In normal women, ovarian function begins to decline only at the age of 45 to 50. If signs of decline appear before the age of 40, it is medically known as premature ovarian failure (POF). Such women often have amenorrhea or oligomenorrhea, increased gonadotropin levels and decreased estrogen levels, and clinical manifestations include varying degrees of hot flashes and sweating, vaginal dryness, decreased libido and other pre- and post-menopausal symptoms. The etiology of premature ovarian failure is complex, mostly due to a combination of factors, and is unknown in the majority of patients. It is usually considered to be related to genetic factors, infectious factors, autoimmune factors, physicochemical factors, metabolic factors, medical factors, environmental and psychological factors, and idiopathic factors. Genetic abnormalities are also heterogeneous and multifactorial, including FSH receptor abnormalities, translocations of homologous sequences on the X and Y chromosomes, and structural abnormalities of FSH (inability to bind to the receptor). It has been found that for normal ovarian function to be maintained, 2 structurally normal X chromosomes must be present, each with a specific locus that maintains ovarian function .Abnormalities in both the number and structure of X chromosomes can cause congenital ovarian hypoplasia and POF. POF is a group of X-linked genetic disorders that are often associated with chromosomal recombination, translocations, or monosomal changes.X chromosomal abnormalities, such as 45X Turner syndrome and its variants are the most common genetic causes of POF. Mo Zhongfu et al. believe that 10% of patients with POF have a family history and can be transmitted vertically. Infectious factors include mumps, viral infections, and bacterial infections. Mumps in young girls can be combined with viral ovarian infections, while 2% to 8% of patients with ovarian infections tend to develop premature ovarian failure, and the risk of premature ovarian failure increases nearly 10-fold in women with previous mumps, and many cases report that POF occurs when these patients fully recover to normal ovarian function. Histologic examination of patients who recover from mumps ovarian disease shows ovarian atrophy and fibrosis with loss of normal follicular structure. The ovaries are remarkably resistant to infections that can cause POF, including tuberculosis, malaria, chickenpox, and Shigella spp. The pathogenic bacteria invade the ovaries and lead to inflammation and fibrosis of the ovaries, causing a decrease in the number of follicles, which can eventually develop into premature ovarian failure. Some pelvic infections such as severe tuberculosis, gonorrhea or septic pelvic inflammatory disease can also cause POF. Autoimmune factors About 20% of patients will have autoimmune diseases, which may occur before the symptoms of ovarian insufficiency become apparent, including autoimmune thyroiditis, hypoparathyroidism, SLE, rheumatoid arthritis, type I diabetes, etc. Premature ovarian failure is often considered to be part of a systemic polyglandular syndrome. Immune ovarianitis has been reported to account for approximately 4% of the etiology of POF. It has been found that lymphocytes and plasma cells infiltrate in developing follicles, atretic follicles and luteal cysts; plasma cells, T cells, B cells and NK cells infiltrate in mature follicles, and immune cells release cytokines to damage follicles and accelerate follicular atresia. In the peripheral blood of POF patients, T helper cells (TH or CD4+) are increased and T suppressor cells (TI or CD8+) are few, and the TH/TI ratio is increased, promoting the production of autoimmune antibodies by B cells and causing ovarian damage. Anti-ovarian antibodies can be measured in the blood of 10%-69% of POF patients. Physicochemical factors The physicochemical factors in the development of premature ovarian failure include: radiation irradiation, chemical drugs and possible infectious factors. Radiation exposure can destroy the ovaries and lead to temporary or permanent amenorrhea. However, Madsen believes that the risk of POF in women undergoing chemotherapy is low. the likelihood of POF is significantly correlated with reversibility and irradiation dose, patient age, and sensitivity, with younger age generally being more resistant to radiation damage. Severely damaged ovaries due to radiation show loss of primordial and developing follicles, interstitial fibrosis and vitellogenic changes, vascular sclerosis, and storage of hilar cells.