The cytoplasm of normal human male and female gingiva contains a receptor capable of specifically binding 17 beta-estradiol and moxestrol (R-2858) with high affinity (Kd = approximately 3.4 X 10(-10) M) and low capacity (4.5 fmol/mg protein). The binding is sensitive to heat (destroyed by warming to 37 C for 60 min), proteolytic enzymes (pronase, trypsin, and chymotrypsin), and exhibits a pattern of competition similar to that obtained with estrogen receptors from other target tissues. Nuclear uptake of [3H]estradiol was demonstrated by using a dry autoradiographic technique. Specific nuclear localization of [3H]estradiol was found predominantly in basal and spinous layers of gingival epithelium, stromal connective tissue cells (fibroblasts), and endothelial cells and pericytes of small blood vessels in the lamina propria. There was no difference between the Kd values in normal and diseased tissue or between the Kd values or number of binding sites and the age or sex of the patient. However, there was a difference between the amount of estrogen binding sites per mg protein in normal tissue compared to gingiva with dilantin hyperplasia. These results provide the first direct evidence that human gingiva may function as a target organ for estrogens.

Binding of 3H‐Methyltrienolone (3H‐R1881) to cytoplasmic androgen receptor protein and its translocation into nuclei in human gingiva was demonstrated. 3H‐R1881 binds to androgen receptors with high affinity (Kd= 1.7−1.9 × 10−9 M) and low capacity (10–16 fmol/mg protein). The binding was specific for DHT binding sites and was destroyed by proteolytic enzymes (pronase and trypsin). These results suggest that 3H‐R1881 can be used as a ligand in combination with nonradioactive DHT to study androgen receptors in the gingiva.

Nuclear localization of 3H-dexamethasone to secretory and duct cells in the rabbit submandibular gland was determined by dry-mount autoradiography. This saturable nuclear binding indicates that glucocorticoid effects on this gland may be mediated by cytosol-nuclear receptors.