Bone Structure at the Distal Radius During Adolescent Growth

Abstract

The incidence of distal forearm fractures peaks during the adolescent growth spurt, but the structural basis for this is unclear. Thus, we studied healthy 6-to 21-yr-old girls (n = 66) and boys (n = 61) using high-resolution pQCT (voxel size, 82 mm) at the distal radius. Subjects were classified into five groups by bone-age: group I (prepuberty, 6-8 yr), group II (early puberty, 9-11 yr), group III (midpuberty, 12-14 yr), group IV (late puberty, 15-17 yr), and group V (postpuberty, 18-21 yr). Compared with group I, trabecular parameters (bone volume fraction, trabecular number, and thickness) did not change in girls but increased in boys from late puberty onward. Cortical thickness and density decreased from pre-to midpuberty in girls but were unchanged in boys, before rising to higher levels at the end of puberty in both sexes. Total bone strength, assessed using microfinite element models, increased linearly across bone age groups in both sexes, with boys showing greater bone strength than girls after midpuberty. The proportion of load borne by cortical bone, and the ratio of cortical to trabecular bone volume, decreased transiently during mid-to late puberty in both sexes, with apparent cortical porosity peaking during this time. This mirrors the incidence of distal forearm fractures in prior studies. We conclude that regional deficits in cortical bone may underlie the adolescent peak in forearm fractures. Whether these deficits are more severe in children who sustain forearm fractures or persist into later life warrants further study.

Rapid growth produces transient cortical weakness: A risk factor for metaphyseal fractures during puberty

“…This relative delay produces incomplete coalescence of trabeculae on the endocortical surface leaving cortical porosity and a reduction in vBMD of cortical bone of the distal radial metaphysis but not so at the distal tibial metaphysis because of regional difference in growth velocity. (6,7) This view is supported by a data from a recent study by Kirmani et al (24) Thus, this temporary decrease in cortical thickness and cortical vBMD is likely the result of incomplete consolidation by bone formation on adjacent trabecular surfaces. Finding lower cortical vBMD at more distal sites of the metaphyses (adjacent to the growth plate) than distally (adjacent to the diaphysis) and greater proximal-distal cortical vBMD difference at the site of more rapid growth (distal radius) than site of slower growth (distal tibia) support this view and is consistent with the report by Tanck et al (12) However, the distal-proximal difference was likely overestimated due to partial volume effect which underestimated the cortical vBMD more at the distal than at the proxmial site because of their difference in cortical thickness.…”

“…In late puberty, cortical vBMD and thickness increased, probably due to reduced porosity. (24) We suggest that this is the result of slowing of external bone growth while trabeculae coalescence continues as bone formation proceeds on trabecular surfaces. Earlier exposure to sex steroids in peri-and post-pubertal girls may enhance the consolidation of metaphyseal cortex at the endocortical surface decreasing the residual cortical porosity.…”

“…(9,10,24,25) However, the morphological basis for this reduction has not been reported. The data presented here suggest the dissociation between growth in size and mineral accrual is accompanied by the occurrence of thinner cortex with lower cortical vBMD.…”

The mutual dependence between bone and gonads

“…They are, at least in part, responsible for the gender differences in bone growth, which emerges during adolescence (Riggs et al 2002, Vanderschueren et al 2004, Clarke & Khosla 2010. Although skeletal size and volume are similar in prepubertal girls and boys (Kelly et al 1990, Seeman 2001, Vanderschueren et al 2004, Kirmani et al 2009, Callewaert et al 2010a, the sexual dimorphism in bone growth becomes apparent during puberty, at which time men reach higher peak bone mass (Clarke & Khosla 2010). This skeletal sexual dimorphism is mainly due to a stimulatory androgen action on periosteal bone formation in men, whereas an inhibitory estrogen-related action occurs in women (Bertelloni et al 1995, Finkelstein et al 1996, Katznelson et al 1996, Seeman 2001, Venken et al 2006, Kirmani et al 2009).…”

“…Although skeletal size and volume are similar in prepubertal girls and boys (Kelly et al 1990, Seeman 2001, Vanderschueren et al 2004, Kirmani et al 2009, Callewaert et al 2010a, the sexual dimorphism in bone growth becomes apparent during puberty, at which time men reach higher peak bone mass (Clarke & Khosla 2010). This skeletal sexual dimorphism is mainly due to a stimulatory androgen action on periosteal bone formation in men, whereas an inhibitory estrogen-related action occurs in women (Bertelloni et al 1995, Finkelstein et al 1996, Katznelson et al 1996, Seeman 2001, Venken et al 2006, Kirmani et al 2009). Since an excess of androgen in women is associated with higher bone mineral density, there is evidence that androgens also affect peak bone mass in women (Buchanan et al 1988, Zborowski et al 2000, Wei et al 2010.…”