Acne vulgaris is an inflammatory disease of the pilosebaceous unit, driven by excess sebum, follicular hyperkeratinisation, the commensal bacterium Cutibacterium acnes, and the inflammation these provoke. For decades, antibiotics were a first reflex. That reflex created a problem now impossible to ignore: antibiotic resistance.
The resistance debt
Widespread, prolonged use of topical antibiotics — often as monotherapy — selected for resistant strains of C. acnes and contributed to the broader burden of antimicrobial resistance. The result is that some antibiotic-based regimens are simply less effective than they were a generation ago, and that dermatology has a duty to use antibiotics sparingly and never alone.
Why benzoyl peroxide is different
Benzoyl peroxide kills C. acnes by a fundamentally different mechanism: it releases reactive oxygen species that oxidise bacterial proteins non-specifically. Because the attack is chemical and multi-target rather than a single enzyme interaction, bacteria do not develop resistance to it — a property that has held true across decades of use. It also has mild comedolytic action, helping clear the follicular plugging that starts a lesion.
The modern role
Current guidance places benzoyl peroxide at the centre of mild-to-moderate acne care — used alone for milder disease and, crucially, combined with topical retinoids or antibiotics where those are indicated, because it suppresses the emergence of resistance in the companion drug. The trade-offs are modest: transient dryness and the well-known tendency to bleach fabric. Improvement is visible by around four weeks and optimal at eight to twelve. It is inexpensive, off-patent and unglamorous — and, on the evidence, one of the most sensible things we can still put on inflamed skin.