Acne Vulgaris: an Inflammatory Disease Even Before the Onset of Clinical Lesions

Abstract

Acne is a chronic self-limited disease, which affects mostly teenagers, without gender difference. In recent years, the incidence has increased in female adults. The factors involved in this epidemiological observation are still under discussion in the literature. Clinically, acne is characterized by different types of lesions. The disease affects the regions rich in sebaceous glands (face, chest and upper back). The clinical lesions are: open and closed comedones, erythematous papules, pustules, nodules and different types of scars. Taking into consideration the general concept of inflammation (redness, pain, heat and loss of function), acne is traditionally classified as non-inflammatory (open and closed comedones) and inflammatory (other primary lesions). With the knowledge advancement this concept seems to be wrong and therefore acne would be an inflammatory disease even before the onset of their clinical lesions.

Reduction of Inflammatory and Noninflammatory Lesions with Topical Tyrothricin 0.1% in the Treatment of Mild to Severe Acne Papulopustulosa: A Randomized Controlled Clinical Trial

“…Referring to acne pathogenesis, hyperproliferation of the follicular epithelium leads to the development of clinically nonvisible microcomedones, which are the precursor lesions of acne vulgaris. This leads to the hypothesis that even macroscopically noninflammatory lesions carry inflammatory potential [3,6,10]. Hence, the antimicrobial effect of tyrothricin might also be effective in the treatment of microcomedones.…”

“…The pathogenesis of acne is multifactorial. There are four primary pathogenic factors, which interact to produce acne lesions: (1) increased sebum production in the sebaceous glands, (2) alterations in the keratinization process, (3) Propionibacterium acnes follicular colonization, and (4) release of inflammatory mediators [1,2,3,4,5]. …”

“…They might develop into noninflammatory lesions (closed and open comedones) and into clinically visible inflamed papules, pustules, and nodules. Despite this differentiation, the inflammatory potential of acne vulgaris is given throughout the course of the disease; hence, acne is an inflammatory disease from its beginning onwards [3,6,7,8,9,10,11]. …”

Measuring acne using Coproporphyrin III, Protoporphyrin IX, and lesion-specific inflammation: an exploratory study

“…The pathogenesis of acne is multifactorial with four primary factors: (1) increased sebum production, (2) alterations in the keratinization process, (3) Propionibacterium acnes ( P. acnes ) follicular colonization, and (4) release of inflammatory mediators [5, 6, 15, 19, 27]. Excess keratin combined with sebum partially obstructs the opening of the follicle forming a microcomedo which is the beginning of comedonal lesion development [21].…”

Antibacterial therapy of vulgar acne

“…Акне -это мультифакториальный дерматоз, в патогенезе которого большую роль играют генетически обусловленная гиперандрогения и генетически детерминированный тип секреции сальных желез [9]. Обыкновенные акне являются распространенным хроническим заболеванием сально-волосяных фолликулов, чаще встречающимся в пубертатном периоде и резко снижающим качество жизни больных [1][2][3]. Пациенты с акне составляют основной контингент врачей -дерматологов и косметологов, при этом лекарственная терапия этого дерматоза требует вложения большого количества денежных средств.…”