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Results for “Bone Remodeling”

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PubMed1986

A critical analysis of mechanical factors correlated with bone remodeling following total elbow arthroplasty.

Thirty elbows were critically reviewed for quantitative evidence of bone remodeling, with demonstrable bone remodeling noted in more than one half of the ulnae and humerii. Bone remodeling was analyzed statistically with independent variables of age, sex, handedness, diagnosis, implant design considerations, and implant alignment. Only implant design and alignment had a statistically significant impact on bone remodeling. Periarticular (zone 1) bone loss was statistically significantly correlated with a high percentage of diaphyseal medullary canal occupied by prosthesis, the presence of assymetric stem cortical contact, and lack of metaphyseal (zone 1) load transfer. Diaphyseal bone hypertrophy (zone 4) was statistically significantly correlated with a high percentage of diaphyseal medullary canal occupied by prosthesis (zone 4) and assymetric stem tip-to-cortical wall contact. Periarticular bone hypertrophy and diaphyseal bone atrophy did not occur. Fractures through the humeral condyles occurred in three elbows undergoing bone atrophy, but no implant loosening or failure could be correlated with bone remodeling. Bone remodeling does occur in a high percentage of stemmed elbow implants but to date has not been a factor in clinical failure.

Atrophy↗

PubMed2004

Long-term prediction of three-dimensional bone architecture in simulations of pre-, peri- and post-menopausal microstructural bone remodeling.

The mechanical behavior of trabecular bone depends on the internal bone structure. It is generally accepted now that the trabecular bone structure is a result of a load adaptive bone remodeling. The mathematical laws that relate bone remodeling to the local state of stress and strain, however, are still under investigation. The aim of this project was to investigate if changes in the trabecular architecture as observed with age-related bone loss and osteoporosis can be predicted from a computer model that simulates bone resorption after hormone depletion based on realistic models of trabecular microstructure using micro-computed tomography (muCT). A compact desktop muCT providing a nominal isotropic resolution of 14 mum was used to measure two groups of seven trabecular bone specimens from pre-menopausal and post-menopausal women respectively. A novel algorithm was developed to simulate age-related bone loss for the specimens in the first group. The algorithm, also referred to as simulated bone atrophy (SIBA), describes a truly three-dimensional approach and is based directly on cellular bone remodeling with an underlying realistic time frame. Bone resorption is controlled by osteoclastic penetration depth and bone formation is governed by the efficiency level of the osteoblasts. The simulation itself describes an iterative process with a cellular remodeling cycle of 197 days. Activation frequency is controllable and can be adjusted for the different phases of pre-, peri- and post-menopause. For our simulations, osteoblastic and osteoclastic activities were in balance until the onset of menopause, set to be at the age of 50 years. In that period, the structure remained almost constant. After the onset of menopause an imbalance in the cell activities was modeled resulting in a net bone loss. The doubling of the activation frequency in the peri-menopausal phase caused a pronounced loss. Using advanced animation tools and quantitative bone morphometry, the changes in bone architecture associated with the bone loss were monitored over an average observation time of 43 years until the age of 80 years. In that time, bone volume density decreased monotonously with the progression of the simulation for all specimens. Right after the onset of menopause, bone was lost fast, where with the progression of age losses slowed down. The structures at the end-point of the simulations were then compared qualitatively and quantitatively to the structures of the post-menopausal group with all morphometric indices being within a narrow margin of error. These results suggest the feasibility of transforming "normal" to "osteopenic" bone on a microstructural level yielding in realistic bone models similar in appearance as well as in structural behavior if compared to a post-menopausal group of women.

Aged↗

PubMed2001

The ratio of messenger RNA levels of receptor activator of nuclear factor kappaB ligand to osteoprotegerin correlates with bone remodeling indices in normal human cancellous bone but not in osteoarthritis.

