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PubMed2005

Computer-simulated bone architecture in a simple bone-remodeling model based on a reaction-diffusion system.

Bone is a complex system with functions including those of adaptation and repair. To understand how bone cells can create a structure adapted to the mechanical environment, we propose a simple bone remodeling model based on a reaction-diffusion system influenced by mechanical stress. Two-dimensional bone models were created and subjected to mechanical loads. The conventional finite element method (FEM) was used to calculate stress distribution. A stress-reactive reaction-diffusion model was constructed and used to simulate bone remodeling under mechanical loads. When an external mechanical stress was applied, stimulated bone formation and subsequent activation of bone resorption produced an efficient adaptation of the internal shape of the model bone to a given stress, and demonstrated major structures of trabecular bone seen in the human femoral neck. The degree of adaptation could be controlled by modulating the diffusion constants of hypothetical local factors. We also tried to demonstrate the deformation of bone structure during osteoporosis by the modulation of a parameter affecting the balance between formation and resorption. This simple model gives us an insight into how bone cells can create an architecture adapted to environmental stress, and will serve as a useful tool to understand both physiological and pathological states of bone based on structural information.

Bone Remodeling↗
PubMed1981

A study of bone remodeling using metal-polymer laminates.

Bone remodeling due to stress-shielding has been studied using a model system consisting of metal-polymer laminated fixation plates securely fixed to canine femurs. The plate stiffness was controlled by varying the ratio of metal facing to polymer core thickness in the laminate design while secure fixation to bone was achieved by providing a porous bone interfacing surface for the ingrowth of bone from the periosteal surface. Observations of laterally and medially placed plates indicated resorption in the area of the periosteal and endosteal bone surfaces respectively, for the higher stiffness composite plates used. The results indicate that plate stiffness greater than approximately 70 GPa (axial) and 6 N m2 (flexural) will result in extensive bone remodeling in the canine femur after a six month implantation period.

Alloys↗
PubMed2003

The pathogenesis of osteodystrophy after renal transplantation as detected by early alterations in bone remodeling.

BACKGROUND: Loss of bone mass after transplantation begins in the early periods after transplantations and may persist for several years, even in patients with normal renal function. While the pathogenesis of these abnormalities is still unclear, several studies suggest that preexisting bone disease, glucocorticoid therapy, and alterations in phosphate metabolism may play important roles. Recent studies indicate that osteoblast apoptosis and impaired osteoblastogenesis play important roles in the pathogenesis of glucocorticoid-induced osteoporosis. OBJECTIVES: To examine the early alterations in osteoblast number and surfaces during the period following renal transplantation. METHODS: Twenty patients with a mean age of 36.5 +/- 12 years were subjected to bone biopsy 22 to 160 days after renal transplantation. In 12 patients, a control biopsy was performed on the day of transplantation. Bone sections were evaluated by histomorphometric analysis and cell DNA fragmentation by the methods of terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end labeling (TUNEL), using immunoperoxidase and direct immunofluorescence techniques. RESULTS: The main alterations in posttransplant biopsies were a decrease in osteoid and osteoblast surfaces, adjusted bone formation rate, and prolonged mineralization lag time. Peritrabecular fibrosis was markedly decreased. None of the pretransplant biopsies revealed osteoblast apoptosis. In contrast, TUNEL-positive cells in the proximity of osteoid seams or in the medullary space were observed in nine posttransplant biopsies of which four had mixed bone disease, two had adynamic bone disease, one had osteomalacia, one had osteitis fibrosa, and one had mild hyperparathyroid bone disease. Osteoblast number in posttransplant biopsies with apoptosis was lower as compared with posttransplant biopsies without apoptosis. In addition, most of them showed a marked shift toward quiescence from the cuboidal morphology of active osteoblasts. Serum phosphorus levels were lower in patients showing osteoblast apoptosis and correlated positively with osteoblast number and negatively with the number of apoptotic osteoblasts. In addition, posttransplant osteoblast surface correlated positively with parathyroid hormone (PTH) levels and negatively with glucocorticoid cumulative dose. CONCLUSION: The data suggest that impaired osteoblastogenesis and early osteoblast apoptosis may play important roles in the pathogenesis of posttransplant osteoporosis. The possible mechanisms involved in the pathogenesis of theses alterations include posttransplant hypophosphatemia, the use of glucocorticoids, and the preexisting bone disease. PTH seems to have a protective effect by preserving osteoblast survival.

