From the Guidelines
Acne vulgaris is a chronic inflammatory skin condition, not primarily an infectious disease, though bacteria play a role in its pathogenesis. The development of acne involves four key pathological processes: excessive sebum production by sebaceous glands stimulated by androgens, abnormal follicular keratinization leading to comedone formation, colonization of the hair follicle by Cutibacterium acnes (formerly Propionibacterium acnes), and subsequent inflammation 1. While C. acnes is a normal skin commensal, it contributes to inflammation by producing enzymes that break down sebum into irritating fatty acids and by triggering immune responses through activation of toll-like receptors.
Pathogenesis of Acne Vulgaris
The process begins when hormonal influences, particularly during puberty, increase sebum production, creating an environment where C. acnes can proliferate, especially in blocked follicles 1. The bacteria then trigger inflammatory responses, resulting in papules, pustules, nodules, or cysts. Key factors in the pathogenesis 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
Treatment Approaches
Treatment approaches target these pathogenic factors through:
- Topical retinoids to normalize follicular keratinization
- Benzoyl peroxide or antibiotics to reduce bacterial load
- Hormonal therapies to decrease sebum production
- Isotretinoin may be used for severe cases as it addresses all pathogenic factors simultaneously 1. Strong recommendations are made for topical benzoyl peroxide, retinoids, and/or antibiotics and their fixed-dose combinations, and for oral doxycycline, with oral isotretinoin strongly recommended for severe acne 1.
Infection Process
While acne is not primarily considered an infectious disease, the role of C. acnes in its pathogenesis indicates an infection process is involved, albeit as part of a multifactorial disease state 1. The use of antibiotics in treatment, especially for moderate to severe cases, further highlights the role of bacterial infection in acne's pathogenesis. However, concerns about antibiotic resistance and the disruption of the microbiome have led to guidelines recommending the limitation of systemic antibiotic use in acne treatment 1.
From the Research
Pathogenesis of Acne Vulgaris
- Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit, resulting from androgen-induced increased sebum production, altered keratinisation, inflammation, and bacterial colonisation of hair follicles by Propionibacterium acnes (now known as Cutibacterium acnes) 2, 3.
- The pathophysiology of acne vulgaris involves the interplay of follicular hyperkeratinization, the presence of Propionibacterium acnes bacteria in the follicular canal, and sebum production 4.
- The disease is characterised by the formation of comedones, inflammatory lesions, and scarring, which can have a significant impact on quality of life and self-image 5.
Infection or Disease State
- Acne vulgaris is not solely an infection, but rather a complex disease state involving multiple factors, including bacterial colonisation, inflammation, and altered keratinisation 2, 6.
- The role of Propionibacterium acnes in the pathogenesis of acne is well established, and immunotherapy targeting this bacterium has shown promise in reducing inflammation and improving symptoms 6.
Infection Process
- The infection process in acne vulgaris involves the colonisation of hair follicles by Propionibacterium acnes, which can lead to inflammation and the formation of acne lesions 2, 3.
- The use of antibiotics in the treatment of acne vulgaris is common, but their effectiveness can be limited by the development of antibiotic-resistant bacterial strains 6.
- Topical and systemic therapies, including retinoids, benzoyl peroxide, and oral antibiotics, can be effective in reducing acne lesions and improving symptoms, but the optimal treatment approach depends on the severity and type of acne, as well as individual patient factors 3, 5.