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ABSTRACT: The aim of our study was to perform trabecular bone structure analysis with images from 64- and 320-slice multidetector computed tomography (MDCT) and to compare these with high-resolution peripheral computed tomography (HR-pQCT).
Twenty human cadaver distal forearm specimens were imaged on a 64- and 320-slice MDCT system at 120 kVp, 200 mA and 135 kVp, 400 mA (in-plane pixel size 234 microm; slice thickness 500 microm). HR-pQCT imaging was performed at an isotropic voxel size of 41 microm. Bone volume fraction (BV/TV), trabecular number (Tb.N), thickness (Tb.Th) and separation (Tb.Sp) were computed.
MDCT-derived BV/TV and Tb.Sp were highly correlated (r = 0.92-0.96, p < 0.0001) with the corresponding HR-pQCT parameters. Tb.Th was the only structure measure that did not yield any significant correlation.
The 64- and 320-slice MDCT systems both perform equally well in depicting trabecular bone architecture. However, because of constrained resolutions accurate derivation of trabecular bone measures is limited to only a subset of microarchitectural parameters.
European Radiology 09/2009; 20(2):458-68. · 3.22 Impact Factor
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ABSTRACT: We studied the feasibility of cancellous bone structure assessment of the proximal femur using multidetector computed tomography (MDCT) in an simulated in vivo experimental model. The proximal femur of 15 intact human cadavers was examined using 64-row MDCT using a thin-section protocol with an in-plane spatial resolution of 273 mum. High-resolution peripheral quantitative computed tomography (HR-pQCT) of the isolated specimens with a voxel size of 82 mum served as a standard of reference. Trabecular bone structure and optimized textural parameters were calculated in MDCT images and compared to measures obtained by HR-pQCT. Significant correlations between MDCT- and HR-pQCT-derived values for bone fraction (r = 0.87), trabecular separation (r = 0.66), and number (r = 0.53) were found. Parameters derived from textural analysis performed better in predicting trabecular separation (up to r = 0.86) and number (up to r = 0.83). Trabecular thickness could not be quantified correctly using MDCT, most likely due to its limited resolution. Individual parameters for assessement of trabecular microarchitecture can be measured using MDCT-derived imaging studies and a simulated in vivo setup. Thus, in vivo assessment of bone architecture in addition to BMD may be feasible in clinical practice.
Calcified Tissue International 11/2008; 83(5):332-41. · 2.38 Impact Factor
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ABSTRACT: We showed that the IGF-IR-null mutation in mature osteoblasts leads to less bone and decreased periosteal bone formation and impaired the stimulatory effects of PTH on osteoprogenitor cell proliferation and differentiation.
This study was carried out to examine the role of IGF-I signaling in mediating the actions of PTH on bone.
Three-month-old mice with an osteoblast-specific IGF-I receptor null mutation (IGF-IR OBKO) and their normal littermates were treated with vehicle or PTH (80 microg/kg body weight/d for 2 wk). Structural measurements of the proximal and midshaft of the tibia were made by microCT. Trabecular and cortical bone formation was measured by bone histomorphometry. Bone marrow stromal cells (BMSCs) were obtained to assess the effects of PTH on osteoprogenitor number and differentiation.
The fat-free weight of bone normalized to body weight (FFW/BW), bone volume (BV/TV), and cortical thickness (C.Th) in both proximal tibia and shaft were all less in the IGF-IR OBKO mice compared with controls. PTH decreased FFW/BW of the proximal tibia more substantially in controls than in IGF-IR OBKO mice. The increase in C.Th after PTH in the proximal tibia was comparable in both control and IGF-IR OBKO mice. Although trabecular and periosteal bone formation was markedly lower in the IGF-IR OBKO mice than in the control mice, endosteal bone formation was comparable in control and IGF-IR OBKO mice. PTH stimulated endosteal bone formation only in the control animals. Compared with BMSCs from control mice, BMSCs from IGF-IR OBKO mice showed equal alkaline phosphatase (ALP)(+) colonies on day 14, but fewer mineralized nodules on day 28. Administration of PTH increased the number of ALP(+) colonies and mineralized nodules on days 14 and 28 in BMSCs from control mice, but not in BMSCs from IGF-IR OBKO mice.