Adult↗
PubMed2003

Bone remodeling after renal transplantation.

Several studies have indicated that bone alterations after transplantation are heterogeneous. Short-term studies after transplantation have shown that many patients exhibit a pattern consistent with adynamic bone disease. In contrast, patients with long-term renal transplantation show a more heterogeneous picture. Thus, while adynamic bone disease has also been described in these patients, most studies show decreased bone formation and prolonged mineralization lag-time faced with persisting bone resorption, and even clear evidence of generalized or focal osteomalacia in many patients. Thus, the main alterations in bone remodeling are a decrease in bone formation and mineralization up against persistent bone resorption, suggesting defective osteoblast function, decreased osteoblastogenesis, or increased osteoblast death rates. Indeed, recent studies from our laboratory have demonstrated that there is an early decrease in osteoblast number and surfaces, as well as in reduced bone formation rate and delayed mineralization after transplantation. These alterations are associated with an early increase in osteoblast apoptosis that correlates with low levels of serum phosphorus. These changes were more frequently observed in patients with low turnover bone disease. In contrast, PTH seemed to preserve osteoblast survival. The mechanisms of hypophosphatemia in these patients appear to be independent of PTH, suggesting that other phosphaturic factors may play a role. However, further studies are needed to determine the nature of a phosphaturic factor and its relationship to the alterations of bone remodeling after transplantation.

Bone Diseases↗
PubMed1998

[Morphology of bone remodeling].

In this review, first the basic structure of bone and the histological and cytological characteristics of bone remodeling are reviewed. Then, topics on the ultrastructural and cytochemical characteristics of the biological mineralization, such as matrix vesicle and advanced collagen mineralization, are discussed. The recent advances in the understanding of the fine structural and cytochemical characteristics of bone cells in bone remodeling and their role in the regulation of bone metabolism, with special focus on the ultrastructural and cytochemical evidences of cell to cell, cell to metrix interaction of bone cells are also reviewed.

Bone Remodeling↗
PubMed1989

Haversian bone remodelling in human fetus.

Haversian bone remodelling used to be considered an attribute of adult bone. In the present paper, typical haversian remodelling was observed in the humerus, ulna, radius, femur, tibia, fibula and 6th and 7th ribs as soon as the 24th week. Its aspect suggests an already ancient occurrence. Remodelling was found in the same bone pieces of the neonate as well as in the clavicle and the other ribs. Mechanical factors may be responsible for starting the remodelling but their effects could be modulated by metabolic needs. Other still unknown factors might play a role too.

Bone Development↗
PubMed2006

Parametric sensitivity analysis applied to a specific one-dimensional internal bone remodelling problem.

The relative importance of the various parameters in inducing bone mass loss and osteoclastic perforations is still controversial. Therefore, there is a significant motivation to better understand the parameters behind such dynamic response, and great interest to carry out a parametric sensitivity study as it can provide useful information. As an application, the widely-accepted bone remodelling equation [M.G. Mullender, R. Huiskes, H. Weinans, A physiological approach to the simulation of bone remodeling as self organizational control process, J. Biomech. 27 (1994) 1389.] is investigated using the "n units" model [M. Zidi, S. Ramtani, Bone remodeling theory applied to the study of n unit-elements model, J Biomech. 32 (1999) 743.]. This analysis pointed out that the power in the modulus density relationship p and the power to which density is raised in normalizing the energy stimulus q, known as strongly implicated in the stability condition of the remodelling process, were also stated as insensitive parameters in the bone loss area.

