaction of these with other factors, lead to the aberrant regulation of calcium and phosphorus. Among other effects, this aberrant regulation leads to pathologic changes in bone metabolism. The pathology of renal bone disease varies along a spectrum from disorders of low turnover to those of high turnover. This spectrum reflects the results of therapeutic intervention, hormone balances, and other causes. Effective management of renal bone disease therefore requires thorough evaluation of relevant risk factors, measurement of biochemical markers of bone remodeling, and determination of the physical status of bone tissue either by bone mineral density or bone biopsy. Subsequent therapeutic intervention with newer vitamin D compounds, novel phosphate binders, calcimimetics, and the use of alternative dialysis modalities offer hope in normalizing bone remodeling and mineral balance. The human skeleton functions in two capacities: the storage of minerals and structural support of the body. It is the only tissue that behaves as both a major source and a sink of calcium (Ca) and phosphorus (P). Healthy bone is a composite of a collagenous matrix embedded with crystals of hydroxyapatite. On the surface of bone and within the calcified matrix are specialized cells that build and maintain the tissue, and facilitate the movement of Ca and P into and out of serum. Bone undergoes remodeling in response to either damage from mechanical strain or as part of the normal cycle of bone renewal. The process involves distinct steps of cellular activation, bone resorption, and subsequent bone formation. It is a relatively slow process that takes several months, and at any one time occurs at many different sites along the bone surface. Systemic factors, such as PTH and vitamin D, regulate the resorption and formation of bone, and thus the systemic movement of Ca and P. However, during conditions of stress and disease, other factors may also play a role. In patients with chronic renal disease, the balance of Ca and P is profoundly disturbed. This disruption and the compensatory changes that occur in response alter the normal processes of bone metabolism.

Biomarkers↗
PubMed1979

An analytical investigation into possible mechanical causes of bone remodelling.

Three-dimensional finite element analyses were carried out on idealisations of two situations where bone remodelling has been reported clinically viz. the malaligned femur and a maxillary central incisor under orthodontic loading. The mechanical responses, i.e. stress, strain and change of curvature, in various directions, are presented. They are compared with the biological response, either bone resorption or bone deposition. The results are discussed in relation to three current theories of bone remodelling.

Alveolar Process↗
PubMed2005

Comparison of zinc excretion and biochemical markers of bone remodelling in the assessment of the effects of alendronate and calcitonin on bone in postmenopausal osteoporosis.

OBJECTIVES: The aim of this study was to determinate the clinical usefulness of urinary bone resorption markers, urinary zinc excretion, and other biochemical markers in postmenopausal women with osteoporosis. We also evaluated the effects of alendronate and calcitonin therapies on biochemical markers of bone remodeling and urinary zinc excretion over a 6-month period. SUBJECTS AND METHODS: The study design was a randomized placebo controlled study. The patients were randomly assigned to receive alendronate (10 mg/day; 45 patients) or calcitonin (200 IU/day; 45 patients) or placebo (45 patients) for 6 months. All patients received supplemental calcium (1000 mg/day). To assess bone resorption, we measured excretion of cross-linked N-telopeptides of Type I collagen (uNTx); urinary zinc concentrations and standard chemistry determinations were also measured; and osteocalcin (sOC) was measured as a marker of bone formation. All parameters were measured before therapy and again after 1, 3, and 6 months in all groups. RESULTS: A statistically significant decrease occurred in the levels of sOC, uZn, and uNTx after 3 and 6 months in patients receiving calcitonin therapy (P < 0.05). sOC, uZn, and uNTx levels in the calcitonin group were significantly lower after three and 6 months from both placebo and baseline values of calcitonin group. In the alendronate group, a statistically significant decrease was observed in the levels of uNTx and uZn after 1 month and in the sOC, uZn, and uNTx after 3 and 6 months from both placebo and baseline values of alendronate group (P < 0.05). uNTx, sOC, and uZn decreased about 44%, 36%, and 33%, respectively, in the calcitonin group and about 53%, 51%, and 38%, respectively, in the alendronate group below baseline values 6 months after initiating treatment. In the placebo group, there was no significant decrease in sOC, uZn, and uNTx during the course of the study. CONCLUSION: Our study suggests that in postmenopausal women with osteoporosis, both alendronate and calcitonin reduce the concentrations of uNTx, uZn, and sOC, the effect of the alendronate dose administered being significantly earlier and more pronounced. Measurement of uNTx, uZn, and sOC might be a useful biochemical method of observing the positive clinical effect following alendronate or calcitonin therapy in postmenopausal women.

