Topical Treatment With an Agent Disruptive to P. acnes Biofilm Provides Positive Therapeutic Response: Results of a Randomized Clinical Trial

June 2016 | Volume 15 | Issue 6 | Original Article | 677 | Copyright © June 2016

Michael J. Bernhardt MDa and Matthew F. Myntti PhDb

aJacksonville Center for Clinical Research, Jacksonville, FL; Private Practice, Jacksonville, FL
bNext Science LLC, Jacksonville, FL

The traditional disease model of acne has been one of follicular plugging due to ‘sticky epithelial cells’ associated with increased sebum production with deep follicular anaerobic conditions favoring P. acnes- generated inflammation. P. acnes biofilms have been found more frequently in patients with acne than controls. Biofilms are genetically coded to create adhesion to the pilosebaceous unit followed by production of a mucopolysaccharide coating capable of binding to lipid surfaces. Traditional therapies for acne have involved mixtures of oral and topical antibiotics admixed with topical keratolytics and retinoids, which are aimed at traditional bacterial reduction as well as downregulating the inflammatory cascade. These approaches are limited by side effect and compliance/tolerability issues. As the P. acnes biofilm may, in fact, be the instigator of this process, we studied the use of a topical agent designed to reduce the P. acnes biofilm to see if reducing the biofilm would be therapeutically efficacious. We present data of a proprietary topical non-prescription agent with a novel pharmaco mechanism designed to attack the biofilm produced by P. acnes. Our data shows a decrease of inflammatory lesions by 44% and non-inflammatory lesions by 32% after 12 weeks and also provided for a meaningful improvement in the quality of life of the patients in the study. These improvements were achieved with a product that was not associated with burning, chafing, irritation, or erythema, which can be seen with topical treatments. It is apparent from this study that by addressing the biofilm which protects the P. acnes bacteria through the use of the Acne Gel, the incidence of acne symptoms can be greatly reduced, while having no negative impacts on the patients’ skin ( registry number NCT02404285).

J Drugs Dermatol. 2016;15(6):677-683.


Acne is the most common condition in dermatological offices, affecting approximately 85% of people aged 12 to 24, 8% of people 25 to 34 and 3% of people 35 to 44.1 In the U.S. over 50 million people will be affected with one third requiring medical attention.
Propionibacterium acnes is slow-growing aero tolerant gram positive rod, that is implicated as a causative agent, although speculation persists because acne genesis is a multi-faceted process. The condition is often tied to early adolescence and its associated surge of androgen levels, accompanied by increased sebum production, desquamation of follicular epithelium, inflammation, and microcomedone formation.
The standard model posits that follicular plugging occurs due to ‘sticky’ epithelium associated with increased sebum and culminating in anaerobic follicular conditions that favor P. acnes, generating inflammation. Some infer that an alternate, reversed sequence may be more accurate.2 In acne patients, subclinical inflammation has been noted prior to microcomedone formation with clinically normal skin displaying increased T-cell and macrophage infiltrate, including increased expression of pro-inflammatory cytokines, E- selectin, and vascular adhesion molecules. In 28% of lesions, inflammatory lesions preceded microcomedone formation.2
Three groups of microorganisms are known to inhabit the pilosebaceous unit; staph and lipophilic yeasts in upper aspects, and P. acnes in deeper areas.3 P. acnes is most numerous, achieving colony growth rates of up to 10^7 organisms/pilosebaceous unit. P. acnes is also a known immune-stimulant, activating the TLR 2 complex and NLRP3 inflammasomes.4
P. acnes exerts such influence by forming sessile aggregates known as biofilms.5 Through formation of biofilms, bacteria are capable of growing and adhering to almost any surface, including human surfaces such as teeth (plaque), skin, and urinary tract which enable chronic infections.6 Compared to control groups, P. acnes biofilms have been found more frequently in patients with acne.2 Biofilms are genetically coded7 to create adhesion to pilosebaceous units, including production of a mucopolysaccharide coating that can bind to lipid surfaces.