Glial implants in gliomatosis peritonei arise from normal tissue, not from the associated teratoma.

Metaplasia of subcoelomic mesenchyme has been implicated, but not proven, in the pathogenesis of common gynecological diseases such as endometriosis and rarer entities such as leiomyomatosis peritonealis disseminata and gliomatosis peritonei (GP). GP is associated with ovarian teratomas and is characterized by numerous peritoneal and omental implants composed of glial tissue. Two theories to explain the origin of GP have been proposed. In one, glial implants arise from the teratoma, whereas in the other, pluripotent Müllerian stem cells in the peritoneum or subjacent mesenchyme undergo glial metaplasia. To address the origin of GP, we exploited a unique characteristic of many ovarian teratomas: they often contain a duplicated set of maternal chromosomes and are thus homozygous at polymorphic microsatellite (MS) loci. In contrast, DNA from matched normal or metaplastic tissue (containing genetic material of both maternal and paternal origin) is expected to show heterozygosity at many of these same MS loci. DNA samples extracted from paraffin-embedded normal tissue, ovarian teratoma and three individual laser-dissected glial implants were studied in two cases of GP. In one case, all three implants and normal tissue showed heterozygosity at each of three MS loci on different chromosomes, whereas the teratoma showed homozygosity at the same MS loci. Similar results were observed in the second case. Our findings indicate that glial implants in GP often arise from cells within the peritoneum, presumably pluripotent Müllerian stem cells, and not from the associated ovarian teratoma. This finding has important implications for more common gynecological entities with debatable pathogenesis, such as endometriosis, by definitively demonstrating the metaplastic potential of stem cells within the peritoneal cavity.