Abstract
Background:
Cutaneous fibrosis and wound healing span a continuum of responses to injury, unified by inflammation, vascular remodeling, and extracellular matrix deposition. The interplay among vascular injury, macrophage activity, and profibrotic signaling determines whether repair resolves or progresses to chronic fibrosis. This study surveys immunohistochemical patterns reflecting vascular activation, macrophage presence, and profibrotic signaling across diverse cutaneous conditions.
Methods:
Formalin-fixed, paraffin-embedded specimens from postoperative scars, keloids, morphea, nephrogenic systemic fibrosis (NSF), and radiation-induced sclerosis were stained for CD163 (macrophages), Collagen IV (basement membrane and vascular-associated matrix), TGF-β1 (profibrotic cytokine), and VCAM (endothelial activation/vascular injury). Staining distribution and intensity were compared across entities.
Results:
Postoperative scars showed temporally dynamic staining with transient VCAM and focal TGF-β1 expression during early healing, returning toward baseline in mature scars.
Keloids lacked significant CD163 positivity, showed reduced intralesional Collagen IV compared to adjacent dermis, minimal VCAM expression, and were negative for TGF-β1.
Morphea demonstrated deeper dermal and interstitial Collagen IV accentuation with sparse VCAM expression and absence of TGF-β1 in both early and mature lesions.
NSF exhibited variable VCAM positivity (endothelial and perivascular dendritic) and focal Collagen IV accentuation in sclerotic areas, with limited TGF-β1 staining.
Radiation sclerosis displayed perivascular and “shaggy” Collagen IV deposition with minimal VCAM and TGF-β1 expression and predominantly dendritic CD163 staining.
Conclusions:
Distinct but intersecting immunohistochemical profiles emerge across fibrosing and wound-healing conditions. These findings suggest that endothelial activation, matrix remodeling, and context-specific macrophage responses variably shape the fibrotic microenvironment across cutaneous entities, providing histologic insight into shared and disease-specific mechanisms of fibrosis and repair.
