GH deficiency is believed to adversely impair skeletal health. In this study bone mass and architecture was assessed using DXA & pQCT. 30 GHD adults (peak GH to stimulation 0.33 to 2.4 mcg/l), 24 GHI adults (peak GH 1.6 to 6.7 mcg/l), and 30 controls comprised the study population.
BMD (areal and volumetric), bone size, and architecture, were not significantly different from those of control subjects in either the GHD or GHI, AO groups. CO GHD adults DXA values (g/cm2) were reduced at the lumbar spine (P = 0.002) and total hip (P < 0.001). At the 4% pQCT site total and cortical/subcortical (g/cm,3 p = 0.001), but not trabecular BMD was lower than control subjects. Total, cortical, and trabecular area were not significantly different from values in controls at the 4% pQCT site. At the 50% site cortical density was 1.9% lower than control subjects (p = 0.045). There was a 19.9% reduction in cortical thickness (p < 0.001) and 23.4% reduction in cortical cross-sectional area (p < 0.001) that contributed to an overall 24.6% reduction in cortical content (p < 0.001). In CO GHI adults DXA measures of BMD (Z-scores) were reduced at the lumbar spine (p < 0.001), femoral neck (p = 0.029), and total hip (p = 0.045). At the 4% pQCT site CO GHI adults were shown to have reduced cortical/subcortical density (p = 0.034), but normal trabecular density. At the 50% pQCT slice all values for volumetric bone density, bone size, and architecture for the CO GHI adults were intermediate between CO GHD adults and control subjects.
This study shows AO GHD adults have normal bone density and architecture, and that lesser degrees of GH deficiency (GHI) of either AO or CO have negligible impact on the skeleton. The reduced bone density of CO GHD adults is accounted for primarily by reduced cortical thickness, whilst volumetric bone density is relatively maintained.