Our results indicate that the IGF-IR null mutation in mature osteoblasts leads to less bone and decreased bone formation, in part because of the requirement for the IGF-IR in mature osteoblasts to enable PTH to stimulate osteoprogenitor cell proliferation and differentiation.
Journal of Bone and Mineral Research 10/2007; 22(9):1329-37. · 6.37 Impact Factor
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Benjamin M Boudignon,
Daniel D Bikle,
Pam Kurimoto,
Hashem Elalieh,
Shigeki Nishida,
Yongmei Wang, Andrew Burghardt,
Sharmila Majumdar,
Benjamin E Orwoll,
Clifford Rosen,
Bernard P Halloran
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ABSTRACT: IGF-I stimulates osteoblast proliferation, bone formation, and increases bone volume in normal weight-bearing animals. During skeletal unloading or loss of weight bearing, bone becomes unresponsive to the anabolic effects of insulin-like growth factor I (IGF-I). To determine whether skeletal reloading after a period of unloading increases bone responsiveness to IGF-I, we examined bone structure and formation in response to IGF-I under different loading conditions. Twelve-week-old rats were divided into six groups: loaded (4 wk), unloaded (4 wk), and unloaded/reloaded (2/2 wk), and treated with IGF-I (2.5 mg x kg(-1) x day(-1)) or vehicle during the final 2 wk. Cortical bone formation rate (BFR), cancellous bone volume and architecture in the secondary spongiosa (tibia and vertebrae), and total volume and calcified volume in the primary spongiosa (tibia) were assessed. Periosteal BFR decreased during unloading, remained low during reloading in the vehicle-treated group, but was dramatically increased in IGF-I-treated animals. Cancellous bone volume decreased with unloading and increased with reloading, but the effect was exaggerated in the tibia of IGF-I-treated animals. Total and calcified volumes in the primary spongiosa decreased during unloading in the vehicle-treated animals. IGF-I treatment prevented the loss in volume. These data show that reloading after a period of skeletal unloading increases bone responsiveness to IGF-I, and they suggest that IGF-I may be of therapeutic use in patients who have lost bone as a consequence of prolonged skeletal disuse.
Journal of Applied Physiology 08/2007; 103(1):125-31. · 3.75 Impact Factor
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ABSTRACT: We investigated the influence of soft tissue (ST) on image quality by high-resolution multidetector computed tomography (MDCT) scans and assessed the effect of surrounding ST on the quantification of trabecular bone structure. Eight bone cores obtained from human proximal femoral heads discarded during hip replacement surgery were scanned with micro-computed tomography (microCT) as well as with MDCT both without (w/o) and with (w) simulated surrounding ST, where a phantom imitated a human torso. Signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) were measured in all scans. Apparent trabecular bone structure parameters were calculated and compared to similar parameters obtained in coregistered sections of the microCT scans. Residual errors were calculated as root-mean-square (RMS) errors relative to the microCT measurements. Compared to microCT results, trabecular structure parameters were overestimated by MDCT both w and w/o ST. SNR and CNR were significantly higher in the scans w/o ST. Significant correlations between microCT and MDCT results were found for bone fraction (r = 0.90 w/o ST, r = 0.84 w ST), trabecular number, and separation. RMS ranged from 10% to 15% for MDCT w/o ST and from 10% to 17% for MDCT w ST. Only bone fraction showed significantly different RMS and correlations for scans w/o vs. w ST (P < 0.05). This study showed that MDCT is able to visualize trabecular bone structure in an in vivo-like setting at skeletal sites within the torso such as the proximal femur. Even though ST scatter compromises image quality substantially, the major characteristics of the trabecular network can still be appreciated and quantified.