Biomechanical Phenomena↗
PubMed2005

Osteoblasts and osteoclasts in bone remodeling and inflammation.

Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts. Osteoblasts not only play a central role in bone formation by synthesizing multiple bone matrix proteins, but regulate osteoclast maturation by soluble factors and cognate interaction, resulting in bone resorption. Osteoclast maturation requires stimulation by RANKL expressed on osteoblasts, and the cognate interaction is mediated by firm adhesion via ICAM-1. During the processes, pro-inflammatory cytokines such as IL-1 and TNF-alpha, cause an imbalance in bone metabolism, by favoring bone resorption via the induction of RANKL and ICAM-1 on osteoblasts. These inflammatory signals originate from the immune system, the largest source of cell-derived regulatory signals, and such immunological signals to the bone are transmitted primarily via osteoblasts to induce osteoclast maturation, resulting in secondary osteoporosis. Actually, such phenomena mainly occur at the interface between proliferating synovium and bone tissue in rheumatoid arthritis (RA). Thus, therapeutic strategies for these conditions, an anti-TNF-alpha antibody and an IL-1 receptor antagonist, effective for treating RA disease activity, also reduce secondary osteoporosis and joint destruction. Based on an improved understanding of immune signals, investigation of the suppression of cell functions may lead to improved understanding and better treatment of diseases of bone metabolism and osteoporosis.

Animals↗
PubMed1995

The 5-lipoxygenase inhibitor BWA4C impairs osteoclastic resorption in a synchronized model of bone remodeling.

The role of leukotrienes on bone resorption was tested in a well-standardized model of bone remodeling by inhibiting their biosynthesis with BWA4C, a specific inhibitor of 5-lipoxygenase. After extraction of their upper molars unilaterally, 30 Wistar rats were divided into three groups; the first remained untreated (control group), the second received 80 mg/kg/day of BWA4C dissolved in polyethylene glycol 300 (experimental group), and the third received only the vehicle (sham-treated group). After four days of experiment, the animals were killed and the resorption profile was assessed along the antagonist mandibular buccal cortex. The main result was a dramatic decrease in the number of TRAP-positive mononucleated preosteoclasts in the experimental group (-69%, p < 0.0005 and p < 0.003 vs. the control and sham-treated groups, respectively). This drop was related to a significant decrease in the number of osteoclasts. Neither the activation of the differentiated osteoclasts nor their mean interface with the bone surface were affected by BWA4C. Concomitantly, the mast cell population residing near the vascular network limiting the periosteum was markedly and significantly increased by the treatment. These mast cells were mostly degranulating, i.e., were in a state of activation that we previously found to related to resorption. These data suggest (1) that the leukotrienes are involved in the recruitment of osteoclast progenitors, and/or their differentiation into preosteoclasts, and (2) that mast cells responded to leukotriene inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1996

Cortical bone remodeling in autosomal dominant osteopetrosis: a study of two different phenotypes.

