Skeletal Fragility in Type 1 Diabetes: Glycemic Control and Bone Strength

T1D is primarily associated with decrements in bone strength due to disrupted microarchitecture occurring during peak bone mass accrual, and this disruption arises from hyperglycemia and glycemic variability. Impaired bone development during this period likely predisposes to an increased fracture risk across the lifespan.

The investigators will compare baseline, 12 month and 24 month changes in High-resolution peripheral quantitative computed tomography/micro-finite element analysis (HR-pQCT/μFEA)-based estimates of bone strength and bone turnover by biochemical measurements in 40 T1D children at the onset of peak bone mineral accretion (n=40) versus sex and puberty-matched healthy controls (n=40). The investigators will determine relationships between changes in bone strength (including trabecular and cortical components) and measures of glycemic control and variability by continuous glucose monitoring (CGM).

Inclusion criteria

(T1D and Controls):

• Children within 2 years preceding the onset of the pubertal growth spurt

Inclusion criteria

(T1D participants):

• documentation of β-cell autoimmunity and need for insulin replacement

Exclusion criteria

• Estimated glomerular filtration rate (eGFR)< 60 ml/mim
• 25(OH)D level < 20 ng/ml.
• Celiac disease
• Autoimmune thyroid disease
• Addison's disease
• History of pathological fractures

-- Disorders associated with altered skeletal structure or function

• Bone active drugs in past year
• Diabetes of other or unclear etiology