Acne vulgaris

PATHOPHYSIOLOGY OF ACNE VULGARIS

Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit [1] (PU) caused by increased sebum production, inflammation, and cellular hyperproliferation. Acne vulgaris is also affected by a disturbed skin barrier which allows cutaneous commensal microorganisms to penetrate the skin, multiply and cause an inflammatory response. The main microorganism involved in the pathophysiology of Acne vulgaris is Cutibacterium acnes (C. acnes) (1, 2).

The sebaceous glands and androgens [2] influence sebum production in acne, with the leading hormonal cause of increased sebum production being dihydrotestosterone (DHT) (3). DHT stimulates the sebaceous glands to increase sebum production in the hair follicle, which leads to an increase in the keratinocytes and pressure within the PU (4). The blockage within the hair follicle reduces the oxygen level leading to anaerobic bacteria growth (i.e., C. acnes) and inflammatory processes (3).

[1] The pilosebaceous unit – The structural, or pilosebaceous, unit of a hair follicle consists of the hair follicle itself with an attached sebaceous gland and arrector pili muscle. The hair follicle begins at the surface of the epidermis. Julianna L. Martel; Julia H. Miao; Talel Badri. Anatomy, Hair Follice. 2022. URL: https://www.ncbi.nlm.nih.gov/books/NBK470321/#:~:text=The%20structural%2C%20or%20pilosebaceous%2C%20unit,the%20surface%20of%20the%20epidermis [24.12.2022].

[2] Androgens are sex hormones that, among other functions, control sebum production (e.g., testosterone, 5-dihydrotestosterone).

ACNE TREATMENTS

Acne treatment aims to alleviate signs and symptoms (i.e., sebum production, inflammation, erythema, lesions, pain), resolve existing lesions to prevent scar formation, and improve the overall quality of life. Existing evidence shows the effectiveness of using topical treatments for mild, mild to moderate and moderate types of acne (5).

The prescribing process depends on Acne’s severity and duration, scar predisposition, skin type, previous treatments used, current medication, hyperpigmentation, patient factors, family and social history, and mental health.

Hyperkeratinisation is the cause of early comedo formation. Topical retinoids have anti-comedogenic properties because they normalise cell keratinisation by reducing excessive cell production. They also accelerate resolution from Acne vulgaris-induced post-inflammatory hyperpigmentation due to their anti-inflammatory properties.

Adapalene is a topical retinoid-like compound used for the treatment of Acne vulgaris. It prevents new comedone formation by controlling cell proliferation and shows a significant anti-inflammatory effect, preventing new inflammatory lesions. Compared to other topical retinoids, Adapalene has similar efficacy but a better tolerance due to a superior safety profile.

Topical use of Adapalene can cause minor skin irritation, such as erythema, dryness and stinging. Therefore, recommendations include sunscreen use before UV light exposure for patients using topical retinoids (6-8).

Benzoyl peroxide (BPO) is a topical agent used to treat Acne vulgaris. It shows antibacterial, keratolytic, comedolytic and anti-inflammatory properties. Benzoyl peroxide also has an irritant effect responsible for an increased cell turnover at the epithelium level, accelerating the resolution of comedones (increased skin peeling). Benzoyl Peroxide can oxidise proteins in bacterial cell membranes, therefore having bactericide properties towards C. acnes. The topical application does not cause a systemic toxic effect as it does not enter the systemic circulation. Like Adapalene, Benzoyl Peroxide can cause local skin reactions, such as stinging and burning sensations (9, 10).

Other treatments include topical Azelaic acid, topical and oral antibiotics (e.g., Clindamycin, Doxycycline, Lymecycline, Erythromycin) and for more severe cases of acne, oral Isotretinoin.

DIAGNOSING ACNE

In some cases, skin conditions known as acneiform eruptions can mimic acne (11):

