Any abnormality in tubal morphology or function may lead to ectopic pregnancy. In normal pregnancy the egg is fertilized in the Fallopian tube, and then it is transported into the uterus. It is believed that the most important cause of ectopic pregnancy is damage to the tubal mucosa, which could obstruct the embryo transport due to scarring. The other possibility is that a small defect in the mucosa attracts implantation in the Fallopian tube [13]. The mucosal damage may be caused by infection or surgical trauma. However, evidence of tubal damage is lacking in many cases of ectopic pregnancy. In these women the cause of ectopic pregnancy may be a dysfunction in the tubal smooth muscle activity. In general, oestrogens stimulate tubal myoelectrial activity and progesterone has an inhibitory effect. An altered oestrogen/progesterone ratio may affect tubal motility in different ways. Abnormally high oestrogen levels may cause tubal spasm, which could block transport of the embryo towards the uterine cavity. This may be an explanation for increased rates of ectopics following ovarian hyperstimulation and post-coital oral contraception. Conversely, pharmacological doses of progesterone in women using progesterone-only contraception could cause complete tubal relaxation leading to retention of the fertilized egg within the tube [14].

Embryonic abnormalities have also been studied in an attempt to explain occurrence of ectopics in the absence of tubal pathology and although the majority of tubal pregnancies are non-viable, the incidence of chromosomal defects is no higher than in samples obtained from intrauterine pregnancies [15].

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