Effects of Ovarian Pathologies and Uterine Inflammations on Adenomyosis in Bitches

In: Acta Scientiae Veterinariae · 2018 · vol. 46 , pp. 7 · doi:10.22456/1679-9216.87473 · W2944699887
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This study investigated the roles of ovarian pathologies and uterine inflammations in the development of adenomyosis in bitches, finding that tissue damage from inflammation or hormonal disturbances may contribute to its occurrence.

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The study examined how ovarian pathologies and uterine inflammations relate to the histopathogenesis of adenomyosis in bitches after ovariohysterectomy, using routine tissue processing, histopathology, immunohistochemistry (including p53, Ki-67, α-smooth-muscle actin, and cytokeratin markers), and receptor staining for estrogen and progesterone. Among 38 uterine samples, 7 were diagnosed with adenomyosis characterized by endometrial glands breaking through the myometrium, sometimes accompanied by fibromyoma and inflammatory changes, with evidence of follicular/parovarian cysts in some ovaries and positive CK19 staining in endometrial glands in a subset. The authors report that four of the seven adenomyotic tissues had inflammation and three showed pre-inflammatory changes, proposing roles for local hormonal imbalance and inflammation-related cellular proliferation/infiltration, while noting an additional possibility that p53 defects may contribute to de novo neoplastic transformation. This paper is centrally about adenomyosis — investigating how ovarian cysts/pathologies and uterine inflammatory changes associate with adenomyosis development in bitches, providing a mechanistic comparison relevant to endometriosis.

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Abstract

Background: Adenomyosis is a non-neoplastic condition, characterized by the presence of endometrial glands or cells in the myometrium. Adenomyosis is defined by post-operative microscopic examination of uterine tissue and a rarely seen infertility problem in bitches. The process of transformation of healthy uterus into adenomiotic uterus is still a mystery. We aimed to determine role of ovarian pathologies and uterine inflammations on pathogenesis of uterine adenomyosis in bitches.Cases: After ovariohysterectomy, the uteri were fixed and processed by routine methods. Sections were stained with HematoxylinEosin, Masson’s trichrome and Periodic-Acid-Schiff and immunohistochemically; with p53 protein, Ki-67, α-smooth-muscle actin, cytokeratin-CK 8, 14, 19 antibodies, estrogen and progesterone receptors by Avidin-Biotin-Complex-Peroxidase method. Histopathologically, 7 of the collected tissue samples (n = 38) were diagnosed as adenomyosis. There were unilateral (n = 6) or bilateral (n = 1) adenomyosis in which endometrial glands had broken through the myometrium, and in some cases there were fibromyoma, inflammation, papillary hyperplasia and cysts in glands. Vaginal fibroma, fibromyoma and benign mix tumor (n = 1), simple carcinoma (n = 3), carcinosarcoma (n = 3) in mammary gland were determinated histopathologically. In addition to these findings, follicular cysts (n = 4), parovarian cyst (n = 1), adenocarcinoma and Rete ovarii adenoma were diagnosed in some ovaries. The CK 19 was scored at endometrial glands (n = 2) positively and also, muscle fibers were stained positively with α-smooth-muscle actin antibody (n = 7).Discussion: Adenomyosis is an infertility problem in adult dogs and is hard to detect with routine gynecological examinations. Adenomyosis can be seen unaccompanied by other gynecological problems such as endometritis or leiomyomas, while mammary tumors with adenomyosis have been previously reported in women and in only one case of a bitch. Little is known of the interrelationships between gross pathological and endocrine features of ovarian cysts in bitches. Due to the local hormonal imbalance, most of these ovarian tumors and cystic structures might be accompanied with uterine-vaginal and mammary gland pathologies, cystic endometrial hyperplasia-pyometra, adenomyosis, vaginal fibroma and mammary tumors. The hyperestrogenic metabolic state may promote both the invagination process and the overall spreading of adenomyosis into the myometrium. Adenomyosis is often associated with polyps, anovulation, hyperplasia without cytological atypia, and uterine leiomyoma which are produced by hyperestrogenic states. Prolactin appears to induce adenomyosis in mice and hyperprolactinemia may cause myometrial degeneration/weakness and subsequent endometrial invasion in the presence of ovarian steroids in women. Premature decline in progesterone, a problem ensues with prolactin release which can promote hyperprolactinemia or endogenous prolactin release. In addition to hormonal problems, uterine infections, immune factors and their products like cytokines and inflammatory mediators, oxidative stress and free radical metabolism also might have roles in the occurrence of adenomyosis. In the present study, four of seven adenomyotic uterine tissues had inflammation and 3 of 7 cases had pre-inflammatory changes. Changes in uterine tissues may increase cell infiltration and proliferation as well as the activity of immune cells which may promote development of adenomyosis in bitches. It is therefore possible that a defect in the p53 tumor suppressor gene may play an important role in the de novo neoplastic transformation of adenomyosis. In conclusion, adenomyosis can be observed bilaterally or unilaterally in dogs. Tissue damage under the influence of inflammation or hormonal disturbances might have a role in the occurrence of uterine adenomyosis.
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Background