Previous analyses of cancellous bone remodeling in autosomal dominant osteopetrosis (ADO) have suggested a diminished osteoclastic resorption at the endocortical surface. Consequently, cortical width increases with age in both ADO type I and II. By means of histomorphometric methods, the remodeling cycle of the Haversian surface in the iliac crest has recently been reconstructed in normal individuals. The aim of the present investigation was to study cortical bone remodeling in ADO type I and II. Transcortical iliac crest bone biopsies obtained from 21 ADO patients were studied. Of these, 14 had ADO type I and seven had ADO type II. Twenty of the patients had received intravital double labeling with tetracycline before the biopsies were obtained. The static histomorphometric parameters for cortical bone mass and structure were compared with a control group of 21 sex- and age-matched individuals. Regarding the dynamic histomorphometric parameters for reconstruction of the cortical bone remodeling cycle, the ADO type I material was compared with control material from 14 sex- and age-matched individuals, whereas the ADO type II material was compared with control material from six sex-matched but younger individuals. Significant increases were seen in absolute as well as fractional cortical widths in both ADO types. Furthermore, an age-related increase was observed in both absolute and fractional cortical widths in ADO type I, whereas ADO type II was nonsignificant with regard to age. The fractional cancellous width was reduced in both type I and type II. However, only in ADO type I did the fractional cancellous width significantly correlate inversely with age. In the control group, neither cortical dimensions nor cancellous width correlated significantly with age. No significant differences were observed between patients and the control group in osteon dimensions; fractional resorptive, formative, or quiescent sites; resorptive or formative remodeling rates; remodeling periods; or activation frequency. An age-related increase in cortical porosity was seen in the group of normal individuals, but not in the two patient groups. The fractional remodeling space was increased in the ADO type II group. In conclusion, cortical dimensions are increased in both ADO type I and II and positively correlated to age in type I. However, cortical remodeling at the Haversian surface is essentially normal in both ADO type I and II. This could be explained by a defective endocortical bone resorption, as no periosteal accretion was observed, and because cancellous bone remodeling previously has been described to be normal.

Adult↗
PubMed2001

The skeleton in primary hyperparathyroidism: a review focusing on bone remodeling, structure, mass, and fracture.

The mechanisms behind the influence of PHPT on the skeleton are closely connected with bone turnover. Throughout life, the skeleton is continuously renewed by bone remodeling, a process which serves the purpose of repairing damaged bone and adapting the skeleton to changes in physical load. In this process, old bone is removed by osteoclastic resorption and new bone is laid down by osteoblastic formation. Bone mass increases with growth in the first decades of life, and around the age of 30 years the peak bone mass is reached. Thereafter, as a result of mechanisms involving bone remodeling, a net bone loss is seen: 1) A reversible bone loss because of increase in the remodeling space, i.e., the amount of bone resorped but not yet reformed during the remodeling cycle. This mechanism leads to decrease in average trabecular thickness and cortical width, and to increase in cortical porosity. 2) An irreversible bone loss caused by negative bone balance, where the amount of bone formed by the osteoblasts is exceeded by the amount of bone resorbed by the osteoclasts at the same remodeling site. Consequently, progressive thinning of trabecular elements, reduced cortical width and increased cortical porosity is seen. 3) Finally, perforation of trabecular plates by deep resorption lacunae leads to complete irreversible removal of structural bone components. Parathyroid hormone, together with vitamin D, are the principal modulators in calcium homeostasis. The main actions of PTH are executed in bone and kidneys. In the kidneys, PTH increases the tubular re-absorption of calcium, thereby tending to increase serum calcium. PTH also induces increased conversion of 25(OH)-D to 1,25(OH)2-D. This last action, enhances intestinal calcium absorption and increased skeletal calcium mobilization, which further adds to the circulating calcium pool. In bone, the "acute" regulatory actions of PTH on serum calcium are probably accompliced via activation of osteocytes and lining cells. A second mechanism of PTH in bone is the regulation of bone remodeling. The action seems to be an increased recruitment from osteoblastic precursor cells and activation of mature osteoclasts. It is supposed that these responses are predominantly mediated indirectly through actions on osteoblast-like or nonosteoblast-like stromal cells, as osteoclasts themselves to not have PTH receptors. Bone metabolism and bone mass are studied by biochemical bone markers, bone histomorphometry, and densitometry. As bone markers and bone histomorphometry give information on bone metabolism from different points of view, these methods are preferably combined. Histomorphometry gives detailed information about bone turnover on cellular level, the whole remodeling sequence is described, and the bone balance can be calculated. However, they focus on a small volume, and may, therefore, not be representative for the whole skeleton. On the other hand, studies of bone markers supply general information about turnover in the whole skeleton, but they do not give facts on the bone turnover on the cellular or tissue level and bone balance. Bone densitometry is the principal method in studying bone mass, but valuable information concerning bone structure also comes from histomorphometry. Bone remodeling is considerably increased in PHPT. Studies of bone markers show increase in both resorptive and formative markers, and the increases seem to be of equivalent size. This is in agreement with histomorphometric findings and shows that the coupling between resorption and formation is preserved. By histomorphometry on iliac crest biopsies, trabecular bone remodeling is found increased by 50%, judged by the increase in activation frequency; a measure of how often new remodeling is initiated on the trabecular bone surface. In PHPT, such remodeling activity is repeated about once every year. Reconstruction of the whole remodeling sequence does not show major deviations in lengths of the resorptive and formative periods compared to normal. Furthermore, the amount of bone removed by the osteoclasts during the resorptive phase is matched by the amount of new bone formed by the osteoblasts leading to a bone balance very close to zero. Compared with trabecular bone, the turnover rate in cortical bone is considerably lower, around 10%. Remodeling of the cortical bone takes place at the endocortical, the pericortical, and the Haversian surfaces. Endocortical bone remodeling activities are very similar to trabecular remodeling activities with good correlation between individual parameters. Periosteal remodeling activity is negligible in PHPT, as it is in the normal state. Cortical porosity, which reflects the remodeling activity on the Haversian surface, is increased by 30-65% in PHPT. (ABSTRACT TRUNCATED)

