Ovariectomy induces regression of hyperplastic uterus in female dogs.

Abstract

Cystic endometrial hyperplasia (CEH) is a common physiological affection in adult female dogs in diestrus, which can make the uterine environment susceptible to bacterial infections. It is known that hormonal interactions, mainly between progesterone and estrogen, are key players for development of the CEH-pyometra complex, but many questions remain regarding its etiopathogenesis. The present study proposes a new approach, to the authors' knowledge not yet described in literature, to add new information for better understanding of this affection and possibly establish new guidelines for obstetric surgery and reproduction in veterinary medicine. It is demonstrated that the absence of steroidal hormones leads to significant regression of uterine tissue and glandular hyperplasia, as well as reduction in estrogen and progesterone receptors and markers of tissue proliferation, in the uterus of female dogs, six months after ovariectomy. Significant involution of endometrial hyperplasia was observed, as the size and macroscopic appearance of the uterus. This study reaffirms the important role played by steroid hormones in demonstrating macroscopically, molecularly and histologically the regression of hyperplastic endometrial and glandular tissue when performing ovariectomy in female dogs. Our findings suggest that ovariectomy may induce regression of endometrial hyperplasia and could represent a potential alternative to ovariohysterectomy. However, larger studies including control groups are required to confirm these results and define the clinical applicability of this approach.