Programmed cell death by apoptosis occurs in fetal and maternal tissues dur
ing early pregnancy and plays an important role during implantation, decidu
alization, and in fetal development. In the regulation of apoptosis, bcl-2
is one of the central controlling genes, and acts by protecting the cell ag
ainst apoptosis, It is postulated that invasiveness of ectopic trophoblast
towards and through the muscularis zone of the tubal wall consequently lead
ing to tubal rupture might be due to disturbed regulation of apoptosis, By
means of immunohistochemistry and a computerized image analysis, bcl-2 immu
nostaining was localized and quantified in 36 randomly selected paraffin-em
bedded ectopic trophoblast tissue specimens collected from women undergoing
surgery for ruptured (n = 18) and non-ruptured (n = 18) tubal ectopic preg
nancies, Immunostaining was found in the villi syncytiotrophoblast in all p
atients, while the percentage of positive bcl-2 immunostained area (%PA) (P
= 0.0009) and staining intensity (P = 0.0042) were consistently greater in
the group of ruptured ectopic pregnancies, Including the variables %PA and
saturation into a logistic regression model for a probability threshold of
0.5 (<0.5 = non-ruptured ectopic pregnancy, >0.5 = ruptured ectopic pregna
ncy) to identify tubal rupture, a sensitivity and specificity of 94.4% were
found, It is suggested that elevated bcl-2 immunostaining in the syncytiot
rophoblast layer reflects unlimited cell survival of ectopic trophoblast an
d could lead to the establishment of a circulating marker for tubal rupture
.