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PubMed2006

[Anisotropic bone remodeling model with mechanostat].

At present, the numerical model of bone remodeling is inadequate to copy the physiological process of bone remodeling. According to the physiological mechanism of bone remodeling and the anisotropy of bone mechanics properties, an anisotropic bone modeling model with mechanostat was developed, and then was applied to a study on the remodeling evolution of 2D squareplate model. Good results were obtained. The model can be used in the study of implant, osteoporosis and other bone diseases.

Anisotropy↗

PubMed2003

Defective bone remodelling in osteoprotegerin-deficient mice.

Previous studies have reported enhanced osteoclastogenesis, increased bone resorption and osteoporosis in osteoprotegerin (OPG)-deficient mice. In the present study, we show that the tibial epiphyses contain abundant, thin trabeculae lined with numerous osteoclasts and cuboidal osteoblasts. The increase in osteoblasts and osteoclasts was associated with a dramatic increase in calcein labelling of the mineralization fronts and replacement of much of the intertrabecular marrow with numerous alkaline phosphatase-positive preosteoblasts. Furthermore, the discrete, linear cement lines seen in wild-type mice were replaced by a randomly oriented meshwork of cement lines that were stained intensely for tartrate-resistant acid phosphatase and osteopontin in the OPG-/- mice. These indices of accelerated bone remodelling in mutant bone were associated with irregular trabecular surfaces, a disorganized collagen matrix interspersed with amorphous ground substance and numerous fissures between old and new bone. In total, these observations indicate that enhanced osteoclastic activity in OPG-/- epiphyses led to a coupled increase in osteoblast differentiation and activity and an increase in bone remodelling. The high bone turnover, disorganized matrix and impaired attachment of new to old bone in the cement lines in OPG-/- mice appear to cause bone fragility.

Animals↗

PubMed1982

Cellular kinetics of the bone remodeling sequence in the rat.

The kinetics of the bone remodeling sequence in the rat has been studied using a system in which well-synchronized remodeling units were induced along the periosteum of rat mandibles. Remodeling of the periosteal surface of the mandibles was induced according to Tran Van (1979) by extraction of the opposing row of teeth; namely, the right maxillary molars were extracted under light ether anesthesia, therefore allowing the right mandibular molars to egress; this, in turn, induced a wave of remodeling activity on the buccal side of the periosteal surface of the alveolar bone. The quantification of the different cellular activities involved in bone remodeling has been performed up to 16 days after induction. This allowed us to demonstrate the sequential activity of the different cell types involved in bone remodeling, to study the cellular kinetics of this sequence of events, and to directly measure the duration of each phase of the bone remodeling sequence. A single wave of osteoclasts appeared 3 days after induction, reached a peak of 4-5 days, and then decreased sharply. This was followed by a single wave of mononuclear cells (Baron et al., 1980) within remodeling sites during the reversal phase; they appeared 4 days after induction, reached a peak by day 7, and then decreased sharply. This reversal activity was then followed by osteoblasts forming new bone on top of a reversal cement line in the remodeling sites, starting 6 days after induction and increasing until the end of the experiment. In addition, the synchronization of the system used in this study allowed direct measurement of the duration of the successive steps of the remodeling sequence. The directly measured values have then been compared to previous data calculated from other systems.

Animals↗

PubMed2005

Thermoelectroelastic solutions for surface bone remodeling under axial and transverse loads.

Theoretical prediction of surface bone remodeling in the diaphysis of the long bone under various external loads are made within the framework of adaptive elastic theory. These loads include external lateral pressure, electric and thermal loads. Two solutions are presented for analyzing thermoelectroelastic problems of surface bone remodeling. The analytical solution that gives explicit formulation is capable of modeling homogeneous bone materials, while the semi-analytical solution is suitable for analyzing inhomogeneous cases. Numerical results are presented to verify the proposed formulation and to show the effects of mechanical, thermal and electric loads on surface bone remodeling process.

Animals↗

PubMed2000

Cyclosporine bone remodeling effect prevents steroid osteopenia after kidney transplantation.

