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PubMed1995

Evaluation of bone loss and the serum markers of bone metabolism in patients with hyperparathyroidism.

Bone loss and the serum markers of bone metabolism were studied in 22 patients with primary hyperparathyroidism and 108 patients with renal hyperparathyroidism. The parameters of bone loss were bone mineral density in the distal radius and lumbar vertebrae, measured by dual energy X-ray absorptiometry, and bone mass index (sigma GS/D) and the metacarpal index, in the second metacarpal bone, measured by the digital image processing method. Alkaline phosphatase (AIP), intact osteocalcin (OC), and the carboxyterminal propeptide of type I procollagen (PICP) were measured as serum markers of bone formation, while tartrate-resistant acid phosphatase (TRACP) and the carboxyterminal pyridinoline cross-linked telopeptide of type I collagen (ICTP) were measured as serum markers of bone resorption. Bone loss and elevated markers of bone metabolism were observed both in patients with skeletal symptoms and in those without. Furthermore, the decrease in the cortical bone mass was more predominant than that of the trabecular bone. As markers of bone formation, AIP and OC seemed to be more sensitive than PICP, and as markers of bone resorption, ICTP appeared to be more sensitive than TRACP. Thus, a close correlation was observed between bone loss and the markers of bone formation and resorption.

Acid Phosphatase↗
PubMed1984

Bone-derived factors active on bone cells.

Effects of systemic calcium regulating hormones have been studied extensively, yet mechanisms of bone volume regulation at the local level are poorly understood. Our laboratory has reported evidence for two locally mediated processes of bone volume regulation which function independently of systemic control: (1) coupling of bone formation and resorption and (2) repletion of resorbed bone. These local regulatory mechanisms have been shown to occur in vivo and in vitro. We have reported that embryonic chick tibiae in culture, stimulated to resorb, release a factor in the serum-free culture medium that stimulates bone cell proliferation and bone matrix formation in vitro. We have postulated that this factor could be involved in the coupling mechanism. Subsequently, a similar factor which stimulates bone cell proliferation, collagen synthesis and bone formation in vitro was extracted from embryonic and adult bones. The factor partially purified from human bone, designated as human skeletal growth factor, has molecular weight, heat sensitivity and biological activity similar to the factor found in bone conditioned medium. Many other biologically active factors have also been extracted from bone cells or demineralized bone by different laboratories. Their actions on bone cells range from chemotactic to mitogenic. These recently discovered bone factors emphasize that there is important regulation of bone metabolism at the local level.

Animals↗
PubMed2005

Tendon reattachment to a metallic implant using an allogenic bone plate augmented with rhOP-1 vs. autogenous cancellous bone and marrow in a canine model.

Functionality of endoprosthetic reconstruction may be improved through secure and lasting soft tissue reattachment directly to the metallic implant surface. Tendon reattachment to the metallic surface of a titanium implant (enhanced tendon anchor, ETA) using autogenous bone plate as an interpositional structure between the tendon and metal, augmented with autogenous bone chips and marrow, provided successful mechanical and functional outcome. However, preparation of the autogenous bone plate is not practical in a clinical setting, but application of an allogenic bone plate could be an alternative. The autogenous cancellous bone and marrow may also be substituted by bone growth factors so that no autogenous bone graft is required. We hypothesized that the reconstitution of the direct tendon-bone insertion morphology in tendon reattachment to metallic implant could be achieved using allogenic cancellous bone plate augmented with autogenous cancellous bone and marrow, and that the autogenous bone grafts could be replaced by recombinant human osteogenic protein-1 (rhOP-1). In two canine groups the supraspinatus tendon was reattached unilaterally to a modified ETA implant with a highly porous metallic surface known as Tritanium Dimensionalized Metal. Allogenic bone plates saturated with rhOP-1-collagen putty were used in the OP-1 (OP) group, while plates saturated with autogenous cancellous bone and marrow were used in the bone marrow (BM) group. Functional, radiographical, mechanical and histomorphological analysis results were compared between both groups. At 15 weeks, gait analysis showed 78% and 81% recovery of preoperative weight-bearing in OP and BM groups, respectively. The calcified area around the tendon in OP group was 5.2 times larger than that in BM group (p<0.001). The ultimate tensile strength of the reattachment was 24% and 38% of the intact contralateral side in OP and BM groups, respectively, without significant difference between them. There was evidence of tendon-bone insertion transitional zones, tissue ingrowth and adhesion to the metallic surface in both groups. In conclusion, the use of the allograft combined with rhOP-1 had a similar effect as combined with autogenous cancellous bone and marrow in the tendon reattachment to the metallic surface.

