Developmental Dental Anomalies

 Anomalies of Number: problems in initiation stage

 Hypodontia: 6% incidence; usually autosomal dominant (50% chance of passing to children) with variable expressivity (e.g., parent has mild while child has severe); most common missing permanent tooth (excluding 3rd molars) is Md 2nd premolar, 2nd most common is X lateral; oligodontia (at least 6 missing), and anodontia

1. Clincial implications: can interfere with function, lack of teeth → ↓ alveolar bone formation, esthetics, hard to replace in young children, implants only after growth completed, severe cases should receive genetic and systemic evaluation to see if other problems

2. Syndromes with hypodontia: Rieger syndrome, incontinentia pigmenti, Kabuki syndrome, Ellis-van Creveld syndrome, epidermolysis bullosa junctionalis, and ectodermal dysplasia (usually X-linked; sparse hair, unable to sweat, dysplastic nails)

Supernumerary teeth: aka hyperdontia; mesiodens when located in palatal midline; occur sporadically or as part of syndrome, common in cleft cases; delayed eruption often a sign that supernumeraries are preventing normal eruption

 

1. Multiple supernumerary teeth: cleidocranial dysplasia/dysostosis, Down’s, Apert, and Crouzon syndromes, etc.

Anomalies of Size: problems in morphodifferentiation stage

Microdontia: most commonly peg laterals; also in Down’s syndrome, hemifacial microsomia

Macrodontia: may be associated with hemifacial hypertrophy

Fusion: more common in primary dentition; union of two developing teeth

Gemination: more common in primary; incomplete division of single tooth bud → bifid crown, one pulp chamber; clinically distinguish from fusion by counting geminated tooth as one and have normal # teeth present (not in fusion)

 Anomalies of Shape: errors during morphodifferentiation stage

Dens evaginatus: extra cusp in central groove/cingulum; fracture can → pulp exposure; most common in Orientals

Dens in dente: invagination of inner enamel epithelium → appearance of tooth within a tooth

Taurodontism: failure of Hertwig’s epithelial root sheath to invaginate to proper level → elongated (deep) pulp chamber, stunted roots; sporadic or associated with syndrome (e.g., amelogenesis imperfecta, Trichodento-osseous syndrome, ectodermal dysplasia)

Conical teeth: often associated with ectodermal dysplasia

Anomalies of Structure: problems during histodifferentiation, apposition, and mineralization stages

Dentinogenesis imperfecta: problem during histodifferentiation where defective dentin matrix → disorganized and atubular circumpulpal dentin; autosomal dominant inheritance; three types, one occurs with osteogenesis imperfecta (brittle bone syndrome); not sensitive despite exposed dentin; primary dentition has bulbous crowns, obliterated pulp chambers, bluish-grey or brownish-yellow teeth that are easily worn; permanent teeth often stained but can be sound

Amelogenesis imperfecta: heritable defect, independent from metabolic, syndromes, or systemic conditions (though similar defects seen with syndromes or environmental insults); four main types (hypoplastic, hypocalcified, hypomaturation, hypoplastic/hypomaturation with taurodontism); proper treatment addresses sensitivity, esthetics, VDO, caries and gingivitis prevention

Enamel hypoplasia: quantitative defect of enamel from problems in apposition stage; localized (caused by trauma) or generalized (caused by infection, metabolic disease, malnutrition, or hereditary disorders) effects; more common in malnourished children; least commonly Md incisors affected, often 1st molars; more susceptible to caries, excessive wearing → lost VDO, esthetic problems, and sensitivity to hot/cold

Enamel hypocalcification: during calcification stage

Fluorosis: excess F ingestion during calcification stage → intrinsic stain, mottled appearance, or brown staining and pitting; mild, moderate, or severe; porous enamel soaks up external stain