Altered bone material properties in HLA-B27 rats include reduced mineral to matrix ratio and altered collagen cross-links.
Spondyloarthropathy and inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, are often associated with severe osteopenia/osteoporosis in both children and adults. HLA-B27 transgenic rats present a phenotype that includes severe colitis and severely accelerated alveolar bone loss. The purpose of this study was to evaluate long bone density status, systemic bone metabolic markers, and intrinsic bone material properties in HLA-B27 transgenic (TG) rats, and compare them with those of age- and sex-matched wild-type (WT) animals. The results indicate that in the HLA-B27 rat, an animal susceptible to both alveolar bone loss (ABL) and long bone osteopenia, there is a statistically significant negative correlation between ABL and long bone bone mineral density (BMD), as well as mineral/matrix ratio at active bone-forming trabecular surfaces. The TG animals had a lower mineral/matrix ratio and higher relative proteoglycan and advanced glycation end product (ϵ-N-Carboxymethyl-L-lysine) content and pyridinoline/divalent collagen cross-link ratio compared with WT. These results may provide better understanding of the interrelationship between osteoporosis and oral bone loss, the underlying causes of the inferior bone strength in the HLA-B27 transgenic animals, and could prove to be a useful model in the elucidation of the pathophysiology of spondyloarthropathy and IBD-associated osteopenia/osteoporosis and in the evaluation of pharmacological intervention(s) against such conditions.
Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK and AUVA Trauma Centre Meidling, 1st Medical Department, Hanusch Hospital, Vienna, Austria.
Sonja
S
Gamsjaeger
Apurva K
AK
Srivastava
Jon E
JE
Wergedal
Jochen
J
Zwerina
Klaus
K
Klaushofer
Eleftherios P
EP
Paschalis
Dimitris N
DN
Tatakis
D016301:Alveolar Bone Loss / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000596:Amino Acids / Q000235:genetics / Q000378:metabolism; D000818:Animals; D015519:Bone Density; D017127:Glycation End Products, Advanced / Q000235:genetics / Q000378:metabolism; D015796:HLA-B27 Antigen / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000150:complications / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010024:Osteoporosis / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D055647:Rats, Transgenic
D000596:Amino Acids; D017127:Glycation End Products, Advanced; D015796:HLA-B27 Antigen; C015484:pyridinoline
Collagen; Genetic animal models; Matrix mineralization