Sexual Dimorphism in Skeletal Size, Density and Strength

Oral presentation: Section A

Long bones grow in length and diameter while the mineralized mass of bone within the periosteal envelope of the long bones is modeled and remodelled though out growth into hollow cylinders with splayed ends containing trabecular bone. These are masterpieces of minimalism, created using the least amount of material needed for optimum yet contradictory function – stiffness for resistance to bending in static loading yet flexibility for energy absorption in dynamic loading, lightness for speed yet strength for loading; features that ensuring the organism can find dinner, rather than be it. BMD increases during the pre and peripubertal years because long bones increase in size. As the bone grows in length and diameter, the mass of bone 'inside' the periosteum increases in proportion to the enlarging volume of the whole bone including the marrow space. This mass of bone is fashioned into a cortex of a given thickness and distance from the neutral axis of the long bone. Volumetric BMD of long bones is independent of age and not different in boys and girls. In young adulthood, men and women have the same volumetric BMD but men have a bigger bone than women. Thus, if the strength of the radius or femur is greater in older than younger children, or greater in males than females, it is due to differences in size, not density. The constancy of volumetric BMD before puberty has important implications. What factors account for the variance in volumetric BMD and the relationship between growth in size and the mass are not known.

The sex difference in leg length is the result of a longer prepubertal period of growth in the male. The difference in height at peak between women and men is primarily in leg length, not trunk length. The absolute and relative movements of the periosteal and endosteal surfaces determine the diameter of the long bone, the mass of cortical bone, cortical thickness, and the distance this cortical mass is placed from neutral axis of the bone. Periosteal apposition increases bone width in boys and girls during prepubertal growth. Most of the increase in cortical thickness is achieved by accelerated periosteal apposition, a process that is likely to be regulated by testosterone directly (via the androgen receptor), growth hormone (GH) and insulin like growth factor 1 (IGF-1). In addition, aromatization of testosterone may influence GH and IGF-1. When females enter puberty, periosteal apposition is inhibited,

Growth produces a bigger not denser skeleton in males and females. Bone fragility in old age begins 9 months before birth by picking the wrong mother and father, it gains expression in the follies of a misspent intrauterine development, youth and the excesses of adulthood, and strikes those forced to endure old age, inheriting its gifts of senility and fractures.

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