ESPE Abstracts

Background: Sclerostin is an inhibitor of the Wnt/b-catenin bone metabolic pathway. Increased sclerostin levels and reduced bone mineral density (BMD) have been documented in adult patients with diabetes mellitus (DM), predominantly in those with T2DM. No relevant data exist on childhood T1DM.

Objective and hypotheses: Our aim was to study plasma sclerostin concentration in children and adolescents with T1DM and controls and to correlate sclerostin levels with metabolic bone markers and BMD.

Method: Forty children and adolescents with T1DM were evaluated (mean±S.D. age: 13.04±3.53 years, T1DM duration: 5.15±3.33 years), along with 40 healthy matched controls (mean±S.D. age 12.99±3.3 years). Sclerostin, osteocalcin, C-telopeptide crosslinks-CTX, electrolytes, PTH, total 25(OH) D and total body BMD were measured.

Results: Sclerostin levels demonstrated a Gaussian distribution (Shapiro-Wilk z=−1.685, P=0.95, kurtosis=2.77, skewness=0.13), with no significant difference between patients and controls (51.56±12.05 vs 50.98±13.55 pmol/l, P=0.84). Lower values were found in girls (49.1±12.7 vs 53.9±12.3 pmol/l, P=0.05) and in prepubertal children (47.3±11.6 vs 53.3±12.9 pmol/l, P=0.02). In both patients and controls sclerostin values significantly and gradually increased in children through pubertal Tanner stages 1 to 3, then they were reduced in stage 4 adolescents and were increased again in pubertal stage 5 adolescents (ANOVA F=4.56, P=0.0024). Sclerostin levels were positively correlated with logCTX (r=0.41, P<0.001), logOsteocalcin (r=0.33, P=0.004), total body BMD (r=0.34, P=0.0018) and BMD Z-score (r=0.27, P=0.015). Total body BMD was not significantly different between patients and controls.

Conclusion: T1DM children and adolescents had similar sclerostin levels and total BMD with controls. In both patients and controls, sclerostin was correlated with both resorption and formation markers and also with bone mass indices, gender and pubertal stage. The decrease in sclerostin values observed in pubertal stage 4 adolescents coincides with the concurrent growth spurt, and is consistent with sclerostin physiology as an inhibiting signal of bone formation.