Calcified Tissue International 07/2007; 80(6):366-73. · 2.38 Impact Factor
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ABSTRACT: Parathyroid hormone (PTH) exerts both catabolic and anabolic actions on bone. Studies on the skeletal effects of PTH have seldom considered the effects of gender. Our study was designed to determine whether the response of mouse bone to PTH differed according to sex. As a first step, we analyzed gender differences with respect to bone mass and structural properties of 4 month old PTH treated (80 microg/kg per day for 2 weeks) male and female CD-1 mice. PTH significantly increased fat free weight/body weight, periosteal bone formation rate, mineral apposition rate, and endosteal single labeling surface, while significantly decreasing medullary area in male mice compared with vehicle treated controls, but induced no significant changes in female mice. We then analyzed the gender differences in bone marrow stromal cells (BMSC) isolated from 4 month old male and female CD-1 mice following treatment with PTH (80 microg/kg per day for 2 weeks). PTH significantly increased the osteogenic colony number and the alkaline phosphatase (ALP) activity (ALP/cell) by day 14 in cultures of BMSCs from male and female mice. PTH also increased the mRNA level of receptor activator of nuclear factor kappaB ligand in the bone tissue (marrow removed) of both females and males. However, PTH increased the mRNA levels of IGF-I and IGF-IR only in the bones of male mice. Our results indicate that on balance a 2-weeks course of PTH is anabolic on cortical bone in this mouse strain. These effects are more evident in the male mouse. These differences between male and female mice may reflect the greater response to PTH of IGF-I and IGF-IR gene expression in males enhancing the anabolic effect on cortical bone.
Journal of Endocrinology 06/2006; 189(2):279-87. · 3.55 Impact Factor
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ABSTRACT: Although trabecular bone structure has been evaluated, variation with knee compartment and depth from joint surface is not completely understood. Cadaver knees were evaluated with microcomputed tomography analysis for these variations. Objective differences were compared between: medial vs. lateral compartments; femoral vs. tibial bone; and normal vs. arthritic knees. Depth dependent changes in the parameters were observed for the first 6 mm of the cores in normal knees: BV/TV, Tb.N and Conn.D gradually decrease, while Tb.Sp and SMI increase. In the first 6 mm of the normal tibia BV/TV, Tb.N, and Tb.Th are greater than in the femur on both the medial and lateral compartments while Tb.Sp, SMI, and Conn.D are lower. The medial compartment values for BV/TV, Tb.N, Tb.Th and Conn.D are generally greater than for the lateral in both the femur and tibia while Tb.Sp and SMI are lower. In comparison of normal vs. arthritic knees significant differences are observed in the first 6 mm of the medial tibia. With arthritis BV/TV and Tb.Th are lower, while SMI and Tb.Sp are higher. Tb.N and Conn.D show no statistically significant difference. The bone structure variations are, thus, most prominent in the first 6 mm of depth and medial compartment bone is generally more structurally sound than lateral. Severely arthritic bone changes are most prominent in the medial compartment of the tibia and bone structure is less sound in severe arthritis.© 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.
Journal of Orthopaedic Research 12/2005; 21(1):6 - 13. · 2.81 Impact Factor
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ABSTRACT: Investigation on architecture of lumbar pedicle.
To determine morphological properties of pedicular cancellous bone.
Many researchers have been stimulated to study trabecular architecture by improvements in stereological technology. Although the structure of vertebral cancellous bone has been well studied in the literature, no information is available about the architecture of pedicular cancellous bone.
Eight cadaveric L3 lumbar vertebrae were harvested. After collecting the bone mineral density (BMD) data on the vertebrae, pedicle isthmuses were removed from the vertebral bodies using a reciprocal hand saw. The BMD measurements were done on the dissected pedicle isthmus specimens. All the specimens were then analyzed using a micro-computed tomography unit. Morphologic parameters of trabecular bone were calculated.
Bone volume was found as 0.209 +/- 0.046, whereas Tb.Th, Tb.Sp, and Tb.N were found to be 0.201 +/- 0.035 mm, 0.930 +/- 0.123 mm, and 1.098 +/- 0.136 mm(-1), respectively. Connectivity density and structure model index were observed to be 3.135 +/- 0.918 mm(-3), 0.37, whereas degree of anisotropy value was 1.241 +/- 0.093. Vertebral BMD could explain 63% of variance in bone density of a pedicle isthmus.
The structure of the pedicular cancellous bone is somewhat different from that of vertebral body. The trabecular architecture within the pedicle isthmus is isotropic and plate-like. The thickness and number of the trabeculae were greater than those of vertebral trabeculae. Decrease in the bone volume with age is mainly by thinning of the trabeculae and increasing in trabecular spacing, but not by loss of mass.
