Hypertrophic and keloid scars fail to progress from the CD 34 − /α‐smooth muscle actin (α‐ SMA ) + immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

作者：Grace C. Limandjaja, J.M. Belien, Rik J. Scheper, Frank B. Niessen, Susan Gibbs · 发表于：British Journal of Dermatology · 年份：2019 · DOI：10.1111/bjd.18219 · 被引用次数：95 · 研究领域：Dermatologic Treatments and Research、Wound Healing and Treatments、Hair Growth and Disorders

Our understanding of the pathogenesis underlying keloid scar formation is still very limited, and the morphological distinction between hypertrophic and keloid scars remains difficult. To test whether hypertrophic and keloid scars may reflect an inability to progress from immaturity to the desired mature normotrophic scar phenotype. Using whole‐biopsy imaging and an objectively quantifiable way to analyse immunoreactivity, we have compared the immunohistopathological profiles of young immature scars with mature normotrophic scars, hypertrophic scars, and keloids with their surrounding‐normal‐skin. Abnormal scars (hypertrophic scars and keloids) maintain the immature scar phenotype, characterized by a CD34− (tumour biomarker) and α‐smooth muscle actin (α‐SMA)+ (myofibroblast) dermal region. This is in contrast to normal skin, surrounding‐normal‐skin and mature normotrophic scars that were CD34+/ α‐SMA−. Immature, hypertrophic and keloid scars showed abnormal epidermal differentiation (involucrin), but only hypertrophic scars and keloids showed increased epidermal thickness. Immature scars did show increased epidermal and dermal proliferation (Ki67), which was absent from abnormal scars, where mesenchymal hypercellularity (vimentin) and senescence (p16) were predominant. Keloidal collagen and α‐SMA were previously considered to distinguish between hypertrophic scars and keloids. However, α‐SMA staining was present in both abnormal scar types, while keloidal collagen was present...