Femoral Trabecular Bone Research Articles

Bone responses to zirconia implants with a thin carbonate‐containing hydroxyapatite coating using a molecular precursor method

Thin carbonate-containing hydroxyapatite (CA) films coating partially stabilized zirconia (Y-TZP) were prepared (CA-Y-TZP) to establish a metal-free implant system. CA was coated using a molecular precursor method. The CA film was deposited on the surface of Y-TZP using a precursor solution, which was a mixture of a calcium-ethylenediaminetetraacetic acid (EDTA) complex and phosphate compounds. The deposited CA film was characterized by X-ray diffraction, Fourier transform infrared spectroscopy, and energy dispersive X-ray spectroscopy measurements. A focus ion beam system technique revealed that the thickness of the CA film was less than 1.0 µm. Biological evaluations of CA-Y-TZP were performed by immersion experiments in simulated body fluid (SBF) and implantation experiments in the tibiae and femoral condyles of rabbits. In the SBF immersion experiment, apatite deposition progressed more on CA-Y-TZP at the early stage of immersion than on Y-TZP without the CA coating. Animal experiments revealed that bone formation on CA-Y-TZP was similar with than on Y-TZP. Histomorphometrical evaluations showed a significantly higher bone-to-implant contact ratio and bone mass on CA-Y-TZP after implantation into the femoral trabecular bone of rabbits. Therefore, CA-Y-TZP appears to be applicable as a metal-free implant.

Hepatic lipase is expressed by osteoblasts and modulates bone remodeling in obesity

A number of unexpected molecules were recently identified as products of osteoblasts, linking bone homeostasis to systemic energy metabolism. Here we identify the lipolytic enzyme hepatic lipase (HL, encoded by Lipc) as a novel cell-autonomous regulator of osteoblast function. In an unbiased genome-wide expression analysis, we find Lipc to be highly induced upon osteoblast differentiation, verified by quantitative Taqman analyses of primary osteoblasts in vitro and of bone samples in vivo. Functionally, loss of HL in vitro leads to increased expression and secretion of osteoprotegerin (OPG), while expression of some osteoblast differentiation makers is impaired. When challenging energy metabolism in a diet-induced obesity (DIO) study, lack of HL leads to a significant increase in bone formation markers and a decrease in bone resorption markers. Accordingly, in the DIO setting, we observe in Lipc−/− animals but not in wild-type controls a significant increase in lumbar vertebral trabecular bone mass and formation rate as well as in femoral trabecular bone mass and cortical thickness. Taken together, we demonstrate that HL expressed by osteoblasts has an impact on osteoblast OPG expression and that lack of HL leads to increased bone mass in DIO. These data provide a novel and completely unexpected molecular link in the complex interplay of osteoblasts and systemic energy metabolism.

Improving bone strength prediction in human proximal femur specimens through geometrical characterization of trabecular bone microarchitecture and support vector regression.

We investigate the use of different trabecular bone descriptors and advanced machine learning tech niques to complement standard bone mineral density (BMD) measures derived from dual-energy x-ray absorptiometry (DXA) for improving clinical assessment of osteoporotic fracture risk. For this purpose, volumes of interest were extracted from the head, neck, and trochanter of 146 ex vivo proximal femur specimens on multidetector computer tomography. The trabecular bone captured was characterized with (1) statistical moments of the BMD distribution, (2) geometrical features derived from the scaling index method (SIM), and (3) morphometric parameters, such as bone fraction, trabecular thickness, etc. Feature sets comprising DXA BMD and such supplemental features were used to predict the failure load (FL) of the specimens, previously determined through biomechanical testing, with multiregression and support vector regression. Prediction performance was measured by the root mean square error (RMSE); correlation with measured FL was evaluated using the coefficient of determination R2. The best prediction performance was achieved by a combination of DXA BMD and SIM-derived geometric features derived from the femoral head (RMSE: 0.869 ± 0.121, R2: 0.68 ± 0.079), which was significantly better than DXA BMD alone (RMSE: 0.948 ± 0.119, R2: 0.61 ± 0.101) (p < 10-4). For multivariate feature sets, SVR outperformed multiregression (p < 0.05). These results suggest that supplementing standard DXA BMD measurements with sophisticated femoral trabecular bone characterization and supervised learning techniques can significantly improve biomechanical strength prediction in proximal femur specimens.