BACKGROUND: It is well established that prednisone above 7.5 mg/day may induce osteopenia in association with decreased bone formation. In contrast, the effect of cyclosporine on bone remodeling and bone mineral density (BMD) is controversial. Multiple confounding factors explain this controversy, especially after renal transplantation. METHODS: Fifty-two renal transplanted patients never exposed to aluminum while on dialysis were selected because they had no rejection and no hypercalcemia for 24 months while being treated with low dose prednisone/cyclosporine A (daily dose at 10 mg and 4.8 mg/kg, respectively, beyond 3 months). Bone remodeling markers (BRMs; plasma osteocalcin, bone and total alkaline phosphatases for formation, and urinary pyridinolines for resorption) were sequentially measured together with plasma creatinine, intact parathyroid hormone (PTH) and 25 OH vitamin D and cyclosporine from day 0 to 24 months. BMD was measured at 3, 6, 12, and 24 months by quantitative computerized tomography (QCT) at the lumbar spine and by double-energy x-ray absorptiometry (DEXA) at this site, as well as at the femoral neck, radius shaft, and ultradistal (UD) radius. RESULTS: Plasma concentrations of creatinine, PTH, and 25 OH vitamin D initially decreased and stabilized beyond three months at 137 micromol/L, 1.5 the upper limit of normal (ULN) and 11 ng/mL, respectively. All BRM increased significantly above the ULN at six months and then decreased. The BMD Z score at three months was low at all sites measured by DEXA and QCT. Follow-up measurements showed stability of absolute value and of Z score at all sites measured by DEXA. A comparison of the lumbar QCT Z score, which was available in 42 patients at 3 and 24 months, showed an increase in 28 and a decrease in 14, so that the increase for the whole group was significant (P < 0.04). Compared with patients with a decreased Z score, those with an increased Z score had significantly higher cyclosporine and lower prednisone dosages and a greater BRM increase at six months, whereas age, sex ratio, and plasma creatinine, PTH and 25 OH vitamin D were comparable and stable from months 3 through 24. The mean trough level of cyclosporine for the first six months was positively correlated to osteocalcin and total alkaline phosphatase increase at six months, and both bone formation and resorption marker increases were significantly correlated to the lumbar QCT Z score increase at 24 months. CONCLUSIONS: Combined low-dose prednisone and cyclosporine immunosuppression are associated with a stabilization of BMD measured at all sites with DEXA 3 to 24 months after renal transplantation and with a prevention of age-related loss of vertebral trabecular bone, as shown by the significant increase in lumbar spine QCT Z score. It is suggested that cyclosporine, together with the decrease of prednisone dosage but independent of renal function, PTH, and vitamin D status, contributes to a transient stimulation of bone remodeling at six months, which counterbalances the deleterious effect of prednisone on bone formation and BMD.

Absorptiometry, Photon↗

PubMed2004

Bone remodeling: new aspects of a key process that controls skeletal maintenance and repair.

Bone remodeling is the concerted interplay of two cellular activities: osteoclastic bone resorption and osteoblastic bone formation. Bone remodeling is the physiologic process that maintains bone mass, skeletal integrity and skeletal function. A molecular understanding of this process is therefore of paramount importance for almost all aspects of skeletal physiology and many facets of bone diseases. Based on the morphological observation of the BMU-"bone multicellular unit" or "bone metabolic unit"-and a wide body of in vitro data, bone remodeling was thought to be controlled locally through functional coupling of resorption and formation and vice versa. However, recent genetic studies have shown that there is no obligatory tight cross-control of bone formation and bone resorption in vivo and that there is also a central axis controlling bone formation, one aspect of bone remodeling. The molecule that inhibits bone formation through a hypothalamic relay is leptin. Following binding to its receptor located on the ventromedial nuclei of the hypothalamus, leptin's action on bone formation is mediated via a neuronal signaling cascade that involves the ss-adrenergic system. The overall goal of this review is to show how the dialogue between clinical medicine and mouse genetics helped to uncover a new concept in skeletal physiology.

Bone Remodeling↗

PubMed1990

[The usefulness of biochemical markers of bone remodelling in the diagnosis and follow-up of Paget's disease of bone, primary hyperparathyroidism, tumoral hypercalcemia and postmenopausal osteoporosis. I. The markers of bone formation].