The determinants of cancellous bone turnover and trabecular structure are not understood in normal bone or skeletal disease. Bone remodeling is initiated by osteoclastic resorption followed by osteoblastic formation of new bone. Receptor activator of nuclear factor kappaB ligand (RANKL) is a newly described regulator of osteoclast formation and function, the activity of which appears to be a balance between interaction with its receptor RANK and with an antagonist binding protein osteoprotegerin (OPG). Therefore, we have examined the relationship between the expression of RANKL, RANK, and OPG and indices of bone structure and turnover in human cancellous bone from the proximal femur. Bone samples were obtained from individuals with osteoarthritis (OA) at joint replacement surgery and from autopsy controls. Histomorphometric analysis of these samples showed that eroded surface (ES/BS) and osteoid surface (OS/BS) were positively associated in both control (p < 0.001) and OA (p < 0.02), indicating that the processes of bone resorption and bone formation remain coupled in OA, as they are in controls. RANKL, OPG, and RANK messenger RNA (mRNA) were abundant in human cancellous bone, with significant differences between control and OA individuals. In coplotting the molecular and histomorphometric data, strong associations were found between the ratio of RANKL/OPG mRNA and the indices of bone turnover (RANKL/OPG vs. ES/BS: r = 0.93, p < 0.001; RANKL/OPG vs. OS/BS: r = 0.80, p < 0.001). These relationships were not evident in trabecular bone from severe OA, suggesting that bone turnover may be regulated differently in this disease. We propose that the effective concentration of RANKL is related causally to bone turnover.

Adult↗

PubMed2004

Computer simulation of an adaptive damage-bone remodeling law applied to three unit-bone bars structure.

It is well admitted that the mechanical loading plays an important role in the growth and maintenance of our skeleton, and that microdamage (i.e.: microcracks) occurs naturally when the bone is overloaded during day-to-day activities. It is also argued, from experimental and theoretical viewpoint, that the cells which built and rebuilt the skeleton are sensitive for both strain and microdamage. The recent damage-bone remodeling theory is employed here to study the mechanical response of the three unit-bone bars that simulate bone trabeculae in the form of truss. It is shown that under constant load, such a structure exhibit inhomogeneous strain and it's response to external applied load depends strongly upon the manner in which the microdamage is distributed.

Bone Remodeling↗

PubMed1984

Mathematical modeling and numerical solutions for functionally dependent bone remodeling.

The phenomenon of bone remodeling is a complex biological process which is dependent on genetic, hormonal, metabolic, and age-related factors as well as functional requirements. The possibility of successfully developing a mathematical model to describe and predict the adaptive response of bone to load will be significantly increased after identification of the nature of the transducer(s) which senses functional requirements and provides signals for the cellular processes responsible for bone synthesis and bone removal. In spite of the present limitations in knowledge about the functional dependence of bone remodeling, a phenomenological model has been developed that assumes that the output signal from the (as yet unspecified) transducer is a remodeling potential that can be modulated by genetic, hormonal, and metabolic factors. An attempt has been made to cast the mathematical model in such a form that the constants and variables appearing in the equations are not mere abstractions, but can be related to biological parameters. In order to use the adaptive hypothesis with specific structural model examples, a numerical procedure has been developed to determine the strain distribution, predict the remodeling (assuming that the remodeling rate is related to the strain history), and update the model by changing the geometry and material properties in response to the remodeling. This numerical procedure is repeatedly iterated to determine the structural architecture at subsequent times. The numerical approach allows use of the remodeling concepts with models of irregular geometry, inhomogeneous material distribution, and anisotropic material properties.

Adaptation, Physiological↗

PubMed1998

Effects of LY-117018 HCl on bone remodeling and mineral density in the oophorectomized rat.

OBJECTIVE: LY-117018 HCl is a recently developed, selective estrogen receptor modulator and an analog of raloxifene. Its mode of action on the skeleton is similar to that of estrogens, although it does not have the same side effects. The aim of the current study was to compare the effects produced by the administration of 17alpha-ethinyl estradiol (0.1 mg/kg/day) and LY-117018 HCl (1 mg/kg/day) on bone remodeling, bone mineral density, and body and uterus weight in sham-operated and oophorectomized rats (experimental model of postmenopausal osteoporosis). STUDY DESIGN: Twelve-week-old female Wistar rats were used. Treatment was given for 3 months after oophorectomy or sham operation. Bone mineral density was determined in the lumbar spine (L2, L3, and L4) and in the left femur with use of a Hologic QDR 1000 (S/N 277) densitometer. Bone remodeling was estimated with use of the formation markers osteocalcin (bone gla protein) and alkaline phosphatase and the resorption markers type I collagen carboxyterminal telopeptide and tartrate-resistant acid phosphatase. RESULTS AND CONCLUSIONS: The newly developed derivative of raloxifene, LY-117018 HCl, offsets the reduction in bone mineral density and the accompanying increase in bone remodeling markers observed in oophorectomized rats compared with control animals. 17Alpha-ethinyl estradiol also prevents the loss of bone mass attributed to oophorectomy, but this is accompanied by an increase in body mass and a greater increase in uterus weight than that observed after treatment with LY-117018 HCl.

