Objective: Individuals with type 2 diabetes have increased fracture risk despite higher bone mineral density (BMD). Our aim was to examine the influence of glucose control on skeletal complications.
Research design and methods: Data of 4,135 participants of the Rotterdam Study, a prospective population-based cohort, were available (mean follow-up 12.2 years). At baseline, 420 participants with type 2 diabetes were classified by glucose control (according to HbA1c calculated from fructosamine), resulting in three comparison groups: adequately controlled diabetes (ACD; n = 203; HbA1c <7.5%), inadequately controlled diabetes (ICD; n = 217; HbA1c ≥ 7.5%), and no diabetes (n = 3,715). Models adjusted for sex, age, height, and weight (and femoral neck BMD) were used to test for differences in bone parameters and fracture risk (hazard ratio [HR] [95% CI]).
Results: The ICD group had 1.1-5.6% higher BMD, 4.6-5.6% thicker cortices, and -1.2 to -1.8% narrower femoral necks than ACD and ND, respectively. Participants with ICD had 47-62% higher fracture risk than individuals without diabetes (HR 1.47 [1.12-1.92]) and ACD (1.62 [1.09-2.40]), whereas those with ACD had a risk similar to those without diabetes (0.91 [0.67-1.23]).
Conclusions: Poor glycemic control in type 2 diabetes is associated with fracture risk, high BMD, and thicker femoral cortices in narrower bones. We postulate that fragility in apparently "strong" bones in ICD can result from microcrack accumulation and/or cortical porosity, reflecting impaired bone repair.