Aging aggravates early scar healing after facial laceration through fibroblast-centered extracellular matrix...

This study examined whether age was associated with early scar outcomes after facial laceration, whether wound characteristics modulate this age effect, and to explore the biological basis of age-related scar worsening through histologic and single-cell analyses of aged skin.

This study enrolled patients presenting with acute maxillofacial lacerations to the emergency center. All wounds received standardized debridement, layered closure, and postoperative care. Scar characteristics were assessed at 1 and 3 months using subjective clinical scoring and objective shear-wave elastography. Gaussian Lasso regression was used to identify the predictors associated with early scar severity, followed by multivariable linear models and interaction analyses. To provide complementary biological context, we reanalyzed publicly available single-cell RNA-sequencing data from young and aged human eyelid skin. Besides, H&E and immunofluorescence analyses were performed on uninjured dorsal skin collected from young and aged mice.

A total of 95 patients were included. Age and wound length were retained in the primary Gaussian LASSO model of 1-month early scarring results. Age demonstrated related associations with scar hardness, peri-scar stiffness and vascularization. Wound characteristics further modified the effect of age: age-related scar worsening was more evident in trans-oral wounds, selected anatomical sites, and short-to intermediate-length wounds. Secondary analysis of the public human eyelid-skin single-cell dataset suggested age-associated changes in epithelial homeostasis and fibroblast-centered extracellular matrix signaling. In mouse experiments, aged skin showed altered epidermal and dermal morphology together with stronger Fibronectin 1 and Periostin immunofluorescence signals.

Early scar outcomes after facial laceration are associated with age, and these associations vary across wound characteristics. Complementary findings from reanalyzed public human skin transcriptomic data and separate mouse experiments are consistent with age-associated fibroblast-centered extracellular matrix remodeling.