Animals↗
PubMed2004

Intermittent ibandronate preserves bone quality and bone strength in the lumbar spine after 16 months of treatment in the ovariectomized cynomolgus monkey.

UNLABELLED: The dose-dependent effect of ibandronate treatment on bone mass and architecture was assessed in a large animal study of OVX monkeys using microCT for quantitative bone morphometry and biomechanical testing for measures of bone strength. The study showed that intermittent ibandronate preserved lumbar spine bone quality and strength in these animals after 16 months of treatment. INTRODUCTION: Ibandronate is a bisphosphonate, which is a class of compounds that, in pharmacologically active doses, not only suppresses bone resorption and turnover but also prevents loss of bone mass and strength in the ovariectomized (OVX) rat. MATERIALS AND METHODS: We evaluated the effects of ibandronate on bone mass and architecture in the OVX cynomolgus macaque. Sixty-one adult female macaques were divided into five groups (N = 11-15): sham control, OVX control, and OVX low- (10 microg/kg), medium- (30 microg/kg), and high- (150 microg/kg) dose ibandronate. Treatment was administered by intravenous bolus injection every 30 days for 16 months starting at ovariectomy. This dosing schedule is equivalent to a 3-monthly dosing regimen in human subjects over 4 years. Animals were killed at the conclusion of the study, and excised bone specimens of the first lumbar vertebra (L1) were evaluated for quantitative bone densitometry, morphometry, and mechanical properties. Architectural parameters were assessed by microCT including direct 3D bone morphometry. A measure of specimen strength was obtained using destructive compression testing. RESULTS AND CONCLUSIONS: A significant loss of bone mass and related changes in bone architecture after ovariectomy resulted in a reduction of whole bone strength as expressed by high correlations between architectural and mechanical properties. In this analysis, BMC was the best single predictor of whole bone strength (r2 = 67%). Nevertheless, including architectural indices in a multiple linear regression analysis increased that prediction to 88%. With respect to the treatment, the medium- and high-dose groups were not significantly different from the sham group for all bone mineral and structural parameters. Additionally, significant differences were seen for all measured parameters between the high-dose group and the OVX group, and for some parameters, between the medium-dose group and the OVX group. Intermittent ibandronate treatment effectively and dose-dependently prevented bone loss, architectural deterioration, and strength reduction in the lumbar spine of OVX monkeys.

Animals↗
PubMed1998

Markers of bone remodelling in metabolic bone disease.

New specific markers of bone remodelling have been developed that allow the evaluation of bone formation (plasma levels of osteocalcin and bone alkaline phosphatases) or bone resorption (collagen crosslink levels in urine). These markers can be used to evaluate bone disease. Their best application is currently in renal osteodystrophy, where there is a broad spectrum of bone abnormalities. In patients with this disease, bone markers can obviate the need for bone biopsy. So far, bone alkaline phosphatase is the most sensitive and specific marker for predicting the type of bone disease and therefore for deciding treatment in dialysed patients, although it is not ideal. Bone markers have also allowed a dramatic improvement in the comprehensive approach to bone loss with aging in women. Monitoring of the marked increase in bone turnover, and its persistence, in older women after menopause may help in the design of treatment strategies for osteoporosis. There is some hope that the measurement of urinary levels of collagen crosslinks will help to predict the clinical outcome of osteoporosis with respect to fractures in postmenopausal women. Bone markers could, besides being a measurement of bone density, help to determine the optimal treatment of postmenopausal women. Bone markers could also be used to predict or ascertain the response to treatment of osteoporosis, but few data are currently available to judge the routine usefulness of these new applications.

