The causes and mechanisms of baldness are still not fully understood. The current view is that pemphigus is an autoimmune disease, which may be the result of the interaction of multiple genetic factors and environmental factors. The pathogenesis of baldness in children has its own characteristics compared to that of adults. This article reviews the status of research on the etiology of childhood pattern baldness in recent years, and is summarized below. 1. Genetics Many genetic epidemiological studies have shown that many patients with baldness have a family history of the disease, with a positive rate of 10% to 42% in foreign countries, and 10% to 18% in children. 215 Kuwaiti children with baldness were observed by Nanda et al. This shows that the prevalence of baldness is related to the level of kinship, and the closer the kinship, the higher the prevalence, indicating that genetic factors have a certain influence on the development of baldness. In another study, 392 children with baldness in Singapore were investigated and only 8.4% of them had a positive family history. The large statistical variation in family history may be related to the Asian and Caucasian genetic background; it may also be the reason why milder cases are often overlooked. Significant associations were found with HLA B21 and B40 in 50 children with a positive family history of baldness, and with HLA B12 and B21 in those without a positive family history. Significant correlations were also found between limited baldness and HL A B21 and between generalized baldness and HL A B21 and B40. However, none of the above observations were statistically different. The relationship between childhood pattern baldness and HL A antigens is less reported, and the relationship with HLA may be related to the geographical area of distribution. Foreign researchers found that 6 of 203 patients with Down syndrome had a combination of baldness, suggesting that a gene on chromosome 21 is important in determining susceptibility to baldness. Further research on the genetic aspects of baldness in children is needed. 2. Immunology Baldness is considered to be a tissue-specific autoimmune disease. Sharma et al. observed T3, T4, TSH levels and antithyroid microsomal antibodies in patients with baldness and concluded that thyroid disorders are rarely associated with baldness, while thyroid clinical observation of 1,032 Chinese patients with baldness revealed a family history of 8.4%, of which 1.6% were first-degree relatives and 0.6% were second-degree relatives. The prevalence was 1.6% in class I relatives, 0.19% in class II relatives, and 0.03% in class III relatives. The heritability of the presentees was 47.16%, 42.53%, and 22.29% in class I, class II, and class III relatives, respectively, which indicates a higher prevalence in class I relatives than in class II and class III relatives, suggesting a clear genetic predisposition for baldness. A new point of view is raised here, how to observe the heritability of baldness in patients with baldness, and the data on baldness in children is still unknown. The genetics of pattern baldness has made considerable progress in recent years, and the correlation between HLA2I class A and B series haplotypes and pattern baldness has been inconsistently reported. A study of 10 members from a three-generation white American family found three patients with HLA2A2, B40, and B40 haplotypes. Valsecal et al. studied a three-generation family from northern Italy and found that the HLA2Aw32 and B18 haplotypes were associated with baldness. Colombe et al. concluded that many diseases, especially those with strong autoimmune factors, mostly show an association with HLA, especially the HLA2 class II gene. It was shown that the class II genes of HLA2DR4, DR5, DR7 and DR3 are associated with baldness, and that more than 80% of all patients who underwent genetic scanning were positive for the DQB1 * 03 (DQ3) antigen, suggesting that this antigen is a marker of general susceptibility to baldness, whereas the DQ * 0301 and DRB * 0401 alleles were only present in patients with total and generalized baldness. This provides a genetic basis for differentiating between the two clinical types of baldness, i.e., patchy baldness and allodynia/primary baldness. The most studied gene in relation to HLA2 class III is TNF2α, a proinflammatory factor associated with several chronic autoimmune inflammatory diseases. the TNF2α gene is intermediate between the HLA2I and HLA2 class II antigen genes. The variable TNF2α allele frequency in plaque baldness reflects the HLA haplotype chain imbalance associated with plaque baldness. Some investigators have found different expression of TNF2α alleles in patchy baldness compared to total and universal baldness, which may be evidence of genetic heterogeneity in these types of disease. However, 14 children were found to have thyroid abnormalities (including 3 with abnormal thyroid function and 11 with elevated thyroid autoantibodies). These results underscore the importance of screening for thyroid abnormalities in children with chronic, recurrent, and/or widespread baldness. Some authors have reported a relationship between childhood baldness and pediatric celiac disease and myasthenia gravis, all of which indirectly suggest that baldness is an autoimmune disease. The rate of atopy in patients with pemphigus vulgaris is high and also correlates with the severity of the disease. It is unanimously believed that atopy is related to the immune function of the person. In a study of 736 patients with pemphigus vulgaris, it was found that the atopic rate differed between children and adults, at 18% and 9%, respectively, and was higher in the more severe types of pemphigus. Sharma et al. observed 201 pediatric baldness patients and found a clear history and evidence of atopic disease in 17.5% of the children. These included: nasal and nasobronchial allergy, bronchial asthma, and atopic dermatitis. In addition, earlier studies abroad have shown that 10% to 52% of patients with baldness are associated with atopic disease, and that atopy is associated with an earlier age of onset, longer duration, and more severe disease. In a recent study by Nanda et al. of 215 children with baldness, 