Adults with type 1 diabetes (T1D) experience an increased lifetime risk of fractures, but the effects of T1D on bone accrual during adolescence are not well established. Puberty is a period of rapid skeletal growth and a major determinant of peak bone mass; disruptions during specific pubertal windows could have long-term consequences for bone health. The authors designed a study to examine whether bone microarchitecture and strength differ between adolescents with T1D and matched controls when assessed at sex-specific stages of pubertal bone accrual.
The primary objective was to compare bone microarchitecture and estimated bone strength between adolescents with T1D and control participants during sex- and pubertal stage–specific periods of bone accrual, and to evaluate relationships between bone measures and glycemic control, advanced glycation end-products, growth factors, and bone turnover markers.
This was a cross-sectional study conducted at a tertiary medical center. The analytic sample included 40 adolescents with T1D and 40 matched control youth. Participants were studied during sex-specific pubertal windows: early-pubertal girls (Tanner stages 2–3) and mid-pubertal boys (Tanner stages 3–4), intervals selected to reflect critical stages of pubertal bone accrual.
Bone assessments included areal bone mineral density by dual-energy X-ray absorptiometry (DXA) and microarchitectural evaluation by high-resolution peripheral quantitative computed tomography (HR-pQCT) with individual trabecula segmentation. Micro-finite element analysis was applied to HR-pQCT images to estimate mechanical competence (failure load). Laboratory and metabolic assessments included glycated hemoglobin (HbA1c), continuous glucose monitoring (CGM), skin autofluorescence (SAF) pentosidine as a surrogate for advanced glycation end-products, insulin-like growth factor-1 (IGF-1), and bone turnover markers.
Compared with control boys, boys with T1D exhibited several microarchitectural and strength deficits. At the distal tibia, boys with T1D had a lower trabecular bone volume fraction (−14%; P = .033), a marked reduction in plate-like trabeculae (−23%; P = .007), and reduced failure load (−12%; P = .008), indicating compromised trabecular structure and mechanical competence. At the proximal tibia, cortical area was lower in boys with T1D (−8%; P = .026). Similar patterns of deficits were reported at the radius.
In contrast to the findings in mid-pubertal boys, early-pubertal girls with T1D did not show detectable deficits in the evaluated bone microarchitecture or strength measures when compared with matched control girls. The study reports no significant bone deficits in this early pubertal female subgroup.
Within mid-pubertal boys, higher HbA1c was associated with fewer plate-like trabeculae (β = −.31, P = .038) and with reduced estimated bone strength. Lower IGF-1 concentrations predicted decreased trabecular bone volume and reduced mechanical strength, linking impaired growth-factor signaling to poorer bone outcomes. Across the entire T1D cohort, markers of hyperglycemia from CGM and higher skin autofluorescence (SAF), a measure related to advanced glycation end-products, correlated with suppressed bone turnover, suggesting systemic metabolic factors associated with diabetes may influence bone remodeling during adolescence.
The study demonstrates sex- and pubertal stage–specific skeletal effects of T1D: mid-pubertal boys show both trabecular and cortical deficits and reduced bone strength, whereas early-pubertal girls in this cohort did not exhibit deficits. These findings indicate that mid-puberty in boys with T1D may represent a critical window of skeletal vulnerability when glycemic control, IGF-1 status, and accumulation of glycation products are linked to adverse bone outcomes. Clinicians caring for adolescents with T1D may consider heightened attention to bone health during mid-puberty in boys, including monitoring and potentially intervening on modifiable factors such as glycemic control and factors affecting IGF-1 and bone turnover.
This report is based on the abstract and metadata provided by the source article. Details beyond those reported in the abstract—such as specific inclusion/exclusion criteria, participant demographics beyond sex and Tanner stage, duration of diabetes, treatment regimens, full statistical models, and absolute values for all measures—were not reported in the provided source text and therefore are not described here. The study design is cross-sectional; causal inferences about longitudinal bone accrual cannot be made from these data alone.
In this cross-sectional evaluation, adolescents with T1D demonstrated sex- and pubertal stage–specific differences in bone microarchitecture and estimated strength: mid-pubertal boys had trabecular and cortical deficits with reduced failure load, whereas early-pubertal girls showed no deficits. Higher HbA1c, CGM-detected hyperglycemia, elevated SAF, and lower IGF-1 were linked to adverse bone measures or suppressed bone turnover, supporting the concept that metabolic control during key windows of pubertal bone accrual may influence skeletal outcomes in youth with T1D.