Biomarkers↗
PubMed2005

The roles of bone mineral density, bone turnover, and other properties in reducing fracture risk during antiresorptive therapy.

Osteoporosis is a skeletal disorder characterized by compromised bone strength and increased risk of fracture. Properties related to bone strength include rate of bone turnover, bone mineral density, geometry, microarchitecture, and mean degree of mineralization. These properties (with or without bone density) are sometimes collectively referred to as bone quality. Antiresorptive agents may reduce fracture risk by several separate but interrelated effects on these individual properties. For example, antiresorptive agents have been reported to reduce bone turnover, stabilize or increase bone density, preserve or improve microarchitecture, reduce the number or size of resorption sites, and improve mineralization. Although changes in bone architecture and mineralization are not currently measurable in clinical practice, bone turnover is assessed easily in vivo and affects the other bone properties. Moreover, antiresorptive therapies that produce larger decreases in bone turnover markers together with larger increases in bone mineral density are associated with greater reductions in fracture risk, especially at sites primarily composed of cortical bone such as the hip. Reductions in fracture risk are the most convincing evidence of good bone quality. Data from well-designed randomized clinical trials with up to 10 years of continuous antiresorptive therapy have shown that certain antiresorptive agents effectively reduce fracture risk and (together with extensive preclinical data) suggest no deleterious effects on bone quality.

Bone Density↗
PubMedDate not supplied

[Correlation of procollagen (I) with prostate specific antigen and bone scan for the diagnosis of bone metastases in patients with prostate carcinoma].

Procollagen (I) carboxyterminal propeptide (PICP) is a metabolite of procollagen, a precursor molecule of collagen type I, which accounts for more than 90% of the organic matrix of the bones. Serum PICP levels indicate the rate of bone collagen synthesis and therefore the osteoblastic activity. In this study we evaluate the clinical usefulness of serum PICP as an indicator of bone metastases in patients with prostate cancer in relation to bone scan and to prostate specific antigen (PSA) measurements. We found no similar study in the literature relating these three tests. Seventy-eight patients (median age 63+/-4,3 years) with prostate adenocarcinoma were examined. The diagnosis was confirmed histologically. Bone metastases were diagnosed in 42 (54%) of them assessed by bone scans (Group A), while the remaining 36 patients (46%) had no bone metastases (negative bone scans and X-rays) (Group B). We also examined 21 patients with benign prostate hyperplasia as a control group (Group C). All patients had serum PICP measurements, bone scans with (99m)Tc-MDP and PSA measurements. None of them had a history of disease or of using drugs known to affect bone metabolism. Serum levels of PICP were assayed by a radioimmunoassay (RIA) kit (Orion Cooperation, Farmos Diagnostics, Finland). Serum PSA was also tested by a RIA kit (Tandem-R, Hybritech Inc, USA). PICP levels in Group A were 265+/-89 microg/l, in Group B 128+/-39 microg/l and in Group C patients 110+/-48 microg/l. High levels of PICP above 170 microg/l, were diagnostic of bone metastases with sensitivity 54%, specificity 93% and accuracy 84%. In comparison, PSA levels above 4 ng/ml were also diagnostic with a sensitivity of 68%, specificity of 91% and accuracy 88%. Patients with low levels of PICP, lower than 90 microg/l, n=31, had no bone metastases. The positive prognostic value of bone scan was 74% with a sensitivity of 76%, specificity of 58% and accuracy 71%. Positive bone scans combined with very high levels of PICP and PSA, had positive prognostic value 97%, with sensitivity of 78%, specificity of 96% and accuracy 97%, while bone scans with levels of PICP lower than 170 microg/l, had positive prognostic value of 32%. Levels of PICP and PSA were significantly higher in patients with prostate cancer and bone metastases in comparison to patients with benign prostate hyperplasia (P<0.0001) respectively. Also, levels of PICP and PSA were higher in patients with prostate cancer without metastases as compared to prostate hyperplasia (P<0.0005 and P<0.0001 respectively) (Wilcoxon-Mann-Whitney test). When metastases were more extensive, PICP levels were higher than PSA. It is concluded that PICP as a marker of osteoblastic activity is useful for diagnosing bone metastases of prostate adenocarcinoma but when co-evaluated with PSA and the bone scan, the diagnostic accuracy of these three diagnostic procedures is much higher.

