Calcifications in Ovary and Endometrium and Their Neoplasms

Abstract

In this study, we investigated the role of hormones in the pathogenesis of calcifications in ovary and in endometrium and their neoplasms of the gynecologic tract and assessed the anatomic location and incidence of these calcifications. The study consists of three parts designed to investigate the pathogenesis, the location, and the incidence of calcifications in ovary and endometrium and their neoplasms. In the first part, 79 female guinea pigs were divided into 10 groups, and different hormones, given weekly for 12 months, were administered to the guinea pigs by group. A control group of 7 guinea pigs received sterile water. Calcifications developed in 5 of 7 guinea pigs treated with prolactin, 10 of 20 treated with human chorionic gonadotropin, 5 of 11 treated with estradiol, 3 of 7 treated with estrone, 1 of 6 treated with growth hormone, and 1 of 10 treated with testosterone; in 20 of the guinea pigs, the calcifications developed in the stroma of the endometrium, and in 5 guinea pigs, they developed in the ovary. The second part of the study consisted of an evaluation of the specific location of calcifications in 43 consecutive human surgical ovaries and endometria. Calcifications were seen only in the stroma in 100% of the ovarian serous adenofibroma specimens; in ovarian serous borderline neoplasms, the stroma contained 70 to 100% of the calcifications, and the epithelium had 0 to 30% of the calcifications. In ovarian serous carcinoma specimens, the calcifications were seen in the stroma in 50 to 60% of the cases, in the epithelium in 40% of the cases, and in areas of necrosis in 10% of the cases.The third part of the study was directed to determine the frequency of calcifications in ovarian lesions. We found that all cases of endosalpingiosis and ovarian low-grade serous carcinoma had calcifications, whereas 80% of the cases of serous borderline tumor had calcifications, and only 50% of the cases of ovarian high-grade serous carcinoma contained calcifications. The results of this study indicate that the majority of the calcifications in the ovary and the endometrium and their neoplasms are present in the stroma. This is most probably secondary to metabolic changes, which could be related to hormones and not caused by degenerative changes in epithelial cells. Pathologic calcifications are classified as either metastatic (associated with hypercalcemia) or dystrophic (associated with normal calcemia) (1, 2). Traditionally, calcifications in neoplasms have been considered to be dystrophic, forming secondary to degeneration of the epithelium or in association with areas of necrosis (2-6). However, a secretory rather than a degenerative etiology has also been suggested on the basis of the absence of stainable DNA and RNA in areas with calcifications (7-9). In this study, we investigated the role of hormones in the pathogenesis of calcifications in the ovary and the endometrium and their neoplasms and assessed the anatomic site and incidence of these calcifications. A novel pathogenetic mechanism to explain the...

Increase in post-therapy tumor calcification on CT scan is not an indicator of response to therapy in low-grade serous ovarian cancer

“…Among different subtypes of ovarian cancer, calcified metastasis tends to occur more often in low-grade serous ovarian cancers [21,13,14,22,16,17,23]. The exact etiology of tumor calcification in ovarian cancer is still unclear.…”

“…The exact etiology of tumor calcification in ovarian cancer is still unclear. It is hypothesized that multiple mechanisms may be involved in the pathogenesis of ovarian tumor calcifications, with dystrophic calcification developing secondary to degeneration of the epithelium or in areas of tumor necrosis or may be related to hormonal influence [23]. …”

Calcification

“…In that study, 96 (79%) of 122 patients with calcification had stages II and III disease, whereas 964 (85%) of 1134 patients without calcification had stages II and III disease. Likewise, in a study involving 35 ovarian cancers, Silva et al 17 found that all of the ovarian low-grade serous cancers had calcifications, whereas 80% of the serous borderline tumors had calcifications, and only 50% of the high-grade serous cancers contained calcifications. Also, Motohara et al 18 revealed the same result.…”

“…22 However, in the case of ovarian cancer, Cheng et al 23 17 found that calcification occurred predominantly in the stroma and could be induced by various hormones in guinea pigs; they suggested that this phenomenon was related to metabolic changes, which were secondary to stromal cell secretion, but not related to necrosis or degenerative changes. 17 The ultrastructural study of meningiomas by Tsuchida et al 24 found that collagen and vesicles secreted by tumor cells formed psammoma bodies. Similar view is also expressed in a study about ovarian cancer, Kiyozuka et al 25 reported that bone morphogenetic protein 2 and type IV collagen can promote the formation of psammoma bodies in ovarian cancer.…”

Erratum to: Psammoma bodies in two types of human ovarian tumours: a mineralogical study

“…(2001) found the formation of PBs in ovarian cancer was closely related to BMP-2 and type-IV collagen. Silva et al (2003) found hormone can affect the formation of PBs. Besides, nanobacteria may also get involved in the crystallization of PBs (Sedivy & Battistutti 2003;Hudelist et al 2004).…”