Spontaneous vertebral fractures are a common occurrence in modern humans, yet these fractures are not documented in other hominoids. Differences in vertebral bone strength between humans and apes associated with trabecular bone microarchitecture may contribute to differences in fracture incidence. We used microcomputed tomography to examine trabecular bone microarchitecture in the T8 vertebra of extant young adult hominoids. Scaled volumes of interest from the anterior vertebral body were analyzed at a resolution of 46 lm, and bone volume fraction, trabecular thickness, trabecular number, trabecular separation, structure model index, and degree of anisotropy were compared among species. As body mass increased, so did trabecular thickness, but bone volume fraction, structure model index, and degree of anisotropy were independent of body mass. Bone volume fraction was not significantly different between the species. Degree of anisotropy was not significantly different among the species, suggesting similarity of loading patterns in the T8 vertebra due to similar anatomical and postural relationships within each species' spine. Degree of anisotropy was negatively correlated with bone volume fraction (r 2 ¼ 0.85, P < 0.05) in humans, whereas the apes demonstrated no such relationship. This suggested that less dense human trabecular bone was more preferentially aligned to habitual loading. Furthermore, we theorize that trabeculae in ape thoracic vertebrae would not be expected to become preferentially aligned if bone volume fraction was decreased. The differing relationship between bone volume fraction and degree of anisotropy in humans and apes may cause less dense human bone to be more fragile than less dense ape bone. Anat Rec, 292:1098Rec, 292: -1106Rec, 292: , 2009. V V C 2009 Wiley-Liss, Inc.

The size and shape of human cervical vertebral bodies serve as a reference for measurement or treatment planning in multiple disciplines. It is therefore necessary to understand thoroughly the developmental changes in the cervical vertebrae in relation to the changing biomechanical demands on the neck during the first two decades of life. To delineate sex‐specific changes in human cervical vertebral bodies, 23 landmarks were placed in the midsagittal plane to define the boundaries of C2 to C7 in 123 (73 M; 50 F) computed tomography scans from individuals, ages 6 months to 19 years. Size was calculated as the geometric area, from which sex‐specific growth trend, rate, and type for each vertebral body were determined, as well as length measures of local deformation‐based morphometry vectors from the centroid to each landmark. Additionally, for each of the four pubertal‐staged age cohorts, sex‐specific vertebral body wireframes were superimposed using generalized Procrustes analysis to determine sex‐specific changes in form (size and shape) and shape alone. Our findings reveal that C2 was unique in achieving more of its adult size by 5 years, particularly in females. In contrast, C3–C7 had a second period of accelerated growth during puberty. The vertebrae of males and females were significantly different in size, particularly after puberty, when males had larger cervical vertebral bodies. Male growth outpaced female growth around age 10 years and persisted until around age 19–20 years, whereas females completed growth earlier, around age 17–18 years. The greatest shape differences between males and females occurred during puberty. Both sexes had similar growth in the superoinferior height, but males also displayed more growth in anteroposterior depth. Such prominent sex differences in size, shape, and form are likely the result of differences in growth rate and growth duration. Female vertebrae are thus not simply smaller versions of the male vertebrae. Additional research is needed to further quantify growth and help improve age‐ and sex‐specific guidance in clinical practice.

The field of evolutionary medicine examines the possibility that some diseases are the result of trade-offs made in human evolution. Spinal fractures are the most common osteoporosis-related fracture in humans, but are not observed in apes, even in cases of severe osteopenia. In humans, the development of osteoporosis is influenced by peak bone mass and strength in early adulthood as well as age-related bone loss. Here, we examine the structural differences in the vertebral bodies (the portion of the vertebra most commonly involved in osteoporosis-related fractures) between humans and apes before age-related bone loss occurs. Vertebrae from young adult humans and chimpanzees, gorillas, orangutans, and gibbons (T8 vertebrae, n = 8–14 per species, male and female, humans: 20–40 years of age) were examined to determine bone strength (using finite element models), bone morphology (external shape), and trabecular microarchitecture (micro-computed tomography). The vertebrae of young adult humans are not as strong as those from apes after accounting for body mass (p<0.01). Human vertebrae are larger in size (volume, cross-sectional area, height) than in apes with a similar body mass. Young adult human vertebrae have significantly lower trabecular bone volume fraction (0.26±0.04 in humans and 0.37±0.07 in apes, mean ± SD, p<0.01) and thinner vertebral shells than apes (after accounting for body mass, p<0.01). Since human vertebrae are more porous and weaker than those in apes in young adulthood (after accounting for bone mass), even modest amounts of age-related bone loss may lead to vertebral fracture in humans, while in apes, larger amounts of bone loss would be required before a vertebral fracture becomes likely. We present arguments that differences in vertebral bone size and shape associated with reduced bone strength in humans is linked to evolutionary adaptations associated with bipedalism.

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