Spine 08/2005; 30(13):1485-90. · 2.08 Impact Factor
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ABSTRACT: HA activates CD44 to stimulate RANKL expression in bone marrow stromal cells. HA stimulation of RANKL is blocked by anti-CD44 antibody and is absent in cells from CD44(-/-) mice. CD44(-/-) mice exhibit thicker cortical bone and a smaller medullary cavity, but indices of bone resorption are not affected.
Hyaluronan (HA), the major nonprotein glycosaminoglycan component of the extracellular matrix in mammalian bone marrow, functions in part through its receptor, CD44, to stimulate a series of intracellular signaling events that lead to cell migration, adhesion, and activation. To determine whether HA activation of CD44 influences RANKL and osteoprotegerin (OPG) expression and whether CD44 is functionally important in bone metabolism, we studied whole bone and bone marrow stromal cells (BMSCs) from wildtype and CD44(-/-) mice.
BMSCs from wildtype and CD44(-/-) mice at 7 weeks of age were cultured and treated with either HA or anti-CD44 antibody. The levels of mRNA of RANKL, OPG, CD44, alkaline phosphatase (ALP), osteocalcin (OC), and alphaI collagen (COLL) were determined by quantitative real-time RT-PCR. Levels of RANKL and CD44 protein were measured by immunoblotting, and expression of CD44 in whole bone was determined by immunohistochemical staining. Double immunofluorescence staining and confocal microscopy were used to study colocalization of Cbfa1, CD44, and HA. Tibias were imaged using muCT, and cancellous and cortical parameters were measured. Osteoblast and osteoclast surface in the distal femoral metaphysis and osteoclast on the endocortical surface at the tibio-fibular junction were measured using quantitative histomorphometry. Differences were analyzed using ANOVA and the Newman-Keuls test.
Addition of HA dose-dependently increased RANKL mRNA (3.6-fold) and protein (3-fold) levels in BMSCs. Stimulation of RANKL by HA could be blocked with anti-CD44 antibody. Treatment of cells with HA or anti-CD44 antibody had no significant effect on OPG mRNA levels. Both CD44 and HA localized on the plasma membrane in cells expressing Cbfa1. HA localization on the cell membrane disappeared when cells were preincubated with anti-CD44 antibody. Compared with control mice, cortical bone of CD44(-/-) was thicker, and medullary area was smaller at both 7 and 17 weeks, but at 7 weeks, indices of bone resorption were normal. At 17 weeks of age, tibial mass of CD44(-/-) mice was higher than control mice. CD44(-/-) animals expressed less RANKL in whole bone (-30%) and in BMSCs (-50%). Cells from CD44(-/-) animals failed to respond to either HA or CD44 antibody treatment.
HA can increase RANKL expression in BMSCs through CD44.
Journal of Bone and Mineral Research 02/2005; 20(1):30-40. · 6.37 Impact Factor
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Loren G Fong,
Jennifer K Ng,
Margarita Meta,
Nathan Coté,
Shao H Yang,
Colin L Stewart,
Terry Sullivan, Andrew Burghardt,
Sharmila Majumdar,
Karen Reue,
Martin O Bergo,
Stephen G Young
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ABSTRACT: Zmpste24 is a metalloproteinase required for the processing of prelamin A to lamin A, a structural component of the nuclear lamina. Zmpste24 deficiency results in the accumulation of prelamin A within cells, a complete loss of mature lamin A, and misshapen nuclear envelopes. Zmpste24-deficient (Zmpste24(-/-)) mice exhibit retarded growth, alopecia, micrognathia, dental abnormalities, osteolytic lesions in bones, and osteoporosis, which are phenotypes shared with Hutchinson-Gilford progeria syndrome, a human disease caused by the synthesis of a mutant prelamin A that cannot undergo processing to lamin A. Zmpste24(-/-) mice also develop muscle weakness. We hypothesized that prelamin A might be toxic and that its accumulation in Zmpste24(-/-) mice is responsible for all of the disease phenotypes. We further hypothesized that Zmpste24(-/-) mice with half-normal levels of prelamin A (Zmpste24(-/-) mice with one Lmna knockout allele) would be subjected to less toxicity and be protected from disease. Thus, we bred and analyzed Zmpste24(-/-)Lmna(+/-) mice. As expected, prelamin A levels in Zmpste24(-/-)Lmna(+/-) cells were significantly reduced. Zmpste24(-/-)Lmna(+/-) mice were entirely normal, lacking all disease phenotypes, and misshapen nuclei were less frequent in Zmpste24(-/-)Lmna(+/-) cells than in Zmpste24(-/-) cells. These data suggest that prelamin A is toxic and that reducing its levels by as little as 50% provides striking protection from disease.
