The risk of a repeat GTD is approximately 1 in 100, compared with approximately 1 in 1000 risk in the general population. Especially women whose hCG levels remain significantly elevated are at risk of developing a repeat GTD.

Most women with GTD can become pregnant again and can have children again. The risk of a further molar pregnancy is low. More than 98% of women who become pregnant following a molar pregnancy will not have a further hydatidiform mole or be at increased risk of complications.

In the past, it was seen as important not to get pregnant straight away after a GTD. Specialists recommended a waiting period of 6 months after the hCG levels become normal. Recently, this standpoint has been questioned. New medical data suggest that a significantly shorter waiting period after the hCG levels become normal is reasonable for approximately 97% of the patients with hydatidiform mole.

Most studies are based on populations of women who have experienced a pregnancy loss and thus do not address the issue of the prevalence in the general population. A screening study by Woelfer et al. of women without a history of reproductive problems found that about 3% of women had a uterine septation; the most common anomaly in their study was an arcuate uterus (5%), while 0.5% were found to have a bicornuate uterus. In contrast, in about 15% of patients with recurrent pregnancy loss anatomical problems are thought to be causative with the septate uterus as the most common finding.

The cause of this condition is not completely understood. Potential risk factors may include defects in the egg, abnormalities within the uterus, or nutritional deficiencies. Women under 20 or over 40 years of age have a higher risk. Other risk factors include diets low in protein, folic acid, and carotene. The diploid set of sperm-only DNA means that all chromosomes have sperm-patterned methylation suppression of genes. This leads to overgrowth of the syncytiotrophoblast whereas dual egg-patterned methylation leads to a devotion of resources to the embryo, with an underdeveloped syncytiotrophoblast. This is considered to be the result of evolutionary competition with male genes driving for high investment into the fetus versus female genes driving for resource restriction to maximise the number of children.

More than 80% of hydatidiform moles are benign. The outcome after treatment is usually excellent. Close follow-up is essential. Highly effective means of contraception are recommended to avoid pregnancy for at least 6 to 12 months.

In 10 to 15% of cases, hydatidiform moles may develop into invasive moles. This condition is named "persistent trophoblastic disease" (PTD). The moles may intrude so far into the uterine wall that hemorrhage or other complications develop. It is for this reason that a post-operative full abdominal and chest x-ray will often be requested.

In 2 to 3% of cases, hydatidiform moles may develop into choriocarcinoma, which is a malignant, rapidly growing, and metastatic (spreading) form of cancer. Despite these factors which normally indicate a poor prognosis, the rate of cure after treatment with chemotherapy is high.

Over 90% of women with malignant, non-spreading cancer are able to survive and retain their ability to conceive and bear children. In those with metastatic (spreading) cancer, remission remains at 75 to 85%, although their childbearing ability is usually lost.

The condition may not be known to the affected individual and not result in any reproductive problems; thus normal pregnancies may occur. However, it is associated with a higher risk for miscarriage, premature birth, and malpresentation. According to the classical study by Buttram there is a 60% risk of a spontaneous abortion, this being more common in the second than in the first trimester. However, there is no agreement on this number and other studies show a lower risk. Woelfer found that the miscarriage risk is more pronounced in the first trimester.

The condition is also associated with abnormalities of the renal system. Further, skeletal abnormalities have been linked to the condition.

Invasive hydatidiform mole, also known as invasive mole and chorioadenoma destruens is a type of neoplasia that grows into the muscular wall of the uterus. It is formed after conception (fertilization of an egg by a sperm). It may spread to other parts of the body, such as the vagina, vulva, and lung.

Circumvallate placenta is a placental morphological abnormalitiy, a subtype of placenta extrachorialis in which the fetal membranes (chorion and amnion) "double back" on the fetal side around the edge of the placenta. After delivery, a circumvallate placenta has a thick ring of membranes on its fetal surface.