Rapid detection of the exact changes in bone remodelling is exceptionally important. In this paper, the latest bone remodelling biochemical markers are reviewed. Some of them have already been used for a long time, and their utility has been widely demonstrated. The newest ones, in experimental stage, can be used as a complement to the others. The bone remodelling markers reviewed are: 1) Alkaline phosphatase; 2) osteocalcin; 3) Other noncollagen of bone matrix such as osteonectin, GLA-protein of the matrix, osteopontine and alpha 2-HS-glycoprotein; 4) Procollagenous and other collagenous peptides of the matrix (C terminal of type-I procollagen and urinary elimination of nondialysis hydroxyproline. Amongst the bone resorption markers studied are: 1) Calcium/creatinine urinary quotient; 2) Tartrate resistant acid phosphatase; 3) Urinary hydroxyproline; 4) Other substances derived from collagen disruption such as hydroxilysin glycoside, piridinolinic intermolecular bridges and the enzymatic activity of proline iminopeptidase. We endeavoured to collect all the most important references on the matter, especially those relating to Paget's disease of the bone, primary hyperparathyroidism, tumoral hypercalcemia and postmenopausal osteoporosis.

Biomarkers↗

PubMed1990

[Usefulness of bone remodelling biochemical markers in the diagnosis and follow-up of Paget's bone disease, primary hyperparathyroidism, tumor hypercalcemia, and postmenopausal osteoporosis. II. Bone resorption markers].

Rapid detection of the exact changes in bone remodelling is exceptionally important. In this paper, the latest bone remodelling biochemical markers are reviewed. Some of them have already been used for a long time, and their utility has been widely demonstrated. The newest ones, in experimental stage, can be used as a complement to the others. The bone remodelling markers reviewed are: 1) Alkaline phosphatase; 2) osteocalcin; 3) other noncollagen of bone matrix such as osteonectin, GLA-protein of the matrix, osteopontine and alpha 2-HS-glycoprotein; 4) Procollagenous and other collagenous peptides of the matrix (C terminal of type I procollagen and urinary elimination of non-dialysis hydroxyproline. Amongst the bone resorption markers studied are: 1) Calcium/creatinine urinary quotient; 2) Tartrate resistant acid phosphatase; 3) Urinary hydroxyproline; 4) Other substance derived from collagen disruption such as hydroxylysine glycoside, piridinolinic intermolecular bridges and the enzymatic activity of proline iminopeptidase. We endeavored to collect all the most important references on the matter, especially those relating to Paget's disease of the bone, primary hyperparathyroidism, tumoral hypercalcemia and postmenopausal osteoporosis.

Acid Phosphatase↗

PubMed1997

Short-term variations in bone remodeling biochemical markers: cyclical etidronate and alendronate effects compared.

Bone-remodeling markers have been proposed to monitor antiosteoporotic therapy, as substantial changes in these markers usually occur in a relatively short time interval. In this study we have evaluated the short term effects of two bisphosphonates on bone-remodeling markers with the aim of 1) defining the shortest reliable time interval after which markers should be measured, and 2) comparing the effects of different bisphophonates. To do so, 74 postmenopausal women with a lumbar spine t score of at least -1 were randomly allocated to 4 different treatments: calcium carbonate (500 mg/day; n = 18), 5 mg/day alendronate (A5; n = 18), 10 mg/day alendronate (A10; n = 20), and cyclical etidronate (CE; n = 18). Serum and 24-h urine samples were collected at baseline and 14, 28, 56, and 84 days after the beginning of therapy. Type I collagen N-terminal (NTx) and C-terminal (CTx) telopeptides and total deoxypyridinoline (tDPD) were measured in urine and normalized for urinary creatinine excretion. Osteocalcin and bone alkaline phosphatase in serum were measured. Alendronate (at both doses) and CE significantly decreased bone-remodeling markers, whereas calcium carbonate did not. Bone resorption markers reduction reached a plateau 14 (A10) or 28 (A5 and CE) days after the beginning of treatment, whereas osteocalcin and bone alkaline phosphatase were significantly reduced at 56 (A10) and 84 (CE) days. The global effects of alendronate and CE on NTx and CTx (calculated as the area under the curve) were significantly different from those of calcium (P < 0.05), but were not significantly different from each other. The percent change from baseline obtained with tDPD, NTx, or CTx during bisphosphonate treatment were significantly different (P < 0.05), but this difference disappeared when the variability in the calcium carbonate group was taken into account. In conclusion, this study shows that 1) etidronate and alendronate induce a significant and rapid reduction in bone-remodeling markers; 2) the changes in NTx, CTx, and tDPD urinary excretions reach a plateau after 2-4 wk of treatment; and 3) short term treatments with CE or alendronate induce similar changes in the urinary excretion of NTx and CTx.

