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Acne vulgaris is one of the most common cutaneous disorders and
occurs in more than 85% of individuals between the ages
of 12 to 24 years.1The degree of involvement
is quite variable. Many individuals have mild to moderate disease
of a transient nature; however, others develop severe disease that can
lead to significant scarring and emotional distress. The
onset of clinical disease usually occurs between the ages of 12 and
14 years, but mild disease may develop as early as 7 to 8 years
of age and tends to occur somewhat earlier in girls than in boys.
This prepubertal acne may be the first sign of pubertal maturation.
Acne in this group is primarily comedonal and midfacial, favoring
the forehead, nose, medial cheeks, and chin.2 Acne generally
resolves in the late teens or early 20s, but persistence into the
third decade or onset in middle age, particularly in women, is not
unusual. Although most acne may be thought of as physiologic, disease
with unusual features such as early onset or severe recalcitrance
to therapy warrants evaluation for underlying abnormalities of the
adrenal or ovarian systems.
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Acne is most commonly localized to areas of highest sebaceous gland
concentration and activity, such as the face, chest, and upper back.
Acne is a multifactorial disease, involving excessive or increased
sebum production, abnormal epithelial cell proliferation and desquamation,
microbial proliferation, and inflammation.3 Acne lesions
begin with the development of the microcomedone, a small cyst plugged
by accumulated sebum, desquamated epithelial cells, vellus hairs, and bacteria.
The formation of closed comedones (whiteheads) and open comedones (blackheads)
is initiated by abnormal cornification of the follicular orifice
(Fig. 365-1). The epidermal cells
lining the orifice form adherent cornified sheets of cells instead
of desquamating as single cells to be carried away with the sebum
flow. These cornified sheets occlude the follicular opening and
lead to cystic dilatation of the follicle. Open comedones have a
widely patent surface orifice.
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Inflammatory lesions (ie, papules, pustules, or nodules) develop when
the intradermal wall of the comedone ruptures, releasing
comedonal contents into the dermis and provoking an intense, suppurative, and
later a foreign-body, granulomatous-type inflammatory reaction.
In cystic acne, the inflammatory reaction is extreme, resulting
in deep nodules, sinus tracts, and cysts.
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The surge of androgen production that occurs in adolescence
leads to increased sebum production. 5-Alpha-reductase, which converts
testosterone to the more potent dihydrotestosterone (DHT), appears
to be more highly concentrated in infrainfundibular keratocinocytes.3 Interleukin-1
located in the hair follicle can also stimulate hypercornification.3
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Sebum serves as a substrate for Propionibacterium acnes. This
anaerobic diphtheroid is a normal resident of the pilosebaceous
unit and overgrows within the blocked sebaceous follicle. Bacterial
lipases liberate free fatty ...