Overview

Acne vulgaris is the result of several pathologic processes that occur within the pilosebaceous unit (i.e., hair follicle plus associated sebaceous glands) located in the dermis (middle layer of the skin). Hyperproliferation of keratinocytes results in cell cohesion and formation of a plug that blocks the follicle orifice. This plug distends the follicle to form a microcomedo, the initial pathologic lesion of acne.

As more cells and sebum accumulate, the microcomedo enlarges and becomes visible as a closed comedo, or whitehead—a small, pale nodule just beneath the skin surface. If the contents of the plug distend the orifice, the plug will protrude from the pore, causing an open comedo or blackhead. Blackheads are dark in color because of the presence of melanin and oxidization of lipids upon exposure to air.

Comedones are the precursor of other acne lesions. Behind the plug, the buildup of sebum is an ideal habitat for proliferation of Propionibacterium acnes. This bacterium breaks sebum down into highly irritating free fatty acids and produces proinflammatory mediators. The irritation and inflammation cause localized tissue destruction and inflammatory acne lesions. Papules are characterized by redness and inflammation in and around the follicular canal. Pustules are similar to papules but have visible purulence in the center of the lesion. Nodules form when the follicle wall is disrupted and releases its contents into the surrounding dermis.

Epidemiology

• Acne affects 40–50 million Americans and is the most common skin condition seen in dermatology practice.
  
• Acne reportedly is more prevalent in male patients before age 16 years and in female patients after the age of 23.
  
• Although the peak prevalence of acne is during the adolescent years (>85% of adolescents are affected), the mean age of patients seeking treatment for acne is 24 years.

Etiology

• The exact cause of acne has not been determined yet. The causes are multifactorial and influenced largely by both genetic and hormonal factors.
  
• Although there is no direct correlation to severity, a patient’s likelihood of developing acne is increased if one or both parents had acne.
  
• Pathologic factors involved in the development of acne are (1) androgenic hormonal triggers, (2) excessive sebum production, (3) alterations in keratinization, (4) proliferation of P. acnes bacteria on the skin, and (5) resultant inflammatory responses.
  
• The timing of the start of puberty and the appearance of acne is not a coincidence. The rise in androgenic hormones triggers these processes.
  
  
  
  • The conversion of testosterone to dihydrotestosterone stimulates an increase in the size and metabolic activity of sebaceous glands.
    
  • The excessive sebum serves as a breeding ground for P. acnes as the comedo develops.
  
  
• A number of factors are known to exacerbate existing acne and cause periodic flare-ups of acne in some patients (see Table 1).

Signs and Symptoms

• Acne lesions can be classified generally as noninflammatory or inflammatory.
  
  
  
  • Noninflammatory lesions consist of either open or closed comedones (i.e., whiteheads or blackheads).
    
  • Inflammatory lesions include papules, pustules, and nodules.
  
  
• Noninflammatory lesions often are the first to manifest in the early stages of puberty and often appear initially on the forehead. With the progression of puberty and with age—especially in women—lesions tend to appear on areas of the body below the neck, such as the chest and back.
  
  
  
  • It is not uncommon for women in their 30s and 40s to have acne that is concentrated on the chin and along the jaw line.
  
  
• If acne lesions persist beyond the mid-20s or develop in the mid-20s or later, the symptoms may signal rosacea rather than acne vulgaris. A differential diagnosis is necessary because the treatment of rosacea, although similar to that for acne, has unique elements.

TABLE 1. Exacerbating Factors in Acne

Complications

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