The fetal surface is divided into a central depressed zone surrounded by a thickened white ring which is incomplete the ring is situated at varying distance from the margin of the placenta. The ring is composed of a double fold of amnion and chorion with degenerated decidua vera and fibrin in between. Vessels radiate from the cord insertion as far as the ring and then disappear from the view.

Complete circumvallate placenta occurs in approximately 1% of pregnancies. It is diagnosed prenatally by medical ultrasonography, although one 1997 study of prenatal ultrasounds found that "of the normal placentas, 35% were graded as probably or definitely circumvallate by at least one sonologist," and "all sonologists misgraded the case of complete circumvallation as normal." The condition is associated with perinatal complications such as placental abruption, oligohydramnios, abnormal cardiotocography, preterm birth, and miscarriage.

It is a rare disease, with an incidence of 1 in 1200 placentas. Women with cardiac problems, disorders of circulation, monosomy, hypertension and diabetes are predisposed to Breus' mole. The mole is formed as a sub-chorionic hematoma, formed out of the intervillous blood, causing progressive accumulation of the clotting substance called fibrin with increasing gestational age. Evidence from Southern blot test reveals that 85 percent of the clotted material is maternal blood. Breus mole is reported to be found in the placetae of macerated stillborn foetuses, indicating that massive subchorionic hematoma could have been the cause of their demise. A massive Breus' mole can cause disturbances in blood flow in the spiral arteries and might result in intrauterine growth restriction of the foetus.

A placental disease is any disease, disorder, or pathology of the placenta. The article also covers placentation abnormalities, which is often used synonymously for placental disease.

In rare cases, inherited bleeding disorders, like hemophilia, von Willebrand disease (vWD), or factor IX or XI deficiency, may cause severe postpartum hemorrhage, with an increased risk of death particularly in the postpartum period. The risk of postpartum hemorrhage in patients with vWD and carriers of hemophilia has been found to be 18.5% and 22% respectively. This pathology occurs due to the normal physiological drop in maternal clotting factors after delivery which greatly increases the risk of secondary postpartum hemorrhage.

Another bleeding risk factor is thrombocytopenia, or decreased platelet levels, which is the most common hematological change associated with pregnancy induced hypertension. If platelet counts drop less than 100,000 per microliter the patient will be at a severe risk for inability to clot during and after delivery.

Trophoblastic neoplasms derive from trophoblastic tissue. Examples include:

- Choriocarcinoma

- Hydatidiform mole

Breus' mole (Ova tuberculosa, massive mole) is a massive, subchorionic, tuberous hematoma, formed out of maternal blood in the uterus in pregnancy. It was first described by Karl Breus in 1892.

A longitudinal vaginal septum develops during embryogenesis when there is an incomplete fusion of the lower parts of the two Müllerian ducts. As a result, there is a "double vagina". There may be associated duplications of the more cranial parts of the Müllerian derivatives, a double cervix, and either a uterine septum or uterus didelphys (double uterus).

The person with a longitudinal vaginal septum may be asymptomatic and not aware of the condition. If dyspareunia is a problem a simple resection of the septum could be performed.

A transverse septum can form during embryogenesis when the Müllerian ducts fuse improperly to the urogenital sinus. A complete transverse septum will block menstrual flow and is a cause of primary amenorrhea. The accumulation of menstrual debris behind the septum is termed cryptomenorrhea. Some transverse septa are incomplete and may lead to dyspareunia or obstruction in labour. A surgical incision will relieve the situation.

Antepartum bleeding (APH), also prepartum hemorrhage, is bleeding during pregnancy from the 24th week (sometimes defined as from the 20th week) gestational age to full term (40th week). The primary consideration is the presence of a placenta previa which is a low lying placenta at or very near to the internal cervical os. This condition occurs in roughly 4 out of 1000 pregnancies and usually needs to be resolved by delivering the baby via cesarean section. Also a placental abruption (in which there is premature separation of the placenta) can lead to obstetrical hemorrhage, sometimes concealed. This pathology is of important consideration after maternal trauma such as a motor vehicle accident or fall.

