The impact of obstructive sleep apnea on skin wound healing - from preclinical perspective to clinical evidence: A narrative review.
Adequate tissue oxygenation is essential for effective skin wound healing. Hypoxia contributes to impaired healing and chronic wound formation. Obstructive sleep apnea (OSA) affects nearly one billion adults worldwide, and up to 80% of cases remain undiagnosed. OSA causes intermittent hypoxia (IH), with repetitive cycles of oxygen desaturation and reoxygenation during sleep. The molecular pathways activated by IH differ from those induced by acute and chronic hypoxia. We propose that OSA may contribute to impaired wound healing in two ways. Indirectly, by promoting comorbidities such as diabetes, hypertension, and obesity. Directly, through IH and its effects at the cellular and tissue level.
PubMed/MEDLINE, Scopus, and Web of Science were searched through August 2026 for preclinical and clinical studies on OSA, IH, and wound healing.
To our knowledge, this is the first review to integrate cellular mechanisms, preclinical evidence, and clinical data on this topic. We describe the IH-driven mechanisms that may contribute to impaired wound healing, including reduced antioxidant capacity, sustained inflammation, sympathetic activation, and endothelial dysfunction. Preclinical evidence is limited and mostly derives from in vitro scratch assays. It shows that IH delays wound closure, downregulates HIF-2α and VEGF, and shifts macrophages toward a pro-inflammatory phenotype. Clinical data are also limited and heterogeneous. In diabetic foot ulcers, high OSA risk doubled the risk of poor healing. Improved ulcer healing after CPAP has been described only in a small case series.
Given its high prevalence and underdiagnosis, OSA may be an overlooked and potentially modifiable factor in impaired wound healing.
PubMed/MEDLINE, Scopus, and Web of Science were searched through August 2026 for preclinical and clinical studies on OSA, IH, and wound healing.
To our knowledge, this is the first review to integrate cellular mechanisms, preclinical evidence, and clinical data on this topic. We describe the IH-driven mechanisms that may contribute to impaired wound healing, including reduced antioxidant capacity, sustained inflammation, sympathetic activation, and endothelial dysfunction. Preclinical evidence is limited and mostly derives from in vitro scratch assays. It shows that IH delays wound closure, downregulates HIF-2α and VEGF, and shifts macrophages toward a pro-inflammatory phenotype. Clinical data are also limited and heterogeneous. In diabetic foot ulcers, high OSA risk doubled the risk of poor healing. Improved ulcer healing after CPAP has been described only in a small case series.
Given its high prevalence and underdiagnosis, OSA may be an overlooked and potentially modifiable factor in impaired wound healing.