What is the pathogenesis of acne vulgaris, and is it an infectious or disease state?

From the Guidelines

Acne vulgaris is a chronic inflammatory skin condition, not primarily an infection, though bacteria play a role in its pathogenesis. The development of acne involves four key processes: excessive sebum production by sebaceous glands, abnormal follicular keratinization leading to clogged pores, colonization by Cutibacterium acnes (formerly Propionibacterium acnes), and subsequent inflammation 1. The process begins when hormones, particularly androgens during puberty, stimulate sebaceous glands to produce more oil. This excess sebum combines with dead skin cells that aren't properly shed, forming a plug in the hair follicle. C. acnes, a normal skin bacterium, thrives in this oxygen-poor, lipid-rich environment, multiplying and triggering an immune response.

While C. acnes is involved, acne is not considered a primary infection but rather a multifactorial disease state where the bacteria contribute to inflammation rather than cause a true infection. This explains why treatments target multiple aspects of pathogenesis, including sebum production (isotretinoin), keratin formation (retinoids), bacterial growth (antibiotics), and inflammation (anti-inflammatory agents), rather than focusing solely on eliminating bacteria as would be done for a true infection 1. The guidelines for the management of acne vulgaris support this approach, recommending a combination of topical and oral therapies to address the various factors involved in the pathogenesis of acne.

Key factors in the pathogenesis of acne include:

• Follicular hyperkeratinization
• Microbial colonization with Cutibacterium acnes
• Sebum production
• Complex inflammatory mechanisms involving both innate and acquired immunity
• Neuroendocrine mechanisms
• Genetic and nongenetic factors 1.

The multifactorial nature of acne pathogenesis is reflected in the guidelines for its management, which emphasize a comprehensive approach to treatment. This approach includes the use of topical benzoyl peroxide, retinoids, and/or antibiotics, as well as oral doxycycline and isotretinoin for severe cases 1. By targeting the various factors involved in the pathogenesis of acne, healthcare providers can effectively manage the condition and improve patient outcomes.

From the FDA Drug Label

CLINICAL PHARMACOLOGY: The exact mechanism by which erythromycin reduces lesions of acne vulgaris is not fully known; however, the effect appears to be due in part to the antibacterial activity of the drug. The pathogenesis of acne vulgaris involves an infection process, as the drug's antibacterial activity plays a role in reducing lesions.

• The drug erythromycin has antibacterial properties, which suggests that acne vulgaris has an infectious component.
• The mechanism is not fully understood, but it is known that erythromycin's effect is due in part to its antibacterial activity 2. The condition can be considered a disease state with an infectious component, rather than a simple infection.

From the Research

Pathogenesis of Acne Vulgaris

• Acne vulgaris is a persistent inflammatory skin condition affecting the pilosebaceous unit, involving a combination of factors including increased sebum production, changes in keratinization, colonization of hair follicles by Propionibacterium acnes (P. acnes), and the release of inflammatory mediators 3, 4.
• The development of acne vulgaris is a complex process, with multiple factors contributing to its pathogenesis, including androgen-induced increased sebum production, altered keratinisation, inflammation, and bacterial colonization of hair follicles 4, 5.
• Acne vulgaris can be classified as mild, moderate, or severe based on the number and type of skin lesions, and treatment selection is based on disease severity, patient preference, and tolerability 5, 6.

Infection or Disease State

• Acne vulgaris is considered a chronic inflammatory disease of the pilosebaceous unit, rather than a simple infection 4, 6.
• While Propionibacterium acnes (P. acnes) plays a role in the development of acne vulgaris, the condition is not solely caused by a bacterial infection 3, 7.
• The presence of P. acnes is a contributing factor to the development of acne vulgaris, but it is not the sole cause of the condition, and other factors such as sebum production, keratinization, and inflammation also play important roles 4, 5.

Infection Process

• The colonization of hair follicles by P. acnes is a key factor in the development of acne vulgaris, and the bacterium produces porphyrins that can activate and lead to inflammation 3, 7.
• The infection process in acne vulgaris is complex, involving the interaction of multiple factors, including bacterial colonization, sebum production, and inflammation 4, 5.
• Treatment of acne vulgaris often involves targeting the bacterial colonization, as well as reducing sebum production and inflammation, to effectively manage the condition 5, 6.