ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2010
Genetically determined phenotype covariation networks control bone strength.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Hdac3 regulates bone modeling by suppressing osteoclast responsiveness to RANKL.The Journal of biological chemistry · 2020Article
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- Advanced Genetic Approaches in Discovery and Characterization of Genes Involved With Osteoporosis in Mouse and Human.Frontiers in genetics · 2019Review
- Femoral Neck External Size but not aBMD Predicts Structural and Mass Changes for Women Transitioning Through Menopause.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- The development of inter-strain variation in cortical and trabecular traits during growth of the mouse lumbar vertebral body.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017Article
- Spontaneous destructive periodontitis and skeletal bone damage in transgenic mice carrying a human shared epitope-codingRMD open · 2016Article
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- Genetic regulation of bone strength: a review of animal model studies.BoneKEy reports · 2015Review
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- Biological regulation of bone quality.Current osteoporosis reports · 2014Review
- Characterization of complex, co-adapted skeletal biomechanics phenotypes: a needed paradigm shift in the genetics of bone structure and function.Current osteoporosis reports · 2014Article
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- Systematic evaluation of skeletal mechanical function.Current protocols in mouse biology · 2013Article
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- Functional interactions among morphologic and tissue quality traits define bone quality.Clinical orthopaedics and related research · 2011Review
- Smaller, weaker, and less stiff bones evolve from changes in subsistence strategy.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2011Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
To identify genes affecting bone strength, we studied how genetic variants regulate components of a phenotypic covariation network that was previously shown to accurately characterize the compensatory trait interactions involved in functional adaptation during growth. Quantitative trait loci (QTLs) regulating femoral robustness, morphologic compensation, and mineralization (tissue quality) were mapped at three ages during growth using AXB/BXA Recombinant Inbred (RI) mouse strains and adult B6-i(A) Chromosome Substitution Strains (CSS). QTLs for robustness were identified on chromosomes 8, 12, 18, and 19 and confirmed at all three ages, indicating that genetic variants established robustness postnatally without further modification. A QTL for morphologic compensation, which was measured as the relationship between cortical area and body weight, was identified on chromosome 8. This QTL limited the amount of bone formed during growth and thus acted as a setpoint for diaphyseal bone mass. Additional QTLs were identified from the CSS analysis. QTLs for robustness and morphologic compensation regulated bone structure independently (ie, in a nonpleiotropic manner), indicating that each trait may be targeted separately to individualize treatments aiming to improve strength. Multiple regression analyses showed that variation in morphologic compensation and tissue quality, not bone size, determined femoral strength relative to body weight. Thus an individual inheriting slender bones will not necessarily inherit weak bones unless the individual also inherits a gene that impairs compensation. This systems genetic analysis showed that genetically determined phenotype covariation networks control bone strength, suggesting that incorporating functional adaptation into genetic analyses will advance our understanding of the genetic basis of bone strength.
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