Acne Vulgaris

Acne vulgaris affects nearly 85% of adolescents, primarily on the face, chest, and back due to hormonal surges during puberty that boost sebum production and clog follicles. Cutaneous Propionibacterium acnes bacteria exacerbate inflammation, leading to lesions like blackheads, whiteheads, and cysts. Risk factors include genetics, diet high in dairy/glycemic foods, and medications like corticosteroids.

Pathophysiology
It stems from four key processes: excess sebum from hyperactive sebaceous glands, follicular hyperkeratinization, bacterial proliferation, and immune-mediated inflammation. Androgens stimulate sebaceous activity, while abnormal desquamation blocks pores, fostering microcomedones as precursors to visible acne.

Clinical Features

Non-inflammatory comedones evolve into inflammatory papules, pustules, or painful nodules; severe cases cause scarring and post-inflammatory hyperpigmentation. Grading ranges from mild (comedonal) to severe nodulocystic, impacting psychosocial well-being.

Treatment Approaches

Mild cases use topical retinoids (adapalene, tretinoin) plus benzoyl peroxide to unclog pores and kill bacteria. Hormonal therapies (spironolactone, oral contraceptives) suit females; adjuncts include chemical peels or phototherapy. Early intervention prevents scarring; consistency yields results in 8-12 weeks.