Diabetic Bone Fracture Repair: A Progenitor Cell-Based Paradigm

Current Stem Cell Research & Therapy
Jessica S Hayes, Cynthia M Coleman

Abstract

Long bone fractures in diabetics are slower to heal, have an increased risk of developing non-union and demonstrate greater potential of infection and perioperative complications compared to non-diabetics. The causative aberrant bone mineral density and insufficient bone microstructure of diabetic patients are thought to result from altered osteoblast and osteocyte function, increased bone marrow adiposity, decreased progenitor osteo- and chondral differentiation potential and increased pro-inflammatory cytokine circulation. It is therefore reasonable to hypothesize that the root cause of faulty diabetic bone homeostasis and fracture repair is a reduced population of bone marrow progenitor cells and/or their decreased osteochondral capacity complicated by their repressed neo-vascular potential. The potential of transplanted mesenchymal stem cells with a scaffold to support callus formation through the creation of de novo bone in hyperglycemia has been reported. However, there are minimal supporting pre-clinical and clinical investigations confirming these findings. Clinical trials have instead examined mesenchymal stem cell transplantation to slow disease progression, support .-cell viability and function and restore glucose ho...Continue Reading

Citations

Oct 4, 2018·Current Stem Cell Research & Therapy·Mukta AgrawalShailendra Saraf
Feb 9, 2018·Frontiers in Endocrinology·Carlos MarinKatleen Vandamme

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