Papillary tubal hyperplasia: the putative precursor of ovarian atypical proliferative (borderline) serous tumors, noninvasive implants, and endosalpingiosis

Abstract

In contrast to the controversy regarding the terminology and behavior of ovarian noninvasive low-grade serous tumors [atypical proliferative serous tumor (APST) and serous borderline tumor], little attention has been directed to their origin. Similarly, until recently, proliferative lesions in the fallopian tube had not been extensively studied. The recent proposal that ovarian high-grade serous carcinomas are derived from intraepithelial carcinoma in the fallopian tube prompted us to evaluate the possible role of fallopian tube in the genesis of low-grade serous tumors. We have identified a lesion, designated "papillary tubal hyperplasia (PTH)," characterized by small rounded clusters of tubal epithelial cells and small papillae, with or without associated psammoma bodies, that are present within the tubal lumen and which are frequently associated with APSTs. Twenty-two cases in this study were selected from a population-based study in Denmark of approximately 1000 patients with low-grade ovarian serous tumors in whom implants were identified on the fallopian tube. Seven additional cases were seen recently in consultation at The Johns Hopkins Hospital (JHH). These 7 cases were not associated with an ovarian tumor. PTH was found in 20 (91%) of the 22 cases in the Danish study. On the basis of this association of PTH with APSTs with implants and the close morphologic resemblance of PTH, not only to primary ovarian APSTs but also to noninvasive epithelial implants and endosalpingiosis, we speculate that the small papillae and clusters of cells from the fallopian tube implant on ovarian and peritoneal surfaces to produce these lesions. The 7 JHH cases of PTH that were not associated with an ovarian tumor support the view that PTH is the likely precursor lesion. We propose a model for the development of ovarian and extraovarian low-grade serous proliferations (APST, noninvasive epithelial implants, and endosalpingiosis) that postulates that all of these lesions are derived from PTH, which appears to be induced by chronic inflammation. If this hypothesis is confirmed, it can be concluded that low-grade and high-grade ovarian tumors develop from tubal epithelium and involve the ovary secondarily.

Fig. 1

A Papillary tubal hyperplasia. Although the overall plical architectural changes are subtle, the plicae are slightly thicker and the overall appearance looks “busy”. B Normal fallopian tube.

Fig. 2

Papillary tubal hyperplasia. Numerous small papillae and psammoma bodies in the tubal lumen.

Fig. 3

Papillary tubal hyperplasia. Multiple small papillae floating in tubal lumen.

Fig. 4

Papillary tubal hyperplasia. A profuse number of small papillae in the tubal lumen.

Fig. 5

Papillary tubal hyperplasia. A “naked” psammoma body lying on surface of tubal epithelium and another one within the core of a small papilla, so-called salpingolith.

Fig. 6

Papillary tubal hyperplasia. Psammoma bodies within a papilla (salpingolith), tubal epithelium (blue thin arrow) and lamina propria (blue block arrow). Numerous intraepithelial lymphocytes are located just above the basement membrane in the mucosa (black arrows).

Fig. 7

Papillary tubal hyperplasia. Papilla arising from mucosa before it becomes pinched off. Secretory cells lie between ciliated cells. Intraepithelial lymphocytes lie just above the basement membrane (arrows). The nucleus is characteristically surrounded by a halo.

Fig. 8

Early tubal hyperplasia. Small elevated tufts of epithelium (arrows) represent the earliest hyperplastic change.

Fig. 9

Early tubal hyperplasia. Papillary bud still attached to tubal mucosa appears to be the next stage of hyperplasia before being pinched off and floating into the tubal lumen.

Fig. 10

A and B. Papillary tubal hyperplasia; C and D. Noninvasive epithelial implant; E and F. Atypical proliferative (borderline) serous tumor. Images are from different cases.