English Abstract↗
PubMed2005

Bone marrow lesions in the knee are associated with increased local bone density.

OBJECTIVE: Bone marrow lesions are associated with pain and compartment-specific progression of joint space narrowing in patients with knee osteoarthritis (OA). Bone marrow lesions occur in regions under increased loading, and excess loading produces increased bone mineral density (BMD). The ratio of BMD in the medial tibial plateau compared with that in the lateral tibial plateau (M:L BMD ratio) reflects loading in the knee. Therefore, we hypothesized that a higher M:L BMD ratio would be associated with medial bone marrow lesions, and that lower ratios would be associated with lateral bone marrow lesions. METHODS: Participants in the Framingham Osteoarthritis Study underwent magnetic resonance imaging (MRI), measurement of bone mineral density (BMD), and knee radiography between 2002 and 2004. MRI was used to define medial and lateral bone marrow lesions in the medial and lateral tibiofemoral compartments, respectively. We performed a logistic regression analysis with medial bone marrow lesions as the outcome, testing M:L BMD ratio groups as predictor variables. We adjusted for age, sex, body mass index, and systemic BMD, using generalized estimating equations to adjust for correlations between knees. An identical analysis evaluating lateral bone marrow lesions was performed. RESULTS: Medial bone marrow lesions were strongly associated with a high M:L BMD ratio. The odds ratios (ORs) for prevalent medial bone marrow lesions, for the lowest to the highest quartile of M:L BMD ratios, were 1.0 (referent), 1.3, 5.0, and infinity (P for trend < 0.0001). Lateral bone marrow lesions were strongly associated with low M:L BMD ratios (the ORs for prevalent lateral bone marrow lesions, for the highest to the lowest quartile, were 1.0 [referent], 3.0, 26.8, and 54.0 [P for trend < 0.0001]). CONCLUSION: Medial bone marrow lesions occur in knees with relatively higher local medial tibial bone density, and lateral bone marrow lesions occur in knees with relatively higher lateral tibial bone density, supporting the hypothesis that local BMD reflects loading within the knee. Our findings emphasize the importance of loading in the pathophysiology of OA.

Aged↗
PubMed1996

Analysis of mechanical properties of cancellous bone under conditions of simulated bone atrophy.

The mechanical properties of cancellous bone have been shown to depend on bone density and on the anisotropy of the trabecular bone structure. By means of high-resolution quantitative computed tomography (QCT), providing a nominal resolution of 0.17 mm, it became possible to assess both apparent density and trabecular microstructure of intact bones. In order to study the influence of age- and disease-related bone loss on the mechanical properties of cancellous bone, a more phenomenological approach was used to develop a novel bone resorption algorithm, called simulated bone atrophy. The algorithm, which is principally based on constrained Gauss filtration of segmented data volumes, was applied to create derived microstructural models. The mechanical behavior of the cancellous bone can be expressed as a function of the anisotropic bone properties of the microstructural model on the continuum level. To study the influence of bone atrophy on bone strength we compared three models: the originally noninvasively measured bone biopsy and two derived models simulating moderate and pronounced atrophy. For the comparison of the three models, the apparent Young's moduli in the three orthogonal directions were predicted for each model with the help of three-dimensional finite-element analysis. Realistic results for the apparent Young's moduli were found for the tissue moduli chosen. The results suggest that the prediction of anisotropic material properties of cancellous bone based on noninvasive measurements of trabecular microstructures and the application of simulated bone atrophy may be helpful to understand the influence of age- and disease-related bone loss on bone strength.

Atrophy↗
PubMed1989

Mechanisms of bone destruction in multiple myeloma: the importance of an unbalanced process in determining the severity of lytic bone disease.

