Deterioration of trabecular plate-rod and cortical microarchitecture and reduced bone stiffness at distal radius and tibia in postmenopausal women with vertebral fractures |
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| Affiliation: | 1. Bone Bioengineering Laboratory, Department of Biomedical Engineering, Columbia University, New York, NY, USA;2. Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, USA;1. Department of Biomedical Engineering, Lund University, Lund, Sweden;2. Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden;1. Laboratory of Genetic Metabolic Diseases, Department of Clinical Chemistry and Pediatrics, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105, AZ, Amsterdam, The Netherlands;2. Department of Pediatrics and Amsterdam Lysosome Centre “Sphinx”, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105, AZ, Amsterdam, The Netherlands;3. Department of Oral Cell Biology ACTA, University of Amsterdam and VU University Amsterdam, Research Institute MOVE, Gustav Mahlerlaan 3004, 1081, LA, Amsterdam, The Netherlands;4. Toin H. van Kuppevelt: Department of Biochemistry, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Postbus 9101, 6500, HB, Nijmegen, The Netherlands;1. Pennsylvania State University, Department of Kinesiology, Noll Laboratory, University Park, PA 16802, United States;2. University of Waterloo, Department of Kinesiology, 200 University Ave W, Waterloo, ON, N2L 3G1, Canada;3. University of Nebraska, Department of Nutrition and Health Sciences, Lincoln, NE 68583, United States;1. Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA;2. Department of Biomedical Engineering, Indiana University–Purdue University at Indianapolis, Indianapolis, IN, USA;3. Richard L. Roudebush VA Medical Center, Indianapolis, IN, USA;1. Department of Internal Medicine, Divison of Endocrinology and Diabetology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria;2. Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria;3. Department of Surgery, Division of Transplantation Surgery, Medical University of Graz, Auenbruggerplatz 29, 8036 Graz, Austria;4. Joanneum Research Health, Elisabethstrasse 5, 8010 Graz, Austria;1. Research Centre “E. Piaggio”, Faculty of Engineering, University of Pisa, Largo Lucio Lazzarino, 2, 56126 Pisa, Italy;2. Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, Via Tronto 10/a, 60126 Ancona, Italy |
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| Abstract: | Postmenopausal women with vertebral fractures have abnormal bone microarchitecture at the distal radius and tibia by HR-pQCT, independent of areal BMD. However, whether trabecular plate and rod microarchitecture is altered in women with vertebral fractures is unknown. This study aims to characterize the abnormalities of trabecular plate and rod microarchitecture, cortex, and bone stiffness in postmenopausal women with vertebral fractures. HR-pQCT images of distal radius and tibia were acquired from 45 women with vertebral fractures and 45 control subjects without fractures. Trabecular and cortical compartments were separated by an automatic segmentation algorithm and subjected to individual trabecula segmentation (ITS) analysis for measuring trabecular plate and rod morphology and cortical bone evaluation for measuring cortical thickness and porosity, respectively. Whole bone and trabecular bone stiffness were estimated by finite element analysis. Fracture and control subjects did not differ according to age, race, body mass index, osteoporosis risk factors, or medication use. Women with vertebral fractures had thinner cortices, and larger trabecular area compared to the control group. By ITS analysis, fracture subjects had fewer trabecular plates, less axially aligned trabeculae and less trabecular connectivity at both the radius and the tibia. Fewer trabecular rods were observed at the radius. Whole bone stiffness and trabecular bone stiffness were 18% and 22% lower in women with vertebral fractures at the radius, and 19% and 16% lower at the tibia, compared with controls. The estimated failure load of the radius and tibia were also reduced in the fracture subjects by 13% and 14%, respectively. In summary, postmenopausal women with vertebral fractures had both trabecular and cortical microstructural deterioration at the peripheral skeleton, with a preferential loss of trabecular plates and cortical thinning. These microstructural deficits translated into lower whole bone and trabecular bone stiffness at the radius and tibia. Our results suggest that abnormalities in trabecular plate and rod microstructure may be important mechanisms of vertebral fracture in postmenopausal women. |
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