Adenomyosis in the bovine uterus: correlation between frequency, age, and 17β-estradiol-progesterone equilibrium.

Adenomyosis of the uterus is characterized by the presence of islands of endometrial glands and stroma within the myometrium. Etiopathology of adenomyosis has not been clearly defined but it potentially interferes reproductive processes in cattle. The aim of this initial study was to evaluate the impact of age on the frequency of adenomyosis in cows. Endometrial tissues collected from cows slaughtered between Day 8 and 12 of the estrous cycle (N = 72) were divided into two age groups: (1) 2 to 4 years old (N = 36) and (2) 5 years old and older (N = 36). The tissues were stained with hematoxylin and eosin. The adenomyosis histopathomorphologic stage was classified on a four-point scale according to the penetration of endometrial structures inside the perimetrium. The protein expression of the 17-β estradiol (E2) and progesterone (P4) receptors were evaluated in the endometrial tissue samples by immunohistochemistry and Western blot analysis, and E2 and P4 concentrations were measured in the peripheral blood and uterine tissue. Adenomyosis was observed in 38 of the cows examined including 13 of the 2- to 4-year-old cows and 25 of the cows 5 years old or older. The frequency and intensity of adenomyosis increased with age. Higher E2 receptor protein expression was observed in adenomyotic cows and increased with disease development and increase of number of glands inside the uterus in the direction of perimetrium, and P4 receptor protein expression were unchanged in healthy and adenomyotic cows. An increase in the expression of E2 receptors and high, supraphysiological levels of E2 was detected in cows with III and IV degree of adenomyosis (P < 0.05). Overexpression of E2 receptor and alternations in E2 secretion might make the bovine uterus susceptible to a growth advantage of adenomyotic tissue over the surrounding myometrium. The pathogenesis and immunoendocrine mechanisms controlling adenomyosis in cattle warrant further study. Published by Elsevier Inc.