Endometriosis consists of the growth of endometrial tissue outside the
uterus. A rat model of endometriosis is available to evaluate the pot
ential for environmental chemicals to promote the disease but may be r
elatively insensitive for the evaluation of the hazard of certain comp
ounds. Our objective, which was to develop a mouse model for endometri
osis, was based on (a) the promotion of endometriosis in primates by 2
, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), (b) the apparent relatio
nship between endometriosis and immunodeficiency, and (c) evidence tha
t humoral immunity is suppressed in mice but not rats following TCDD e
xposure. In the mouse model, slices of uterus were sutured to intestin
al mesenteric vessels. By 3 weeks after surgery, these sites were cyst
-like structures, The growth of the sites was hormone dependent. In in
tact mice, sites measured 3.60 +/- 0.22 mm; vehicle and estrone (0.5 m
u g/day) treatments produced site diameters of 0.95 +/- 0.128 and 5.28
+/- 0.355 mm, respectively. This new mouse model provides a sensitive
and useful technique for future studies of the potential for specific
xenobiotics to promote the development of endometriosis.