Acid Phosphatase↗

PubMed2006

Nutritional modulators of bone remodeling during aging.

Bone mass declines progressively with age in both men and women from the age of approximately 30 y. Increased longevity will inevitability be associated with an increase in the incidence of osteoporosis, its associated complications, and incurred health care costs. Current pharmacologic approaches focus on inhibiting bone resorption in those with osteoporosis but do little to improve bone mass. Increased understanding of the cellular events responsible for normal bone formation has led to multiple pathways that can be targeted to positively influence bone mass. Bone morphogenetic proteins (BMPs) have been shown to stimulate bone formation, and the BMP2 gene was recently linked to osteoporosis. BMP-2 therefore represents one potential molecular target to identify new agents to simulate bone formation. Research is accumulating on the positive effects of dietary sources that stimulate the BMP2 promoter and their effects on bone formation. Flavonoids and statins occur naturally in food products and have been shown to promote bone formation. It may be possible to influence peak bone mass by dietary means and to decrease the risk of osteoporosis in later life. To ease the future burden of osteoporosis, focusing on prevention will be key, and this could include dietary interventions to stimulate bone formation.

Aged↗

PubMed1995

[An experimental study of the effects of stress-relaxation plate on bone remodeling].

An ideal bone plate would provide rigid fixation to ensure stabilization of bone fragments at the early stage after fracture, while at the late stage osteoporosis induced by stress shielding effect of the plate should be prevented. However, there is no report of such a plate that could meet with all these requirements. Twenty-eight adult New Zealand rabbits were used in this experiment. Ordinary stainless-steel plate (no washer plate) and similar plate padded with ultrahigh molecular polyethylene washers in its screw holes (washer plate) were fixed respectively on mid-shelf of each side of tibiae. The animals were killed at 2, 4, 8, 12, 16, 20 and 24 weeks after operation, and the fixed bone segments of both tibiae were removed for light microscopy, polarized light microscopy and fluoroscopy. The results showed that the tibiae fixed with plate fixation both appeared bone resorption, but there was more severe resorption in bone with no washer plate fixation than that with washer plate fixation. Cancelization of cortical bone was seen in the former but not in the latter at 12 weeks postopertively. This demonstrated that the washer might creep and damage with fixation time, resulting in gradual decrease in the rigidity of the plate-screw system and thus reducing bone resorption as caused by stress shielding.

Animals↗

PubMed1991

On the significance of remodeling space and activation rate changes in bone remodeling.

This paper quantifies the relative contributions of the remodeling space and the accumulation of Haversian canals to bone porosity at various ages. It also examines the importance of variations in the rate of bone remodeling that occur during growth and aging, and as a result of trauma and disease. The dependence of the remodeling space (cavities due to resorbing, reversing, and refilling BMUs) and the Haversian canal components of porosity on the Basic Multicellular Unit (BMU) activation frequency are mathematically formulated. A graph is developed using data for the cortex of the human rib which shows the extent to which porosity is primarily due to the remodeling space in children, and to accumulated Haversian canals in adults. It is shown that the diminution of activation frequency between birth and age 35 contributes to the concurrent increase in bone volume fraction, and the increase in activation frequency after age 35 contributes to the subsequent decline of bone volume fraction. An equation is derived for determining the time rate of change of activation frequency using two fluorochrome labels.

Aging↗

PubMed1985

The effects of continuous progestogen treatment on cortical bone remodeling activity in beagles.

Cortical bone remodeling measurements were carried out on the ribs of 6 spayed and 5 progestogen-treated spayed Beagle dams which had been subjected to a period of observation equal to more than 1 sigma of intact canine bone remodeling activity. Analyses of static and dynamic features indicated that continuous medroxyprogesterone acetate replacement therapy altered the rates of cortical bone remodeling activity. In the progestogen-treated dams, more Basic Multicellular Units (BMUs) were activated, exhibiting shortened resorption and formation times. Thus, this progestogen appears to play a significant role in regulating cortical bone cell activity and, as such, suggests that progesterone may play a part in the prevention or slowing down of cortical bone loss in females following menopause or oophorectomy.

Animals↗

PubMed2007

The multiple roles of osteoclasts in host defense: bone remodeling and hematopoietic stem cell mobilization.

