Topical Retinoid and Antibiotic Combination Therapy for Acne Management

March 2004 | Volume 3 | Issue 2 | Original Article | 146 | Copyright © 2004

Jonathan S. Weiss, MD and Joel S. Savin, MD

Gwinnett Clinical Research Center, Inc., Snellville, Georgia


The agents most commonly used in combination for the management of acne include topical retinoids and antibiotics. Topical retinoids normalize desquamation of the follicular epithelium, whereas antibiotics inhibit the growth of P. acnes and the production of free fatty acids. This therapeutic combination decreases comedogenesis, bacterial growth, and inflammation, thus targeting three of the four pathogenic factors associated with acne. Efficacy and tolerance are maximized with combination therapy, and the degree of skin irritation is minimized. Furthermore, adjunctive therapy with topical retinoids and antibiotics tends to produce results more quickly than single-agent therapy.

This article will examine the individual agents used in combination for acne management, and discuss the mechanisms by which they achieve efficacy. The rationale of utilizing topical retinoids with antibiotics will be highlighted, particularly in relation to improved tolerance and reduced irritation.

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Acne is the most common of all skin disorders, afflicting 30% to 85% of adolescents and, in lesser proportions, mature individuals as well1. In recent years, advances in the understanding of the pathophysiology of acne and acne inflammation, retinoid receptor biology, and Propionibacterium acnes (P. acnes) microbiology has led to the development of new therapeutic agents and new management regimens. As a result, the disease can be targeted somewhat more precisely than in the past. Consequently, many patients can hope to negotiate adolescence with fewer of the embarrassing stigmata of acne that impact so adversely on quality of life in this age group. Moreover, we now have the potential to prevent the lasting sequelae of the disease – scarring and post-inflammatory hyperpigmentation – in many of our patients.

A brief summary of the newest understanding of the pathophysiology of acne is useful for the clinician in order to optimize patient care. Acne is a chronic inflammatory process that begins within the pilosebaceous canal and affects areas of the skin with the highest densities of sebaceous follicles: the face,back and chest2. At pubarche, increased androgen production triggers the enlargement of the sebaceous glands, which then produce increased amounts of sebum. Epithelial cell turnover increases, and hyperproliferation of corneocytes lining the follicular canal begins to occur. The abnormally desquamated corneocytes and excessive sebum form a bulging follicular plug, known as a microcomedo. Normal drainage from the follicle is blocked, creating an ideal microenvironment for the growth of P. acnes, an anaerobic bacterium normally present in the follicle.


Jonathan S Weiss MD

Gwinnett Clinical Research Center

2383 Pate Street

Snellville, GA 30078

Phone: (770) 972-4845

Fax: (770) 972-0358

The mechanisms controlling the abnormal desquamation are still unclear. However, there is some evidence that changes in sebum composition or secretion may irritate follicular keratinocytes, leading to the release of interleukins and the initiation of comedogenesis3,4.

The microcomedo is the invisible precursor to all acne lesions including closed and open comedones – non-inflammatory lesions inside pilosebaceous follicles – as well as later inflammatory papules and pustules that arise from comedones. In one study, biopsies of papules revealed a microcomedone in 52%, a whitehead in 22%, and a blackhead in 10%5. About 28% of biopsy sections of normal-appearing skin in an individual with acne show histological features of microcomedos6.

Current best practice dictates that acne management focus strongly on preventing microcomedo formation and resolving existing ones. Closed comedos (whiteheads) and open comedos (blackheads) develop from microcomedos and are the first visible acne lesions. It is now believed that the dark color of open comedos results from blockage of light transmission

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