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Placental examination has been proved to be of clinical value in cases selected because of gestational complications, unusual disorders of mother or infant, perinatal death, problems in perinatal diagnosis, and multiple pregnancy. Ten percent to 15% of births meet these criteria for selection. Causes of perinatal death, such as placental abruption, cord accidents, placental infarction, infection, and hematologic disorders, have been demonstrated. Clinically occult abnormalities, including chronic infections, maternal vascular disease, neoplasms, and storage diseases, have been recognized. Amniotic lesions and single umbilical artery have directed attention to fetal malformations. Monozygosity has been documented by monochorionic placentation. As a diagnostic source, the placenta has contributed to clinical care, understanding of disabilities among surviving children, and insight of forensic value. Limitations of placental studies stem from their qualitative nature and from gaps in current knowledge of gestational pathophysiology.

Nine cases of congenital cytomegalovirus infection were diagnosed at Brigham and Women's Hospital in Boston from September 1977 through July 1982. The majority of infected fetuses and newborn infants had intrauterine growth retardation, congenital malformations, microcephaly, or hydrops fetalis. In four cases, cytomegalovirus was recovered from placentas. Eight placentas were examined morphologically. Varying degrees of chronic villitis were noted in all. The most frequent lesion, found in six cases, was focal villous inflammation with mononuclear cell infiltrates. Lymphocytes predominated in this reaction. In three cases, however, the villi were also intensely infiltrated by plasma cells. Typical cytomegalic inclusion bodies were noted in these three placentas. The fetus and infants in whose placentas the plasmacytic villitis and inclusion bodies were discovered displayed the most severe manifestations of cytomegalovirus infection.

Alkaline phosphatase electrophoretic patterns characteristic of three phases in early human trophoblast development are described in this preliminary communication. Phase 1 (6 to 10 weeks) consists entirely of two heat-sensitive, L-homoarginine-inhibited bands, the slower one of which possesses antigenic determinants of live-bone-type alkaline phosphatase, whereas the fast band lacks any of the known alkaline phosphatase antigenic determinants. Phase 2 pattern (11 to 13 weeks) is that of a mixture of Phase 1 and Phase 3 isozyme components, the latter exhibiting two isozyme bands with the characteristics of term placental alkaline phosphatases correspond in order to non-Regan isoenzyme, a mixture of Regan and non-Regan isoenzymes and Regan isoenzyme in a variety of human cancer tissues. The biochemical profile characteristic of trophoblast developmental Phase 1 alkaline phosphatase is expressed as 78.5% heat-sensitive inhibition (5 min at 65 degrees), 66.3% L-homoarginine inhibition, and 17.3% L-phenylalanine inhibition where n = 12. It is hypothesized that the alkaline phosphatase of human tumor tissues reflects the expression of placental genes corresponding to one or more phases of trophoblastic development.

The unusual lesion of gestational trophoblast, variously termed "placental site tumor" and "placental site trophoblastic tumor," may complicate or follow seemingly normal pregnancy, abortion or hydatidiform mole. Posing indeterminate risks of malignant behavior, those lesions must be differentiated from the banal processes of implantation-site reaction, on the one hand, and from choriocarcinoma and other poorly differentiated uterine neoplasms, on the other. A history of antecedent pregnancy, serum assay of chorionic gonadotropin and human placental lactogen, and immunohistochemical studies of tumor tissue lead to a correct diagnosis. Assessment of the degree of malignancy may be problematic in individual cases, and treatment is not always successful. With an origin in the chorionic epithelium at the implantation site, this condition may be termed "placental-site chorioma." Refined diagnostic criteria may then provide a basis for designating some lesions benign chorioma and others malignant--i.e., placental-site choriocarcinoma.

Unlike the normal human placenta, the normal rabbit placenta, near term, is essentially free of such stigmas of aging as infarcts and syncytial knots. When experimental toxemia is produced in the pregnant rabbit by ligating the terminal aorta to a specific degree of stricture, placental lesions resembling those found in human toxemia are observed; namely, diffuse congestion, old and recent infarcts, and syncytial knots. All the treated animals who exhibited anatomical and clinical signs of toxemia presented, in association, obvious placental lesions; there were, however, some animals which showed infarct but no other signs of toxemia.

We investigated the presence of ureaplasmas, mycoplasmas, chlamydiae, fungi, aerobic and anaerobic bacteria, and cytomegalovirus in fetal membranes and evaluated their association with perinatal morbidity and mortality. We cultured 801 placentas from three groups of subjects (144 who died in the perinatal period, 452 neonates admitted to the intensive-care unit, and 205 controls). Ureaplasma urealyticum, Mycoplasma hominis, or both were isolated from 21 per cent of placentas of premature and term infants who died in the perinatal period, 25 per cent of those admitted to intensive care, and 11 per cent of controls. Gestational age and birth weight were inversely related to isolation of ureaplasma, and chorioamnionitis was positively related to isolation. The presence of ureaplasmas in the placenta suggests the transcervical migration of these microorganisms from the lower genitourinary tract. These data show a strong association between ureaplasma infection of the placenta and low birth weight of the neonate and suggest that the association is causal.

From 1982-1986, seven patients with pathologically confirmed placental site trophoblastic tumors underwent treatment at the New England Trophoblastic Disease Center. All seven patients presented with nonmetastatic disease; the presenting symptom was vaginal bleeding in six patients and amenorrhea in one patient. Mitotic counts of the tumor may vary among endometrial curettings, hysterectomy specimens, and metastatic lesions. When placental site trophoblastic tumor is diagnosed on endometrial curettage, a thorough metastatic workup should be undertaken. Because of this tumor's poor response to chemotherapy, a diagnosis of nonmetastatic placental site trophoblastic tumor should be followed by prompt hysterectomy.

Lesions of the uteroplacental vasculature may be involved in the pathogenesis of "placental insufficiency" in pregnancies complicated by hypertension, diabetes, systemic lupus erythematosus, and idiopathic fetal growth retardation. The decidual arteries of the placental bed of normotensive, hypertensive, and diabetic women were studied by histologic examination and direct immunofluorescence for immunoglobulins and complement. Decidual tissue was obtained by curettage and snap frozen immediately after delivery of the placenta in 21 normal pregnant control subjects, 73 nondiabetic women with hypertensive disorders, and 41 women with insulin-dependent diabetes. Lesions of fibrinoid necrosis and/or atherosis were observed in some of the decidual arteries of 53% of women with preeclampsia (primary or superimposed) and also in a proportion of women with stable chronic hypertension or normotensive diabetes. Thus, fibrinoid necrosis/atherosis of the decidual arteries is not specific for preeclampsia. Immunoglobulins and complement were detected in arteries with lesions in subjects of all clinical groups. The findings do not support the concept that immunoprotein deposition in pathologic decidual arteries is related to a hypothetical immunologic reaction specific for preeclampsia. In preeclampsia, vascular deposition of immunoglobulin and complement may be related to local intravascular coagulation.