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      Microfocus Computed Tomography Analysis of Early Changes in Bone Microstructure in Rats with Chronic Renal Failure

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          Background/Aims: Little is known about the microstructural changes in bone tissue in the early phase of chronic renal failure (CRF). In this study, we analyzed the bone tissue in a rat model of early CRF using a high-resolution X-ray tomographic system, i.e. microfocus computed tomography (MXCT), which is capable of detecting microscopic structural changes in bone tissue. Methods: CRF rats were created by 7/8 nephrectomy by ligation of the renal artery branches, and were sacrificed 24 weeks after surgery. MXCT and bone mineral densitometry by single-energy X-ray absorptiometry (SXA) were performed using extracted bone samples. Images obtained by MXCT were further analyzed by node-strut morphometry. Results: Biochemical analysis confirmed that CRF was induced in 7/8-renal artery-ligated rats. MXCT demonstrated a significant decrease in trabecular bone in uremic rats, whereas SXA was unable to detect the difference. The node-strut method revealed decreased trabecular connectivity, with little change in the thickness of the trabecular bone in uremic rats. Conclusion: MXCT was able to detect significant changes in trabecular bone at an early stage of renal failure. The observed structural changes differed from those found in long-term dialysis patients. MXCT is a practical and promising device used for the non-invasive evaluation of early bone changes in uremic patients.

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          Most cited references 13

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          The temporal changes of trabecular architecture in ovariectomized rats assessed by MicroCT.

          To study the short- and long-term effects of estrogen deficiency on trabecular bone, three-dimensional measurements of proximal tibiae of ovariectomized rats were performed by micro-computed tomography (MicroCT). New three-dimensional (3D) techniques were employed to characterize the trabecular architecture from 0 to 110 days post-ovariectomy (OVX). These new methods no longer assume a plate or rod model of bone, but calculate trabecular thickness, separation, and number and their distribution by placing maximal spheres into the 3D representation of the structure. The model type of bone was quantified with the Structure Model Index (SMI). Utilizing these methods we found a rapid loss of trabecular bone in the first week after OVX. After the first week bone mass declined further, although the rate of loss was lower. In addition there was a complete change in model type from plate-like to rod-like within 7 days post-OVX, and then a very constant SMI after 12 days. After an initial thinning of trabecular structure, further bone loss seems to occur through removal of trabeculae, while the trabecular plate thickness remains constant. The heterogeneity of the network could be quantified by intra-individual standard deviation of local separations, which showed a stair-like progression, with a plateau between 12 and 60 days post-OVX. This study provides new insights into ovariectomy-related changes in cancellous bone structure evaluated by 3D MicroCT. In addition, these data suggest that the rapid change of model from plate-like to rod-like post-OVX may potentially introduce biases in the parameters that are determined using model-based algorithms, and these biases may modify the impact of age-related or therapeutic changes.
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            Morphometric Analysis of Human Bone Biopsies: A Quantitative Structural Comparison of Histological Sections and Micro-Computed Tomography

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              Disparate effects of mild, moderate, and severe secondary hyperparathyroidism on cancellous and cortical bone in rats with chronic renal insufficiency.

              The subtotally nephrectomized rat has often been used to investigate the etiology and treatment of secondary hyperparathyroidism (secondaryHPT), but it has been used less frequently to study the effects of secondaryHPT on bone. The recent development of a reliable and specific rat parathyroid hormone (PTH) immunoradiometric assay has provided an opportunity for a thorough investigation of the relationship between circulating, biologically active PTH, and the skeletal abnormalities that occur in chronic renal insufficiency (CRI). Rats were 5/6 nephrectomized (Nx) or sham operated and fed diets with varying levels of Ca and P for 12-14 weeks to induce differing magnitudes of secondaryHPT. Parathyroid gland volume increased by 80%-90% in 5/6 Nx rats in the mild and moderate secondaryHPT groups (2.3- and 7.7-fold higher PTH levels, respectively) and by 3.3-fold in the severe secondaryHPT group (12-fold increase in PTH). The increases in gland volume were caused primarily by cell hyperplasia. Mild secondaryHPT resulted in a 12% decrease in bone mineral density (BMD) across the entire femur, increased osteoclast numbers (N.Oc), unchanged osteoblast numbers (N.Ob), and decreased cancellous bone volume (Cn.BV) in the tibial metaphysis but, apart from increased marrow area, no major changes in cortical bone at the tibio-fibular junction. Moderate secondaryHPT was associated with no changes in femoral BMD, or in tibial Cn.BV, but N.Ob and bone formation rate (BFR) were markedly elevated. Increased periosteal, intracortical, and endocortical BFR and turnover were evident, and contributed to increased cortical porosity (Ct.Po). The changes were exaggerated in the severe secondaryHPT group; BMD was lower in the proximal, but higher in the distal femur, and Cn.BV, N.Ob, N.Oc, and BFR were increased by six-, seven-, three-, and 30-fold, respectively. Endocortical BFR was elevated 31-fold and the extensive Ct.Po (10%) decreased bone strength. However, Ct.Po was not apparent until PTH levels exceeded 500 pg/mL. Thus, in rats with CRI of similar magnitude, progressive secondaryHPT is associated with dramatically different effects on bone. Mild secondaryHPT caused loss of cancellous and endocortical bone, and moderate secondaryHPT tended to maintain both types of osseous tissue, whereas PTH levels >500 pg/mL resulted in substantial cortical bone loss, but cancellous bone gain.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                December 2003
                17 November 2004
                : 95
                : 4
                : e152-e157
                aDivision of Clinical Intensive Care Medicine, Niigata University Medical Hospital, Niigata; bDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, and Oita University of Nursing and Health Care, Oita; cKureha Biomedical Research Laboratories, Tokyo; dInstitute for Medical Sciences, Tokai University, Isehara, and eDivision of Nephrology and Dialysis Center, Kobe University School of Medicine, Kobe, Japan
                74842 Nephron Exp Nephrol 2003;95:e152–e157
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 2, References: 29, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74842
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