Finite Element Simulation: The Effects of Loading Modes at Different Anatomical Sites of Trabecular Bone on Morphological Indices

The relationship between morphological parameter and different type of loading orientation on elastic behavior and yielding of trabecular may provide insight towards osteoporotic bone losses during normal activities. This paper attempts to predict the elastic and failure behavior of different loading modes (tensile and compression) on anatomic sites and morphological indices through finite element (FE) simulation. Specimens extracted from bovine femoral trabecular bone were imaged using micro computed tomography (μCT). Morphological studies were done followed by FE analysis. Results demonstrated differences between yield behaviors on anatomic sites were reflected onto the morphological indices and the type of loading modes. The yield initiated earlier in rod-like than plate-like trabecular in both loading condition but showed different failure behavior in rod-like trabecular with small differences in maximum stress between tensile and compressive. However, in many cases, trabecular models tend to have oblique fracture pattern in all anatomic sites. Through these findings, improved prediction of elastic properties and yield behavior by computational means provide insight in the development of bone substitute material depending on the anatomic site as well as in osteoporotic bone pathological treatment to monitor losses in trabecular struts.

Low-Bone-Mass Phenotype of Deficient Mice for the Cluster of Differentiation 36 (CD36)

Bone tissue is continuously remodeled by bone cells and maintenance of its mass relies on the balance between the processes of resorption and formation. We have reported the expression of numerous scavenger receptors, namely scavenger receptor (SR) class B type I and II (SR-BI and SR-BII), and CD36, in bone-forming osteoblasts but their physiological roles in bone metabolism are still unknown. To unravel the role of CD36 in bone metabolism, we determined the bone phenotype of CD36 knockout (CD36KO) mice and characterized the cell functions of osteoblasts lacking CD36. Weights of CD36KO mice were significantly lower than corresponding wild-type (WT) mice, yet no significant difference was found in femoral nor tibial length between CD36KO and WT mice. Analysis of bone architecture by micro-computed tomography revealed a low bone mass phenotype in CD36KO mice of both genders. Femoral trabecular bone from 1 to 6 month-old CD36KO mice showed lower bone volume, higher trabecular separation and reduced trabeculae number compared to WT mice; similar alterations were noticed for lumbar vertebrae. Plasma levels of osteocalcin (OCN) and N-terminal propeptide of type I procollagen (PINP), two known markers of bone formation, were significantly lower in CD36KO mice than in WT mice, whereas plasma levels of bone resorption markers were similar. Accordingly, histology highlighted lower osteoblast perimeter and reduced bone formation rate. In vitro functional characterization of bone marrow stromal cells and osteoblasts isolated from CD36KO mice showed reduced cell culture expansion and survival, lower gene expression of osteoblastic Runt-related transcription factor 2 (Runx2) and osterix (Osx), as well as bone sialoprotein (BSP) and osteocalcin (OCN). Our results indicate that CD36 is mandatory for adequate bone metabolism, playing a role in osteoblast functions ensuring adequate bone formation.

Effects of unfractionated heparin on renal osteodystrophy and vascular calcification in chronic kidney disease rats

Unfractionated heparin (UFH) is the most widely used anticoagulant in hemodialysis for chronic kidney disease (CKD) patients. Many studies have verified that UFH can induce bone loss in subjects with normal bone, but few have focused on its effect on renal osteodystrophy. We therefore investigated this issue in adenine-induced CKD rats. As CKD also impairs mineral metabolism systemically, we also studied the impacts of UFH on serum markers of CKD–mineral and bone disorder (CKD–MBD) and vascular calcification. We administered low and high doses of UFH (1U/g and 2U/g body weight, respectively) to CKD rats and compared them with CKD controls. At sacrifice, the serum markers of CKD–MBD did not significantly differ among the two UFH CKD groups and the CKD control group. The mean bone mineral densities (BMDs) of the total femur and a region of interest (ROI) constituted of trabecular and cortical bone were lower in the high-dose UFH (H-UFH) CKD group than in the CKD control group (P<0.05 and P<0.01, respectively). The BMD of the femoral ROI constituted of cortical bone did not differ between the H-UFH CKD group and the CKD control group. Histomorphometrical changes in the CKD rats indicated secondary hyperparathyroidism, and the femoral trabecular bone volume, but not cortical bone volume, significantly decreased with increasing UFH dose. The same decreasing trend was found in osteoblast parameters, and an increasing trend was found in osteoclast parameters; however, most differences were not significant. Moreover, no distinct statistical differences were found in the comparison of vascular calcium or phosphorus content among the CKD control group and the two UFH CKD groups. Therefore, we concluded that UFH could induce bone loss in CKD rats with secondary hyperparathyroidism, mainly by reducing the trabecular volume and had little effect on cortical bone volume. The underlying mechanism might involve inhibition of osteoblast activity and promotion of osteoclast activity by UFH. We did not find any effect of UFH on vascular calcification in CKD rats with secondary hyperparathyroidism.