Animals↗
PubMed2006

[Bone remodeling markers in saliva as compared to serum in rats].

Bone markers are useful tools to measure bone remodeling; currently they are assessed in serum and urinary samples; however there is little information concerning their measurement in saliva. The present experimental study evaluates the possibility to measure collagen type I carboxiterminal telopeptide (CTX) and bone alkaline phosphatase (b-AP) in saliva, its correlation with serum samples in normal conditions and in the increase of the bone remodeling due to estrogen deficiency. Twenty four normal adult Wistar rats (300 +/- 20 g) [12 SHAM and 12 rats after 1 week of bilateral ovariectomy (OVX)] were studied. Fasting serum and total saliva after stimulation with pilocarpine were collected. In both samples were measured: CTX (ng/ml) by ELISA (RatLabs, Osteometer Bio Tech, Denmark) and b-AP (IU/L) (Wiener, colorimetrically). Both CTX and b-AL in serum samples were significantly higher in OVX than in SHAM rats (15.3 +/- 4.0 vs. 21.8 +/- 6.4, p < 0.05 y 71 +/- 29 vs. 104 +/- 23; p < 0.01, respectively). Saliva presented the same behaviour (3.6 +/- 0.5 vs. 6.4 +/- 2.9; p < 0.02 y 73 +/- 29 vs. 90 +/- 8; p < 0.003, respectively). When saliva CTX and b-AP were plotted against serum concentration significant positive correlations were obtained: r = 0.58, p < 0.05 and r = 0.59; p < 0.05, respectively. In conclusion, the present results are promisory in the sense of the potential use of a salivary-based test for evaluating bone remodeling. However, the use of this methodology for clinical practice needs extensive additional investigations.

Alkaline Phosphatase↗
PubMed1993

Cytokines and growth factors in the regulation of bone remodeling.

