eMedicine Specialties > Dermatology > Diseases of the Adnexa

Acne Vulgaris

Author: Julie C Harper, MD, Assistant Program Director, Assistant Professor, Department of Dermatology, University of Alabama at Birmingham
Coauthor(s): James Fulton Jr, MD, PhD, Medical Director, Fulton Skin Institute
Contributor Information and Disclosures

Updated: Jul 15, 2008

Introduction

Background

Acne vulgaris is a common skin disease that affects 85-100% of people at some time during their lives. It is characterized by noninflammatory follicular papules or comedones and by inflammatory papules, pustules, and nodules in its more severe forms. 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.

The following are other eMedicine articles on acne:

Additionally, the news article Acne Treatment Linked to Depression and the Medscape Acne Resource Center may be helpful.

Pathophysiology

The pathogenesis of acne vulgaris is multifactorial. Four key factors are responsible for the development of an acne lesion. These factors are follicular epidermal hyperproliferation with subsequent plugging of the follicle, excess sebum, the presence and activity of Propionibacterium acnes, and inflammation.

Follicular epidermal hyperproliferation is the first recognized event in the development of acne. The exact underlying cause of this hyperproliferation is not known. Currently, the 3 leading hypotheses have been proposed to explain why the follicular epithelium is hyperproliferative in individuals with acne.

First, androgen hormones have been implicated as the initial trigger. Comedones, the clinical lesion that results from follicular plugging, begin to appear around adrenarche in persons with acne. Furthermore, the degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S). Additionally, androgen hormone receptors are present in the portion of the follicle where the comedone forms; individuals with malfunctioning androgen receptors do not develop acne.

Second, changes in lipid composition have been implicated in the development of acne vulgaris. Persons with acne frequently have excess sebum production and oily skin. This excess sebum may dilute the normal epidermal lipids and result in a change in the relative concentrations of the various lipids. Diminished concentrations of linoleic acid have been demonstrated in individuals with acne and, interestingly, these levels normalize after successful treatment with isotretinoin. This relative decrease in linoleic acid may be what initiates comedone formation.

Inflammation is the third hypothesized factor incriminated in comedone formation.1 Interleukin (IL)–1–alpha is a proinflammatory cytokine. It has been used in a tissue model to induce follicular epidermal hyperproliferation and comedone formation. Although inflammation is not apparent microscopically or clinically in early lesions of acne, it may still play a pivotal role in the development of acne vulgaris and the comedones.

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. Androgen hormones, in particular, promote sebum production and release. 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 a microaerophilic organism present in many acne lesions. Although, it has not been shown to be present in the earliest lesions of acne, the microcomedo, its presence in later lesions is almost certain. 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. Recent studies have shown that P acnes activates the toll-like receptor 2 on monocytes and neutrophils.2 Activation of the toll-like receptor 2 then leads to the production of multiple proinflammatory cytokines, including IL-12, IL-8, and tumor necrosis factor. Hypersensitivity to P acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.3

Inflammation may be a primary phenomenon or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to P acnes as mentioned above. However, IL-1-alpha expression has been identified in the microcomedone, and it may play a role in the development of acne.4

Frequency

United States

Acne vulgaris affects 85-100% of people at some time during their lives.

Mortality/Morbidity

  • Acne can cause physical pain and psychosocial suffering.
  • Acne can lead to scarring.
  • A severe inflammatory variant of acne, acne fulminans, can be associated with fever, arthritis, and other systemic symptoms.

Race

  • The prevalence of acne in North Americans of African ancestry and whites is similar.

Sex

  • Acne vulgaris is more common in males than in females during adolescence.
  • It is more common in women than in men during adulthood.

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 resolves spontaneously.
  • Adolescent acne usually begins prior to the onset of puberty, when the adrenal gland begins 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.

Clinical

History

  • Local symptoms may include pain or tenderness.
  • Systemic symptoms are most often absent in acne vulgaris.
  • Severe acne with associated systemic signs and symptoms is referred to as acne fulminans.
  • Acne may have a psychological impact on any patient, regardless of the severity or the grade of the disease.

Physical

Acne vulgaris is characterized by comedones, papules, pustules, and nodules in a sebaceous 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, the back, and the 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.
  • Mild inflammatory acne is characterized by inflammatory papules and comedones.
  • Moderate inflammatory acne has comedones, inflammatory papules, and pustules. Greater numbers of lesions are present than in milder inflammatory acne.
  • Nodulocystic acne is characterized by comedones, inflammatory lesions, and large nodules greater than 5 mm in diameter. Scarring is often evident.

Causes

An external cause is seldom identifiable in acne vulgaris.

  • Some cosmetic agents and hair pomades may worsen acne.
  • Medications that can promote acne include steroids, lithium, some antiepileptics, and iodides.
  • Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrine disorders with excess androgens may trigger the development of acne vulgaris.
  • Acne vulgaris may also be influenced by genetic factors.5

More on Acne Vulgaris

Overview: Acne Vulgaris
Differential Diagnoses & Workup: Acne Vulgaris
Treatment & Medication: Acne Vulgaris
Follow-up: Acne Vulgaris
Multimedia: Acne Vulgaris
References
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References

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Further Reading

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Keywords

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

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Contributor Information and Disclosures

Author

Julie C Harper, MD, Assistant Program Director, Assistant Professor, Department of Dermatology, University of Alabama at Birmingham
Julie C Harper, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Stiefel Honoraria Speaking and teaching; Allergan Honoraria Speaking and teaching; Intendis Honoraria Speaking and teaching; Coria Honoraria Speaking and teaching; Sanofi-Aventis Honoraria Speaking and teaching

Coauthor(s)

James Fulton Jr, MD, PhD, Medical Director, Fulton Skin Institute
James Fulton Jr, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Cosmetic Surgery, American Academy of Dermatology, Phi Beta Kappa, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Alexa F Boer Kimball, MD, MPH, Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital and Brigham and Women's Hospital
Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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