Proceedings of the National Academy of Sciences 01/2005; 101(52):18111-6. · 9.68 Impact Factor
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ABSTRACT: Apparent yield strains for trabecular bone are uniform within an anatomic site but can vary across site. The overall goal of this study was to characterize the contribution of inter-site differences in trabecular architecture to corresponding variations in apparent yield strains. High-resolution, small deformation finite element analyses were used to compute apparent compressive and tensile yield strains in four sites (n = 7 specimens per site): human proximal tibia, greater trochanter, femoral neck, and bovine proximal tibia. These sites display differences in compressive, but not tensile, apparent yield strains. Inter-site differences in architecture were captured implicitly in the model geometries, and these differences were isolated as the sole source of variability across sites by using identical tissue properties in all models. Thus, the effects inter-site variations in architecture on yield strain could be assessed by comparing computed yield strains across site. No inter-site differences in computed yield strains were found for either loading mode (p > 0.19), indicating that, within the context of small deformations, inter-site variations in architecture do not affect apparent yield strains. However, results of ancillary analyses designed to test the validity of the small deformation assumption strongly suggested that the propensity to undergo large deformations constitutes an important contribution of architecture to inter-site variations in apparent compressive yield strains. Large deformations substantially reduced apparent compressive, but not tensile, yield strains. These findings indicate the importance of incorporating large deformation capabilities in computational analyses of trabecular bone. This may be critical when investigating the biomechanical consequences of trabecular thinning and loss.
Journal of Biomechanics 09/2004; 37(9):1413-20. · 2.43 Impact Factor
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ABSTRACT: The goal of this study was to explore the role of diffraction enhanced X-ray imaging (DEI) for assessing changes in osteoarthritic cartilage and correlating the findings with concurrent changes in the underlying bone imaged using micro-computed tomography (microCT). DEI was used to image femoral head specimens at various beam energies. DEI utilizes a monochromatic, highly collimated beam, with an analyzer crystal that selectively weights out photons according to the angle they have been deviated with respect to the original direction. This provides images of very high contrast, with the rejection of X-ray scatter. The underlying bone was imaged using microCT and measures quantifying the bone structure were derived. Confirmation of cartilage degeneration was obtained from histology and polarized light microscopy. DEI allowed the visualization of articular cartilage and reflected the fibrillations and fissures in tissues from degenerated joints. The trabecular bone underlying the most degenerated articular cartilage showed increased bone volume fraction and more plate-like characteristics, compared with that underlying normal appearing cartilage. The histology and polarized light microscopy images reflected the DEI based features of cartilage architecture. These data reflect the ability of X-ray based emerging technologies to depict cartilage-bone interactions in joint degeneration.
