Aging-induced osteopenia in avian cortical bone

Cortical bone loss contributes substantially to the degradation of skeletal integrity associated with aging. However, animal models that closely mimic age-related alterations in cortical bone are limited. The objective of this study was to determine if aged rooster cortical bone demonstrates phenoty...

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Bibliographic Details
Published in:Bone (New York, N.Y.) N.Y.), 2000-04, Vol.26 (4), p.361-365
Main Authors: Srinivasan, S., Keilin, S.A., Judex, S., Bray, R.C., Zernicke, R.F., Gross, T.S.
Format: Article
Language:English
Subjects:
Age Factors
Age-related osteopenia
Aging - pathology
Animals
Biological and medical sciences
Bone Diseases, Metabolic - pathology
Bone envelope expansion
Chickens
Cortical bone
Cortical porosity
Diaphyses - pathology
Diseases of the osteoarticular system
Male
Medical sciences
Osteoporosis. Osteomalacia. Paget disease
Periosteum - pathology
Rooster
Ulna - pathology
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Summary:Cortical bone loss contributes substantially to the degradation of skeletal integrity associated with aging. However, animal models that closely mimic age-related alterations in cortical bone are limited. The objective of this study was to determine if aged rooster cortical bone demonstrates phenotypic alterations similar to those observed in aged human cortical bone (i.e., expansion of the endocortical and periosteal envelopes and elevated cortical porosity). When compared with young adult roosters, aged roosters demonstrated significant expansion of the endocortical (16%) and periosteal (10%) envelopes, resulting in significantly increased cross-sectional moments of inertia. In addition, aged rooster bone demonstrated significantly elevated cortical porosity (51%) and average area of porosity (83%). We conclude that rooster bone demonstrates age-related adaptations similar to those of humans at both tissue and cellular levels, and may therefore represent a relatively useful, inexpensive animal model for investigating the mechanisms of age-related bone loss.
ISSN:8756-3282
1873-2763
DOI:10.1016/S8756-3282(00)00237-4