Correlations of linear and nonlinear ultrasound parameters with density and microarchitectural parameters in trabecular bone

In the present study, correlations of linear and nonlinear ultrasound parameters (speed of sound, normalized broadband ultrasound attenuation, and nonlinear parameter B/A) with bone mineral density and microarchitectural parameters were investigated in 28 bovine femoral trabecular bone samples in vitro. All three ultrasound parameters exhibited relatively high correlation coefficients with the indexes of bone quantity (bone mineral density and bone volume fraction) and lower correlation coefficients with the remaining microarchitectural parameters. These results suggest that B/A, in addition to speed of sound and attenuation, may have potential as an index for the assessment of bone status and osteoporosis.

Dependences of the backscatter coefficient on the frequency, the bone volume fraction, and the trabecular thickness in bovine femoral trabecular bone in Vitro

The present study aims to provide insight into the dependences of the backscatter coefficient on the frequency, the bone volume fraction (BV/TV), and the trabecular thickness (Tb.Th) in bovine femoral trabecular bone in vitro. The frequency-dependent backscatter coefficient was measured in 20 bovine femoral trabecular bone samples over a frequency range from 0.2 to 0.7 MHz. The backscatter coefficient measured at 0.5 MHz exhibited significant positive correlations with the BV/TV (r = 0.76) and the Tb.Th (r = 0.77). The power-law fits to the measurements showed that the backscatter coefficient was empirically proportional to the frequency, the BV/TV, and the Tb.Th with exponents of n = 2.9, 1.3, and 1.8, respectively. The present study also used a scattering model, in which the scattering coefficient was proportional to the product of the mean velocity fluctuation and the correlation function integrated over the volume, to predict the measurements. The measurements were found to largely fall within the range of the predictions obtained from the scattering model.

The Influence of implant geometry and surface composition on bone response

The implant design and surface modification are independent conditions that can alter the implant bone response. The objective of this study is to compare the bone response to roughened tapered and cylindrical screw-type implants with and without hydroxyapatite (HA) surface coating in the femoral trabecular bone of rabbits. Thirty-two implants (8×3.5mm) consisting of four different types (eight implants in each group), that is, tapered implants, cylindrical implants, HA-coated tapered implants, and HA-coated cylindrical implants were installed in the femoral condyle of 16 rabbits. After 8weeks of healing, the femoral condyles were retrieved and studied histologically. The bone-to-implant contact percentage was assessed and analyzed statistically. The histomorphometric analysis revealed that the bone-to-implant contact (BIC) values seemed to be higher for HA-coated tapered implants (65.62±13.02) followed by cylindrical non-coated implants. All four types of implants showed wide distribution of BIC with no statistical significance between different types of implants. It can be concluded that under the current experimental conditions, implant design and surface composition had little effect on the bone-to-implant interface.

Trabecular bone deterioration at the greater trochanter of mice with unilateral obstructive nephropathy

Our previous study showed the early molecular responses of bone in response to obstructive nephropathy in a unilateral ureteral obstruction (UUO) mouse model. Here, we addressed the changes in trabecular bone properties at greater trochanter, the proximal and the distal metaphysis of femur in UUO mice. The male mice were subjected to UUO (n=10) or sham operation (n=10). All mice were killed on day 7 after the surgical operation. The micro-computed tomography (micro-CT) analysis for different femoral trabecular bone sites demonstrated pathological alterations of trabecular bone mass and micro-networks at greater trochanter as shown by decreases in bone mineral density/bone volume (P<0.05) and trabecular number (P<0.05) and increases in trabecular separation (P<0.01) and bone surface/bone volume (P<0.05) in UUO mice. The present study demonstrates that UUO-induced unilateral obstructive nephropathy has markedly detrimental effects on the trabecular trochanter of the femur.