Alendronate↗
PubMed1995

Osteopontin and the bone remodeling sequence. Colloidal-gold immunocytochemistry of an interfacial extracellular matrix protein.

Relative to other noncollagenous, extracellular matrix proteins in mineralized tissues, colloidal-gold immunocytochemistry has demonstrated that the ultrastructural distribution of osteopontin (OPN) is unique in that this protein preferentially accumulates at mineralized tissue interfaces. In bone, this protein is present as a major component of cell-matrix and matrix-matrix interfacial structures called cement lines and laminae limitantes. In the present article, the implications of this distinct tissue distribution are discussed in terms of the bone remodeling sequence, and a detailed account of the secretion, accumulation and potential role of OPN is presented and related to current theory on the cellular and extracellular matrix events associated with basic multicellular unit (BMU)-based bone remodeling. In this context, a proposal is made describing the production of this protein as one of the earliest, and latest, secretory activities of the osteoblastic lineage, and that this activity manifests itself morphologically as a cement line ('plane') and a lamina limitans, respectively, at bone matrix interfaces. When integrated with other, known functional characteristics of this protein, the present morphological and compositional data indicate that OPN in cement lines and laminae limitantes may participate in initial and late extracellular matrix organization and mineralization, matrix-matrix/mineral adhesion and/or cell adhesion at bone interfaces.

Animals↗
PubMed2006

Bone remodelling around HA-coated acetabular cups : a DEXA study with a 3-year follow-up in a randomised trial.

This study was designed to investigate bone remodelling around the cup in cementless THA. Previous studies indicate an advantage of better sealing of the bone-prosthesis interface by HA/TCP coating of implants, inhibiting polyethylene-induced osteolysis. One hundred patients gave informed consent to participate in a controlled randomized study between porous coated Trilogy versus Trilogy Calcicoat (HA/TCP coated). The cup was inserted in press-fit fixation. The femoral component was a cementless porous coated titanium alloy stem (Bi-Metric), with a modular 28-mm CrCo head. The Harris Hip Score (HHS) and bone mineral density (BMD) determined by DEXA scanning were used to study the effect. Measurements revealed no difference between the two groups after 3 years either in the clinical outcome or in terms of periprosthetic bone density. Patients with a body mass index above normal regained more bone mineral than patients with normal weight. This finding supports the assumption that load is beneficial to bone remodelling.

Absorptiometry, Photon↗
PubMed1991

Partial inhibition of bone resorption by disodium cromoglycate in a synchronized model of bone remodeling.

In a previous study we observed that mast cell degranulation might be associated to bone resorption. To verify this assumption, the efficiency of cromoglycate was assessed on a synchronized sequence of bone remodeling induced in male Wistar rats along the mandibular cortex. After 4 days (time of osteoclastic peak in this model), cromoglycate (15/mg/kg and 30 mg/kg/d per os) decreased the number of degranulating mast cells, especially in the population adjacent to the bone surface. Concomitantly the extent of resorption surface was decreased vs untreated animals. Active osteoclasts were lower whereas the total number of osteoclasts (both active and inactive) was not statistically modified. The mean osteoclast-bone interface was not modified. No dose effect was found. These data indicate that mast cell degranulation is involved in the events leading to osteoclast resorption, presumably in the mechanisms providing osteoclast access to bone surface.

Animals↗
PubMed2003

[Bone remodelling using the boundary element method].

An algorithm for the mathematical representation of external bone remodeling is proposed. The Boundary element method is used for the numerical analysis of trabecular bone, together with the remodeling algorithm presented by Fridez. The versatility and power of the algorithm discussed herein are shown by some numerical examples. As well, the method converges very fast to the solution, which is one of the main advantages of the proposed numerical scheme.

Algorithms↗
PubMed1981

Effects of thyroxine on cortical bone remodeling in adult dogs: a histomorphometric study.