Osteoporosis and periodontal disease both represent examples of abnormal bone remodeling. As knowledge of the cellular and molecular events in the normal bone remodeling process has accumulated in the last decade, better understanding of the pathophysiology of bone loss associated with periodontal disease and with aging has occurred. This short review does not attempt to include all aspects of this topic but covers specific areas in which there have been recent advances. (1) Observations made in the last few years have indicated that a hierarchy of both receptor and nonreceptor tyrosine kinases may be involved in normal osteoclastic bone resorption and that certain members of these tyrosine kinase families may mediate cytokine effects. Studies in the op/op variant of murine osteopetrosis have shown that normal production of monocyte-macrophage colony-stimulating factor 1 (M-CSF, also called CSF-1) and activation of its receptor (the receptor tyrosine kinase c-fms) are required for normal osteoclast formation. (2) Studies in mice made deficient in nonreceptor tyrosine kinase by gene knockout have shown that expression of this nonreceptor tyrosine kinase is required for normal osteoclast action and ruffled border formation, although not for osteoclast formation. (3) Recent studies have shown that in addition to prostaglandins of the E series, other arachidonic acid metabolites may be involved in normal and abnormal osteoclastic bone resorption. 5-Lipoxygenase metabolites, the leukotrienes, stimulate isolated osteoclasts to form resorption pits as well as cause osteoclastic bone resorption in organ cultures of neonatal mouse calvariae. These compounds, which are unstable in tissue culture media, are readily inhibitable by agents that inhibit 5-lipoxygenase enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2003

[Effect of cyclophosphamide on bone remodeling in rats].

Neoplasms, with or without metastases in bones, can induce pathological bone remodeling, leading to systemic bone resorption and hypercalcemia or osteomalacia and normocalcemia. The aim of the present study was to investigate the effect of a cytostatic--cyclophosphamide on the skeletal system in rats. The experiments were carried out in male Wistar rats with initial body weight of 212-229 g, divided into 3 groups (n = 6): I--Control, II--Cyclophosphamide (10 mg/kg m.c. i.m. daily for 14 days, and after a 7-day break, for 7 days), III--Cyclophosphamide (20 mg/kg m.c.p.o. daily for the initial 14 days). After 30 days of the experiment, the animals were killed and bone mass, length and diameter of long bones, mineral content in bones, transverse cross-section surfaces of the cortical diaphysis and of the marrow cavity, transverse growth, width of endosteal and periosteal osteoid in the tibia, width of trabeculae, width of epiphyseal cartilage and mechanical features of the femur were examined. Cyclophosphamide caused disorders of bone tissue remodeling. Decreases in bone mass, length, diameter, mineral content in bones, width of trabeculae in the femur, transverse growth, width of osteoid, transverse cross-section surface of the cortical diaphysis, and worsening of mechanical properties of the femur were observed.

Animals↗
PubMed1989

[Hormonal regulation of bone remodeling].

In the adult skeleton a continuous turnover of bone matrix and mineral takes place at discrete foci throughout life (bone remodeling). This process ensures the mechanical integrity of the skeleton and plays an important role in calcium homeostasis. It constitutes a very complex sequence of events, involving activation of several different stem cell populations and rigid regulation of two contrasting processes: bone resorption and bone formation. The study of factors involved in the control of bone remodeling is complicated by the involvement of local factors (growth factors, prostaglandins, inorganic ions) and systemic factors (calcitropic hormones), that interact at several different levels (cellular, tissue, and organ-levels). Most metabolic bone diseases, including osteoporosis, are caused by disturbances in the regulation of bone remodeling leading to an imbalance between resorption and formation. To understand these disturbances fully, it is necessary to study the different levels of skeletal organization, and the effect of different hormones and local factors on bone resorption and formation. In this review are described the effects of calcitropic hormones on bone cells at the cellular and tissue levels, and their interaction with local factors.

Bone and Bones↗
PubMed2000

Application of bone remodeling theories in the simulation of orthodontic tooth movements.