Bone remodeling by bone-forming osteoblasts and bone-resorbing osteoclasts dynamically alters the bone inner wall and the endosteum region, which harbors osteoblastic niches for hematopoietic stem cells. Investigators have recently elucidated mechanisms of recruitment and mobilization; these mechanisms consist of stress signals that drive migration of leukocytes and progenitor cells from the bone marrow reservoir to the circulation and drive their homing to injured tissues as part of host defense and repair. The physical bone marrow vasculature barrier that is crossed by mobilized cells actively transmits chemotactic signals between the blood and the bone marrow, facilitating organ communication and cell trafficking. Osteoclasts play a dual role in regulation of bone resorption and homeostatic release or stress-induced mobilization of hematopoietic stem/progenitor cells. In this review, we discuss the orchestrated interplay between bone remodeling, the immune system, and the endosteal stem cell niches in the context of stem cell proliferation and migration during homeostasis, which are accelerated during alarm situations.

Animals↗

PubMed2001

Cancellous bone remodeling occurs in specialized compartments lined by cells expressing osteoblastic markers.

We describe a sinus, referred to as a bone remodeling compartment (BRC), which is intimately associated with cancellous bone remodeling. The compartment is lined on its marrow side by flattened cells and on its osseous side by the remodeling bone surface, resembling a roof of flattened cells covering the bone surface. The flat marrow lining cells are in continuity with the bone lining cells at the margins of the BRC. We examined a large number of diagnostic bone biopsy specimens received during recent years in the department. Furthermore, 10 patients (8 women and 2 men, median age 56 [40-69] years) with the high turnover disease of primary hyperparathyroidism who were treated with parathyroidectomy and followed for 3 years were included in the histomorphometric study. Bone samples for the immuno-enzyme staining were obtained from an amputated extremity of child. The total cancellous bone surface covered by BRC decreases by 50% (p < 0.05) following normalization of turnover and is paralleled by a similar 50% decrease in remodeling surface (p < 0.05). The entire eroded surface and two-thirds of the osteoid surface are covered by a BRC. BRC-covered uncompleted walls are 30% (p < 0.05) thinner than those without a BRC. This indicates that the BRC is invariably associated with the early phases of bone remodeling, that is, bone resorption, whereas it closes during the late part of bone formation. Immuno-enzyme staining shows that the flat marrow lining cells are positive for alkaline phosphatase, osteocalcin, and osteonectin, suggesting that they are bone cells. The first step in cancellous bone remodeling is thought to be the lining cells digesting the unmineralized matrix membrane followed by their disappearance and the arrival of the bone multicellular unit (BMU). We suggest that the lining cell barrier persists during bone remodeling; that the old lining cells become the marrow lining cells, allowing bone resorption and bone formation to proceed under a common roof of lining cells; that, at the end of bone formation, new bone lining cells derived from the flattened osteoblasts replace the marrow lining cells thereby closing the BRC; and that the two layers of lining cells eventually becomes a single layer. The integrity of the osteocyte-lining cell system is reestablished by the new generation of lining cells. The BRC most likely serves multiple purposes, including efficient exchange of matrix constituents and minerals, routing, monitoring, or modulating bone cell recruitment, and possibly the anatomical basis for the coupling of bone remodeling.

Adult↗

PubMed1997

Longitudinal evaluation of time related bone remodeling after cementless total hip arthroplasty.

Bone remodeling after cementless total hip arthroplasty was evaluated by dual energy x-ray absorptiometry in a longitudinal study of 32 hips. After insertion of a fully porous surface anatomic stem made of cobalt chromium, bone mineral density was analyzed until at least 2 years postoperatively. Bone remodeling was evaluated in terms of regional bone density changes in the seven adjacent periprosthetic zones as well as the global change in bone density distribution over the entire periprosthetic area. At 12 months after the operation, the averaged regional bone mineral density in all seven zones showed a rapid decrease, ranging from 9% to 24% of the bone mineral density present at 2 weeks postoperatively. Thereafter, the bone density change appeared to be stabilized. The global change in the bone density distribution was expressed as two summarizing statistical indexes derived from principal component analysis: the first index represents the change of average bone mineral density over the entire periprosthetic area, and the second represents the severity of bone mineral density decrease in the proximal area versus the distal area. The second index proved that more bone density reduction occurred in the proximal area, but this was variable among patients and correlated significantly with the stem size and the initial bone mineral density in the distal part of the periprosthetic area. This longitudinal dual energy x-ray absorptiometry study suggests that a large part of the bone remodeling after cementless hip arthroplasty ceases within 1 year postoperatively, and stem size and the initial bone density around the distal portion are important considerations for predicting the proximal bone density decrease during the early rapid remodeling period.