24.7% had a history of atopic disease, but these data were not statistically significant when compared to the control group, so it was concluded that atopic disease was not related to age of onset or severity of baldness. In a survey of baldness, Tan et al. found that 60.7% of patients had a personal or family history of atopic disease, but there was no significant association between atopy and the severity of baldness. Further studies are needed to investigate the relationship between atopy and immune function in children with pemphigus vulgaris and whether there is an association with severity of the disease. The study of various cytokines related to immune regulation in pemphigus is remarkable. For example, TNF2α, IFN2γ, IL210, etc. The important regulatory role of growth factors and cytokines on hair growth is receiving increasing attention. The hair follicle and its surrounding tissues produce some specific factors by autocrine and paracrine means, which play a role in hair growth and development and cycle . Recent studies have demonstrated that Th1 lymphocytes play a key role in the pathogenesis of baldness and that Th2 lymphocyte responses can suppress tissue damage by Th1. In organ-specific autoimmune diseases, Th1-type cytokines can induce disease onset and accelerate the disease process, while Th2-type cytokines can prevent disease onset and alleviate the disease. It can be used as a prognostic indicator for baldness. In addition, IL210 has recently been considered as an immunomodulator of Th1 cells. In China, Luo Min et al. measured serum levels of IFN2γ and IL210 in patients with baldness (including children), and concluded that IFN2γ may be associated with the development of severe alopecia areata, while IL210 may not be associated with the development of baldness. The latter conclusion is inconsistent with another scholar’s report and may be related to case selection and experimental error. The relationship between childhood baldness and immunological aspects is a new topic for future research in the field of baldness etiology. 3. Microcirculation In China, Qu Rui et al. conducted a study on blood rheology and microcirculatory changes in nail folds in patients with pemphigus vulgaris, indicating that abnormal blood rheology and microcirculatory dysfunction play an important role in the pathogenesis of pemphigus vulgaris. Shapiro et al. concluded that nail dystrophy is associated with baldness. Shapiro et al. suggest that nail dystrophy is associated with pemphigus, with an incidence of 10 to 66%, and may involve one, more or all nails. It can occur before or after the baldness has subsided. Nail changes are usually more common in children with pemphigus vulgaris. In a study of 272 children with pemphigus vulgaris, 46% had abnormal nail development, including 92 cases of nail dents and 37 cases of total or universal baldness. The abnormal nail development in pemphigus may be related to local blood circulation disorders. Whether this indicates that the onset of baldness is related to microcirculatory dysfunction, or whether it is an indication for the severity of baldness, remains to be studied. 4. Psychiatric factors Psychoneurological factors play an important role in the development of baldness. In a clinical observation as early as 1998, Zeng Jingshi and others found that 28.15% of the cases were caused by psychiatric factors. It is generally believed that psychological factors have a greater influence on the occurrence and development of adult pattern baldness. A few years later, together with other scholars, he observed 340 cases of childhood baldness and found that 21 of the school-aged children had been in a constant state of mental stress due to studying or taking tests. Therefore, attention should be paid to the influence of mental factors on school-aged children. Overseas data suggest that various emotional stressors such as maternal illness and hospitalization, sibling rivalry, death of a family member, and parental conflict are associated with the development of baldness. The children with baldness were found to have more psychiatric symptoms compared to the control group. The lack of positive life events in the pre-alopecia period was also found to play a causative role. In contrast, the opposite view was held by another scholar, which may be related to the small sample size observed. CMV infection directly affects the immune function of the body, causing abnormalities in cellular and humoral immunity. The rate of infection was significantly higher than that of normal controls. Therefore, it is believed that the development of baldness may be related to human cytomegalovirus infection. However, Offidini et al. denied this idea, stating that HCMV infection is neither a direct cause of baldness nor a trigger for its autoimmune consequences, and Jackow et al. also confirmed that baldness in twins was not associated with CMV infection in a study of 24 twins with baldness, and that the association of HCMV infection with the onset of baldness in children is less well studied and needs to be further investigated. The association between HCMV infection and the onset of baldness in children needs further investigation. The etiology and pathogenesis of childhood pattern baldness are complex and related to a variety of factors. In particular, the genetic family history and the relationship with HLA antigens. Recent studies have focused on the search for more family lines of baldness, trying to perform a lineage chain analysis or to further investigate some susceptibility genes. In addition, the development of childhood pattern baldness is closely related to immune function. The relationship between its atopy and immune function status, as well as the relationship with the development of pemphigus vulgaris, needs to be explored in more studies. In addition to the above two factors, microcirculatory disorders, psychological factors and cytomegalovirus infection may also be related to the development of pemphigus vulgaris. With the rapid development of genetics, molecular immunology and molecular biology, research on the causes of childhood pattern baldness should be more in-depth and extensive in order to take better preventive and therapeutic measures.