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Abstract Intracortical microstructure influences crack
propagation and arrest within bone cortex. Genetic variation
in intracortical remodeling may contribute to
mechanical integrity and, therefore, fracture risk. Our aim
was to determine the degree to which normal populationlevel
variation in intracortical microstructure is due to
genetic variation. We examined right femurs from 101
baboons (74 females, 27 males; aged 7–33 years) from a
single, extended pedigree to determine osteon number,
osteon area (On.Ar), haversian canal area, osteon population
density, percent osteonal bone (%On.B), wall thickness
(W.Th), and cortical porosity (Ct.Po). Through
evaluation of the covariance in intracortical properties
between pairs of relatives, we quantified the contribution of
additive genetic effects (heritability [h2]) to variation in
these traits using a variance decomposition approach.
Significant age and sex effects account for 9 % (Ct.Po) to
21 % (W.Th) of intracortical microstructural variation.
After accounting for age and sex, significant genetic effects
are evident for On.Ar (h2 = 0.79, p = 0.002), %On.B
(h2 = 0.82, p = 0.003), and W.Th (h2 = 0.61, p = 0.013),
indicating that 61–82 % of the residual variation (after
accounting for age and sex effects) is due to additive
genetic effects. This corresponds to 48–75 % of the total
phenotypic variance. Our results demonstrate that normal,
population-level variation in cortical microstructure is
significantly influenced by genes. As a critical mediator of
crack behavior in bone cortex, intracortical microstructural
variation provides another mechanism through which
genetic variation may affect fracture risk.
Keywords Primate  Osteoporosis  Biomechanics 
Population studies  Bone histomorphometry