Endometrial metaplasias are of two types, epithelial metaplasia which is commonly encountered and stromal metaplasia, unusually seen. This includes formation within endometrial stroma, islands of smooth muscle, cartilage, and bone. Endometrial stromal (cartilaginous) metaplasias are conditions frequently overlooked and misdiagnosed. Hence, a careful clinical and histopathological examination is required to avoid the misinterpretation of non-tumor cartilaginous foci as a component of malignant neoplasm. Herein, we report a rare case of endometrial cartilaginous metaplasia which was an incidental finding in a 38-year-old female with third degree uterovaginal prolapse
Epithelial metaplasia refers to the replacement of normal epithelium at a given site by mature benign epithelium inappropriate to that site. The endometrium is not unique in that it too demonstrates a spectrum of metaplastic epithelia. Some of these cytoplasmic alterations are better termed “changes” as they are thought not to represent true metaplastic transformation of the endometrial epithelium. The terminology is rather confusing as these two terms have been used interchangeably in the literature. This process may be encountered in benign conditions but can also be seen in association with endometrial hyperplasia and adenocarcinoma. The presence of endometrial metaplasia can significantly complicate the histological interpretation of endometrial biopsy material due to glandular architectural complexity and crowding which can lead to an erroneous diagnosis of endometrial hyperplasia or even carcinoma if the pathologist is unaware of the potential pitfalls. Endometrial metaplasia although commonly seen involving endometrial epithelium may also on occasions involve the stroma. This review will describe the spectrum of histological features that can be seen in endometrial metaplasia of both epithelium and stroma and will aim to emphasize those histopathological features that will be helpful in distinguishing endometrial metaplasia from hyperplasia and carcinoma.
Endometrial mesenchymal metaplasias are less frequent than epithelial metaplasia. Endometrial metaplasias have been classified by Hendrickson and Kempson into three groups-epithelial, mesenchymal, and glial.[1]
The newer World Health Organization (WHO) classification divides them into those with epithelial and non-epithelial changes.[1]
WHO classification of endometrial metaplasias and related changes:[1]
Epithelial metaplasias and related changes
Smooth muscle metaplasia
Osseous metaplasia
Cartilaginous metaplasia
Fatty change
Glial tissue
- Foam cell change
Non-epithelial metaplastic and related changes
Heterotopia is the occurrence of a mature tissue at an abnormal location. Heterotopic uterine cartilage can be of metaplastic origin or it can result from the displacement and retention of fetal tissues in the uterine wall. The multipotent cells present in normal endometrial stroma can show metaplastic transformation into various elements, including the cartilage.[7] Such cartilaginous metaplasia usually follows trauma secondary to childbirth.[8] The history of multiparity in our case supports the concept of metaplasia.
Heterotopic uterine cartilage of metaplastic origin may occur as solitary or multiple foci, and may be located in the endometrium or even in the stroma of endometrial polyp. The lesion may be an incidental finding as was in our case. However, even menorrhagia may occur.[8]
Genital tuberculosis, unspecific chronic endometritis, or pyometra are other sources of chronic inflammation such as that occurring after retained embryonic tissue, and this inflammation acts as a promoter of secondary changes.[5] In India, endometrial tuberculosis should be ruled out as it can cause infertility as well as chondrogenesis.[4]
Chronic endometritis also stimulates the proliferation of mesenchymal cells that have the inherent property of metaplasia and can differentiate into chondroblasts or osteoblasts.[4]
Other mechanisms proposed for uterine cartilage formation include hypercalcemia and hyperoestrinism. Dystrophic calcification and cartilage formation may be secondary to chronic inflammation in pyometra. Another interesting mechanism is the iatrogenic implantation of the fetal tissue, including the cartilage, into the uterine wall following dilatation and curettage.[7]
