Acne is a chronic inflammatory skin disease of the follicular sebaceous glands with a prevalence of 70% to 87%, and has a psychological and social impact on adolescents that exceeds that of asthma and epilepsy. Treatment options for acne vary widely among clinicians, with some treatments having uncertain efficacy, lacking evidence-based medical evidence to support them, and individual approaches even causing damage to patients. Therefore, it is essential to develop a set of proven guidelines for the treatment of acne to standardize its treatment. Of course, guidelines are not set in stone and need to be updated regularly as new evidence-based medical evidence and new drugs are developed. This guideline is based on the acne guideline published in 2008 and has been revised based on user feedback and advances in domestic and international acne research. Pathophysiology of acne Acne is a chronic inflammatory disease of the sebaceous units of the hair follicles, and the pathogenesis remains incompletely elucidated. Genetics, androgen-induced sebum production in large amounts, follicular sebaceous gland duct keratinization, Propionibacterium acnes colonization, inflammation and immune response may all be involved. The rapid development of sebaceous glands under the action of androgens and the massive secretion of lipids are the pathophysiological basis for the development of acne. The development of adrenal glands and gonads after puberty leads to increased secretion of androgen precursors such as dehydroepiandrosterone sulfate (DHEAs), which are converted to active dihydrotestosterone by a series of androgen metabolizing enzymes such as 5α-reductase, stimulating enhanced sebaceous gland function. Enhanced expression or activity of androgen receptors or related androgen metabolizing enzymes in the skin in a genetic background is also an important factor contributing to sebaceous gland hypersensitivity to androgens and lipid overproduction. In addition, there are changes in the lipid composition of sebum in acne patients such as increased content of peroxisqualene, wax vinegar, free fatty acids, increased proportion of unsaturated fatty acids and decreased content of linoleic acid, which can lead to impaired skin barrier function, keratinization of follicular sebaceous ducts and inflammatory responses. Abnormal keratinization of follicular sebaceous ducts is another important factor and a major pathological phenomenon in acne. Epithelial cell keratinization leads to blockage of follicular sebaceous ducts and impaired sebum drainage, resulting in microcomedema visible under the microscope and acne visible to the naked eye. Propionibacterium acnes is closely associated with acneogenesis. The formation of microcomedones and acne creates a favorable local environment for the proliferation of P. acnes with anaerobic growth characteristics. It is now believed that P. acnes may be involved in the development of acne inflammation through natural immunity, acquired immunity, and direct induction. Early inflammation in acne may be the result of Toll-like receptor (TLR)-mediated natural immune response, which induces the release of pro-inflammatory factors, especially IL-lα. As the disease progresses, the acquired immune response amplifies the inflammatory process, further leading to the release of inflammatory factors and neutrophil aggregation. In the later stages of the disease, the hair follicle wall breaks down and lipids and hairs from the follicle enter the dermis, further aggravating the inflammatory response. Acne Classification Acne classification is an important basis for acne treatment and efficacy evaluation. Whether acne is graded according to the number of lesions or the nature of the lesion, the treatment options are basically the same. For the sake of simplicity and convenience in clinical use, this guideline classifies acne into 3 and 4 grades based mainly on the nature of the lesions: mild (grade I): acne only; moderate (grade II): inflammatory papules; moderate (grade III): pustules; and severe (grade IV): nodules and cysts.