The etiology of prostate enlargement remains incompletely understood. It is now unanimously accepted that old age and functioning testes are two important factors in the development of prostatic hyperplasia. The development and normal physiological function of the prostaglandins require adequate androgens to maintain them. In the presence of androgens, the prostate gradually increases in size. Although increasing age leads to a decrease in the overall level of androgens, the prostate gland in the elderly has an increased ability to locally take up testosterone and convert it to dihydrotestosterone, so the prostate volume gradually increases and the development of prostatic hyperplasia shows a time-related progression. The functioning testes continue to secrete androgens that stimulate hypertrophy of the prostate gland. Histologically the incidence of prostatic hyperplasia increases with age. Men can have varying degrees of prostate enlargement after the age of 45, with clinical symptoms mostly appearing after the age of 50. The binding of dihydrotestosterone to androgen receptors on prostate cells also prompts the secretion of various growth factors, and these factors can contribute to nodule formation and cellular hyperplasia. It also interferes with the apoptosis of cells within the prostate tissue, again leading to an increase in prostate size. As we age, the imbalance of sex hormones in the body and the synergistic effect of estrogen and androgen may also be important causes of prostate enlargement.