The effects of thyroxine on cortical bone remodeling were studied under conditions of normal and accelerated remodeling induced by surgical elevation of the periosteum. Six adult female beagle dogs were administered orally 1.0 mg of L-thyroxine per kg body weight daily for 60 days. Static and dynamic changes were evaluated using tetracycline and DCAF (2,4-bis-N,N'-dicarboxymethyl aminomethyl fluorescein) in vivo double labeling of rib specimens taken before treatment and after 60 days. Thyroxine administered in moderate pharmacologic doses increased the activation frequency, number of bone-forming and -resorbing sites, and the osteoid seam circumference in unaltered bone. Thyroxine, by activating skeletal remodeling, increased bone turnover and both formation and resorption at the tissue level. In ribs with periosteal elevation and accelerated remodeling, thyroxine increased the activation frequency, number of bone resorption and formation sites, and ratio of bone resorptive-to-formative surfaces. In addition, thyroxine under these conditions resulted in an increase in the osteoid seam circumference, radial closure rate, and bone formation rate at the tissue level but decreased the osteon formation time. Under conditions of accelerated remodeling, thyroxine increased osteoblastic and resorptive activity to a greater degree than in unaltered bone and resulted in bone changes similar to that described in human beings with thyrotoxicosis. The increased serum calcium and phosphorus levels and urinary hydroxyproline excretion at several intervals during thyroxine administration were consistent with the morphometric evidence of increased bone turnover and resorption. These findings suggest that thyroxine is a potent activator of skeletal remodeling under conditions of both normal and accelerated remodeling.

Animals↗
PubMed2002

A contact model with ingrowth control for bone remodelling around cementless stems.

This work presents a computational model for bone remodelling around cementless stems. The problem is formulated as a material optimisation problem considering the bone and stem surfaces to be in contact. To emphasise the behaviour of the bone/stem interface, the computer model detects the existence of bone ingrowth during the remodelling; consequently, the contact conditions are changed for a better interface simulation. The trabecular bone is modelled as a strictly orthotropic material with equivalent properties computed by homogenisation. The distribution of bone relative density is obtained by the minimisation of a function that considers both the bone structural stiffness and the biological cost associated with metabolic maintenance of bone tissue. The situation of multiple load conditions is considered. The remodelling law, obtained from the necessary conditions for an optimum, is derived analytically from the optimisation problem and solved numerically using a suitable finite element mesh. The formulation is applied to an implanted femur. Results of bone density and ingrowth distribution are obtained for different coating conditions. Bone ingrowth does not occur over the entire coated surfaces. Indeed, we observed regions where separation or high relative displacement occurs that preclude bone ingrowth attachment. This prediction of the model is consistent with clinical observations of bone ingrowth. Thus, this model, which detect bone ingrowth and allow modification of the interface conditions, are useful for analysis of existing stems as well as design optimisation of coating extent and location on such stems.

Animals↗
PubMed2005

The effect of muscle loading on the simulation of bone remodelling in the proximal femur.

A large number of finite element analyses of the proximal femur rely on a simplified set of muscle and joint contact loads to represent the boundary conditions of the model. In the context of bone remodelling analysis around hip implants, muscle loading affects directly the spatial distribution of the remodelling signal. In the present study we performed a sensitivity analysis on the effect of different muscle loading configurations on the outcome of the bone remodelling simulation. An anatomical model of the femur with the implanted stem in place was constructed using the CT data of the Visible Human Project dataset of the National Institute of Health. The model was loaded with three muscle force configurations with increasing level of complexity. A strain adaptive remodelling rule was employed to simulate the post-operative bone changes around the implant stem and the results of the simulation were assessed quantitatively in terms of the bone mineral content changes in 18 periprosthetic regions of interest. The results showed considerable differences in the amount of bone loss predicted between the three cases. The simplified models generally predicted more pronounced bone loss. Although the overall remodelling patterns observed were similar, the bone conserving effect of additional muscle forces in the vicinity of their areas of attachment was clear. The results of this study suggest that the loading configuration of the FE model does play an important role in the outcome of the remodelling simulation.

Adaptation, Physiological↗
PubMed1998

Bone remodelling.

Explore the source record for details and available documents.

Bone Remodeling↗
PubMed2003

Effects of calcitriol on parathyroid function and on bone remodelling in secondary hyperparathyroidism.