European Radiology 09/2004; 14(8):1440-8. · 3.22 Impact Factor
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ABSTRACT: Osteoclasts, the only bone-resorbing cells, are central to the pathogenesis of osteoporosis, yet their development and regulation are incompletely understood. Multiple receptors of the immune system use a common signaling paradigm whereby phosphorylated immunoreceptor tyrosine-based activation motifs (ITAMs) within receptor-associated adapter proteins recruit the Syk tyrosine kinase. Here we demonstrate that a similar mechanism is required for development of functional osteoclasts. Mice lacking two ITAM-bearing adapters, DAP12 and the Fc receptor gamma-chain (FcRgamma), are severely osteopetrotic. DAP12(-/-)FcRgamma(-/-) bone marrow cells fail to differentiate into multinucleated osteoclasts or resorb bone in vitro and show impaired phosphorylation of the Syk tyrosine kinase. syk(-/-) progenitors are similarly defective in osteoclast development and bone resorption. Intact SH2-domains of Syk, introduced by retroviral transduction, are required for functional reconstitution of syk(-/-) osteoclasts, whereas intact ITAM-domains on DAP12 are required for reconstitution of DAP12(-/-) FcRgamma(-/-) cells. These data indicate that recruitment of Syk to phosphorylated ITAMs is critical for osteoclastogenesis. Although DAP12 appears to be primarily responsible for osteoclast differentiation in cultures directly stimulated with macrophage-colony stimulating factor and receptor activator of NF-kappaB ligand cytokines, DAP12 and FcRgamma have overlapping roles in supporting osteoclast development in osteoblast-osteoclast cocultures, which mirrors their overlapping functions in vivo. These results provide new insight into the biology of osteoclasts and suggest novel therapeutic targets in diseases of bony remodeling.
Proceedings of the National Academy of Sciences 05/2004; 101(16):6158-63. · 9.68 Impact Factor
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[show abstract]
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ABSTRACT: Osteoclasts, the only bone-resorbing cells, are central to the pathogenesis of osteoporosis, yet their development and regulation
are incompletely understood. Multiple receptors of the immune system use a common signaling paradigm whereby phosphorylated
immunoreceptor tyrosine-based activation motifs (ITAMs) within receptor-associated adapter proteins recruit the Syk tyrosine
kinase. Here we demonstrate that a similar mechanism is required for development of functional osteoclasts. Mice lacking two
ITAM-bearing adapters, DAP12 and the Fc receptor γ-chain (FcRγ), are severely osteopetrotic. DAP12
-/-
FcRγ-/- bone marrow cells fail to differentiate into multinucleated osteoclasts or resorb bone in vitro and show impaired phosphorylation of the Syk tyrosine kinase. syk
-/- progenitors are similarly defective in osteoclast development and bone resorption. Intact SH2-domains of Syk, introduced
by retroviral transduction, are required for functional reconstitution of syk
-/- osteoclasts, whereas intact ITAM-domains on DAP12 are required for reconstitution of DAP12
-/-
FcRγ-/- cells. These data indicate that recruitment of Syk to phosphorylated ITAMs is critical for osteoclastogenesis. Although DAP12
appears to be primarily responsible for osteoclast differentiation in cultures directly stimulated with macrophage-colony
stimulating factor and receptor activator of NF-κB ligand cytokines, DAP12 and FcRγ have overlapping roles in supporting osteoclast
development in osteoblast–osteoclast cocultures, which mirrors their overlapping functions in vivo. These results provide new insight into the biology of osteoclasts and suggest novel therapeutic targets in diseases of bony
remodeling.
Proceedings of the National Academy of Sciences 04/2004; 101(16):6158-6163. · 9.68 Impact Factor
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ABSTRACT: A micro-computed tomography (CT) study of the trabecular bone structure on loaded mice tail vertebral bodies was conducted.
To depict and characterize changes in the trabecular bone structure of mice tail vertebral bodies after in vivo application of static compressive load.
Static compressive loading leads to significant structural changes in murine tail intervertebral discs, such as disorganization of the anulus fibrosus, increase in apoptosis, and associated loss of cellularity. Wolff's Law suggests that alterations in spinal loading will also influence the architecture of the adjacent vertebral bodies. Because of biomechanical and biologic interdependencies between the disc and vertebra, these tissues should be considered simultaneously when investigating the etiology of degenerative spinal conditions.
Mice tail discs between the ninth and 10th caudal vertebrae were compressed in vivo for 7 days with static axial loads using external fixators. Micro-CT scans of the vertebral bodies were performed at an isotropic resolution of 18 microm, to obtain trabecular bone structural parameters. Random effects models were used to evaluate statistical significance of these parameters in different compressed conditions.
With loading, the connectivity density of the trabecular network increases significantly. After a period of in vivo recovery on load removal, the trabeculae become more rod-like; corresponding changes such as disorganization of the anulus fibrosus and loss of nuclear and inner-anular cellularity are also seen.
In vivo compressive loading leads to significant architectural changes within vertebral bodies. These observations may be helpful in understanding the pathologic processes and the chronology of degenerative spinal conditions.
