Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy
Objective. To investigate the nature of osteopenia/osteoporosis in spondyloarthropathy, an inflammatory disorder, using the HLA-B27 transgenic rat model. Methods. HLA-B27 transgenic rats were housed individually and sacrificed at the peak of their disease (8-month-old). The spine and femurs were rem...
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Veröffentlicht in: | Rheumatology (Oxford, England) England), 2007-08, Vol.46 (8), p.1258-1262 |
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description | Objective. To investigate the nature of osteopenia/osteoporosis in spondyloarthropathy, an inflammatory disorder, using the HLA-B27 transgenic rat model. Methods. HLA-B27 transgenic rats were housed individually and sacrificed at the peak of their disease (8-month-old). The spine and femurs were removed and stored in saline at −20°C until analysis. The bone structure and strength were determined using a micro-computed tomography (micro-CT) device (Scanco Medical) and mechanical testing (Instron 5543). Vertebral bodies and femurs were scanned to determine trabecular structural properties in terms of bone volume (BV/TV), trabecular thickness, and spacing. After scanning, the mid-shaft femurs were subjected to a 3-point bending test (along anterior-posterior direction), the femoral necks were tested in bending, and the vertebral bodies (L4) were tested in compression. Structural (ultimate/yield load, stiffness) and apparent material (ultimate/yield stress, modulus) strength parameters were then determined. Results. The majority of the bone structural and strength parameters were significantly lower (P < 0.05) in the HLA-B27 transgenic rats as compared with control littermates. Micro-CT data suggested that the transgenic animals had lower BV/TV and trabecular thickness in their vertebral bodies. The poor trabecular structure observed in HLA-B27 rats is also indicative of the poor biomechanical strength properties in the vertebral bodies as well. Conclusion. The HLA-B27 transgenic rats develop bone fragility similar to that seen in spondyloarthropathy and may be an important model for the study of osteoporosis in spondyloarthropathy. |
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fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70736983</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/rheumatology/kem104</oup_id><sourcerecordid>70736983</sourcerecordid><originalsourceid>FETCH-LOGICAL-c513t-f42eb96e71887207bd16e8e88c4ce0abefbbd4e5647cd8573783ae1d42a7c96c3</originalsourceid><addsrcrecordid>eNqN0U1v1DAQBmALUdGy8AuQkIUEt7T-SGzn2G5pF2lVQAKBuFiOM9lNm8Sp7Ujdf4-rrNqKS7nYPjzv2J5B6B0lx5SU_MRvYepNdJ3b7E5uoKckf4GOaC5YRjhnLx_OLD9Er0O4JoQUlKtX6JDKgomSySN0dQ7WgwlQ48oNgEP0MGziFrcDXq1PszMmcfRmCBsYWou9ibh3NXTYNTiMbqh3nTM-br0bTdzu3qCDxnQB3u73Bfp58fnHcpWtv15-WZ6uM5teELMmZ1CVAiRVSjIiq5oKUKCUzS0QU0FTVXUOhcilrVUhuVTcAK1zZqQtheUL9GmuO3p3O0GIum-Dha4zA7gpaEkkF6Xiz0JaqnsnEvzwD7x2kx_SJ5IphKBFThPiM7LeheCh0aNve-N3mhJ9PxT9dCh6HkpKvd-Xnqoe6sfMfgoJfNwDE6zpmtRv24ZHp0rOSVoW6Hh2bhr_8-ZsDrQhwt1DxPgbLVJTC736_Ud_56vzs1-XS_2N_wXjQLkW</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>195661541</pqid></control><display><type>article</type><title>Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy</title><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Akhter, M. P. ; Jung, L. K. L.</creator><creatorcontrib>Akhter, M. P. ; Jung, L. K. L.</creatorcontrib><description>Objective. To investigate the nature of osteopenia/osteoporosis in spondyloarthropathy, an inflammatory disorder, using the HLA-B27 transgenic rat model. Methods. HLA-B27 transgenic rats were housed individually and sacrificed at the peak of their disease (8-month-old). The spine and femurs were removed and stored in saline at −20°C until analysis. The bone structure and strength were determined using a micro-computed tomography (micro-CT) device (Scanco Medical) and mechanical testing (Instron 5543). Vertebral bodies and femurs were scanned to determine trabecular structural properties in terms of bone volume (BV/TV), trabecular thickness, and spacing. After scanning, the mid-shaft femurs were subjected to a 3-point bending test (along anterior-posterior direction), the femoral necks were tested in bending, and the vertebral bodies (L4) were tested in compression. Structural (ultimate/yield load, stiffness) and apparent material (ultimate/yield stress, modulus) strength parameters were then determined. Results. The majority of the bone structural and strength parameters were significantly lower (P < 0.05) in the HLA-B27 transgenic rats as compared with control littermates. Micro-CT data suggested that the transgenic animals had lower BV/TV and trabecular thickness in their vertebral bodies. The poor trabecular structure observed in HLA-B27 rats is also indicative of the poor biomechanical strength properties in the vertebral bodies as well. Conclusion. The HLA-B27 transgenic rats develop bone fragility similar to that seen in spondyloarthropathy and may be an important model for the study of osteoporosis in spondyloarthropathy.