This can aid in predicting growth changes, allowing dentists, especially orthodontists, to develop a suitable treatment plan. Coupled with that, findings consistent among individuals include:

Anterior hypodontia associated with hyper divergent craniofacial pattern;
A tendency toward a class III malocclusion identified in maxillary hypodontia, and;
Reduced lower posterior facial height in children with posterior and mandibular hypodontia. Associated anomalies
Reduction in coronal or radical dimensions
Retained primary teeth
Ectopic canine eruption
Abnormal morphology such as peg-shaped maxillary lateral incisors and taurodontism, characterized by an enlarged tooth body and roots that are reduced in size
Extracted teeth

Cause
Several theories regarding the aetiology of hypodontia have been proposed in existing literature. There have been various theories mostly looking into genetic and environmental aspects and how they may both be involved. However, the exact cause remains unclear. The extent of individual influences of genetic and environmental factors is still widely debated.Theories regarding the mechanism through which hypodontia occurs can be categorised into evolutional or anatomical.Preliminary studies focused on an evolutionary approach which suggested shortening of the intermaxillary complex and thus shorter arches may contribute to a decrease in number of teeth. This was also suggested in 1945 by Dahlberg using Butlers Field Theory that focused on evolution and development of mammalian teeth into human dentition in an attempt to analyse different of agenesis. In each jaw, four morphological sites were identified (incisors, canines, premolars and molars). The tooth at the end of each region was less genetically stable and hence more prone to absence.
Congenital rubella syndrome (CRS) can occur in a developing fetus of a pregnant woman who has contracted rubella, usually in the first trimester. If infection occurs 0–28 days before conception, the infant has a 43% risk of being affected. If the infection occurs 0–12 weeks after conception, the risk increases to 81%. If the infection occurs 13–26 weeks after conception, the risk is 54% of the infant being affected by the disease. Infants are not generally affected if rubella is contracted during the third trimester, or 26–40 weeks after conception. Problems rarely occur when rubella is contracted by the mother after 20 weeks of gestation and continues to disseminate the virus after birth. It was discovered in 1941 by Australian Norman McAlister Gregg. Signs and symptoms
The classic triad for congenital rubella syndrome is:
Sensorineural deafness (58% of patients)
Eye abnormalities—especially retinopathy, cataract, glaucoma, and microphthalmia (43% of patients)
Congenital heart disease—especially pulmonary artery stenosis and patent ductus arteriosus (50% of patients)Other manifestations of CRS may include:

Spleen, liver, or bone marrow problems (some of which may disappear shortly after birth)
Intellectual disability
Small head size (microcephaly)
Low birth weight
Thrombocytopenic purpura
Extramedullary hematopoiesis (presents as a characteristic blueberry muffin rash)
Enlarged liver
Small jaw size
Skin lesions Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of:

Developmental delay
Autism
Schizophrenia
Growth retardation
Learning disabilities
Diabetes mellitus

Diagnosis
Prevention
Vaccinating the majority of the population is effective at preventing congenital rubella syndrome.