Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy

Mohammed P. Akhter, L. K L Jung

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1258-1262
Number of pages5
JournalRheumatology
Volume46
Issue number8
DOIs
StatePublished - Aug 2007

Fingerprint

Transgenic Rats
Spondylarthropathies
HLA-B27 Antigen
Bone and Bones
Femur
Osteoporosis
Genetically Modified Animals
Metabolic Bone Diseases
Femur Neck
Spine
Tomography
Equipment and Supplies

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Rheumatology

Cite this

Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy. / Akhter, Mohammed P.; Jung, L. K L.

In: Rheumatology, Vol. 46, No. 8, 08.2007, p. 1258-1262.

Research output: Contribution to journalArticle

@article{927c36d70e37434ebee59bbdc7442b67,
title = "Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy",
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.",
author = "Akhter, {Mohammed P.} and Jung, {L. K L}",
year = "2007",
month = "8",
doi = "10.1093/rheumatology/kem104",
language = "English",
volume = "46",
pages = "1258--1262",
journal = "Rheumatology",
issn = "1462-0324",
publisher = "Oxford University Press",
number = "8",

}

TY - JOUR

T1 - Decreased bone strength in HLA-B27 transgenic rat model of spondyloarthropathy

AU - Akhter, Mohammed P.

AU - Jung, L. K L

PY - 2007/8

Y1 - 2007/8

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=34547840157&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34547840157&partnerID=8YFLogxK

U2 - 10.1093/rheumatology/kem104

DO - 10.1093/rheumatology/kem104

M3 - Article

VL - 46

SP - 1258

EP - 1262

JO - Rheumatology

JF - Rheumatology

SN - 1462-0324

IS - 8

ER -