Diabetes and Bone
Towards more Quality – Deciphering the Sweet Bone Phenomenon
Bone in patients with diabetes breaks easily and heals poorly. Sometimes, it does not heal at all. For the patients, this means immobility over months and as a consequence less life quality. Type 2 diabetes mellitus and osteoporosis may affect half of the aging European population. However, the ‘sweet bone phenomenon’ remains a conundrum, since bone mineral density is paradoxically high or normal. Therefore, we set out to answer the fundamental question “How is bone weakened by diabetes?”
We believe that bone material strength is affected by direct and indirect effects of type 2 diabetes mellitus on bone. In the last four years, our group has found that bone microarchitecture and accumulation of advanced glycosation endproducts (AGE) contribute to poor bone quality in diabetes. In our ongoing studies, we test how microvascular damage and persistent low-grade inflammation may contribute to impaired bone cell function. To tackle these research questions, we use preclinical models and comprehensively assess intact and regenerating bone with a spectrum of high-resolution imaging modalities and advanced cell biology methods.
We expect to uncover the cause of poor bone quality in diabetes by focussing on vascular and inflammatory mechanisms and to deliver better bone therapies for patients with diabetes.
Principal Investigators
Lorenz Hofbauer, MD
«I am trying to find the missing link.»
Juliane Salbach-Hirsch, PhD
«Research is going up all alleys to see if they are blind.»
Martina Rauner, PhD
«It is an important research area as it concerns so many people worldwide.»
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- Stephanie Zeiler
Research Question
In diabetes, patients display a paradox finding. Although their bone mass is normal or even increased, they encounter more fragility fractures that tend to heal poorly. We suspect that the bone quality is severely compromised in diabetes and that this may be the result of vascular and inflammatory mechanisms.
Approach
Our team analyzes the contribution of microvascular damage, chronic inflammation, and osteocytic alterations to impaired bone strength and bone repair. We use preclinical models of T2DM both intact and regenerating bone recovering from fractures and employ a spectrum of high-resolution technologies.
Projects
- Effects of T2DM on bone vasculature
- Role of Dkk1 in diabetic bone disease
- Investigating the role of Wnt signalling in type 2 diabetes induced bone disease
- Role of Dkk-1 in type 1 diabetes bone fragility
Funding
Funded by DFG SFB/Transregio-67 and the EU MSCA ITN Fidelio.