BACKGROUND: Secondary hyperparathyroidism (2HPT) develops in chronic renal failure due to disturbances of calcium, phosphorus and vitamin D metabolism. It is characterized by high turnover bone disease and an altered calcium-parathyroid hormone (PTH) relationship. Calcitriol has been widely used for the treatment of 2HPT. However, it remains controversial whether calcitriol is capable of inducing changes of the calcium-PTH curve. The aim of the present study was to examine this issue and to determine the effect of calcitriol on bone remodelling in patients with severe 2HPT. METHODS: We evaluated 16 chronic haemodialysis patients with severe 2HPT (PTH 899+/-342 pg/ml). Each patient underwent a dynamic parathyroid function test (by infusion of calcium gluconate and sodium citrate) and a bone biopsy before and after a 6 month period of i.v. calcitriol therapy (CTx). RESULTS: After treatment, eight patients were identified as calcitriol responders and the other eight as non-responders, based on plasma PTH level (<300 pg/ml for responders and >300 pg/ml for non-responders). The first group had higher plasma 25OHD(3) levels (39+/-8 vs 24+/-7 ng/ml, P<0.005). As to the calcium-PTH curve, we found differences in slope (-12.7+/-5.2 vs -21.7+/-11.4, P=0.05), basal/maximum PTH ratio (48.8+/-14.9 vs 71.05+/-20.1%, P=0.01) and time to achieve hypocalcaemia (79.0+/-13.5 vs 94.3+/-13.7 min, P<0.001). Initial histomorphometric parameters did not allow identification of the different groups. After the 6-month CTx, alterations in the calcium-PTH curve were clearly seen in responders [a drop in maximum PTH (from 1651+/-616 to 938+/-744 pg/ml, P<0.05) and minimum PTH (from 163+/-75.4 to 102.2+/-56.7 pg/ml, P<0.005)], associated with an increase in minimum/basal PTH ratio (from 23.3+/-11.6 to 34.5+/-20.4%, P<0.05) and maximum calcium (from 0.99+/-0.07 to 1.1+/-0.09 mmol/l, P<0.05). Set point and slope were not altered after calcitriol treatment, in responders (set point=1.17+/-0.08 vs 1.15+/-0.1 mmol/l, ns; slope=-12.7+/-5.2 vs -12.9+/-9.3, ns) or non-responders (set point=1.21+/-0.05 vs 1.21+/-0.2 mmol/l, ns; slope=-21.7+/-11.4 vs -17.3+/-8.4, ns). Bone formation parameters were reduced in all patients [osteoid surface (OS/BS)=from 57.1+/-21.6 to 41.6+/-26%, P<0.05 for responders, and from 76.7+/-12 to 47.1+/-15%, P<0.001 in non-responders], but non-responders had increased bone resorption [eroded surface (ES/BS)=7.1+/-3.4 vs 16.6+/-4.9, P<0.05]. CONCLUSION: Calcitriol had non-uniform effects on parathyroid function and bone remodelling in uraemic patients. Non-responders exhibited a decoupled remodelling process that could further influence mineral balance or possibly also bone structure. To avoid such undesirable effects, early identification of non-responder patients is crucial when using calcitriol for the treatment of 2HPT.

Adult↗
PubMed1994

Effect of long-term tamoxifen therapy on cancellous bone remodeling and structure in women with breast cancer.

The effects of long-term tamoxifen therapy on bone remodeling were studied in 41 women with breast cancer, 22 treated with tamoxifen for a minimum of 15 months (mean 33) and 19 untreated. Transiliac crest bone biopsies were obtained and a comprehensive histomorphometric analysis performed using a semiautomatic image analysis system. There were no statistically significant differences between the two groups in bone area, osteoid perimeter and area, or osteoid width. Mineral appositional rate, adjusted appositional rate, and mineralization lag time were also similar in the two groups; however, tissue-based bone formation rate was significantly lower in the tamoxifen-treated women (p = 0.05) and the remodeling period significantly longer (p < 0.05). Mean and maximum resorption cavity depth and cavity area were significantly reduced in the tamoxifen-treated patients compared to the untreated patients (p < 0.01, p < 0.01, and p < 0.03, respectively). Calculated and directly measured indices of cancellous bone structure were similar in the two groups, although the data indicated a trend toward greater connectedness in the tamoxifen-treated group. These data indicate that tamoxifen does not exert an antiestrogenic effect on bone remodeling in the human and are consistent with a weak estrogenic effect.

Aged↗
PubMedDate not supplied

Bone remodeling in experimental total hip arthroplasty.

Experimental studies of cementless porous-coated total hip arthroplasty indicate that the most important design variable for femoral remodeling is stem stiffness. In the long-term (2 years) in the canine model, other variables including the presence, type and placement of the porous coating did not significantly affect the pattern of bone remodeling when tested with metallic stems. The basic pattern of bone remodeling was characterized by proximal cortical atrophy, and distal cortical and medullary bone hypertrophy. The use of low stiffness stems altered this pattern, leading to reduced proximal bone loss and no distal cortical hypertrophy.

Animals↗
PubMed2004

The role of subchondral bone remodeling in osteoarthritis: reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model.