Adenomyosis is a non-neoplastic condition, characterized by the presence of endometrial glands or cells in the myometrium. Adenomyosis is defined by post-operative microscopic examination of uterine tissue and a rarely seen infertility problem in bitches. The process of transformation of healthy uterus into adenomiotic uterus is still a mystery. We aimed to determine role of ovarian pathologies and uterine inflammations on pathogenesis of uterine adenomyosis in bitches. Cases: After ovariohysterectomy, the uteri were fixed and processed by routine methods. Sections were stained with HematoxylinEosin, Masson’s trichrome and Periodic-Acid-Schiff and immunohistochemically; with p53 protein, Ki-67, α-smooth-muscle actin, cytokeratin-CK 8, 14, 19 antibodies, estrogen and progesterone receptors by Avidin-Biotin-Complex-Peroxidase method. Histopathologically, 7 of the collected tissue samples (n = 38) were diagnosed as adenomyosis. There were unilateral (n = 6) or bilateral (n = 1) adenomyosis in which endometrial glands had broken through the myometrium, and in some cases there were fibromyoma, inflammation, papillary hyperplasia and cysts in glands. Vaginal fibroma, fibromyoma and benign mix tumor (n = 1), simple carcinoma (n = 3), carcinosarcoma (n = 3) in mammary gland were determinated histopathologically. In addition to these findings, follicular cysts (n = 4), parovarian cyst (n = 1), adenocarcinoma and Rete ovarii adenoma were diagnosed in some ovaries. The CK 19 was scored at endometrial glands (n = 2) positively and also, muscle fibers were stained positively with α-smooth-muscle actin antibody (n = 7).

Discussion

Adenomyosis is an infertility problem in adult dogs and is hard to detect with routine gynecological examinations. Adenomyosis can be seen unaccompanied by other gynecological problems such as endometritis or leiomyomas, while mammary tumors with adenomyosis have been previously reported in women and in only one case of a bitch. Little is known of the interrelationships between gross pathological and endocrine features of ovarian cysts in bitches. Due to the local hormonal imbalance, most of these ovarian tumors and cystic structures might be accompanied with uterine-vaginal and mammary gland pathologies, cystic endometrial hyperplasia-pyometra, adenomyosis, vaginal fibroma and mammary tumors. The hyperestrogenic metabolic state may promote both the invagination process and the overall spreading of adenomyosis into the myometrium. Adenomyosis is often associated with polyps, anovulation, hyperplasia without cytological atypia, and uterine leiomyoma which are produced by hyperestrogenic states. Prolactin appears to induce adenomyosis in mice and hyperprolactinemia may cause myometrial degeneration/weakness and subsequent endometrial invasion in the presence of ovarian steroids in women. Premature decline in progesterone, a problem ensues with prolactin release which can promote hyperprolactinemia or endogenous prolactin release. In addition to hormonal problems, uterine infections, immune factors and their products like cytokines and inflammatory mediators, oxidative stress and free radical metabolism also might have roles in the occurrence of adenomyosis. In the present study, four of seven adenomyotic uterine tissues had inflammation and 3 of 7 cases had pre-inflammatory changes. Changes in uterine tissues may increase cell infiltration and proliferation as well as the activity of immune cells which may promote development of adenomyosis in bitches. It is therefore possible that a defect in the p53 tumor suppressor gene may play an important role in the de novo neoplastic transformation of adenomyosis. In conclusion, adenomyosis can be observed bilaterally or unilaterally in dogs. Tissue damage under the influence of inflammation or hormonal disturbances might have a role in the occurrence of uterine adenomyosis. Downloads

