Introduction
Acne is a common skin condition that affects most people at some point in their lives. It occurs when hair follicles under the skin become plugged with oil and dead skin cells. The medical term for acne is acne vulgaris. Acne usually appears on the face, forehead, chest, upper back and shoulders. It is non-contagious but often results in scarring of the skin. The severity of acne can range from mild to moderate or severe cystic acne. Understanding the pathogenesis and evaluating treatment options is important in managing the condition effectively. This research paper provides an in-depth review of acne including its causes, pathophysiology, clinical presentation, complications and various treatment modalities.
Causes and Risk Factors
The exact causes of acne are multifactorial. The main factors that are thought to contribute to the development of acne include:
Increased sebum (oil) production: Sebaceous glands attached to hair follicles produce an oily substance called sebum. Excess sebum clogs hair follicles and leads to acne lesions. Hormonal changes during adolescence and menstruation stimulate sebum production.
Hyperkeratinization: Increased skin cell production inside the hair follicles can result in pores becoming blocked more easily.
Propionibacterium acnes bacteria: P. acnes is a common skin bacterium that lives in everyone’s skin. When pores are blocked, P. acnes bacteria multiply rapidly within the follicle resulting in inflammation.
Genetics: Acne tends to run in families. Having a parent or sibling with acne increases one’s risk.
Hormonal factors: Fluctuating hormone levels during puberty, premenstrual periods and pregnancy can trigger acne breakouts in susceptible individuals.
Medications: Certain medications like corticosteroids, lithium, bromocriptine and iodides may induce or worsen acne.
Stress: Stress does not directly cause acne but may exacerbate existing acne or induce breakouts in acne-prone individuals due to increased sebum production.
Lifestyle: Greasy cosmetics, frequent skin scrubbing, dirty cellphones held against the face and facial hair that rubs against the skin can all negatively impact acne.
Pathophysiology
The pathological process underlying acne involves proliferation of sebum production, blockage of follicles, bacterial colonization and local inflammation. In detail:
Increased sebum secretion from enlarged sebaceous glands blocks the pores and hair follicles.
Accumulation of excess keratin and sebum within the follicular canal forms a microcomedo (non-inflammatory lesion).
P. acnes bacteria within occluded follicles metabolize sebum into fatty acids that attract white blood cells.
Inflammation occurs when neutrophils and lymphocytes infiltrate in response to P. acnes antigens and fatty acid byproducts.
This leads to papules (pinhead sized, inflamed lesions) and pustules (papules filled with pus) forming on the skin surface.
Deeper nodulocystic lesions form when inflammation involves the deeper dermis, manifesting as very painful nodules or cysts.
Clinical Presentation
The clinical manifestations of acne depend on the severity and type of lesions. Some key presenting features are:
Comedones – Open (blackheads) or closed (whiteheads) comedones are non-inflammatory lesions.
Papules – Small, solid, pink or red, tender bumps 2-3mm in size with definite elevation above the skin.
Pustules – Papules containing non-purulent or purulent material appearing yellowish-white in color.
Nodules – Larger boggy lesions >5mm diameter arising deeper in the dermis.
Cysts – Cavities filled with pus arising from enlarged, inflamed follicles. May cause scarring.
Location – Commonly seen on face, upper back and chest but can occur anywhere with sebaceous glands.
Tenderness – Lesions may cause discomfort especially during flare-ups or when squeezed.
Scarring – Severe, long-standing nodulocystic acne can lead to pitted scars and hyperpigmentation.
Differential Diagnoses
Other conditions that show similar skin lesions to acne need to be excluded, such as:
Folliculitis – Superficial infection of hair follicles seen as red papules/pustules.
Rosacea – Persistent central facial erythema with transient papules/pustules, especially in adults.
Hidradenitis suppurativa – Painful abscesses/nodules in axillary and inguinal regions.
Drug eruptions – Medication may induce acneiform lesions elsewhere on the body.
Severe stress – Emotional stress cannot directly cause but exacerbate acne symptoms.
Pseudofolliculitis barbae – Ingrowm hairs cause papules/pustules on areas of shaving.
Dermatoses papulosa nigra – Skin-colored papules commonly seen on face of darkly-pigmented individuals.
Complications
Most acne cases are mild and resolve without complications. Severe, resistant acne can lead to:
Scarring – Irregular textured scars (ice pick, boxcar and rolling scars) develop due to damage to dermal collagen and elastin fibers from inflammation.
Post-inflammatory hyperpigmentation – Darkening of the skin occurs at sites of healed lesions especially in darker skin types.
Infection – P picking at lesions risks secondary infection, cellulitis, abscess or spread to other areas.
Cystic acneform nodules or conglobata – Severe deep nodular inflammation occurs especially on back, resulting in cording and bridging scars.
Psychological issues – Moderate to severe acne can cause psychological distress, low self-esteem and depression, particularly during adolescence. Rarely suicidal thoughts.
Chronic infections – Deep nodulocystic acne may lead to prolonged infections needing long-term antibiotics and/or hospitalization.
Diagnosis
No special tests are usually required to diagnose typical acne. Diagnosis is generally based on:
Characteristic clinical presentation of lesions – Open/closed comedones, papules, pustules, nodules or cysts.
History of onset and course, including temporal association with hormones or medications.
Exclusion of possible differential diagnoses based on distribution and features of lesions.
Grading of severity – Scales used include Leeds acne grading technique and the Physician’s Global Assessment scale.
Wood’s lamp examination – Can detect P. acnes bacteria within uninflamed comedones that fluoresce apple-green.
Treatment
Treatment is aimed at reducing inflammation, treating infections, preventing scarring and improving the patient’s quality of life. The three main treatment strategies include:
Topical Therapy
over-the-counter topicals with benzoyl peroxide or retinoids are first line for mild to moderate acne.
Topical retinoids (tretinoin, adapalene) work by unclogging pores, speeding skin cell turnover and reducing inflammation.
Benzoyl peroxide kills P. acnes bacteria and has mild keratolytic effects. It is usually combined with antibiotics.
Topical antibiotics (clindamycin, erythromycin) control P. acnes infection but do not address blocked pores or inflammation on their own.
Oral Therapy
Systemic antibiotics are used for moderate to severe acne – tetracyclines, macrolides or trimethoprim-sulfamethoxazole depending on severity.
Spironolactone acts as an androgen blocker and is useful specifically in females with acne. It is not teratogenic.
Oral contraceptives or spironolactone with estrogen-containing contraceptives may help treat acne in females via hormonal effects.
Isotretinoin (Accutane) is reserved for severe nodulocystic or scarring acne resistant to other therapies due to its teratogenicity risks.
Procedural Therapy
Comedone extraction and incision/drainage of inflamed lesions by a dermatologist.
Chemical peels, dermabrasion, laser therapy (IPL, fractional resurfacing) to reduce scarring and pigmentation.
Photodynamic therapy with topical photosensitizing medications and light exposure.
Combination therapies are often most effective, especially for more severe types of acne. Adjuvant measures like stress reduction, proper skin hygiene and cosmetic use are also encouraged. Long-term low dose antibiotic maintenance may be needed.
Prognosis
Most acne cases respond well to treatment. Prognosis depends on:
Type and severity – Mild-moderate cases usually resolve in months, severe cases may take 6-12 months or longer.
Adherence to treatment plan – Strict compliance with medications and lifestyle changes is important for optimal outcomes.
Early effective treatment
Andrew Stroud