In order to clarify the mechanisms involved in the occurrence of lytic bone lesions (BL) in multiple myeloma (MM), we have compared the presenting myeloma-induced histological bone changes of 14 previously untreated MM patients with lytic BL with those of seven MM patients lacking lytic BL at presentation despite similar myeloma cell mass. A major unbalanced bone remodeling (increased bone resorption with normal to low bone formation) was the characteristic feature of patients presenting lytic BL. Furthermore, this unbalanced process was associated with a significant reduction of bone mass. Unexpectedly, a balanced bone remodeling (increase of both bone resorption and bone formation, without bone mass reduction) rather than a true lack of an excessive bone resorption was the usual feature of patients lacking lytic BL. Our current work clearly shows that a majority (72%) of patients with MM present an important unbalanced bone remodeling at diagnosis, leading to bone mass reduction and bone destruction (unbalanced MM). Some patients (20%) retain a balanced bone remodeling with initial absence of bone destruction (balanced MM). Few (8%) patients have pure osteoblastic MM without bone destruction.

Bone Diseases↗
PubMed1989

Calcitonin receptors as markers for osteoclastic differentiation: correlation between generation of bone-resorptive cells and cells that express calcitonin receptors in mouse bone marrow cultures.

The osteoclast is the cell that resorbs bone. It is known to derive from hemopoietic precursors, but analysis of lineage and regulation of differentiation has been hampered by lack of a specific marker that enables identification of cells of osteoclastic phenotype. Previously used markers, such as multinuclearity, that are specific for osteoclasts in bone become less specific in culture. Uniquely among bone and bone marrow cells, osteoclasts possess abundant calcitonin (CT) receptors. We therefore tested the correlation between the generation of bone-resorptive function and the formation of CT receptor-positive cells from hemopoietic tissue in vitro. Without 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3], a hormone that induces osteoclastic differentiation in vitro, bone marrow cultures showed very little bone resorption, and only small numbers of CT receptor-positive cells developed. When 1,25-(OH)2D3 was added to the cultures, CT receptor-positive cells developed within 1 day and reached a peak after 7 days. Bone resorption commenced within 2 days of hormone addition. There was a strong parallelism between the cumulative number of CT receptor-positive cells and the extent of bone resorption. The capacity of cultures to generate bone-resorptive activity and CT receptor-positive cells declined progressively when 1,25-(OH)2D3 was added to hemopoietic tissue after a 7- to 21-day hormone-free incubation period. The number of CT receptor-positive cells in these cultures correlated strongly (r = 0.96) with bone resorption. The behavior of these cultures suggests that 1,25-(OH)2D3 acts to induce terminal differentiation of osteoclast precursors present in the cultures, and that precursor cell numbers decreased with increasing time in vitro. All of the CT receptor-positive cells in control cultures and all of those seen shortly after 1,25-(OH)2D3 addition were mononuclear, despite considerable bone resorption; the majority of CT receptor-positive cells remained mononuclear throughout the incubation period. This suggests that mononuclear cells with characteristics of osteoclasts exist that are able to excavate bone. CT receptor-positive cells slightly preceded the development of bone-resorptive function, implying that CT receptors develop before the acquisition of bone-resorptive capacity by osteoclasts. Peritoneal macrophages, blood mononuclear cells, and cells of the J774 macrophage cell line failed to either resorb bone or express CT receptors, even after incubation with 1,25-(OH)2D3 for 14 days. These results show a strong and specific correlation between the generation of bone-resorptive cells and CT receptor-positive cells, and suggest that CT receptor express

Animals↗
PubMed2002

Circulating estradiol and osteoprotegerin as determinants of bone turnover and bone density in postmenopausal women.

