“Skin Purging” vs. Breakouts: A Scientific Review of Exfoliation-Related Flares

By Wendy Ouriel, M.S. • Updated Oct 12, 2025

Many people observe a breakout after starting a new product and label it a “purge.” In biology, only increased epidermal turnover can unmask pre-existing lesions. Non-exfoliating products cannot “purge”—they irritate or clog, causing true breakouts. Below is a structured, citation-led review and a practical protocol to manage flares the right way.

Abstract

The term “skin purging” is widely used to justify product-induced breakouts. Here we review clinical and mechanistic evidence indicating that exfoliation-related flares arise when accelerated desquamation exposes pre-existing microcomedones and inflammatory foci within acne-prone skin. Histological studies demonstrate inflammatory signaling present at lesion initiation and within comedones. In contrast, flares from non-exfoliating products represent irritant or comedogenic breakouts. We propose a management algorithm built on controlled chemical exfoliation, barrier-compatible hydration, and avoidance of sensitizers. Practical guidance references OUMERE resources and products designed to minimize inflammation while normalizing turnover.

Introduction

Myths in skincare often start with a real observation and end with a mistaken mechanism. The observation: after starting certain products, breakouts increase. The misunderstanding: the skin is “detoxing” by pushing acne out. In reality, non-inflamed whiteheads often regress without rupture as the immune system resolves the lesion internally over time.

Inflammatory cells in early acne lesions (Jeremy et al., 2003) — Inflammatory events in lesion initiation (Jeremy et al., 2003).

When exfoliation begins—via topical chemical exfoliants (e.g., No. 9 Daily Liquid Exfoliant) or systemic retinoids—retained corneocytes are shed, revealing underlying pathology. This can transiently increase visible lesions. By contrast, non-exfoliating products cannot reveal what lies beneath; they can only irritate, occlude, or disrupt the barrier, provoking new breakouts.

Methods (Scope of Review)

This narrative review synthesizes histological and immunological findings on acne lesion initiation and comedone biology, and integrates practical observations from controlled exfoliation protocols in the clinic. Key sources include studies demonstrating pro-inflammatory cytokines within comedones and early lesions, as well as TLR2-mediated inflammatory responses in acne skin.

Results (Key Evidence)

Inflammation precedes or accompanies comedogenesis. Inflammatory mediators are present within open comedones and during lesion initiation, indicating that “silent” pathology can exist beneath intact stratum corneum (Ingham 1992; Jeremy 2003; Layton 1998; Tanghetti 2013).
Innate immune activation contributes to flares. TLR2 activation in acne triggers cytokine cascades, priming skin for inflammatory expression once occlusion is relieved (Kim 2002).
Exfoliation reveals, it does not create, pre-existing lesions. Accelerated turnover removes the masking corneocyte layer, transiently increasing visible papules/pustules until equilibrium is reached.
Non-exfoliating “purges” are misnomers. If a cleanser, serum, or moisturizer without turnover effects causes bumps, the mechanism is irritation, barrier injury, or comedogenesis—not purging.

Clinical flare during early exfoliation period — Early flare during exfoliation: unmasking, not “toxins.”

Discussion

Exfoliation-associated flares reflect exposure of pre-existing inflammatory microenvironments. With consistent, barrier-compatible care, lesion counts typically decline as ductal architecture normalizes and the inflammatory burden decreases. Conversely, fragranced or alcohol-heavy routines, essential oils, and occlusive, comedogenic creams prolong inflammation and perpetuate the “try more products” loop.

Core claim clarified: The only context in which a “purge” is biologically coherent is when epidermal turnover increases. Non-exfoliating products cannot purge; they can only provoke breakouts through damage or clogging.

Clinical-Style Guidance: Managing an Exfoliation Flare

Choose a controlled, gentle acid system. Start with No. 9 Daily Liquid Exfoliant (PHA/AHA/BHA; fragrance-free). For active rosacea/redness, calm first: Sensitive Skin: The Cellular Response.
Support the barrier. Layer UV-R™ Concentrate (anti-inflammatory hydration) and seal with Serum Bioluminelle (non-occlusive oils).
Eliminate sensitizers. Avoid fragrance/essential oils, drying alcohols, harsh scrubs/brushes, and unstable vitamin C cocktails. See: Essential Oils Are Not Essential.
Be consistent for several weeks. Expect transient increases in visible lesions as microcomedones surface, then steady decline.
Keep cleansing non-stripping. Use Oil Dissolution Theory® Cleanser nightly.

Prefer a map? Follow The OUMERE Routine and, for flare triage, see Acne & Inflammation: Biological Origin and Barrier Repair After Retinoid/Acid Damage.

Limitations

This article synthesizes mechanistic literature and practical experience; it is not a randomized clinical trial. Individual variability in sebaceous output, microbiome composition, and sensitivity will influence flare amplitude and duration.

Conclusion

“Purging” is not a universal explanation for product-induced breakouts. It is a specific, temporary outcome of increased turnover unmasking pre-existing lesions. If a non-exfoliating product triggers bumps, it is not purging—it’s a breakout. Replace irritants with a minimal, science-led routine to restore barrier integrity and reduce inflammatory load.

References

Ingham, E., et al. (1992). Pro-inflammatory IL-1α-like activity in open comedones. J Invest Dermatol 98(6):895–901.
Jeremy, A. H., et al. (2003). Inflammatory events in acne lesion initiation. J Invest Dermatol 121(1):20–27.
Kim, J., et al. (2002). TLR2 activation in acne triggers cytokines. J Immunol 169(3):1535–1541.
Layton, A. M., et al. (1998). Evolving inflammation in acne lesions. Exp Dermatol 7(4):191–197.
Tanghetti, E. A. (2013). The role of inflammation in acne. J Clin Aesthet Dermatol 6(9):27–35.