acne vulgaris

Pathophysiology of Acne vulgaris

Acne vulgaris

Acne is a common, usually self-limiting disease involving inflammation of the sebaceous follicles of the face and upper trunk.


Acne usually begins in the prepubertal period and progresses as androgen production and sebaceous gland activity increase with gonad development. Acne progresses through four stages: (1) increased follicular keratinization, (2) increased sebum production, (3) bacterial lipolysis of sebum triglycerides to free fatty acids, and (4) inflammation.

Circulating androgens cause sebaceous glands to increase their size and activity. There is increased keratinization of epidermal cells and development of an obstructed sebaceous follicle, called a microcomedone. Cells adhere to each other, forming a dense keratinous plug. Sebum, produced in increasing amounts, becomes trapped behind the keratin plug and solidifies, contributing to open or closed comedone formation.

Acne vulgaris

Pooling of sebum in the follicle facilitates proliferation of the anaerobic bacterium Propionibacterium acnes, which generates a T-cell response resulting in inflammation. P. acnes produces a lipase that hydrolyzes sebum triglycerides into free fatty acids that may increase keratinization and lead to microcomedone formation.

The closed comedone (whitehead) is the first visible lesion of acne. It is almost completely obstructed to drainage and has a tendency to rupture. An open comedone (blackhead) is formed as the plug extends to the upper canal and dilates its opening. Acne characterized by open and closed comedones is termed noninflammatory acne


Pus formation occurs due to recruitment of neutrophils into the follicle during the inflammatory process and release of P. acnes–generated chemokines. P. acnes also produces enzymes that increase permeability of the follicular wall, causing it to rupture, thereby releasing keratin, lipids, and irritating free fatty acids into the dermis. Inflammatory lesions that may form and lead to scarring include pustules, nodules, and cysts.

Clinical presentation

Lesions usually occur on the face, back, upper chest, and shoulders. Severity varies from a mild comedonal form to severe inflammatory acne. The disease is categorized as mild, moderate, or severe, depending on the type and severity of lesions. Lesions may take months to heal completely, and fibrosis associated with healing may lead to permanent scarring.


Diagnosis is established by patient assessment, which includes observation of lesions and excluding other potential causes (eg, drug-induced acne). Several different systems are in use to grade acne severity. 

Acne treatment ( phamacological and non-pharmacological)

2009 Global Alliance to Improve Outcomes in Acne consensus statements:

  • Acne should be approached as a chronic disease.
  • Strategies to limit antibiotic resistance are important in acne management.
  • Combination retinoid-based therapy is first-line therapy.
  • Topical retinoids should be first-line agents in maintenance therapy.
  • Early, appropriate treatment is best to minimize potential for acne scars.
  • Adherence should be assessed via verbal interview or use of a simple tool.

Non-pharmacologic therapy

Encourage patients to avoid aggravating factors, maintain a balanced diet, and control stress. Patients should wash no more than twice daily with a mild, non-fragranced opaque or glycerin soap or a soap-less cleanser. Scrubbing should be minimized to prevent follicular rupture. Comedone extraction results in immediate cosmetic improvement but has not been widely tested in clinical trials.

Pharmacologic therapy

Comedonal noninflammatory acne: Select topical agents that target the increased keratinization by producing exfoliation. Topical retinoids (especially adapalene) are drugs of choice. Benzoyl peroxide or azelaic acid can be considered.

Mild to moderate papulopustular inflammatory acne: It is important to reduce the population of P. acnes. Either the fixed-dose combination of adapalene and benzoyl peroxide or the fixed-dose combination of topical clindamycin and benzoyl peroxide is first choice therapy. As alternatives, a different topical retinoid used with a different topical antimicrobial agent could be used, with or without benzoyl peroxide. Azelaic acid or benzoyl peroxide can also be recommended

In more widespread disease, combination of a systemic antibiotic with adapalene is recommended for moderate papulopustular acne. If there are limitations in use of first-choice agents, alternatives include fixed-dose combination of erythromycin and tretinoin, fixed-dose combination of isotretinoin and erythromycin, or oral zinc. In cases of widespread disease, a combination of a systemic antibiotic with either benzoyl peroxide or adapalene in fixed combination with benzoyl peroxide can be considered.

Severe papulopustular or moderate nodular acne: Oral isotretinoin monotherapy is first choice. Alternatives include systemic antibiotics in combination with adapalene, with the fixed-dose combination of adapalene and benzoyl peroxide or in combination with azelaic acid. If there are limitations to use of these agents, consider oral antiandrogens in combination with oral antibiotics or topical treatments, or systemic antibiotics in combination with benzoyl peroxide.


Nodular or conglobate acne: Monotherapy with oral isotretinoin is first choice. An alternative is systemic antibiotics in combination with azelaic acid. If limitations exist to these agents, consider oral antiandrogens in combination with oral antibiotics, systemic antibiotics in combination with adapalene, benzoyl peroxide, or the adapalene-benzoyl peroxide fixed-dose combination.

Maintenance therapy for acne: Topical retinoids are most commonly recommended (adapalene, tazarotene, or tretinoin). Topical azelaic acid is an alternative. Maintenance is usually begun after a 12-week induction period and continues for 3 to 4 months. A longer duration may be necessary to prevent relapse upon discontinuation.


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