Osteoprotegerin (OPG) is a recently identified cytokine that acts as a decoy receptor for the receptor activator of NF kappa B ligand. OPG has been shown to be an important inhibitor of osteoclast differentiation and activation in rodent models. Estrogen is known to suppress bone resorption, and the action of estrogen on bone may be mediated by OPG. The relationship between endogenous estrogen and circulating OPG levels and bone status in human populations is unclear. Thus, the aim of this study was to investigate the relationship between biochemical markers of bone turnover and bone density and circulating OPG and endogenous estradiol levels in a population-based cohort of postmenopausal women. Subjects were 180 women ages 55-91 yr (mean age, 67 yr). Serum estradiol was measured using an auto-analyzer. Serum concentrations of OPG were determined by ELISA. Markers of bone formation and resorption were measured by standard methods. Bone mineral density at total body, total hip, femoral neck, and lumbar spine was measured by dual energy x-ray absorptiometry. There was a significant inverse relationship between estradiol and all bone turnover markers (r-values from -0.46 to -0.23; P < 0.05). Serum estradiol was positively related to absolute bone density at all sites and to change in bone density at the hip and femoral neck by univariate analysis (r-values from 0.15-0.29; P < 0.05). We observed a weak inverse association between OPG and serum-based bone turnover markers (r-values -0.18 and -0.16; P < 0.05). There was a significant positive relationship between OPG and bone mineral density at total body, total hip, and femoral neck (r-values from 0.17-0.2; P < 0.05) by univariate analysis, which was lost after adjustment for age and body mass index. There was a significant weak positive relationship between circulating OPG and serum estradiol (r = 0.18; P < 0.02). We observed no significant relationships between OPG and bone turnover markers measured in urine. We conclude that the variation in circulating endogenous estradiol levels is an important factor contributing to levels of bone turnover and bone density at the menopause. Our observations also suggest that circulating levels of OPG may reflect OPG activity in bone and are related to circulating endogenous levels of estradiol. We have previously reported high levels of variability in urine markers of bone resorption, and we suggest that this could account for the absence of a significant association between these markers and circulating OPG.

Aged↗
PubMed2003

Fracture characteristics of acrylic bone cement-bone composites.

In this study, the fracture properties of Perspex, acrylic bone cement prepared using a commercially available reduced pressure mixing system and a bone cement-bone composite were compared under different test conditions. The method used was the double-torsion (DT) test. The observations made from this investigation are as follows. The fracture toughness and critical crack length for Perspex significantly increased (ANOVA, p = 0.001) when tested in water compared to air. An increase in test temperature from 19 to 37 degrees C resulted in a decrease in the fracture properties in water, this reduction being also statistically significant (ANOVA, p = 0.02). The mean fracture toughness and standard deviation of CMW3 bone cement when mixed under reduced pressure was 2.19 +/- 0.11 MN m(-3/2) compared to 3.89 +/- 0.10 MN m(-3/2) for the cement-bone composite (ANOVA, p = 0.004). The crack length determined for CMW3 bone cement and the cement bone composite were 0.323 +/- 0.031 and 1.1434 +/- 0.61 mm respectively. The plateau loads of the composite material were higher than measured for the monolithic acrylic bone cement, 249.66 +/- 67.75 N compared with 140.83 +/- 6.82 N. The high level of variation recorded for the plateau loads of the bone cement bone composite is due to the orientation and volume fraction of the cancellous bone. It can be concluded from this investigation that acrylic bone cement interdigitation into the cancellous bone results in a superior material with respect to crack resistance in comparison with the bone cement as a lone entity. Therefore it is an advantage if there is sufficient cancellous bone stock available within the intermedullary canal to allow bone cement penetration to occur, for the transfer of loads during daily activity. Additionally, it is paramount that the clinician ensures that adequate pressure is applied and maintained for an appropriate time during cement injection and prosthesis insertion in order to ensure optimum cement penetration into the pore openings of the cancellous bone, thus improving the resistance of the cement mantle to fracture and ultimately improving the longevity of the joint replacement.

Animals↗
PubMed1997

Expression of nitric oxide synthase isoforms in bone and bone cell cultures.

