<HashMap><database>biostudies-literature</database><scores/><additional><submitter>He P</submitter><funding>Guangdong Basic and Applied Basic Research Foundation</funding><funding>Basic and Applied Basic Research Foundation of Guangdong Province</funding><funding>National Natural Science Foundation of China</funding><funding>National Natural Science Foundation of China (NSFC)</funding><pagination>e70643</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12759167</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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.&lt;h4>Conclusions&lt;/h4>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.</pubmed_abstract><journal>Journal of cosmetic dermatology</journal><pubmed_title>Optimizing Wound Care: The Mechanistic Role of Dressing Change Frequency in Acute and Diabetic Wound Healing.</pubmed_title><pmcid>PMC12759167</pmcid><funding_grant_id>2024A1515013286</funding_grant_id><funding_grant_id>82472586</funding_grant_id><pubmed_authors>Mo C</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Qi X</pubmed_authors><pubmed_authors>Han Y</pubmed_authors><pubmed_authors>He P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Optimizing Wound Care: The Mechanistic Role of Dressing Change Frequency in Acute and Diabetic Wound Healing.</name><description>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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.&lt;h4>Conclusions&lt;/h4>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.</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-06-09T05:16:18.6Z</modification><creation>2026-06-09T03:07:40.389Z</creation></dates><accession>S-EPMC12759167</accession><cross_references><pubmed>41482679</pubmed><doi>10.1111/jocd.70643</doi></cross_references></HashMap>