Testosterone, Saliva

Testosterone, Saliva (salivary testosterone; free/bioavailable testosterone surrogate) is used to assess androgen excess or deficiency and to investigate tumor activity related to gonadal or adrenal sources. In males, results aid the diagnosis and monitoring of hypogonadism, hypopituitarism, infertility, erectile dysfunction, and late-onset androgen deficiency; they also support evaluation of Klinefelter syndrome and monitoring of antiandrogen therapy in prostate cancer. In females, testing contributes to the workup of hirsutism, virilization, anovulation, amenorrhea or oligomenorrhea, polycystic ovary syndrome, androgen-secreting ovarian or adrenal tumors, and congenital adrenal hyperplasia. In children, measurement supports evaluation of pubertal and developmental disorders, including precocious puberty. When sex hormone–binding globulin (SHBG) is altered (eg, hypothyroidism, hyperandrogenism, obesity), salivary testosterone may better reflect the bioactive fraction than total testosterone.

Testosterone synthesis is regulated by luteinizing hormone and occurs predominantly in testicular Leydig cells, with smaller contributions from the ovaries and adrenal cortex. In circulation, most hormone is protein bound: roughly 60% tightly to sex hormone–binding globulin (SHBG) and a substantial portion loosely to albumin, leaving only about 2% to 3% in the free state. The unbound fraction is biologically active and traverses cell membranes; salivary testosterone closely approximates this free component. Within target tissues, 5α-reductase converts testosterone to dihydrotestosterone, which has greater androgenic potency, while aromatase generates estradiol in multiple sites. Secretion follows a circadian pattern with peak concentrations in the morning and a decline with aging in males. In females, levels vary during the menstrual cycle, increase during pregnancy, and decrease after menopause. Androgen excess produces virilization and other hyperandrogenic features in females and can lead to precocious puberty in boys; marked elevations may arise from congenital adrenal hyperplasia or androgen-producing tumors. Deficiency causes hypogonadal manifestations in males and may be associated with nonspecific symptoms in females. When SHBG is increased, bioavailable testosterone may fall more than total testosterone.