Specialization for a locomotor behaviour may affect limb bone morphology throughout ontogeny. Ontogenetic development of the limb skeletons of two mammalian species, which are behaviourally specialized for the half-bounding gait (Chinchilla lanigera and Oryctolagus cuniculus), were compared to two similarly-sized species which are not specialized for half-bounding (Rattus norvegicus and Monodelphis domestica). Limb bone lengths and anteroposterior diameters (mediolateral diameters for the radius and metacarpal) were measured from radiographs taken throughout the ontogeny of each species. Body mass was also measured repeatedly during growth. Bone measurements were regressed against body mass, as well as forelimb bone length vs serially homologous hindlimb bone length, bone length vs total limb length and bone length vs width. Similar comparisons were made among adults of each species using ratios. Although there were many significant differences among species, overall there were few consistent differences in adult scaling ratios or ontogenetic allometry slopes between specialized and generalized groups. Adult specialized half-bounders had significantly narrower tibiae and metatarsals than the gait-generalized runners. Specialized half-bounders usually had similar slopes for hindlimb length vs width ontogenetic comparisons, but the non-specialized species did not group together. However, there were two patterns that occurred among all four species: (1) hindlimb bone lengths nearly always grew faster than the serially homologous forelimb bone lengths in all species; (2) proximal elements usually increased in length proportionally faster than distal elements. In conclusion, small mammals may share strong developmental constraints that govern their relative growth rates. It is also likely that there are different selective pressures on juveniles and adults, but that these selective pressures may not be different between specialized and unspecialized runners during ontogeny.

Adequate provision of nutrients composing the bone matrix and regulating bone metabolism should be provided from birth in order to achieve maximal bone mass, compatible with individual genetic background, and to prevent osteoporosis later in life. Low calcium intake (<250 mg day−1) in children is associated with both a reduced bone mineral content and hyperparathyroidism. Optimal calcium intake is, however, still a matter of controversy. The minimisation of fracture risk would be the ideal functional outcome on which to evaluate lifetime calcium intakes, but proxy indicators, such as bone mass measurements or maximal calcium retention, are used instead. Calcium recommendations in Europe and the United States are based on different concepts as to requirements, leading to somewhat different interpretations of dietary adequacy. Minerals and trace elements other than calcium are involved in skeletal growth, some of them as matrix constituents, such as magnesium and fluoride, others as components of enzymatic systems involved in matrix turnover, such as zinc, copper and manganese. Vitamins also play a role in calcium metabolism (e.g. vitamin D) or as co-factors of key enzymes for skeletal metabolism (e.g. vitamins C and K). Physical activity has different effects on bone depending on its intensity, frequency, duration and the age at which it is started. The anabolic effect on bone is greater in adolescence and as a result of weight-bearing exercise. Adequate intakes of calcium appear necessary for exercise to have its bone stimulating action.

Angiogenesis is essential for the replacement of cartilage by bone during growth and repair. In order to obtain a better understanding of the mechanisms regulating vascular invasion at sites of endochondral ossification we have investigated the expression of the endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), by chondrocytes in human neonatal growth plates. VEGF was absent from chondrocytes in the resting zone and only weakly expressed by occasional chondrocytes in the proliferating region. In the hypertrophic zone the number of chondrocytes stained and the intensity of staining for VEGF increased with chondrocyte hypertrophy, maximum expression of VEGF being observed in chondrocytes in the lower hypertrophic and mineralised regions of the cartilage. These observations provide the first demonstration of the presence of VEGF in situ in developing human bone and are consistent with in vitro observations demonstrating the upregulation of proangiogenic growth factor production with increasing chondrocyte hypertrophy. The presence of numerous small blood vessels and vascular structures in the subchondral region where VEGF expression was maximal indicates that VEGF produced by hypertrophic chondrocytes may play a key role in the regulation of vascular invasion of the growth plate.