Epidemiological studies have found that patients with Type 2 Diabetes Mellitus (T2D) have a higher incidence of fragility fractures relative to non-diabetic individuals. Given the substantial morbidity, mortality and costs that emanate from T2D-related fractures, proper recognition of T2D individuals at increased fracture risk is indispensable. Although fracture risk in type 2 diabetics is routinely assessed with WHO-FRAX scores or DXA these methods show limitations. This highlights that other mechanisms, independent of BMD, might be driving the pathophysiology of diabetic bone disease. In this context, microRNAs (miRNAs) are of special interest. MicroRNAs (miRNAs) are small non-coding RNAs that orchestrate gene expression on a post-transcriptional level and emerged as masterregulators of many cell processes including e.g. cell differentiation and senescence. They get secreted into the blood stream from cells of various tissues proportional to local disease severity where they remain stably expressed. Recent evidence has shown that miRNAs are crucial to bone homeostasis (osteomiRs) and T2D etiology. This talk will focus on how studying miRNA expression may provide novel insights into the pathophysiology and morphological correlates of increased bone fragility in T2DM patients.
14 May 2016 - 17 May 2016