Recent work has shown that nitric oxide (NO) acts as an important mediator of the effects of proinflammatory cytokines and mechanical strain in bone. Although several bone-derived cells have been shown to produce NO in vitro, less is known about the isoforms of NO synthase (NOS), which are expressed in bone or their cellular distribution. Here we investigated the expression, cellular localization, and regulation of NOS mRNA and protein in cultured bone-derived cells and in bone tissue sections. We failed to detect inducible NOS (iNOS) protein in normal bone using immunohistochemical techniques, even though low levels of iNOS mRNA were detected by sensitive reverse transcribed polymerase chain reaction (RT-PCR) assays in RNA extracted from whole bone samples. Cytokine stimulation of bone-derived cells and bone explant cultures caused dramatic induction of iNOS mRNA and protein in osteoblasts and bone marrow macrophages, but no evidence of iNOS expression was seen in osteoclasts by immunohistochemistry or in situ hybridization. Endothelial NOS (ecNOS) mRNA was also detected by RT-PCR in whole bone, and immunohistochemical studies showed widespread ecNOS expression in bone marrow cells and trabecular lining cells in vivo. Related studies in vitro confirmed that ecNOS was expressed in cultured osteoblasts, stromal cells, and osteoclasts. Neuronal NOS mRNA was detected by RT-PCR in whole bone, but we were unable to detect nNOS protein in bone cells in vivo or in studies of cultured bone-derived cells in vitro. In summary, our data show that mRNAs for all three NOS isoforms are expressed in bone and provide evidence for differential expression and regulation of the enzymes in different cell types. These findings confirm the likely importance of the L-arginine-NO pathway as a physiological mediator of bone cell function and demonstrate that it may be possible to exert differential effects on osteoblast and osteoclast activity in vivo by differential targeting of constitutive and inducible NOS isoforms by selective NOS inhibitors.

Animals↗
PubMed2002

Soft tissue movement and stress shielding do not affect bone ingrowth in the bone conduction chamber.

A variety of bone chambers are used in orthopedic research to study bone and tissue ingrowth in small and large animals. If different bone chambers are placed in one species, differences in bone ingrowth are observed. For instance, bone ingrowth in the bone conduction chamber (BCC) is high, but is low or absent in the repeated sampling bone chamber (RSBC). This difference may be explained by the design and fixation of these chambers. It is known that stress shielding and micromovement can influence bone formation. The objective of the study reported here was to determine whether stress shielding or soft tissue movement affected bone ingrowth in the BCC in the goat. Two types of caps were made, with fixation similar to that of the fixation plate of the RSBC. By placing the caps over the BCCs and fixating the caps directly to the tibial bone, the effect of stress shielding was studied. One cap was in direct contact with the bone chamber underneath, the other cap did not touch the chamber. This difference was used to observe whether movement of the soft tissue on top of the chamber and cap would affect bone ingrowth. Each limb received one control chamber without a cap and a chamber with a cap, either with or without contacting the BCC, yielding four implants per goat. After 12 weeks, bone and total tissue ingrowths were measured. Bone ingrowth was seen in 38 of 40 chambers. Total tissue and bone ingrowths were comparable between control chambers and BCCs with a cap, irrespective of type. Neither stress shielding, nor lack of movement of soft tissue affected bone ingrowth. Other factors in the design of the chambers were responsible for the difference in bone ingrowth between the BCC and the RSBC.

Animals↗
PubMed1997

Histomorphology and bone morphometry of the bone marrow edema syndrome of the hip.