</description><identifier>ISSN: 1462-0324</identifier><identifier>EISSN: 1462-0332</identifier><identifier>DOI: 10.1093/rheumatology/kem104</identifier><identifier>PMID: 17526927</identifier><identifier>CODEN: BJRHDF</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Animals, Genetically Modified ; Biological and medical sciences ; Bone ; Bone strength ; Compressive Strength ; Disease Models, Animal ; Diseases of the osteoarticular system ; Elasticity ; Femur ; Femur - physiopathology ; HLA-B27 Antigen - genetics ; Inflammatory joint diseases ; Lumbar Vertebrae - physiopathology ; Male ; Medical sciences ; Osteoporosis - etiology ; Osteoporosis - genetics ; Osteoporosis - physiopathology ; Rats ; Spondylarthropathies - complications ; Spondylarthropathies - genetics ; Spondylarthropathies - physiopathology ; Spondyloarthropathy ; Stiffness ; Stress, Mechanical ; Transgenic rat ; Vertebral body</subject><ispartof>Rheumatology (Oxford, England), 2007-08, Vol.46 (8), p.1258-1262</ispartof><rights>The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2007</rights><rights>2007 INIST-CNRS</rights><rights>The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-f42eb96e71887207bd16e8e88c4ce0abefbbd4e5647cd8573783ae1d42a7c96c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1584,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18933089$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17526927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Akhter, M. P.</creatorcontrib><creatorcontrib>Jung, L. K. L.</creatorcontrib><title>Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy</title><title>Rheumatology (Oxford, England)</title><addtitle>Rheumatology (Oxford)</addtitle><description>Objective. To investigate the nature of osteopenia/osteoporosis in spondyloarthropathy, an inflammatory disorder, using the HLA-B27 transgenic rat model. Methods. HLA-B27 transgenic rats were housed individually and sacrificed at the peak of their disease (8-month-old). The spine and femurs were removed and stored in saline at −20°C until analysis. The bone structure and strength were determined using a micro-computed tomography (micro-CT) device (Scanco Medical) and mechanical testing (Instron 5543). Vertebral bodies and femurs were scanned to determine trabecular structural properties in terms of bone volume (BV/TV), trabecular thickness, and spacing. After scanning, the mid-shaft femurs were subjected to a 3-point bending test (along anterior-posterior direction), the femoral necks were tested in bending, and the vertebral bodies (L4) were tested in compression. Structural (ultimate/yield load, stiffness) and apparent material (ultimate/yield stress, modulus) strength parameters were then determined. Results. The majority of the bone structural and strength parameters were significantly lower (P < 0.05) in the HLA-B27 transgenic rats as compared with control littermates. Micro-CT data suggested that the transgenic animals had lower BV/TV and trabecular thickness in their vertebral bodies. The poor trabecular structure observed in HLA-B27 rats is also indicative of the poor biomechanical strength properties in the vertebral bodies as well. Conclusion. The HLA-B27 transgenic rats develop bone fragility similar to that seen in spondyloarthropathy and may be an important model for the study of osteoporosis in spondyloarthropathy.</description><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Biological and medical sciences</subject><subject>Bone</subject><subject>Bone strength</subject><subject>Compressive Strength</subject><subject>Disease Models, Animal</subject><subject>Diseases of the osteoarticular system</subject><subject>Elasticity</subject><subject>Femur</subject><subject>Femur - physiopathology</subject><subject>HLA-B27 Antigen - genetics</subject><subject>Inflammatory joint diseases</subject><subject>Lumbar Vertebrae - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Osteoporosis - etiology</subject><subject>Osteoporosis - genetics</subject><subject>Osteoporosis - physiopathology</subject><subject>Rats</subject><subject>Spondylarthropathies - complications</subject><subject>Spondylarthropathies - genetics</subject><subject>Spondylarthropathies - physiopathology</subject><subject>Spondyloarthropathy</subject><subject>Stiffness</subject><subject>Stress, Mechanical</subject><subject>Transgenic rat</subject><subject>Vertebral body</subject><issn>1462-0324</issn><issn>1462-0332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0U1v1DAQBmALUdGy8AuQkIUEt7T-SGzn2G5pF2lVQAKBuFiOM9lNm8Sp7Ujdf4-rrNqKS7nYPjzv2J5B6B0lx5SU_MRvYepNdJ3b7E5uoKckf4GOaC5YRjhnLx_OLD9Er0O4JoQUlKtX6JDKgomSySN0dQ7WgwlQ48oNgEP0MGziFrcDXq1PszMmcfRmCBsYWou9ibh3NXTYNTiMbqh3nTM-br0bTdzu3qCDxnQB3u73Bfp58fnHcpWtv15-WZ6uM5teELMmZ1CVAiRVSjIiq5oKUKCUzS0QU0FTVXUOhcilrVUhuVTcAK1zZqQtheUL9GmuO3p3O0GIum-Dha4zA7gpaEkkF6Xiz0JaqnsnEvzwD7x2kx_SJ5IphKBFThPiM7LeheCh0aNve-N3mhJ9PxT9dCh6HkpKvd-Xnqoe6sfMfgoJfNwDE6zpmtRv24ZHp0rOSVoW6Hh2bhr_8-ZsDrQhwt1DxPgbLVJTC736_Ud_56vzs1-XS_2N_wXjQLkW</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Akhter, M. P.