OBJECTIVE: It has been suggested that subchondral bone remodeling plays a role in the progression of osteoarthritis (OA). To test this hypothesis, we characterized the changes in the rat anterior cruciate ligament transection (ACLT) model of OA and evaluated the effects of alendronate (ALN), a potent inhibitor of bone resorption, on cartilage degradation and on osteophyte formation. METHODS: Male Sprague-Dawley rats underwent ACLT or sham operation of the right knee. Animals were then treated with ALN (0.03 and 0.24 microg/kg/week subcutaneously) and necropsied at 2 or 10 weeks postsurgery. OA changes were evaluated. Subchondral bone volume and osteophyte area were measured by histomorphometric analysis. Coimmunostaining for transforming growth factor beta (TGF beta), matrix metalloproteinase 9 (MMP-9), and MMP-13 was performed to investigate the effect of ALN on local activation of TGF beta. RESULTS: ALN was chondroprotective at both dosages, as determined by histologic criteria and collagen degradation markers. ALN suppressed subchondral bone resorption, which was markedly increased 2 weeks postsurgery, and prevented the subsequent increase in bone formation 10 weeks postsurgery, in the untreated tibial plateau of ACLT joints. Furthermore, ALN reduced the incidence and area of osteophytes in a dose-dependent manner. ALN also inhibited vascular invasion into the calcified cartilage in rats with OA and blocked osteoclast recruitment to subchondral bone and osteophytes. ALN treatment reduced the local release of active TGF beta, possibly via inhibition of MMP-13 expression in articular cartilage and MMP-9 expression in subchondral bone. CONCLUSION: Subchondral bone remodeling plays an important role in the pathogenesis of OA. ALN or other inhibitors of bone resorption could potentially be used as disease-modifying agents in the treatment of OA.

Acid Phosphatase↗
PubMed2005

Interleukin-11 receptor signaling is required for normal bone remodeling.

UNLABELLED: IL-6 and -11 regulate bone turnover and have been implicated in estrogen deficiency-related bone loss. In this study, deletion of IL-11 signaling, but not that of IL-6, suppressed osteoclast differentiation, resulting in high trabecular bone volume and reduced bone formation. Furthermore, IL-11 signaling was not required for the effects of estradiol or estrogen deficiency on the mouse skeleton. INTRODUCTION: Interleukin (IL)-6 and -11 stimulate osteoclastogenesis and bone formation in vitro and have been implicated in bone loss in estrogen deficiency. Because of their common use of the gp130 co-receptor signaling subunit, the roles of these two cytokines are linked, and each may compensate for the absence of the other to maintain trabecular bone volume and bone cell differentiation. MATERIALS AND METHODS: To determine the interactions in bone between IL-11 and IL-6 in vivo and whether IL-11 is required for normal bone turnover, we examined the bone phenotype of mature male and female IL-11 receptor knockout mice (IL-11Ralpha1-/-) and compared with the bone phenotype of IL-6-/- mice and mice lacking both IL-6 and IL-11Ralpha. To determine whether IL-11 is required for the effects of estrogen on trabecular bone, mature IL-11Ralpha1-/- mice were ovariectomized and treated with estradiol. RESULTS: In both male and female IL-11Ralpha1-/- mice, trabecular bone volume was significantly higher than that of wildtype controls. This was associated with low bone resorption and low bone formation, and the low osteoclast number generated by IL-11Ralpha1-/- precursors was reproduced in ex vivo cultures, whereas elevated osteoblast generation was not. Neither trabecular bone volume nor bone turnover was altered in IL-6-/- mice, and compound IL-6-/- :IL-11Ralpha1-/- mice showed an identical bone phenotype to IL-11Ralpha1-/- mice. The responses of IL-11Ralpha1-/- mice to ovariectomy and estradiol treatment were the same as those observed in wildtype mice. CONCLUSIONS: IL-11 signaling is clearly required for normal bone turnover and normal trabecular bone mass, yet not for the effects of estradiol or estrogen deficiency on the skeleton. In the absence of IL-11Ralpha, increased trabecular bone mass seems to result from a cell lineage-autonomous reduction in osteoclast differentiation, suggesting a direct effect of IL-11 on osteoclast precursors. The effects of IL-11Ralpha deletion on the skeleton are not mediated or compensated for by changes in IL-6 signaling.

Animals↗
PubMedDate not supplied

[Morphofunctional characteristics of the endosteum in connection with bone remodeling].

Current information on the endost structure at different stages of bone remodelling is given on the basis of the original data and literature. Possible causes and character of the bone cells activity changes during the cycle of remodelling at the decreased functional stimulation on the bone structures and under pathological conditions are discussed.

Animals↗