Contemporary acne treatment options: Achieving optimal results

Contemporary acne treatment options: Achieving optimal results

Aug 18, 2007
Alan R. Shalita, MD
Patient Care

Key Points
-Pathogenesis of acne: Four factors are involved: abnormal keratinization in pilosebaceous follicles leading to the formation of microcomedones, increased sebum production, accumulation of Propionibacterium acnesthat releases proinflammatory factors, and perifollicular inflammation.
-Treatment options: Mild acne may respond to OTC products containing salicylic acid, a mild comedolytic agent, or 2.5% to 5% benzoyl peroxide.
-Topical retinoids are particularly effective for noninflamed lesions.
-A short course of oral antibiotics may be needed to treat patients with moderate/severe inflammatory acne.
-Treatment with isotretinoin is reserved for patients with resistant, disfiguring acne.

In Western societies, acne develops in an estimated 85% of the adolescent population and affects 8% of 25- to 34-year-olds and 3% of 35- to 44-year-olds. Occurring in all racial groups, it tends to appear slightly earlier in girls than in boys. If treatment is delayed or not taken seriously early in the course of the disease, a significant number of patients suffer from cutaneous and emotional scars that can result in chronic problems with self-esteem, social withdrawal, depression, and unemployment.

PATHOGENESIS AND SEVERITY

Acne is a chronic inflammatory disease of the pilosebaceous follicles, which are most common on the face, neck, and upper trunk. These pilosebaceous units consist of large sebaceous glands associated with small hair follicles. Sebaceous glands excrete sebum, a complex lipid mixture of triglycerides, squalene, cholesterol, and wax esters. Sebum is transported up the follicular canal to the skin surface, carrying with it desquamated cells from the follicular epithelium.

When the normal flow of sebum onto the skin surface is obstructed by follicular hyperkeratosis, microcomedones are formed. Early stages of acne typically manifest 1 to 2 years before the onset of puberty as a result of androgenic stimulation of the sebaceous glands. The microcomedo, the precursor of all acne lesions, evolves into either a noninflammatory closed comedo (whitehead), an open comedo (blackhead), or an inflammatory pustule, papule, or nodule. Acne arises from the interaction of the following 4 factors:

Comedogenesis due to sebaceous follicle obstruction resulting from increased cohesiveness of follicular epithelial cells, hyperproliferation of ductal keratinocytes, or both
Excessive sebum production caused by androgenic stimulation of sebaceous glands
Proliferation of Propionibacterium acnes, an anaerobic diphtheroid that populates sebaceous follicles as a normal constituent of cutaneous flora and that produces chemotactic factors and proinflammatory mediators
Inflammation as a result of P acnes proliferation, follicular rupture, and extension of inflammation into the dermis. The result is formation of the inflammatory lesions of acne: papules, pustules, and nodules.

Teens and preteens with genetically susceptible follicles will develop acne. Acne usually resolves in the third decade as adrenal androgen levels decline, although the condition may persist or develop de novo in adulthood. Postadolescent acne mainly affects women, about one-third of whom have features of hyperandrogenicity.

Therapies for acne are directed at the multiple factors that combine to cause it and are individualized according to the fluctuating severity of the disorder. The principle of treatment is to disrupt the cycle of follicular plugging, increased sebum production, colonization of P acnes, and inflammation. When these processes are targeted early, the microcomedo can be significantly reduced and the inflammatory stages of disease that produce scarring can be prevented. While oral estrogen therapy and oral isotretinoin are the only available treatments that affect sebum production, P acnes proliferation and microcomedones can be well managed with antimicrobials and topical retinoids.

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