Fluorosis

Anomalies in tooth structure occur after the tooth germ has formed. Knowledge of tooth development timing is important. Review the development tables of the teeth of the primary and secondary dentitions.

Fluorosis is caused by systemic intake of fluoride in excess of 1 ppm (parts per million) for some period of time. It is called "mottled enamel". It can result in a significant aesthetic problem if it occurs during the 2nd or 3rd year of age because secondary (permanent) anterior teeth are forming at this time. The severity of fluorosis is dose-dependent and time-dependent. Teeth are caries-resistant with enamel that is discoloured (white, yellow, brown) and can result from young children swallowing toothpaste.

Generalized fluorosis (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Generalized fluorosis (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Turner's tooth

This condition is also called Turner's hypoplasia and results in an abnormally shaped secondary (permanent) tooth. Trauma is a common cause for Turner's hypoplasia in secondary (permanent) maxillary incisors. Infection (periapical abscess) of the primary (deciduous) molars is a common etiological factor in secondary (permanent) premolars with Turner's hypoplasia. The appearance of Turner's hypoplasia can vary from discoloured areas to severe hypoplasia.

Panoramic radiograph on the left illustrates a Turner's tooth in the third quadrant (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Turner's tooth permanent mandibular left first premolar

(courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Amelogenesis Imperfecta

This is an ectodermal disorder and therefore affects the enamel only. The incidence ranges from .01% to .14% depending on the population At least 18 subtypes (Witkop, CJ, 1988) have been identified based on clinical features, light microscopic appearance and the inheritance pattern. This defect affects both the primary and secondary dentitions. Multiple modes of inheritance including autosomal dominant and autosomal recessive are possible.

Features of amelogenesis imperfecta include openbite due to attrition, eruption may be normal or late and the dentinoenamel junction is scalloped. Affected teeth are discoloured (exogenous pigment) and may be pitted, rough or smooth enamel. Enamel is thin or mottled radiographically. Problems include aesthetics, abrasion, sensitivity and caries susceptibility. Pathogenesis is a progressive, functional defect of ameloblasts. Management may include crowns (full coverage) and possibly full mouth osteoplasty (recontouring of bone) to increase the length of the clinical crowns for retention of full veneer crowns.

Pitted form of amelogenesis imperfecta

(courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Snow-capped form of amelogenesis imperfecta (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

A case study of a Type IE X-linked (dominant) smooth hypoplastic amelogenesis imperfecta (Witkop's classification) is presented to illustrate the inheritance pattern of one type of amelogenesis imperfecta. This subtype of AI (amelogenesis imperfecta) was diagnosed through the use of a pedigree and examination of all the members of the M family. The father Chris M had severe, generalized hypoplastic defects of the enamel. A pedigree illustrated that this defect was only transferred to the female children (Katrina M and Maria M). Son Marcus M had a normal dentition. The defects in the teeth of the female children were somewhat less severe than in the father but resulted in vertical banding of the enamel. A diagnosis of Type IE X-linked (dominant) smooth hypoplastic amelogenesis imperfecta was made based on a pedigree and clinical examination of all family members. The pattern of enamel defects in the family are illustrated below.

Chris M

Amelogenesis Imperfecta

Father Chris M as he initially presented. Maxillary teeth had been treated with metal ceramic crowns. Mandibular teeth are virtually devoid of enamel (courtesy of Dr. BM Cleghorn, Dalhousie University).

Occlusal view of Chris M illustrating normal tooth morphology and hypoplastic enamel

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Right BW radiograph

Chris M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Left BW radiograph

Chris M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Right PA radiograph

Chris M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Left PA radiograph

Chris M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Katrina M

Pre-treatment frontal view of daughter Katrina M aged 12 years 9 months

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Maxillary left quadrant close-up of vertical banding of enamel in patient Katrina M illustrating severely hypoplastic enamel

Right BW radiograph

Katrina M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Left BW radiograph

Katrina M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Post-treatment frontal view of Katrina M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Post-treatment view of maxillary arch of Katrina M with full coverage of all teeth

Vickie M

Pre-treatment frontal view of Vickie M aged 5 years 4 months

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Pre-treatment view of maxillary left quadrant of patient Vickie M

Pre-treatment occlusal view of maxillary arch of Vickie M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Pre-treatment occlusal view of mandibular arch of Vickie M

Marcus M

Marcus and brother Chris Jr. were unaffected by this sex-linked Type IE X-linked (dominant) smooth hypoplastic amelogenesis imperfecta.

Frontal view of Marcus M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Right BW

Marcus M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Left BW

Marcus M

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Chris Jr.

Frontal view of Chris Jr. aged 3 years 5 months

(courtesy of Dr. BM Cleghorn, Dalhousie University).

Dentinogenesis imperfecta

This is a mesodermal defect that affects the dentin. The condition is also called hereditary opalescent dentin and can be seen in isolation or associated with a systemic defect (osteogenesis imperfecta). Both the primary and secondary dentitions are affected. Dentinogenesis Imperfecta (DI) is a genetic disorder with an autosomal dominant mode of inheritance. The teeth are blue or brown and translucent. The incidence is approximately 1 in 8,000 in the USA. The classification system for this entity is less than perfect.

