Higher BMC and areal BMD in children and grandchildren of individuals with hip or knee replacement.

The relationship between aBMD and osteoarthritis (OA) remains unclear. We compared aBMD, BMC and bone size among children and grandchildren of Hutterites with hip or knee replacement (n=23 each) to children and grandchildren of age- and sex-matched controls (178 children and 267 grandchildren). There were no differences in anthropometric measures or activity levels between case and control probands, but femoral neck (FN) and spine (LS) aBMD and Z-scores were greater in cases than controls (0.89 vs. 0.80 g/cm2; 1.15 vs. 1.03 g/cm2; 1.5 vs. 0.8; 2.4 vs. 1.2: all p<0.05). Hip, FN and LS aBMD (1.05 vs. 0.97, 0.92 vs. 0.84, 1.15 vs. 1.03 g/cm2), BMC (34.1 vs. 32.0, 4.58 vs. 4.27, 69.5 vs. 62.4 g) and Z-scores (1.0 vs. 0.4; 0.9 vs. 0.2; 1.3 vs. 0.2) were greater in daughters of cases than controls (hip BMC p=0.06, others p<0.05); there were no differences between sons. Grandchildren (aged 8-39 years) were categorized as growing (premenarcheal or male<14 years) or not growing (> or =2 years post-menarcheal or males> or =18 years): 33 were not classified. Post-menarcheal, but not premenarcheal, granddaughters of cases had greater hip, FN and LS aBMD Z-scores (0.7 vs. -0.1; 0.6 vs. -0.1; 0.8 vs. -0.3); greater hip and spine aBMD (1.03 vs. 0.95, 1.10 vs. 0.98 g/cm2); greater femoral neck and spine BMC (4.77 vs. 4.21, 66.7 vs. 55.4 g); and greater spine bone area (60.7 vs. 56.6 cm2) compared to granddaughters of controls (all, p<0.05), which remained significant when height, weight, and age were included as covariates. Growing grandsons of cases were taller and heavier than control grandsons, and a greater hip aBMD among grandsons of cases (0.88 vs. 0.76 g/cm2) was the only bone difference that remained significant after taking into account body size differences. Grandsons who were not growing had greater spine bone area (1.19 vs. 1.08 cm2) if their grandparent had OA compared to grandsons whose grandparents did not have OA. We speculate that there is a genetic basis for OA that leads to early differences in growth patterns among boys and greater peak bone mass and aBMD among girls.