Optimizing Wound Care: The Mechanistic Role of Dressing Change Frequency in Acute and Diabetic Wound Healing

Dressing change frequency is fundamental to wound care yet governed by tradition, creating a clinical paradox: protecting acute wounds versus debriding diabetic, biofilm-laden ones. Because "one-size-fits-all" protocols ignore this pathophysiological divide, the mechanistic principles for tailoring frequency to the specific wound state remain critically undefined.

We established parallel full-thickness wound models in normal (acute) and diabetic mice, randomized to high-, intermediate-, or low-frequency dressing change regimens. Healing was evaluated via macroscopic closure, histology, and qRT-PCR analysis of key genes regulating inflammation, macrophage polarization, and matrix remodeling.

An intermediate-frequency regimen drove superior healing in acute wounds, with accelerated closure and organized collagen deposition. In stark contrast, diabetic wounds required high-frequency treatment; low-frequency intervention was actively detrimental. These opposing outcomes were governed by a common mechanism: the optimal frequency orchestrated a rapid resolution of LBP-mediated inflammation and triggered a decisive M1-to-M2 macrophage shift, driving effective collagen synthesis.

This study challenges the static paradigm in wound care. We establish that dressing frequency is a dynamic therapeutic variable that must be tailored to the wound's pathophysiology. Our findings provide the first evidence-based rationale for modulating intervention rhythm based on a wound's inflammatory state-a critical strategy to accelerate acute repair and rescue diabetic nonhealing wounds.