Acne vulgaris is a multifactorial disease whose onset is related to endocrine, bacterial infection, abnormal skin keratinization, and immune response. 1. Endocrine. The development and secretion of sebaceous glands are regulated by androgens. When the level of androgens, the number or sensitivity of androgen receptors, and enzymes in the process of androgen metabolism are abnormal, it leads to increased secretion of sebaceous glands. 2. Abnormal keratinization of hair follicle sebaceous gland ducts. Excessive keratinization can lead to thin openings in the sebaceous gland ducts, blocking the excretion of sebum and follicular epithelial cells and causing blockage, resulting in acne. 3. Microbial infection. Bacteria such as Propionibacterium acnes, Staphylococcus epidermidis, and oval furfur spores secrete esterases, which cause the breakdown of triglycerides to produce free fatty acids. The nonspecific inflammation in turn draws in neutrophils to participate, leading to increased inflammation. The formation of papules, pustules, abscesses, nodules. 4. Immune factors. Elevated IgG levels in the serum of some patients, Propionibacterium acnes-mediated cellular immunity and allergic reactions are involved in the development of the disease. 5, Other. Genetic factors, dietary factors (sugar, cocoa, fat, chili peppers, fried foods, strong alcohol), mental stress, and overexertion all influence the development of the disease.