Common Features of Dentinogenesis Imperfecta

all teeth are discoloured (types 2 and 3 more prominent)

bell-shaped crowns

attrition

obliteration of root canals in Type 1 and 2 (more marked in the permanent dentition)

enamel is lost early in Types 1 & 2 due to a defect in the DEJ (no scalloping of the DEJ)

difficult to differentiate Types 1 and 2 clinically and radiographically

Type 1 is always associated with osteogenesis imperfecta while Type 2 is never associated unless by chance

Frontal view of dentinogenesis imperfecta (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

PA radiograph of dentinogenesis imperfecta illustrating bell-shaped crown on mandibular first molar (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Occlusal view of a patient with dentinogenesis imperfecta illustrating the severe attrition of all of the maxillary teeth (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

BW radiograph of dentinogenesis imperfecta illustrating obliterated pulps (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

PA radiograph of dentinogenesis imperfecta illustrating shell teeth (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Dentin Dysplasia

There are two forms of this condition and they are Type 1 and Type 2. The radicular form or Type 1 is the most common form. Short roots are a feature due to abnormal formation of root dentin. This is a genetic disorder with an autosomal dominant inheritance. Enamel and coronal dentin are essentially normal in Type 1. The incidence is 1 in 100,000 in North America. Teeth may exfoliate prematurely. Radiographic evidence of obliterated pulps assists in the diagnosis of this condition. Treatment includes extraction of those teeth with periapical pathosis.

PA radiograph of Type 1 dentin dysplasia illustrating short roots, and crescent-shaped pulp chambers (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

PA radiograph of Type 2 dentin dysplasia illustrating pulp stones, normal root length, and "thistle tube-shaped" enlargements of the pulp chambers (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Regional Odontodysplasia

This is a localized condition, usually with a non-hereditary cause. Sometimes regional odontodysplasia is associated with syndromes or growth abnormalities.It tends to occur in segments of the dentition.

Most Common Location for Regional odontodysplasia

Maxillary anterior teeth (occurs in segments of neighbouring teeth)

Enamel is hypoplastic and hypocalcified and the teeth appear "ghost-like" in their radiographic appearance due to their thin shell of enamel. The teeth often fail to erupt. Very large pulp chambers are evident in this condition. The aetiology is thought to be a vascular or viral problem

PA radiograph of the mandibular right quadrant illustrating the "ghost-like" appearance of the affected teeth (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

PA radiograph of the mandibular right quadrant illustrating the "ghost-like" appearance of the affected teeth (courtesy of Dr. John Perry, University of Manitoba).

Periapical cemental dysplasia (cementoma)

This presents initially as multiple periapical radiolucencies usually in the mandibular anterior region. It is important to diagnose this condition correctly as no treatment is required. The pulps of the involved teeth will be vital.

Most Common Location for Periapical Cemental Dysplasia

Secondary (permanent) Mandibular incisors

Follow up of this condition radiographically will confirm the diagnosis as the radiolucency(ies) will change to a mixed radiolucency/radiopacity then to apical radiopacities associated with the affected teeth over a period of years. Differentiation from a periapical abscess or granuloma is critical, as these conditions require root canal therapy while there is no treatment required for periapical cemental dysplasia.

Periapical cemental dysplasia initially presents as periapical radiolucencies in the mandibular incisor region

(courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Periapical cemental dysplasia at a later stage; the apical lesions become radiopaque over time; teeth remain vital (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Hypercementosis

Deposits of secondary cementum on the root surface characterize this condition. The aetiology can be due to local or systemic factors.

PA radiograph illustrating hypercementosis in the apical third of both the mesial and distal roots of the permanent mandibular right first molar (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Extracted permanent maxillary left second premolar with hypercementosis on the apical half of the root (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Impacted Teeth

These are teeth that are prevented from erupting by some physical barrier. The aetiology can be due to a lack of space (crowding) or a rotated tooth germ (so that the tooth is 'aimed' in the wrong direction).

Most Common Impacted Teeth

third molars

maxillary canines

premolars

supernumerary teeth

PA of impacted permanent mandibular right third molar (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

PA of impacted permanent mandibular right canine; the crown is undergoing resorption (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Panoramic radiograph of impacted third molars; the maxillary right third molar is both impacted and inverted; both of the mandibular third molars exhibit a 90 degree horizontal rotation (courtesy of Dr. BM Cleghorn, Dalhousie University).

Panoramic radiograph of a patient with multiple impacted and supernumerary teeth (courtesy of Dr. BM Cleghorn, Dalhousie University).

Ankylosis

This is a condition where teeth are fused to bone teeth are below the plane of occlusion.They are sometimes referred to as "submerged" teeth. However, this terminology is not really correct. The ankylosed tooth has failed to erupt while the surrounding teeth have continued to erupt. Radiographically, the periodontal ligament (PDL) will not be visible in the ankylosed area.

Most Common Ankylosed Teeth

primary (deciduous) mandibular second molars

These teeth are infra-erupted (not submerged). The aetiology can be due to trauma, genetics, infection or a disturbance in local metabolism. Treatment is usually a surgical extraction of the ankylosed tooth. Otherwise eruption of the secondary (permanent) tooth may be prevented.

PA of ankylosed and infra-erupted primary mandibular right second molar (courtesy of Drs. Steve Ahing and John Perry, University of Manitoba).

Tetracycline Staining

This is a type of anomaly caused by the ingestion of tetracycline as teeth are developing. The group of tetracycline antibiotics has an affinity for calcifying tissues such as bone and teeth. Horizontal bands of yellow or brown staining occur as teeth form. Examination of the location of the banding on the affected teeth can determine the approximate age and duration that the tetracycline was given.

Horizontal banding on this mandibular third molar indicates that the drug was ingested in the early or middle teens as the root was forming at this time. Acne is a common condition at this age and is often treated by one of the tetracycline group of antibiotics. This is the most likely aetiology of the staining on the root of this third molar. Devastating aesthetic defects can occur to tooth crowns if tetracyclines are ingested as they are developing. Therefore no tetracyclines should be administered to children under 8 years old. By this age the crown of all of the permanent teeth will have developed. Only the third molars are developing at this time.

Extracted mandibular third molar with tetracycline staining on the cervical half of the root (courtesy of Dr. BM Cleghorn, Dalhousie University).