Adult↗

PubMed2006

A mathematical model for simulating the bone remodeling process under mechanical stimulus.

OBJECTIVES: Among the current mathematical models for bone remodeling, few can consider bone resorption due to overload. The objective of this paper is to develop a new bone remodeling model which can simulate both underload and overload resorptions that often occur in dental implant treatments. METHODS: Based on the traditional model, a new mathematical equation relating the density change rate with mechanical stimulus has been developed. The new equation contains an additional quadratic term which can produce reduction in bone density at high load levels. In addition, to fully exploit the characteristics of this model, a range of different bone remodeling behaviors were studied under the load cases with both constant and varying stress magnitudes. Finally, the model was applied in conjunction with the finite element method to a practical case of dental implant treatment. RESULTS: The FE analysis results showed that bone resorption at the neck of the implant occurred due to occlusal overload but then resorption stopped after some time before reaching the coarse threads. Meanwhile, the density of the bone deeper into the mandible increased slightly due to the additional mechanical stimulus provided by the occlusal load. This phenomenon is observable in some clinical situations. SIGNIFICANCE: The new model can describe the bone overload resorption, a feature which is absent in most of the current models. And by simulating the dental implant treatment using FE method, the ability of the new mathematical model to simulate overload bone resorption has been clearly demonstrated.

Biomechanical Phenomena↗

PubMed1991

Bone remodeling in W/Wv mast cell deficient mice.

Strong experimental evidence exists for a relationship between mast cells and bone disease, but the role of mast cells in the regulation of bone remodeling is unknown. In order to address this question, mast cell deficient mice (W/Wv) were paired with their mast cell sufficient (+/+) littermates and evaluated for differences in response to an induced cycle of bone remodeling. This was achieved using a tooth egression protocol, in which a synchronous cycle of bone remodeling was induced in the mandibular buccal alveolar periosteum by extraction of the opposing dentition. Quantitative histomorphometric changes during the activation, resorption, reversal, and formation phases of bone remodeling were documented using standard techniques. Most cell deficient mutants exhibited the following defects in response to an induced cycle of bone remodeling: (a) the onset of the remodeling cycle was delayed by a prolonged activation phase, (b) the duration and extent of the active formation phase was decreased, and (c) the amount of new bone matrix synthesized was diminished while mineralization rates were found to be normal. These results suggest that mast cells and their mediators provide a paracrine mechanism which influences the recruitment of osteoclast and osteoblast progenitors and their participation in bone remodeling. Nonetheless, since bone remodeling occurs in mast cell deficient mice, albeit less efficiently, this mechanism is most likely one of several redundant mechanisms that provide for adequate skeletal homeostasis.

Animals↗

PubMed2003

Regulation of bone remodeling and emerging breakthrough drugs for osteoporosis and osteolytic bone metastases.

Major advances have been made in the past 10 years in our understanding of the molecular basis of bone cell formation and bone remodeling. For example, the discovery of osteoprotegerin, the decoy receptor and inhibitor of receptor activator of NF-kappaB ligand (RANKL), and the RANKL/receptor activator of NF-kappaB (RANK) signaling pathway that is essential for osteoclastogenesis, has helped clarify the mechanisms regulating osteoclast formation, activation, and survival. PTH, like most other osteoclast stimulating factors, promotes RANKL production by osteoblast/stromal cells when they are exposed to it continuously, but when given intermittently it stimulates bone formation and reduces fracture risk in postmenopausal women. This anabolic effect is associated with increased expression of insulin-like and fibroblast growth factors and decreased osteoblast apoptosis. Src tyrosine kinase is essential for osteoclast activation and also negatively regulates osteoblast activity. Thus, it is a well-validated therapeutic target for the prevention of postmenopausal and other forms of bone loss. Preliminary in vitro and in vivo studies of specifically designed, bone targeted, non-peptide Src inhibitors have shown that these compounds inhibit bone resorption and stimulate new bone formation. The design of drugs using structure/function approaches such as this should lead to the development of novel therapeutics that could be used to counteract the negative effects of chronic renal failure on the skeleton.

Animals↗

PubMed1991

Effects of neonatal sympathectomy and capsaicin treatment on bone remodeling in rats.