A numerical model that calculates bone apposition and resorption around a tooth root on the basis of bone remodeling theories was developed to simulate orthodontic tooth movements. The model was used to calculate different kinds of orthodontic tooth movements, that were then compared with the expected movements based on clinical experience. For simulation of the movements the root of a canine was modeled in an idealized way in the form of an elliptical paraboloid and was processed with a finite element program. The finite element model was loaded with defined force systems. Two model assumptions were used to calculate the bone remodeling process. The mechanical loads firstly in the periodontal ligament and secondly in the alveolar bone were taken to simulate the following tooth movements: 1. mesial tipping around the center of resistance (force system at the bracket: isolated torque MY = 5 Nmm), 2. rotation around the long axis of the tooth (MZ = 5 Nmm), 3. uncontrolled tipping around the root tip (FX = 1 N, MZ = 5 Nmm), 4. canine retraction (FX = 1 N, MY = -9.5 Nmm, MZ = 5 Nmm), 5. and 6. extrusion/intrusion (FZ = +/- 0.5 N, MX = +/- 2.5 Nmm). Comparison with clinical experience was performed by calculating the orthodontic tooth movements based on the assumption of a fixed position of the center of resistance. It could be demonstrated that the numerical model of orthodontic bone remodeling can be used to calculate orthodontic tooth movements. However, the results are strongly dependent on the model assumptions. The model simulating the bone remodeling on the basis of the loading of the periodontal ligament delivers results that are in very good accordance with the biomechanical assumptions of the position of the center of resistance. However, marked side effects occurred with the second model, especially in the simulations of uncontrolled tipping, translation and intrusion/extrusion. Clinically, these side effects cannot be observed.

Bone Remodeling↗
PubMed1993

Adaptive bone remodeling around bonded noncemented total hip arthroplasty: a comparison between animal experiments and computer simulation.

Severe loss of bone related to stress-shielding is one problem threatening the long-term integrity of noncemented total hip arthroplasty. It is widely accepted that this phenomenon is caused by adaptive bone remodeling according to Wolff's law. Recently, quantitative bone-remodeling theories have been proposed, suitable for use in computer-simulation models in combination with finite-element codes, which can be applied to simulate the long-term effect of the remodeling process. In the present paper, the results of such a computer simulation are compared with those in an animal experiment. A three-dimensional finite-element model was constructed from an animal experimental configuration concerning the implantation of a fully coated femoral hip prosthesis in dogs. The simulation results of the adaptive bone-remodeling process (geometric adaptations at the periosteal surface and density adaptations within the cancellous bone) were compared with cross-sectional measurements of the canine femurs after 2 years of follow-up. The detailed comparison showed that long-term changes in the morphology of bone around femoral components of total hip replacements can be fully explained with the present quantitative adaptive bone-remodeling theory.

Adaptation, Physiological↗
PubMed2004

Drugs used to treat osteoporosis: the critical need for a uniform nomenclature based on their action on bone remodeling.

There continues to be uncertainty about the classification of available drugs for treating osteoporosis. We find that grouping them into anti-catabolic and anabolic classes based on the mechanisms of their action on bone remodeling and fracture reduction removes ambiguities and provides a relatively straightforward classification. The recent introduction of teriparatide into clinical practice initiated the era of anabolic therapy for osteoporosis, but it is still unclear how to define an anabolic drug. All drugs that increase bone mass do so by affecting bone remodeling. When their mechanisms of action on bone remodeling and on fracture reduction are considered, we find that anti-osteoporotic drugs fall naturally into either anti-catabolic or anabolic classes. Anti-catabolic drugs increase bone strength and reduce fractures mainly by decreasing the number of bone multicellular units (BMUs). This reduces perforative resorption and preserves skeletal microarchitecture (by preventing further structural damage to trabecular bone and increased porosity in cortical bone induced by high bone remodeling). Reduction in bone remodeling by anti-catabolic drugs may increase bone mass moderately during the interval in which previously initiated BMUs are completing mineralization. Some anti-catabolic drugs may also enhance the formation phase of the remodeling cycle, but their major action is to reduce overall bone turnover (i.e., the number of BMUs in bone). In contrast, anabolic drugs increase bone strength and reduce fractures by substantially increasing bone mass as a result of an overall increase in the number of BMUs combined with a positive BMU balance (the magnitude of the formation phase is greater than that of the resorption phase). Some anabolic drugs also induce renewed modeling, increase periosteal apposition and repair of trabecular microstructure. We hope that this classification will serve as a starting point for continued discussion on the important issue of nomenclature.

Adult↗