A 32-year-old woman with a history of early pregnancy loss followed by a full-term pregnancy presented to her gynecologist with difficulty conceiving and amenorrhea. Her second pregnancy, the live birth, had resulted in a vaginal birth followed by the manual removal of an attached posterior placenta. Twenty months after delivery, she had an ongoing amenorrhea, despite not breastfeeding. Endocrine investigations for follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, and prolactin were normal.
We requested a transvaginal ultrasound, which showed a hyperechoic endometrial band (Figure 1). We performed a hysteroscopy and resected bone spicules found on the posterior wall and uterotubal regions (Figure 2). Pathological examination showed multifocal calcific deposits and metaplasia, with a background atrophic endometrium. We diagnosed bone metaplasia with secondary infertility. Her periods resumed later; she conceived spontaneously and had a lively and healthy birth.
The prevalence of bone metaplasia is estimated to be 0.02% among women with infertility.1 More than 80% of reported cases occur after pregnancy.2 Bone metaplasia causes a sterile foreign body reaction similar to that caused by an intrauterine contraceptive device (IUCD). ). Risk factors include prior uterine instrumentation, presence of an IUD, infection, uterine abnormalities, and retained conception products.3 Physicians should consider bone metaplasia when ultrasounds show echogenic bands with acoustic shadow. Hysteroscopy is recommended, with resection of calcifications that often restore menstruation and fertility.2,3.
Several pathophysiological explanations for the development of bone metaplasia have been suggested. Multipotent stromal cells can occur in response to chronic endometritis, an emerging risk factor for recurrent pregnancy loss and implantation failure. In addition, bone differentiation of mesenchymal stem cells may occur secondary to osteogenesis after fetal bone retention, dystrophic calcification of retained necrotic tissues, and disorders of calcium and vitamin D.3 metabolism.
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