</creator><creator>Jung, L. K. L.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7QO</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20070801</creationdate><title>Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy</title><author>Akhter, M. P. ; Jung, L. K. L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-f42eb96e71887207bd16e8e88c4ce0abefbbd4e5647cd8573783ae1d42a7c96c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Biological and medical sciences</topic><topic>Bone</topic><topic>Bone strength</topic><topic>Compressive Strength</topic><topic>Disease Models, Animal</topic><topic>Diseases of the osteoarticular system</topic><topic>Elasticity</topic><topic>Femur</topic><topic>Femur - physiopathology</topic><topic>HLA-B27 Antigen - genetics</topic><topic>Inflammatory joint diseases</topic><topic>Lumbar Vertebrae - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Osteoporosis - etiology</topic><topic>Osteoporosis - genetics</topic><topic>Osteoporosis - physiopathology</topic><topic>Rats</topic><topic>Spondylarthropathies - complications</topic><topic>Spondylarthropathies - genetics</topic><topic>Spondylarthropathies - physiopathology</topic><topic>Spondyloarthropathy</topic><topic>Stiffness</topic><topic>Stress, Mechanical</topic><topic>Transgenic rat</topic><topic>Vertebral body</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Akhter, M. P.</creatorcontrib><creatorcontrib>Jung, L. K. L.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Rheumatology (Oxford, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Akhter, M. P.</au><au>Jung, L. K. L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy</atitle><jtitle>Rheumatology (Oxford, England)</jtitle><addtitle>Rheumatology (Oxford)</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>46</volume><issue>8</issue><spage>1258</spage><epage>1262</epage><pages>1258-1262</pages><issn>1462-0324</issn><eissn>1462-0332</eissn><coden>BJRHDF</coden><abstract>Objective. To investigate the nature of osteopenia/osteoporosis in spondyloarthropathy, an inflammatory disorder, using the HLA-B27 transgenic rat model. Methods. HLA-B27 transgenic rats were housed individually and sacrificed at the peak of their disease (8-month-old). The spine and femurs were removed and stored in saline at −20°C until analysis. The bone structure and strength were determined using a micro-computed tomography (micro-CT) device (Scanco Medical) and mechanical testing (Instron 5543). Vertebral bodies and femurs were scanned to determine trabecular structural properties in terms of bone volume (BV/TV), trabecular thickness, and spacing. After scanning, the mid-shaft femurs were subjected to a 3-point bending test (along anterior-posterior direction), the femoral necks were tested in bending, and the vertebral bodies (L4) were tested in compression. Structural (ultimate/yield load, stiffness) and apparent material (ultimate/yield stress, modulus) strength parameters were then determined. Results. The majority of the bone structural and strength parameters were significantly lower (P < 0.05) in the HLA-B27 transgenic rats as compared with control littermates. Micro-CT data suggested that the transgenic animals had lower BV/TV and trabecular thickness in their vertebral bodies. The poor trabecular structure observed in HLA-B27 rats is also indicative of the poor biomechanical strength properties in the vertebral bodies as well. Conclusion. The HLA-B27 transgenic rats develop bone fragility similar to that seen in spondyloarthropathy and may be an important model for the study of osteoporosis in spondyloarthropathy.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>17526927</pmid><doi>10.1093/rheumatology/kem104</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Animals, Genetically Modified Biological and medical sciences Bone Bone strength Compressive Strength Disease Models, Animal Diseases of the osteoarticular system Elasticity Femur Femur - physiopathology HLA-B27 Antigen - genetics Inflammatory joint diseases Lumbar Vertebrae - physiopathology Male Medical sciences Osteoporosis - etiology Osteoporosis - genetics Osteoporosis - physiopathology Rats Spondylarthropathies - complications Spondylarthropathies - genetics Spondylarthropathies - physiopathology Spondyloarthropathy Stiffness Stress, Mechanical Transgenic rat Vertebral body |
title | Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy |
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