From a prospective study of patients with MR imaging proven bone marrow edema syndrome of the hip, bone biopsies that were retrieved at core decompression treatment of 32 femoral heads (from 28 men and 3 women; age range, 25-63 years) were evaluated microscopically. The undecalcified microtome sections showed diffuse or spotty areas of interstitial and intrasinusoidal fluid in the marrow cavities, together with fat cell destruction or fibrovascular regeneration or both in exactly the regions exhibiting the magnetic resonance signals for bone marrow edema. The vital bone trabeculae in these edematous regions showed more or less continuous, partly osteoblast covered osteoid seams, and often, formation of irregular woven bone (microcallus), pointing to increased bone formation activity. Preceding or active osteoclastic resorption was rarely seen. Computer assisted bone morphometry revealed age related normal to elevated bone volume densities (above 20% bone volume of tissue volume); thus, no evidence for osteoporosis was present. In addition to increased osteoid volumes, a decreased maximal hydroxyapatite content and a shift to undermineralized bone was found by mineral densitometry of corresponding microradiographs, when compared with age matched femoral heads without bone pathology. These bone mineral changes, but not transient bone loss, could be the explanation for the more or less subtle and transient radiolucency in hips affected by bone marrow edema syndrome. Live trabeculae and active bone formation, however, point to increased repair capacity, which seems the key for the spontaneously reversible course of this syndrome. There is still controversy whether the bone marrow edema syndrome represents a distinct transient disease or an early reversible phase of avascular necrosis, but because of the similarities in histopathology reported for early classic avascular necrosis and bone marrow edema in the literature and in the authors' own material, a common pathophysiology is discussed for these seemingly different diseases.

Adult↗
PubMed2006

Discontinuing antiresorptive therapy one year after cardiac transplantation: effect on bone density and bone turnover.

BACKGROUND: We have previously reported that subjects randomized to alendronate or calcitriol immediately after cardiac transplantation sustained minimal bone loss during the first year, significantly less than a concurrently transplanted reference group that received calcium and parent vitamin D. In this extension, we evaluated the effect of discontinuing alendronate or calcitriol on bone loss and biochemical markers of bone turnover during the second year. We hypothesized that subjects who discontinued alendronate, which has a long half-life in bone, would not sustain significant bone loss. As the half-life of calcitriol is short, we hypothesized that there would be significant bone loss after discontinuing calcitriol. METHODS: We measured bone density (BMD), calciotropic hormones and bone turnover markers at 12, 18, and 24 months after transplantation in adherent subjects who completed the randomized trial on alendronate or calcitriol, and in reference subjects who had received no preventive therapy. RESULTS: In all, 75 subjects (34 alendronate, 25 calcitriol, 16 reference) participated. During the second year, the bone resorption marker, serum N-telopeptide, rose by 27% in the calcitriol group (P< or =0.001). Bone alkaline phosphatase, a bone formation marker, increased by 54% in the calcitriol group (P< or =0.001) and by 32% in the alendronate group (P< or =0.001). BMD did not change significantly at any site in either randomized group. CONCLUSIONS: After discontinuing alendronate or calcitriol, BMD remained stable during the second year after cardiac transplantation, despite a significant increase in a biochemical marker of bone resorption in the calcitriol group. This suggests that antiresorptive therapy may be discontinued at the end of the first posttransplantation year in cardiac transplant recipients without resumption of rapid bone loss. However, as increased bone turnover may predict future bone loss and fractures, such patients warrant observation to ensure that BMD remains stable long-term.

Adult↗
PubMed1993

Bone quality: a determinant for certain risk factors for bone fragility.

Low bone quantity alone is insufficient cause for fragility fractures. This paper examines the role of bone quality in the fracture risk associated with age, sex, and race. Aspects of bone quality to be considered are bone architecture, matrix, mineralization, and fatigue damage. The trabecular network becomes progressively disconnected and weaker with age. Death of old osteocytes leads to hypermineralization and brittleness of bone. The stability of bone collagen declines with age, and unremodeled bone accumulates fatigue damage. The lower bone fragility rates in males than in females may be due to a combination of the larger male skeleton, greater cortical bone density after age 60 years, and greater bone turnover which would replace fatigue damaged bone. Fragility fracture rates in American and African blacks are lower than in whites, bone mineral density (BMD) is greater in American but not in African blacks (except for hip BMD), and American blacks have lower and African blacks higher bone turnover compared to whites. In South African blacks, trabeculae are thicker and better connected and trabecular bone undergoes less destructive age changes than in whites. To reconcile the disparate findings in American and African blacks we suggest that both groups have a genetic tendency to greater BMD than whites; American blacks realize this potential and African blacks do not, possibly because of calcium deficiency. Consequent high turnover removes fatigue damage and so improves bone quality. Weight-bearing activity in African blacks may be responsible for good hip bone density and thick trabeculae.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