Other considerations to include when assessing antepartum bleeding are: sterile vaginal exams that are performed in order to assess dilation of the patient when the 40th week is approaching. As well as cervical insufficiency defined as a midtrimester (14th-26th week) dilation of the cervix which may need medical intervention to assist in keeping the pregnancy sustainable.

Ultraviolet light from the sun causes premature aging of the skin and skin damage that can lead to melanoma. Some scientists hypothesize that overexposure to UV, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed to determine the complex interaction between genetic makeup and overall exposure to ultraviolet light. Some strong indications that this is so (but falling short of proof), are:

- The relative lack of moles on the buttocks of people with dysplastic nevi.

- Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.

Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is "in addition to" those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring "benign" moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever one's shadow is shorter than one's height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses.

Placental site trophoblastic tumor is a form of gestational trophoblastic disease, which is thought to arise from intermediate trophoblast.

It may secrete human placental lactogen (human chorionic somatomammotropin), and result in a false-positive pregnancy test.

Placental site trophoblastic tumor is a monophasic neoplasm of the implantation site intermediate trophoblast, and usually a benign lesion, which comprises less than 2% of all gestational trophoblastic proliferations. Preceding conditions include molar pregnancy (5%). Compared to choriocarcinoma or invasive mole, hemorrhage is less conspicuous and serum β-HCG level is low, making early diagnosis difficult.

Immunohistochemistry: Often stains with hPL, keratin, Mel-CAM, EGFR.

Prognosis: 10–20% of cases metastase leading to death.

Treatment: Because chemotherapy is ineffective; the patient should undergo hysterectomy.

Links between maternal smoking and TDS are tenuous, but there are stronger associations between maternal alcohol consumption and incidences of cryptorchidism in sons. Smoking does however affect the growth of a fetus, and low birth weight is shown to increase the likelihood of all the disorders encompassed by TDS. Maternal obesity, resulting in gestational diabetes, has also been shown to be a risk factor for impaired testes development and TDS symptoms in sons.

Midline cervical clefts are a rare congenital anomaly resulting from incomplete fusion during embryogenesis of the first and second branchial arches in the ventral midline of the neck. The condition presents as a midline cutaneous defect of the anterior neck with a skin projection or sinus, or as a subcutaneous erythematous fibrous cord. Surgical excision is the preferred treatment.

Poor semen quality is measured not only by the number of sperm a man produces but also by how effective the sperm is at fertilising an egg. The motility and shape of the sperm are important for this role. A man with poor semen quality will often present with fertility problems which is defined as a couple trying to conceive for over 1 year with no success. Diagnosis can be made from semen analysis, taking a sample of the man’s semen and running tests to count numbers and quality of the individual sperm.

The cause of Goldenhar syndrome is largely unknown. However, it is thought to be multifactorial, although there may be a genetic component, which would account for certain familial patterns. It has been suggested that there is a branchial arch development issue late in the first trimester.

An increase in Goldenhar syndrome in the children of Gulf War veterans has been suggested, but the difference was shown to be statistically insignificant.

Hormonal changes during pregnancy and diabetics (i.e. insulin) are often contributing to mole formation.

Prevalence ranges from 1 in 3500 to 5600 live births. Male-female ratio is found to be 3:2.

Hand-foot-genital syndrome is inherited in an autosomal dominant manner. The proportion of cases caused by de novo mutations is unknown because of the small number of individuals described. If a parent of the proband is affected, the risk to the siblings is 50%. When the parents are clinically unaffected, the risk to the sibs of a proband appears to be low. Each child of an individual with HFGS has a 50% chance of inheriting the mutation. Prenatal testing may be available through laboratories offering custom prenatal testing for families in which the disease-causing mutation has been identified in an affected family member.