A 32-year-old woman with a history of early pregnancy followed by a premature birth presented herself to her gynecologist with difficulty conceiving and amenorrhea. Her second pregnancy, a live birth, led to a vaginal birth, followed by manual removal of the adjacent posterior placenta. Twenty months after giving birth, she had persistent amenorrhea even though she was not breastfeeding. Endocrine tests for follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone and prolactin are normal.
We ordered a transvaginal ultrasound that showed a hyperechoic endometrial band (Figure 1). We performed hysteroscopy and resected bone spicules covering the posterior wall and uterotubal areas (Figure 2). Pathological examination showed multifocal calcification deposits and metaplasia, with background atrophic endometrium. We diagnosed bone metaplasia with secondary infertility. Subsequently, her menstruation resumed; she conceived spontaneously and gave birth to a healthy living.
The prevalence of bone metaplasia is estimated at about 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 intrauterine contraception device (IUCD). Risk factors include previous uterine instruments, the presence of IUCD, infection, uterine abnormalities, and retained conception products.3 Clinicians should consider bone metaplasia when sonographs show echogenic acoustic shading bands. Hysteroscopy is recommended, as resection of calcifications often restores menstruation and fertility.2,3
Several pathophysiological explanations for the development of bone metaplasia have been proposed. Multipotent stromal cells may occur in response to chronic endometritis, an emerging risk factor for recurrent pregnancy loss and implant failure. In addition, bone differentiation from mesenchymal stem cells may occur secondary to osteogenesis after fetal bone retention, dystrophic calcification of retained necrotic tissue, and disturbances in calcium and vitamin D.3 metabolism.
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