References

Bergeron C., Amant F. & Ferenczy A. 2006. Pathology and physiopathology of adenomyosis. Best Practice & Research Clinical Obstetrics & Gynaecology. 20: 511-521. Bulman-Fleming J. 2008. A rare case of uterine adenomyosis in a Siamese cat. The Canadian Veterinary Journal. 49: 709-712. Concannon P.W. 2011. Reproductive cycles of the domestic bitch. Animal Reproduction Science. 124: 200-210. Di Donato N., Montanari G., Benfenati A., Leonardi D., Bertoldo V., Monti G., Raimondo D. & Seracchioli R. 2014. Prevalence of adenomyosis in women undergoing surgery for endometriosis. The European Journal of Obstetrics & Gynecology and Reproductive Biology. 181: 289-293. Ferenczy A. 1998. Pathophysiology of adenomyosis. Human Reproduction Update. 4: 312-322.6 Ficicioglu C., Tekin H.I., Arioglu P.F. & Okar I. 1995. A murine model of adenomyosis: the effects of hyperprolactinemia induced by fluoxetine hydrochloride, a selective serotonin re-uptake inhibitor, on adenomyosis induction in Wistar albino rats. Acta Europaea Fertilitatis. 26: 75-79. Guttner J. 1980. Adenomyosis in mice. Zeitschrift Fur Versuchstierkunde. 22: 249-251. Habiba M. & Benagiano G. 2016. Adenomyosis and endometrial carcinoma. In: Habiba M. & Benagiano G. (Eds). Uterine Adenomyosis. Switzerland: Springer International Publishing, pp.153-161. Ilha M.R., Newman S. J., Van Amstel S., Fecteau K.A. & Rohrbach B.W. 2010. Uterine lesions in 32 female miniature pet pigs. Veterinary Pathology. 47: 1071-1075. Katkiewicz M., Wierzchon M. & Boryczko Z. 2005. Adenomyosis cows’ uterus – latent cause of infertility? Medycyna Weterynaryjna. : 1378-1381. Knauf Y., Bostedt H., Failing K., Knauf S. & Wehrend A. 2014. Gross pathology and endocrinology of ovarian cysts in bitches. Reproduction in Domestic Animals. 49: 463-468. Knauf Y. & Wehrend A. 2010. Ovarian cysts in the bitch. Tierärztliche Praxis. 38: 333-340. Koike N., Tsunemi T., Uekuri C., Akasaka J., Ito F., Shigemitsu A. & Kobayashi H. 2013. Pathogenesis and malignant transformation of adenomyosis. Oncology Reports. 29: 861-867. Korzekwa A.J., Bah M., Gęstwicka M., Socha B. & Skarżyński D.J. 2013. Adenomyosis in the bovine uterus: correlation between frequency, age, and 17β-estradiol–progesterone equilibrium. Theriogenology. 79: 165-172. Li B., Chen M., Liu X. & Guo S.W. 2013. Constitutive and tumor necrosis factor-α-induced activation of nuclear factor- B in adenomyosis and its inhibition by andrographolide. Fertility and Sterility. 100: 568-577. Łupicka M., Socha B., Szczepańska A. & Korzekwa A. 2015. Expression of pluripotency markers in the bovine uterus with adenomyosis. Reproductive Biology and Endocrinology. 13: 110-123. Mackenzie W.F. & Casey H.W. 1975. Animal model of human disease. Endometriosis. Animal model: endometriosis in rhesus monkeys. The American Journal of Pathology. 80: 341-344. Mir F., Fontaine E., Albaric O., Greer M., Vannier F., Schlafer D.H. & Fontbonne A. 2013. Findings in uterine biopsies obtained by laparotomy from bitches with unexplained infertility or pregnancy loss: an observational study. Theriogenology. 79: 312-322. Mori T. & Nagasawa H. 1983. Mechanisms of development of prolactin-induced adenomyosis in mice. Acta Anatomica. 116: 46-54. Olson P.N., Wrigley R.H., Husted P.W., Bowen R.A. & Nett T.A. 1989. Persistent estrus in the bitch. In: Ettinger S.J., Feldman E.C. & Cote E. (Eds). Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders, pp.1792-1796. Perez-Marin C.C., Molina L., Dominguez J.M., Millan Y. & De Las Mulas J.M. 2008. Incidental finding of uterine adenomyosis in a bitch with reproductive disorders: a case report. Veterinarni Medicina. 53: 636-640. Polat İ.M., Alçi ir E., Pekcan M., Vural S.A., Özenç E., Canatan H.E., Yazlik M.O. & Vural M.R. 2015. Characterization of transforming growth factor beta superfamily, growth factors, transcriptional factors, and lipopolysaccharide in bovine cystic ovarian follicles. Theriogenology. 84: 1043-1052. Silva E., Leitão S., Henriques S., Kowalewski M.P., Hoffmann B., Ferreira-Dias G. & Mateus L. 2010. Gene transcription of TLR2, TLR4, LPS ligands and prostaglandin synthesis enzymes are up-regulated in canine uteri with cystic endometrial hyperplasia–pyometra complex. Journal of Reproductive Immunology. 84: 66-74. Sotnikova N., Antsiferova I. & Malyshkina A. 2002. Cytokine network of eutopic and ectopic endometrium in women with adenomyosis. American Journal of Reproductive Immunology. 47: 251-255. Stockun‐Gautschi N.M., Guscetti F., Reichler I.M., Geissbuhler U., Braun S.A. & Arnold S. 2001. Identification of focal adenomyosis as a uterine lesion in two dogs. Journal of Small Animal Practice. 42: 413-416. Struble J., Reid S. & Bedaiwy M.A. 2016. Adenomyosis: A clinical review of a challenging gynecologic condition. Journal of Minimally Invasive Gynecology. 23: 164-185. Taskin M., Lallas T.A., Shevchuk M. & Barber H.R. 1996. P53 expression in adenomyosis in endometrial carcinoma patients. Gynecologic Oncology. 62: 241-246. Yotov S., Simeonov R., Dimitrov F., Vassilev N., Dimitrov M. & Georgiev P. 2005. Papillary ovarian cystadenocarcinoma in a dog: clinical communication. Journal of the South African Veterinary Association. 76: 43-45. Published How to Cite Issue Section License This journal provides open access to all of its content on the principle that making research freely available to the public supports a greater global exchange of knowledge. Such access is associated with increased readership and increased citation of an author's work. 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