The advent of improved glucose control with insulin and oral medications has allowed for the diabetic population to live longer and healthier lives. Unfortunately diabetes remains a worldwide epidemic with multiple health implications. Specifically, its affects upon fracture healing have been well studied and shown to have negative effects on bone mineral density, biomechanical integrity, and fracture healing. Multiple animal models have been used for research purposes to gain further insight into the effects and potential treatments of this disease process. The diabetic BB Wistar rat is one model that replicates a close homology to human type-1 diabetes and has been used as a fracture model to study the effects of diabetes on bone integrity and healing. In particular, the effects of tight glucose control, ultrasound therapy, platelet-rich plasma (PRP), platelet-derived growth factor (PDGF), bone morphogenetic protein 2 (BMP-2), and allograft bone incorporation have been studied extensively. We present a review of the literature using the BB Wistar rat to elucidate the implications of diabetes on fracture healing. 1. Clinical Significance In the United States, over 13 million Americans have been diagnosed with diabetes mellitus (DM) and an estimated 40 million Americans will develop DM over the next 10 years [1]. The advent of the improved insulin regiment and/or oral hypoglycemics has led to a DM population that is more active and ultimately lives longer. Unfortunately, treatment of DM fractures presents a challenge to the orthopaedic surgeon. Several clinical series, analyzing fracture healing in patients with DM, demonstrated a significant incidence of delayed union, nonunion, and pseudarthrosis [2–5]. Diabetic osteopathy, as one of the diabetes-induced complications, leads to diminished bone formation [6], retardation of bone healing [2], and osteoporosis [7–9]. Bone mineral density [10] and biomechanical integrity [3, 11] are referential predictors of fracture, and patients with type-1 diabetes (T1D) also incur a higher incidence of fractures than healthy individuals. In addition to altered biomechanical properties, diabetic fracture callus has shown to have reduced cell proliferation and collagen synthesis during early states of fracture healing [2, 12, 13]. Patients with T1D are particularly vulnerable to hip fracture [14]. Women with T1D have a 6.9 to 12-fold likelihood of hip fractures compared to women without DM [15, 16]. Fracture healing in patients with all forms of DM may also take twice as long as nondiabetic patients [5, 17]. Likewise,
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