Absorptiometry, Photon↗

PubMed1989

Osteocalcin and bone remodelling in Paget's disease of bone, primary hyperparathyroidism, hypercalcaemia of malignancy and involutional osteoporosis.

We have measured classic markers of bone turnover, serum alkaline phosphatase (sAP), urinary hydroxyproline/creatinine ratio (uOH-Prol/creatinine) and osteocalcin (sBGP), in two bone disorders characterized by an increase in bone remodelling, namely Paget's disease of bone and primary hyperparathyroidism (PHPT) and in two other bone diseases characterized by an increase in bone resorption without the concomitant increase in bone formation, hypercalcaemia of malignancy (HM) and involutional osteoporosis (IO). Serum BGP was increased in patients with Paget's disease of bone (6.7 +/- 3.1; n = 25; p less than 0.01) and in PHPT patients (8.3 +/- 5.3; n = 20; p less than 0.005) with respect to control patients (4.2 +/- 1.2 ng/ml; n = 12). Two subgroups of patients with high and normal levels of sBGP were found in both pathologies. Serum BGP was decreased in HM patients (2.1 +/- 1.7; n = 9; p less than 0.01) and in IO patients (1.9 +/- 1.4; n = 31; p less than 0.001). Two subgroups of patients with normal and low sBGP values were found in these two last disorders. A positive linear correlation was found between sBGP and sAP (y = 14.6x + 73.7; r = 0.44; p less than 0.05) and between sBGP and uOH-Prol/creatinine (y = 0.008x + 0.007; r = 0.67; p less than 0.001) in Paget's disease of bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2001

[Leptin: factor in the central nervous system regulation of bone mass. Development of a new understanding of bone remodeling, skeletal reconstruction, skeletal preservation and skeletal repair].

Bone remodeling is the physiologic process used by vertebrates to maintain a constant bone mass between the end of puberty and gonadal failure. Besides the well-characterized and critical local regulation of bone remodeling, recent genetic studies have shown that there is a central control of bone formation, one aspect of bone remodeling. This central regulation involves leptin, an adipocyte-secreted hormone that controls body weight, reproduction, and bone remodeling following binding to its receptor located on the hypothalamic nuclei. This genetic result in rodents is in line with clinical observations in humans and offers a whole new direction for research in bone physiology.

Adolescent↗

PubMed1993

Short-term oral phosphate and bone remodeling in beagles.

Attempts to increase bone volume in osteoporotic patients are still in the experimental stage. The coherence therapy, proposed by Frost, suggests that the activated bone units can remodel bone matrix in tandem. The cells (i.e., osteoclast and osteoblast which compose the remodeling units) are manipulated through specific medications timed to each of their duration of actions. The current study was to examine the effect of withdrawal of oral phosphate on bone in ovariectomized dogs. The present report demonstrates the capability of short-term oral phosphate to activate bone remodeling in the ovariectomized animal model. Results from biochemical and histomorphometric analyses confirm that remodeling units are activated following the release of parathyroid hormone. This transient scenario inflicts a shift of mineral density distribution in cancellous bone matrix of the iliac crest. Nevertheless, the bone remodeling units appear to be synchronized with each other and thus their resorptive and formative phases should be amenable to further pharmacological manipulation.

Administration, Oral↗

PubMed1993

Bone remodeling and the osteoclast.

Bone remodeling is a process initiated by the osteoclast, and thus, its understanding is prerequisite to regulation of bone turnover. The last decade has witnessed major advances in our understanding of osteoclast biology, specifically as relates to the ontogeny of the cell and the mechanisms by which it degrades bone. It is now possible to isolate and generate osteoclasts and maintain them in relative purity. Using these models, a number of laboratories have shown that ion transport by the osteoclast plays a major role in its ability to resorb bone. Furthermore, osteoclast-bone matrix attachment, mediated at least in part by integrins, is pivotal to the resorptive process. These discoveries are likely to lead to insight into control of the remodeling process.

Animals↗

PubMed2005

Identifying genes that regulate bone remodeling as potential therapeutic targets.

Bone remodeling, a coupled process involving bone resorption and formation, is initiated by mechanical signals and is controlled by local and systemic factors that regulate osteoblast and osteoclast differentiation and function. An excess of resorption over formation leads to the bone loss and increased propensity to fracture that is characteristic of osteoporosis. A newly described inhibitor of osteoblast differentiation, Ciz, interferes with bone morphogenic protein signaling. As a consequence, Ciz-deficient mice develop increased bone mass.

Animals↗