Bone metabolism may be influenced by the innervation of skeletal tissues. Neuropeptides such as vasoactive intestinal peptide, from sympathetic nerves, and calcitonin gene-related peptide, from sensory nerves, have been implicated as local modulators of bone metabolism. The effect of neonatal sympathectomy and of capsaicin-induced sensory denervation in rats was studied on the following: (i) the radial bone growth and apposition rate in tibiae (normal growth and modeling) and (ii) the percentage of periosteal surface of the mandible occupied by osteoclasts during induced remodeling. Neonate rats were treated with guanethidine, capsaicin, or appropriate vehicle. At seven weeks, maxillary molars were removed to induce remodeling on the buccal surface of the mandible. Animals were killed four days after surgery. Cross-sectional cortical area, medullary area, and periosteal apposition rate were measured by histomorphometry in ground sections of tibiae. The percentage of periosteal surface at the remodeling site occupied by osteoclasts (stained for acid phosphatase) was measured in frozen, undecalcified sections. There was no significant difference in cortical or medullary area or periosteal apposition rate in tibiae between each drug treatment and its control. However, the mandibular bone surface occupied by osteoclasts was increased 45.5% (P less than or equal to 0.005) in animals treated neonatally with guanethidine compared to controls. In contrast, the mandibular surface occupied by osteoclasts was decreased 21.2% (P less than or equal to 0.04) in animals treated neonatally with capsaicin compared to controls. The alteration of bone remodeling (osteoclast surface) by both treatments indicates that sensory and sympathetic nerves play a role in focal metabolism of bone.

Animals↗

PubMed1996

Long term bone remodeling around the Charnley femoral prostheses.

Femoral bone remodeling after total hip replacement was studied by following patients who received 326 Charnley femoral prostheses for 10 to 20 years (mean, 13.3 years). The radiographic state of the bone remodeling was visually assessed and measured with a digitizer. Demineralization that started proximally and then progressed distally caused cortical thinning, which correlated with widening of the intramedullary canal, not with changes that developed in the periosteal width, and occurred in the medial femoral neck, around the proximal half of the stem, and around the distal half in 87%, 33%, and 10%, respectively. Cortical thinning around the distal half of the stem was always accompanied by proximal thinning, and extensive cortical thinning (both proximal and distal) correlated with both lower clinical scores and radiologic loosening of the femoral prosthesis. A low canal flare index of Noble, a large canal width, and a patient age of 60 years or more were risk factors for extensive cortical thinning. Accelerated polyethylene wear was related to resorption of the medial femoral neck but not to cortical thinning or radiological loosening. Cortical thickening occurred only around the distal half of the stem in 29%. These findings establish a basis for the performance of cemented femoral prostheses, and allow comparison of bone remodeling when evaluating other femoral prostheses.

Adolescent↗

PubMed1995

Bone remodeling rates and skeletal maturation in three archaeological skeletal populations.

Cortical bone remodeling rates for rib samples from three archaeological populations and a modern autopsy sample were determined using an algorithm developed by Frost (Frost [1987a] Calcif. Tissue Res. 3:211-237). When plotted against the relative antiquities for population samples, histomorphometric variables; i.e., activation frequency (mu rc), net bone formation (netVf,r,t), and mean annual bone formation rate (Vf,r,t), exhibit a concordant trend of increased cortical bone remodeling activity levels over time. Two intensive foraging populations, Windover and Gibson, are similar for all bone remodeling parameters and have the lowest remodeling activity levels among the samples. The more recent Ledders sample, which is reported to practice agricultural subsistence, is consistently intermediate between these and a modern autopsy sample. Although there appear to be differences in bone formation rates among the populations it is concluded that these differences cannot be attributed to differences in bone remodeling rates among the populations, but rather are reflecting different effective ages of adult compacta for their ribs. These findings suggest that the earlier populations, particularly Windsor and Gibson, appear to have reached skeletal maturity at an older age than observed for modern.

Algorithms↗

PubMed2005

A preliminary in vitro and in vivo study of the effects of new anthraquinones on neutrophils and bone remodeling.