Feasibility of bone assessment by using the nonlinear parameter in trabecular bone

The purpose of the present study is to investigate the feasibility of assessing bone status and osteoporosis by using the nonlinear parameter B/A in bovine trabecular bone in vitro. The B/A values measured in 18 bovine femoral trabecular bone samples by using a finite-amplitude through-transmission method ranged from 63.3 to 122.6. The apparent bone density was highly correlated with the B/A and with the existing quantitative ultrasound parameters of the speed of sound (SOS) and the normalized broadband ultrasound attenuation (nBUA), with Pearson’s correlation coefficients of r = 0.83 to 0.96. The best univariate predictor of the apparent bone density was the B/A, with an adjusted squared correlation coefficient of r 2 = 0.91. These results suggest that the B/A, in addition to the SOS and the nBUA, may have potential as an index for the assessment of bone status and osteoporosis.

In vivo microdamage is an indicator of susceptibility to initiation and propagation of microdamage in human femoral trabecular bone

Microdamage has been cited as an important element of trabecular bone quality and fracture risk, as materials with flaws have lower modulus and strength than equivalent undamaged materials. However, the magnitude of the effect of damage on failure properties depends on its tendency to propagate. Human femoral trabecular bone from the neck and greater trochanter was subjected to one of compressive, torsional, or combined compression and torsion. The in vivo, new, and propagating damage were then quantified in thick sections under epifluorescent microscopy. Multiaxial loading, which was intended to represent an off-axis load such as a fall or accident, caused much more damage than either simple compression or shear, and similarly caused the greatest stiffness loss. In all cases, initiation of new damage far exceeded the propagation of existing damage. This may reflect stress redistribution away from damaged trabeculae, resulting in new damage sites. However, the accumulation of new damage was positively correlated with quantity of pre-existing damage in all loading modes, indicating that damaged bone is inherently more prone to further damage formation. Moreover, about 50% of in vivo microcracks propagated under each type of loading. Finally, damage formation was positively correlated to decreased compressive stiffness following both axial and shear loading. Taken together, these results demonstrate that damage in trabecular bone adversely affects its mechanical properties, and is indicative of bone that is more susceptible to further damage.

Jump exercise during hindlimb unloading protect against the deterioration of trabecular bone microarchitecture in growing young rats

Three-dimensional femoral trabecular architecture was investigated in tail-suspended young growing rats and the effects of jump exercise during the period of tail-suspension were also examined. Eight-week-old male Wistar rats (n = 24) were randomly assigned to three body weight-matched groups: a tail suspended group (SUS, n = 8); a sedentary control group (CON, n = 8) and rats primed with jump exercise during the period of tail suspension (JUM, n = 8). The jump exercise protocol consisted of 30 jumps/day, five days/week with a 40 cm jump height. After 3 weeks of jump exercise, bone mineral density (BMD) of the entire right femur was measured using dual energy X-ray absorptiometry. Three-dimensional trabecular bone architecture at the distal femoral metaphysis was evaluated using microcomputed tomography (micro-CT). Tail suspension caused a decrease in femoral BMD (−5%, p < 0.001) and trabecular bone architectural deterioration. Deterioration in the trabecular network during hindlimb unloading was mostly attributed to the reduction of trabecular number (−32%, p < 0.001) in the distal femoral metaphysis. Jump exercise during the tail suspension period increased trabecular thickness (14%, p < 0.001) and the reduction of trabecular number was suppressed. The present data indicate that jump exercise applied during hindlimb unloading could be able to inhibit bone loss and trabecular bone architectural deterioration caused by tail suspension.

The Preventive Effect of Biochanin A on Bone Loss in Ovariectomized Rats: Involvement in Regulation of Growth and Activity of Osteoblasts and Osteoclasts

Biochanin A (BCA) is a major isoflavone abundant in red clover (Trifolium pretense). The protective effect of BCA on bone loss in an ovariectomized (OVX) animal model has never been clarified. The objective of this study was to investigate the biological effects of BCA on bone loss in OVX rats in vivo and on the development of osteoblasts and osteoclasts in vitro. Ovariectomy resulted in a marked increase in body weight and a decrease in femoral bone mineral density and trabecular bone volume that was prevented by BCA or 17β-estradiol (E2) treatment. However, an increase in uterine weight was observed in E2-treated OVX rats, but not in response to BCA treatment. Treatment with BCA increased the mRNA expression of osterix, collagen type I, alkaline phosphatase (ALP), and osteocalcin and decreased the mRNA expression of tartrate-resistant acid phosphatase (TRAP) and the receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) ratio in the femur of OVX rats. Treatment with BCA or E2 prevented the OVX-induced increase in urinary deoxypyridinoline (DPD) and serum tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β). In vitro, BCA induced preosteoblasts to differentiate into osteoblasts and increased osteoblast mineralization. BCA inhibited preosteoclasts and osteoclast proliferation and decreased osteoclast bone resorption. These findings suggest that BCA treatment can effectively prevent the OVX-induced increase in bone loss and bone turnover possibly by increasing osteoblastic activities and decreasing osteoclastic activities.

