Maintenance Therapy for Acne Vulgaris: The Fine Balance Between Efficacy, Cutaneous Tolerability, and Adherence

John E. Wolf, Jr., MD


Skinmed. 2004;3(1) 

In This Article

Pathophysiology of the Microcomedo

Comedogenesis involves the accumulation of corneocytes within the pilosebaceous duct due to hyperproliferation of ductal keratinocytes, increased cohesion of the keratinocytes, or a combination of both pathophysiologic factors.[2] It appears that the cytokine interleukin 1 (IL-1) is involved in keratinocyte proliferation and hypercornification of the infundibulum.[4] This finding provides support for the idea that all forms of acne vulgaris constitute immune system-mediated disorders.

The microcomedo is not a clinically visible lesion. Histologic examination has demonstrated that the ducts of microcomedos show minimal but definite distension, with a prominent granular layer in the ductal epithelium.[5]

Researchers performed skin biopsies on normal-appearing skin sections in patients with comedonal acne. The biopsies revealed that microcomedos were the most common variety of comedones; histologic evidence of microcomedos was found in 28% of samples.[2] Microcomedos can also coexist with inflammatory lesions. Thus, these researchers recommend that topical therapies be applied to obvious acne lesions as well as the adjacent, normal-appearing skin area.[2] Subclinical microcomedos may lurk beneath normal-appearing skin, making treatment of such areas especially relevant to maintenance treatment.


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