Osteolysis, that is, progressive periprosthetic bone loss, is responsible for approximately 70% of aseptic loosening and implant failure. Usually, it is due to a granulomatous reaction wear-induced, leading to macrophage and osteoclast-mediated bone resorption. At present, there is no established prophylaxis or treatment for this process. For this purpose, as a preliminary investigation, we aimed to study the effects in two directions, inhibition of proinflammatory signals, and bone remodeling activity, of two newly synthesized anthraquinone molecules [N,N'-Diethylamino-2,6-anthraquinone-disulfonamide (GR375) and N,N'-(p-ethoxyphenyl)-2,6-anthraquinone-disulfon amide (GR377)]. Among the pro-inflammatory signals, the ability of the two anthraquinones to interfere with the production of superoxide anion (O(2) (-)), which was assumed as a marker of reactive oxygen species (ROS), was evaluated in an in vitro cell model by testing phagocytes, such as human neutrophils, challenged by the chemotactic agent N-formylmethionyl-leucyl-phenylalanine (FMLP). Both compounds inhibited O(2) (-) production, in a dose-dependent way, without exerting scavenger effects. An in vivo model was applied to investigate their effect on bone remodeling. Fifty-four female Wistar rats were divided into eight groups of six animals each, and a 4-week treatment was applied in two phases. A 25 mg/kg/os dose in the first phase and 12.5-6.25 mg/kg/os doses in the second one were employed. The tibia trabecular bone at the secondary spongiosa level was analyzed, and trabecular bone volume (%TBV), trabecular thickness (TbTh), and apatite lattice parameters were measured. At the highest doses of GR375 and GR377 the %TBV and the TbTh increased by 33.2, 34.6%, and 3.6 and 9.1%, respectively, whereas crystallographic parameters were not significantly different from the untreated group. Our results suggest a simultaneous antiinflammatory and antiosteoclastic activity of both drugs that encourages to perform further research. If it will be confirmed, they could be proposed in a variety of bone diseases, in particular, when acute inflammation is associated to osteolytic processes and, eventually, in the prevention and treatment of periprosthetic osteolysis.

Animals↗

PubMed2004

[The expression of MMP-9, MMP-2 in the remodeling bone tissue around implant during unloaded period].

OBJECTIVE: To discuss the function of MMP-9, MMP-2 in the remodeling bone tissue around implant during unloaded period. METHODS: At the anterior of the maxilla and mandibular of the Beagle dog, implants were placed at different periods, so the implant specimens of different periods were obtained after dogs were killed. The implant specimens were removed, fixed in 4% paraformaldehyde for 24 hours at 4 degrees C, decalcified with 10% EDTA at pH 7.2, embedded in paraffin wax and sectioned. The observation of the expression changes of the MMP-2, MMP-9 in the milien bone tissue of the implant at different periods were taken by immunohistochemical staining. RESULTS: Matrix metalloprotainase (MMP-9) was mostly expressed at the peripheral cytoplasmic of osteoclast, macrophage, lining cell and fibroblast. MMP-2 was mostly expressed at the peripheral cytoplasmic of osteoblast, fibroblast, some osteoclast also expressed this enzyme. CONCLUSION: MMP-2 and MMP -9 have an important function at the injured bone absorption, healing and bone remodeling after dental implant placement.

Animals↗

PubMed2005

The role of markers of bone remodeling in multiple myeloma.

Osteolytic bone disease is a frequent complication of multiple myeloma, resulting in skeletal complications that are a significant cause of morbidity and mortality. A characteristic feature of myeloma bone disease is that the lesions rarely heal and bone scans are often negative in myeloma patients who have extensive lytic lesions, offering very little in the follow-up of bone disease. X-rays are also of limited value in monitoring bone destruction during anti-myeloma or anti-resorptive treatment. Biochemical markers of bone turnover, such as N- and C-terminal cross-linking telopeptide of type I collagen (NTX, CTX/ICTP, respectively), and newer ones such as the tartrate resistant acid phosphatase isoform 5b, provide information on bone dynamics that in turn may reflect disease activity in bone. Several studies have shown bone markers to be elevated in myeloma patients and reflect the extent of bone disease, while in some of them bone resorption markers correlate with survival. These markers may also be helpful in identifying those patients likely to respond to bisphosphonate treatment, and monitoring the effectiveness of bisphosphonate therapy in the management of myeloma bone disease. This review attempts to summarize the existing data for the role of markers of bone remodeling in assessing the extent of bone destruction in myeloma and monitoring bone turnover during specific anti-myeloma treatment. We also discuss some novel markers that may be of particular interest in the near future.

Bone Remodeling↗