Micro-computed tomography assessment of human femoral trabecular bone for two disease groups (fragility fracture and coxarthrosis): Age and gender related effects on the microstructure

The aim of this study was to identify three-dimensional microstructural changes of trabecular bone with age and gender, using micro-computed tomography. Human trabecular bone from two disease groups, osteoporosis and osteoarthritis was analyzed. A prior analysis of the effects of some procedure variables on the micro-CT results was performed. Preliminary micro-CT scans were performed with three voxel resolutions and two acquisition conditions. On the reconstruction step, the image segmentation was performed with three different threshold values. Samples were collected from patients, with coxarthrosis (osteoarthritis) or fragility fracture (osteoporosis). The specimens of the coxarthrosis group include twenty females and fifteen males, while the fragility fracture group was composed by twenty three females and seven males. The mean age of the population was 69 ± 11 (females) and 67 ± 10 years (males), in the coxarthrosis group, while in the fragility fracture group was 81 ± 6 (females) and 78 ± 6 (males) years. The 30 μm voxel size provided lower percentage difference for the microarchitecture parameters. Acquisition conditions with 160 μA and 60 kV permit the evaluation of all the volume’s sample, with low average values of the coefficients of variation of the microstructural parameters. No statistically significant differences were found between the two diseases groups, neither between genders. However, with aging, there is a decrease of bone volume fraction, trabecular number and fractal dimension, and an increase of structural model index and trabecular separation, for both disease groups and genders. The parameters bone specific surface, trabecular thickness and degree of anisotropy have different behaviors with age, depending on the type of disease. While in coxarthrosis patients, trabecular thickness increases with age, in the fragility fracture group, there is a decrease of trabecular thickness with increasing age. Our findings indicate that disease, age and gender do not provide significant differences in trabecular microstructure. With aging, some parameters exhibit different trends which are possibly related to different mechanisms for different diseases.

Influence of the pore fluid on the phase velocity in bovine trabecular bone In Vitro: Prediction of the biot model

The present study aims to investigate the influence of the pore fluid on the phase velocity in bovine trabecular bone in vitro. The frequency-dependent phase velocity was measured in 20 marrow-filled and water-filled bovine femoral trabecular bone samples. The mean phase velocities at frequencies between 0.6 and 1.2 MHz exhibited significant negative dispersions for both the marrow-filled and the water-filled samples. The magnitudes of the dispersions showed no significant differences between the marrow-filled and the water-filled samples. In contrast, replacement of marrow by water led to a mean increase in the phase velocity of 27 m/s at frequencies from 0.6 to 1.2 MHz. The theoretical phase velocities of the fast wave predicted by using the Biot model for elastic wave propagation in fluid-saturated porous media showed good agreements with the measurements.

Osteoblast Lineage-Specific Effects of Notch Activation in the Skeleton

Transgenic overexpression of the Notch1 intracellular domain inhibits osteoblast differentiation and causes osteopenia, and inactivation of Notch1 and Notch2 increases bone volume transiently and induces osteoblastic differentiation. However, the biology of Notch is cell-context-dependent, and consequences of Notch activation in cells of the osteoblastic lineage at various stages of differentiation and in osteocytes have not been defined. For this purpose, Rosa(Notch) mice, where a loxP-flanked STOP cassette placed between the Rosa26 promoter and the NICD coding sequence, were crossed with transgenics expressing the Cre recombinase under the control of the Osterix (Osx), Osteocalcin (Oc), Collagen 1a1 (Col2.3), or Dentin matrix protein1 (Dmp1) promoters. At 1 month, Osx-Cre;Rosa(Notch) and Oc-Cre;Rosa(Notch) mice exhibited osteopenia due to impaired bone formation. In contrast, Col2.3-Cre;Rosa(Notch) and Dmp1-Cre;Rosa(Notch) exhibited increased femoral trabecular bone volume due to a decrease in osteoclast number and eroded surface. In the four lines studied, cortical bone was either not present, was porous, or had the appearance of trabecular bone. Oc-Cre;Rosa(Notch) and Col2.3-Cre;Rosa(Notch) mice exhibited early lethality so that their adult phenotype was not established. At 3 months, Osx-Cre;Rosa(Notch) and Dmp1-Cre;Rosa(Notch) mice displayed increased bone volume, and increased osteoblasts although calcein-demeclocycline labels were diffuse and fragmented, indicating abnormal bone formation. In conclusion, Notch effects in the skeleton are cell-context-dependent. When expressed in immature osteoblasts, Notch arrests their differentiation, causing osteopenia, and when expressed in osteocytes, it causes an initial suppression of bone resorption and increased bone volume, a phenotype that evolves as the mice mature.

