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Impaired wound healing for patients with diabetes is due to a constellation of structural, biochemical, cellular and microbial factors. Hyperglycaemia and its associated inflammation contribute to immune dysfunction, vascular damage, neuropathy, cellular senescence, impaired transition beyond the inflammatory stage, microbiome disruptions, failed extracellular matrix formation, growth factor and cytokine imbalance, limited re-epithelialisation, and alterations in fibroblast migration and proliferation. Optimising glycaemic control remains the primary intervention to prevent continual dysfunction and comorbid disease progression.
Swoboda et al. (Sun,) studied this question.