Spine 02/2003; 28(2):123-8. · 2.08 Impact Factor
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ABSTRACT: Although trabecular bone structure has been evaluated, variation with knee compartment and depth from joint surface is not completely understood. Cadaver knees were evaluated with microcomputed tomography analysis for these variations. Objective differences were compared between: medial vs. lateral compartments; femoral vs. tibial bone; and normal vs. arthritic knees. Depth dependent changes in the parameters were observed for the first 6 mm of the cores in normal knees: BV/TV, Tb.N and Conn.D gradually decrease, while Tb.Sp and SMI increase. In the first 6 mm of the normal tibia BV/TV, Tb.N, and Tb.Th are greater than in the femur on both the medial and lateral compartments while Tb.Sp, SMI, and Conn.D are lower. The medial compartment values for BV/TV, Tb.N, Tb.Th and Conn.D are generally greater than for the lateral in both the femur and tibia while Tb.Sp and SMI are lower. In comparison of normal vs. arthritic knees significant differences are observed in the first 6 mm of the medial tibia. With arthritis BV/TV and Tb.Th are lower, while SMI and Tb.Sp are higher. Tb.N and Conn.D show no statistically significant difference. The bone structure variations are, thus, most prominent in the first 6 mm of depth and medial compartment bone is generally more structurally sound than lateral. Severely arthritic bone changes are most prominent in the medial compartment of the tibia and bone structure is less sound in severe arthritis.
Journal of Orthopaedic Research 02/2003; 21(1):6-13. · 2.81 Impact Factor
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ABSTRACT: To determine whether the mouse loses bone with aging and whether the changes mimic those observed in human aging, we examined the changes in the tibial metaphysis and diaphysis in the male C57BL/6J mouse over its life span using microcomputed tomography (microCT). Cancellous bone volume fraction (BV/TV) decreased 60% between 6 weeks and 24 months of age. Loss was characterized by decreased trabecular number (Tb.N), increased trabecular spacing (Tb.Sp), and decreased connectivity. Anisotropy decreased while the structure model index increased with age. Cortical bone thickness increased between 6 weeks and 6 months of age and then decreased continuously to 24 months (-12%). Cortical bone area (Ct.Ar) remained constant between 6 and 24 months. Fat-free weight reached a peak at 12 months and gradually declined to 24 months. Total mass lost between 12 and 24 months reached 10%. Overall, the age-related changes in skeletal mass and architecture in the mouse were remarkably similar to those seen in human aging. Furthermore, the rapid early loss of cancellous bone suggests that bone loss is not just associated with old age in the mouse but rather occurs as a continuum from early growth. We conclude that the C57BL/6J male mouse maybe a useful model to study at least some aspects of age-related bone loss in humans.
Journal of Bone and Mineral Research 07/2002; 17(6):1044-50. · 6.37 Impact Factor
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ABSTRACT: To determine whether the mouse loses bone with aging and whether the changes mimic those observed in human aging, we examined the changes in the tibial metaphysis and diaphysis in the male C57BL/6J mouse over its life span using microcomputed tomography (μCT). Cancellous bone volume fraction (BV/TV) decreased 60% between 6 weeks and 24 months of age. Loss was characterized by decreased trabecular number (Tb.N), increased trabecular spacing (Tb.Sp), and decreased connectivity. Anisotropy decreased while the structure model index increased with age. Cortical bone thickness increased between 6 weeks and 6 months of age and then decreased continuously to 24 months (−12%). Cortical bone area (Ct.Ar) remained constant between 6 and 24 months. Fat-free weight reached a peak at 12 months and gradually declined to 24 months. Total mass lost between 12 and 24 months reached 10%. Overall, the age-related changes in skeletal mass and architecture in the mouse were remarkably similar to those seen in human aging. Furthermore, the rapid early loss of cancellous bone suggests that bone loss is not just associated with old age in the mouse but rather occurs as a continuum from early growth. We conclude that the C57BL/6J male mouse maybe a useful model to study at least some aspects of age-related bone loss in humans.
Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 05/2002; 17(6):1044 - 1050. · 6.04 Impact Factor