• Perioral dermatitis is characterised by itchy and tender papules and is localised to the area around the mouth, eyes and nose (11). It is commonly caused by topical steroids applied to the face (11).
• Keratosis pilaris is rough to the touch, with a goose-flesh appearance on the skin. It can affect any skin surface where hair grows (12), characterised by erythematous follicular papules present on the cheek area, upper arms and thighs (11).
• Drug-induced acne [3] has a similar presentation to acne and is caused by certain drugs (13).
• Folliculitis is an infection of the hair follicle caused by bacteria (Staphylococcus aureus), characterised by red and tender papular-pustular lesions (14). Folliculitis can affect any skin area with hair and can be located on the beard area, lower legs, trunk, buttocks and scalp and can often be itchy (14). A yellow crust can be seen around the lesions, and they are often pierced by hair strands (14).
• Pseudo-folliculitis looks like bacterial folliculitis, but the lumps that form at the bases of hairs do not contain pus, and the inflammation is not caused by an infection (15). These lumps are due to ingrowing hairs and are more common in people with curly or Afro-Caribbean hair (16). Pseudo-folliculitis mainly affects the neck and the jaw, frequently causing scarring, keloid formation and hyperpigmentation (14).
• Rosacea is a chronic facial dermatosis predominantly seen in adults (11), characterised by red patches of erythema, dry skin, inflammatory lesions and telangiectasia [4]. Rosacea can be seen on the forehead, cheeks, nose and chin (11, 17). Although papules and pustules are present in rosacea, the absence of comedones can be noted (11). According to National Institute for Health and Care Excellence – Clinical Knowledge Summaries (NICE-CKS) (18), to diagnose rosacea, at least one ‘diagnostic’ (phyma [5], persistent erythema) or two ‘major’ clinical features (flushing, papules, pustules, telangiectasia and eye symptoms) need to be identified.
• Seborrheic dermatitis is a dry, scaly rash with mild erythema (19). It is a chronic form of eczema that mainly affects the sebaceous regions of the scalp, face (nose area, behind ears, eyebrows), and upper trunk (20, 21). The clinical features of seborrheic dermatitis include scales, pruritus of the affected areas (19, 22), and the absence of papules, pustules and comedones (11). Typical clinical features include flares during winter, which improve after sun exposure (summertime) (21).

[3] Drug-induced acne can be caused by corticosteroids, phenytoin, carbamazepine, lithium, isoniazid, vitamin B1, B6, B12 (13).

[4] Telangiectasia is a condition in which broken or dilated capillaries can be seen on the skin. Oakley A. Telangiectasia. 2014. URL: https://dermnetnz.org/topics/telangiectasia/ [18 April 2021].

[5] Phyma represents the thickening of the skin seen in rosacea and is due to chronic inflammation and oedema (18).

According to NICE-CKS (13), non-inflammatory lesions (comedones) must be present to diagnose acne, and a different diagnosis must be considered in the absence of these lesions.

NATURAL HISTORY AND PROGRESSION OF ACNE VULGARIS

According to World Health Organisation, acne is a chronic skin condition with a prolonged course, a recurrent relapsing clinical presentation, and a psychological and social impact affecting life quality (23). Acne vulgaris mainly affects children near puberty and adolescents, but it can also affect adults as the disease continues through adulthood in many cases (24). Acne can change its distribution and severity throughout the years and lead to considerable scarring, depression and anxiety (25, 26).

The onset of this skin condition often occurs during prepubertal age and sometimes progresses into adulthood (27). Acne begins as a non-inflammatory skin condition (comedonal acne) that progresses to a mild-moderate inflammatory stage (papulopustular acne) (28). It then evolves to a more inflammatory and severe stage (nodulocystic acne), leading to hyperpigmentation and scars (28). Acne can be persistent, starting from puberty and extending into adulthood, and can have a late onset, appearing in people 25 years of age or older (24). It typically resolves by 25, but several studies (24, 28) have demonstrated that it can develop in the mid and late 20s and persist until the mid-40s and beyond (24, 28). The inflammatory stages of acne lead to more scarring and post-inflammatory hyperpigmentation, which can have psychological, social and economic consequences (28).

PUBLIC HEALTH AND ACNE VULGARIS

Acne is a common inflammatory condition affecting people worldwide and represents a global burden that can impair many aspects of individuals’ lives (29). Therefore, acne can affect mental health, leading to comorbidities such as anxiety, depression and a higher suicide rate among acne patients (29). It has been suggested that acne has a substantial impact on social relationships, socioeconomic aspects of life and mental health (29).

The primary concern with acne is related to appearance. The extent of acne’s impact on the emotional state is similar to the psychological impairment identified in other chronic diseases such as diabetes, asthma or epilepsy (30). A systematic review and meta-analysis researching the link between acne vulgaris, depression and anxiety concluded that these psychological disorders are more common in teenagers 12 to ≤19 years of age and adults >19 years of age suffering from acne than those without acne, with a more significant impact on adults (31). Recent studies have also pointed out that depression and social phobia affect many people with acne and can negatively impact the patients’ occupational, social, and family lives (32, 33).

REFERENCES

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