Introduction
Background
Acne vulgaris is a common skin disease that affects 60-70% of Americans at some time during their lives. Twenty percent will have severe acne, which results in permanent physical and mental scarring. Acne vulgaris is American's most common disease and is characterized by noninflammatory, open or closed comedones and by inflammatory papules, pustules, and nodules. Acne vulgaris affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back.
Other eMedicine articles on acne include Acne Conglobata, Acne Fulminans, Acne Keloidalis Nuchae, and Acneiform Eruptions. Also see the Medscape Acne Resource Center.
Pathophysiology
The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics.1 If both parents had acne, 3 of 4 children will have acne. If 1 parent had acne, then 1 of 4 of the children will have acne. However, similar to other genetic conditions, not every family will have the same pattern, with acne vulgaris sometimes skipping generations. What is inherited is the propensity for follicular epidermal hyperproliferation with subsequent plugging of the follicle. Additional aggravating factors include excess sebum, the presence and activity of Propionibacterium acnes, and inflammation.
Retention hyperkeratosis is the first recognized event in the development of acne vulgaris.2 The exact underlying cause of this hyperproliferation is not known. Currently, 3 leading hypotheses have been proposed to explain why the follicular epithelium produces cells at a rapid rate that are retained in individuals with acne.
First, androgen hormones have been implicated as the initial trigger.3 Comedones, the clinical lesion that results from follicular plugging, begin to appear around adrenarche in persons with acne in the T-zone area. Furthermore, the degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S).4 Additionally, androgen hormone receptors are present in sebaceous glands; individuals with malfunctioning androgen receptors do not develop acne.5
Excess sebum is another key factor in the development of acne vulgaris. Sebum production and excretion are regulated by a number of different hormones and mediators. In particular, androgen hormones promote sebum production and release.6 Still, most men and women with acne have normal circulating levels of androgen hormones. An end-organ hyperresponsiveness to androgen hormones has been hypothesized. Androgen hormones are not the only regulators of the human sebaceous gland. Numerous other agents, including growth hormone and insulinlike growth factor, also regulate the sebaceous gland and may contribute to the development of acne.
P acnes is an anaerobic organism present in acne lesions. The presence of P acnes promotes inflammation through a variety of mechanisms. P acnes stimulates inflammation by producing proinflammatory mediators that diffuse through the follicle wall. Studies have shown that P acnes activates the toll-like receptor 2 on monocytes and neutrophils.7 Activation of the toll-like receptor 2 then leads to the production of multiple proinflammatory cytokines, including interleukins 12 and 8 and tumor necrosis factor. Hypersensitivity to P acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.8
Inflammation may be a primary phenomenon or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to P acnes. However, interleukin 1-alpha expression has been identified in microcomedones, and it may play a role in the development of acne.9
Frequency
United States
Acne vulgaris affects 60-70% of Americans at some time during their lives. Twenty percent have severe acne with permanent physical and mental scarring.10
International
Persons of some races are affected more than others. Cystic acne is prevalent in the Mediterranean region from Spain to Iran.11,12
Mortality/Morbidity
Acne can cause psychosocial suffering.13 Acne can lead to physical scarring. A severe inflammatory variant of acne, acne fulminans, can be associated with fever, arthritis, and other systemic symptoms.
Race
Acne is common in North American whites. Spanish persons tend to more commonly develop cystic acne. African Americans have a higher prevalence of pomade acne, likely stemming from the use of hair pomades.
Sex
During adolescence, acne vulgaris is more common in males than in females. In adulthood, acne vulgaris is more common in women than in men.14
Age
Acne vulgaris may be present in the first few weeks and months of life, when a newborn is still under the influence of maternal hormones and when the androgen-producing portion of the adrenal gland is disproportionately large. This neonatal acne tends to resolve spontaneously. However, the neonate should be treated with a mild retinoid to clear out the impacted follicles.
Adolescent acne usually begins with the onset of puberty, when the gonads begin to produce and release more androgen hormone.
Acne is not limited to adolescence. Twelve percent of women and 5% of men at age 25 years have acne. By age 45 years, 5% of both men and women still have acne.15
Clinical
History
Local symptoms of acne vulgaris may include pain or tenderness.
Systemic symptoms are most often absent in acne vulgaris. Severe acne with associated systemic signs and symptoms such as fever is referred to as acne fulminans. Additionally, acne vulgaris may have a psychological impact on any patient, regardless of the severity or the grade of the disease.16
Physical
Acne vulgaris is characterized by comedones, papules, pustules, and nodules in a sebaceous gland distribution. A comedone is a whitehead (closed comedone) or a blackhead (open comedone) without any clinical signs of inflammation. Papules and pustules are raised bumps with obvious inflammation. The face may be the only involved skin surface, but the chest, back, and upper arms are often involved.
In comedonal acne, no inflammatory lesions are present. Comedonal lesions are the earliest lesions of acne, and closed comedones are the precursor lesion of inflammatory lesions. Note the image below.
Acne, grade I; multiple open comedones.
Mild acne is characterized by comedones and a few papulopustules. Note the image below.
Acne, grade II; closed comedones.
Moderate acne has comedones, inflammatory papules, and pustules. Greater numbers of lesions are present than in milder inflammatory acne. Note the image below.
Acne, grade III; papulopustules.
Nodulocystic acne is characterized by comedones, inflammatory lesions, and large nodules greater than 5 mm in diameter. Scarring is often evident. Note the image below.
Acne, grade IV; multiple open comedones, closed comedones, and papulopustules, plus cysts.
Causes
The main underlying cause of acne is a genetic predisposition. The condition is inherited in an autosomal dominant pattern with incomplete penetrance. For example, acne vulgaris may skip a generation. The following aggravating factors are recognized:
- Cosmetic agents and hair pomades may worsen acne.
- Medications that can promote acne development include steroids, lithium, some antiepileptics, and iodides.
- Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrinological disorders associated with excess androgens may trigger the development of acne vulgaris. Even pregnancy may cause a flare-up.17
- Mechanical occlusion with headbands, shoulder pads, back packs, or under-wire bras can be aggravating factors
- Excessive sunlight may either improve or flare acne. In any case, the ultraviolet exposure ages the skin.
More on Acne Vulgaris |
 Overview: Acne Vulgaris |
| Differential Diagnoses & Workup: Acne Vulgaris |
| Treatment & Medication: Acne Vulgaris |
| Follow-up: Acne Vulgaris |
| Multimedia: Acne Vulgaris |
| References |
| Further Reading |
| Next Page » |
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Keywords
acne vulgaris, acne lesion, follicular papules, comedones, inflammatory papules, inflammatory pustules, inflammatory nodules, follicular epidermal hyperproliferation and hyperkeratinization, excess sebum, Propionibacterium acnes, P acnes, microcomedo, microcomedone, acne fulminans, comedonal acne, nodulocystic acne, congenital adrenal hyperplasia, polycystic ovary syndrome
