Genetic selection for fast growth generates bone architecture characterised by enhanced periosteal expansion and limited consolidation of the cortices but a diminution in the early responses to mechanical loading.
Bone strength is, in part, dependent on a mechanical input that regulates the (re)modelling of skeletal elements to an appropriate size and architecture to resist fracture during habitual use. The rate of longitudinal bone growth in juveniles can also affect fracture incidence in adulthood, suggesting an influence of growth rate on later bone quality. We have compared the effects of fast and slow growth on bone strength and architecture in the tibiotarsi of embryonic and juvenile birds. The loading-related biochemical responses (intracellular G6PD activity and NO release) to mechanical load were also determined. Further, we have analysed the proliferation and differentiation characteristics of primary tibiotarsal osteoblasts from fast and slow-growing strains. We found that bones from chicks with divergent growth rates display equal resistance to applied loads, but weight-correction revealed that the bones from juvenile fast growth birds are weaker, with reduced stiffness and lower resistance to fracture. Primary osteoblasts from slow-growing juvenile birds proliferated more rapidly and had lower alkaline phosphatase activity. Bones from fast-growing embryonic chicks display rapid radial expansion and incomplete osteonal infilling but, importantly, lack mechanical responsiveness. These findings are further evidence that the ability to respond to mechanical inputs is crucial to adapt skeletal architecture to generate a functionally appropriate bone structure and that fast embryonic and juvenile growth rates may predispose bone to particular architectures with increased fragility in the adult.
Rawlinson
Simon C F
SC
Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Institute of Dentistry, Turner Street, London E1 2AD, UK.
Murray
Dianne H
DH
Mosley
John R
JR
Wright
Chris D P
CD
Bredl
John C
JC
Saxon
Leanne K
LK
Loveridge
Nigel
N
Leterrier
Christine
C
Constantin
Paul
P
Farquharson
Colin
C
Pitsillides
Andrew A
AA
D000818:Animals; D001696:Biomechanical Phenomena; D001846:Bone Development / Q000235:genetics*; D002138:Calibration; D002452:Cell Count; D002454:Cell Differentiation; D049109:Cell Proliferation; D002642:Chick Embryo; D002645:Chickens; D018483:Diaphyses / Q000033:anatomy & histology / Q000254:growth & development; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010006:Osteoblasts / Q000166:cytology / Q000201:enzymology; D010011:Osteocytes / Q000166:cytology; D010521:Periosteum / Q000033:anatomy & histology / Q000254:growth & development* / Q000502:physiology*; D012641:Selection, Genetic; D013314:Stress, Mechanical; D013977:Tibia / Q000033:anatomy & histology / Q000254:growth & development; D016474:Weight-Bearing
D009569:Nitric Oxide; D005954:Glucosephosphate Dehydrogenase