What are our pimples really saying?

By Ana Espino | Published on February 17, 2026 | 3 min read



Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit, highly prevalent in adolescents but also common in adults. It is characterized by comedonal and inflammatory lesions, typically affecting the face, chest, and back, with significant impact on quality of life, self-esteem, and mental health.  

Current management relies on combinations of topical and systemic treatments—antibiotics, retinoids, benzoyl peroxide—aimed at reducing inflammation, bacterial proliferation, and hyperkeratinization. However, these strategies have major limitations: cutaneous or systemic adverse effects, development of antimicrobial resistance, limited long-term efficacy, and lack of personalization. They primarily target symptoms rather than addressing deeper imbalances within the skin ecosystem.  

A central challenge is understanding the role of the skin microbiome in the onset and persistence of lesions. Recent studies suggest that certain strains of Cutibacterium acnes, previously regarded as uniform pathogens, may coexist with beneficial or pro-inflammatory bacteria within a fragile microbial balance.  

In this context, this review was undertaken to examine the interactions between acne and the skin microbiome, analyze the impact of conventional treatments on microbial diversity, and identify new therapeutic avenues based on targeted modulation of this ecosystem—toward a more precise, sustainable, and less iatrogenic dermatology.

Who truly rules our skin?

Twenty-six primary human studies were included. Animal studies and those focusing exclusively on the gut microbiome were excluded. A qualitative assessment of findings was complemented by a meta-analysis of microbial diversity.

The results confirm the direct involvement of the skin microbiome in acne pathophysiology. Cutibacterium acnes is the dominant species in inflammatory lesions, particularly ribotypes RT4, RT5, and RT8, whereas RT6 is more frequently found in healthy individuals. Other bacteria, such as Staphylococcus epidermidis, S. aureus, and C. granulosum, play complementary roles—sometimes protective, sometimes pathogenic—by modulating the cutaneous microbial balance. Dysbiosis, defined as an imbalance in bacterial composition and diversity, is strongly associated with increased inflammation and disruption of the skin barrier.

Conventional treatments significantly alter the microbiome. Doxycycline reduces C. acnes load while increasing overall bacterial diversity. Benzoyl peroxide has a marked effect on microbial composition. Isotretinoin acts indirectly by reducing sebum production, with variable effects on the microbiome. Supramolecular salicylic acid reduces inflammation and certain pathogenic species. Photodynamic therapy (ALA-PDT) promotes a more balanced bacterial diversity while decreasing C. acnes abundance.

At the same time, emerging therapies aim to restore a healthy microbiome rather than eradicate it. Probiotics such as Lactobacillus and Enterococcus faecalis, plant extracts like Rhodomyrtus tomentosa, and antimicrobial peptides such as poly-L-lysine show promising effects on dysbiosis, inflammation, and clinical skin appearance. These approaches suggest the possibility of more targeted, less invasive treatments with reduced risk of bacterial resistance and improved tolerability.

A microbial revolution ahead?

Acne vulgaris is a common inflammatory disorder whose impact extends far beyond visible skin lesions. A major challenge lies in persistent forms resistant to conventional therapies, often poorly tolerated and lacking durable solutions that address underlying causes.