Abstract

Recurrent pregnancy loss, defined as two or more failed pregnancies by the American Society for Reproductive Medicine [1], is a clinical problem because known effective treatment is limited. Effective treatment depends on the cause of the reproductive failure. Thus, attention has been focused on determining causes of recurrent pregnancy loss. Even so, to date, only chromosomal abnormalities of the conceptus and immunologic risk factors have been generally accepted as etiologies of recurrent pregnancy loss. Recently, a novel pathologic pathway that involves impaired decidualization of endometrial stromal cells has been proposed as a cause of recurrent pregnancy loss [2]. Further, it has been hypothesized that the impaired decidualization is manifested by the prolongation of the window of implantation allowing for increased fecundity and Bsuperfertility^ [2–7]. The following paragraphs will describe the evidence for these notions.

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