Both spontaneous Ins2+/− and streptozotocin‐induced type I diabetes cause bone loss in young mice

The adolescent skeleton undergoes accelerated growth determining overall bone density, length, and quality. Diseases such as type 1 diabetes (T1D), most often diagnosed in adolescents, can alter bone processes and promote bone loss. Studies examining type 1 diabetic (T1D) bone pathologies typically utilize adult mice and rely on pharmacologic models such as streptozotocin (STZ)-induced diabetic rodents. To test the effect of T1D on adolescent bone growth/density we used a novel juvenile genetic model (Ins2(+/-) mice) that spontaneously develop T1D at approximately 5 weeks of age and compared our findings with STZ-induced T1D mice. Compared to controls, both Ins2(+/-) and STZ-induced T1D mice displayed blood glucose levels greater than 300 mg/dl and reduced body, fat and muscle mass as well as femur trabecular bone density. STZ mice exhibited greater bone loss compared to Ins2(+/-) mice despite having lower blood glucose levels. Cortical bone was affected in STZ but not Ins2(+/-) mice. Osteocalcin serum protein and bone RNA levels decreased in both models. Consistent with studies in adult mice, STZ adolescent mice displayed increased marrow adiposity, however this was not observed in the Ins2(+/-) mice. Reduced femur length, decreased growth plate thickness and decreased collagen II expression in both model simplies impaired cartilage formation. In summary, both pharmacologic and spontaneous adolescent T1D mice demonstrated a bone synthesis and growth defect. STZ appears to cause a more severe phenotype. Thus, the Ins2(+/-) mouse could serve as a useful model to study adolescent T1D bone loss with fewer complications.

Impaired osteoclast differentiation and function and mild osteopetrosis development in Siglec-15-deficient mice

Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) is a cell surface receptor for sialylated glycan ligands. Recent in vitro studies revealed upregulated Siglec-15 expression in differentiated osteoclasts and inhibition of osteoclast differentiation by anti-Siglec-15 polyclonal antibody, demonstrating Siglec-15 involvement in osteoclastogenesis. To discern the physiological role of Siglec-15 in skeletal development and osteoclast formation and/or function in vivo, we generated Siglec-15-deficient (siglec-15−/−) mice and analyzed their phenotype. The siglec-15−/− mice developed without physical abnormalities other than increased trabecular bone mass in lumbar vertebrae and metaphyseal regions of the femur and tibia, causing mild osteopetrosis. Histological analyses demonstrated that the number of osteoclasts present on the femoral trabecular bone of the mutant mice was comparable to that of the wild-type mice. However, urinary deoxypyridinoline, a systemic bone resorption marker, decreased in the siglec-15−/− mice, indicating that impaired osteoclast function was responsible for increased bone mass in the mutant mice. In addition, the ability of bone marrow-derived monocytes/macrophages from the siglec-15−/− mice to differentiate into osteoclasts was impaired, as determined in vitro by cellular tartrate-resistant acid phosphatase activity in response to the receptor activator of nuclear factor-κB ligand or tumor necrosis factor-α. These results reveal the importance of Siglec-15 in the regulation of osteoclast formation and/or function in vivo, providing new insights into osteoclast biology.

Influence of cortical endplate on speed of sound in bovine femoral trabecular bone in vitro

Speed of sound (SOS) was measured in 14 bovine femoral trabecular bone samples with and without the cortical endplates with various thicknesses of 1.00, 1.31, 1.47, 1.75, and 2.00 mm. The presence of the cortical endplates resulted in an increase in the mean SOS of 16 m/s (+0.9%) to 91 m/s (+5.3%). The mean SOS measured in the samples with and without the cortical endplates exhibited similar significant correlations with apparent bone density (r = 0.86-0.91). All the SOS measurements were also found to be highly correlated with each other (r = 0.89-0.99).