Diabetes is a systemic disease in which the body cannot regulate the amount of sugar, namely glucose, in the blood. High glucose toxicity has been implicated in the dysfunction of diabetic wound healing, following insufficient production (Type 1) or inadequate usage (Type 2) of insulin. Chronic non-healing diabetic wounds are one of the major complications of both types of diabetes, which are serious concerns for public health and can impact the life quality of patients significantly. In general, diabetic wounds are characterized by deficient chemokine production, an unusual inflammatory response, lack of angiogenesis and epithelialization, and dysfunction of fibroblasts. Increasing scientific evidence from available experimental studies on animal and cell models strongly associates impaired wound healing in diabetes with dysregulated fibroblast differentiation to myofibroblasts, interrupted myofibroblast activity, and inadequate extracellular matrix production. Myofibroblasts play an important role in tissue repair by producing and organizing extracellular matrix and subsequently promoting wound contraction. Based on these studies, hyperglycaemic conditions can interfere with cytokine signalling pathways (such as growth factor-β pathway) affecting fibroblast differentiation, alter fibroblast apoptosis, dysregulate dermal lipolysis, and enhance hypoxia damage, thus leading to damaged microenvironment for myofibroblast formation, inappropriate extracellular matrix modulation, and weakened wound contraction. In this review, we will focus on the current available studies on the impact of diabetes on fibroblast differentiation and myofibroblast function, as well as potential treatments related to the affected pathways.

Background As the aging population increases in the United States, so has the prevalence of osteoporosis (10.2 million adults aged 50 years and older in 2010). Programs to manage the increased incidence of fragility fractures in such patients particularly the postmenopausal women are the priority. Programs such as the Fracture Liaison Service (FLS) might be the answer. Methods Data of 256 postmenopausal women with vertebral compression fractures treated with vertebroplasty between 2012 and 2017 were divided into 2 groups. Group A were patients seen between 2012 and 2014 before the establishment of the FLS program at the clinic. Group B were patients seen between 2015 and 2017 who presented to the FLS program in our clinic. Data collected included demographics, refracture rates, dual-energy X-ray absorptiometry (DEXA) scan T-scores, fracture risk score (FRAX), serum calcium and vitamin D levels, and comorbid conditions. Results There were 103 female patients with a mean age of 79.75 years (standard deviation [SD] ± 10.86) in group A, while group B had 153 patients with a mean age of 75.66 years (SD ± 10.78). There was no significant difference in the DEXA scan T-scores, FRAX scores, and mean serum calcium and vitamin D levels; however, there was a significant reduction in the refracture rate for vertebral compression fractures ( P = .003). Conclusion FLS programs, when implemented, will have a beneficial effect in reducing refracture rates of postmenopausal women with osteoporotic fragility fractures.