What is the pathogenesis of post-acne erythema (PAE) from the initial inflammation of acne to its formation in individuals with a history of severe or inflammatory acne?

Pathogenesis of Post-Acne Erythema: From Initial Inflammation to PAE Formation

Initial Acne Inflammation and Pathogenic Cascade

Post-acne erythema develops as a direct consequence of the inflammatory cascade initiated during active acne vulgaris, where the multifactorial pathogenesis involving follicular hyperkeratinization, Cutibacterium acnes colonization, sebum production, and complex inflammatory mechanisms involving both innate and acquired immunity ultimately damages the dermal microvasculature and triggers persistent erythema even after lesion resolution. 1

The pathogenic sequence begins with:

• Follicular hyperkeratinization creates the initial microcomedone, where abnormal keratinization of the follicular epithelium leads to ductal obstruction 1
• Sebum accumulation within the obstructed follicle provides a lipid-rich environment that promotes bacterial proliferation 1, 2
• Cutibacterium acnes colonization triggers the inflammatory response through bacterial metabolites and cell wall components 1, 2
• Inflammatory mediator release occurs when keratinocytes secrete chemokines and cytokines in response to bacterial stimuli, recruiting inflammatory cells including macrophages, Langerhans cells, T cells, mast cells, and neutrophils 1

The Inflammatory Infiltrate and Vascular Damage

The histopathological hallmark of inflammatory acne demonstrates a dense, periadnexal, leucohistiocytic inflammatory infiltrate with marked clustering of immune cells that directly damages surrounding dermal structures 1. This inflammatory process:

• Creates a periadnexal inflammatory environment where macrophages, T cells, and neutrophils cluster around the pilosebaceous unit 1
• Releases inflammatory cytokines that cause collateral damage to the papillary dermis and its microvasculature 3, 4, 5
• Induces epidermal thinning through inflammatory mediators that disrupt normal keratinocyte differentiation 5
• Triggers microcapillary dilatation within the papillary dermis as a direct response to inflammatory cytokine release 3, 4, 5

Formation of Post-Acne Erythema

PAE represents persistent telangiectasia and erythematous lesions that remain after acne treatment, resulting from permanent or prolonged microvascular changes and inflammatory sequelae. 3, 6 The transition from active inflammation to PAE involves:

• Persistent vascular dilatation where the inflammatory insult causes lasting changes in dermal microcapillaries that fail to return to baseline after lesion resolution 3, 4, 5
• Telangiectasia formation occurs when chronic inflammation damages vessel walls, leading to permanent capillary ectasia visible as persistent erythema 3, 5
• Epidermal thinning makes the dilated dermal vessels more visible through the overlying skin, amplifying the erythematous appearance 5
• Hemoglobin deposition in the papillary dermis contributes to the red appearance, measurable by increased average hemoglobin levels and hemoglobin variation on objective assessment 6

Critical Distinction from Active Inflammation

PAE differs fundamentally from active acne inflammation in that:

• No active inflammatory infiltrate is present histologically, distinguishing it from ongoing acne lesions 3, 4
• Vascular changes predominate rather than cellular inflammation, with the primary pathology being microvascular rather than inflammatory 3, 5
• Time course extends beyond lesion resolution, with PAE persisting for months after the inflammatory acne lesion has healed 3, 6, 5

Clinical Implications for Treatment Selection

Understanding this pathogenesis explains why:

• Vascular-targeted therapies (pulsed dye lasers, IPL) are most effective, as they directly address the underlying microvascular pathology 3, 4, 5
• Anti-inflammatory agents alone are insufficient, since PAE represents post-inflammatory vascular sequelae rather than active inflammation 3
• Tranexamic acid shows efficacy through its anti-angiogenic and vascular stabilizing properties, addressing the underlying vascular pathology 6
• Combination approaches targeting both residual inflammation and vascular changes provide superior outcomes 4