Dental anomalies Flashcards
What cells are involved in tooth development and what are the stages?
There are ectodermal cells from facial processes and mesenchymal cells from the neural crest. There are epithelial and mesenchymal interactions which lead to ameloblasts and odontoblasts. The interactions are sequential and reciprocal and lead to differentiation.
How does the tooth develop from the primary epithelial band?
The stages of dental development are lamina, thickening, cap, early bell and late bell.
There is the appearance of a thickened band of ectoderm along each dental arch called the primary epithelial band. From the this the epithelium proliferates and grows down into the lamina propria. There is condensation of ecto-mesenchyme beneath the band. The epithelial band divides and there is the vestibular and dental lamina. Both lamina continue to deepen and the deepest cells of the dental lamina proliferate to form a ball-bud stage. Superficial cells or vestibular lamina degenerate to form a groove. There is advanced specialisation of cells and signalling between cells. The cells need to develop normally and produce products normally. Ectoderm forms enamel organ and ectomesenchymal components form the dental papilla. The enamel organ partially encloses the dental papilla and this is a tooth germ
What are the stages of tooth development?
- Initiation - starts tooth formation and ensures the right number of teeth in the correct location in the jaws
- Morphodifferentiation - formation of teeth of the correct shape
- Cytodifferentiation - differentiation of cells to produce specific dental tissues
Tooth formation occurs in two phases. The crown is formed first then there is root formation.
What are the types of anomalies and the aetiology?
The anomalies can be in number, size, shape and structure in that order. The aetiology can be genetic or environmental and it is multifactorial so can be a combination of both. Environmental factors can be localised or generalised. Localised can be trauma and infection and generalised can be drugs or infection. The genetic component is polygenic so many genes have an impact to produce an additive effect.
What are some occasional major influences?
- Chromosomal anomalies (chromosome gain, loss) e.g. down syndrome
- Single gene syndromes e.g. ectodermal dysplasia
- Single genes of localised effect e.g. maxillary lateral incisors
- Environmental insults e.g. rubella, thalidomide, irradiation
What does the cellular response to stimuli depend on?
- Developmental stage
- Adaptive range
- Stimulus, severity, duration, interaction
- Individuals response capacity
What are the anomalies of tooth number?
Hypodontia, supernumerary teeth, anodontia and oligodontia (6 or more teeth missing).
What is hypodontia and the most common teeth?
This is missing teeth and the types are mild (1 or 2), moderate (3-5) and severe (oligo >6). In the primary dentition it is more common in the maxilla and the maxillary B is the most common. In the permanent dentition the 8 is the most common and it is so common that it may not be classified as hypodontia. In the permanent dentition maxilla is equal to mandible and the most common is 8>5>upper2, 4.
What is the prevalence of hypodontia?
In the primary dentition female is equal to male and it makes up 0.1-0.9% of the Caucasian population. In the permanent dentition female and male are 4:1. The prevalence is 3.5-6.5% (9-37% if including third molars).
What is the aetiology of hypodontia?
- Obscure
- Polygenic plus intrauterine systemic factor
- Frequency increases in low birth weight, multiple births and increased maternal age
- Single gene mainly for upper 2
PAX9, MSX1 genes have been identified
What conditions can be associated with hypodontia?
It is seen with down syndrome, rubella, thalidomide, embryopathy. Severe hypodontia and microdontia are seen with X-linked hypohidrotic ectodermal dysplasia, anhydrotic ectodermal dysplasia and AR chondroectodermal dysplasia and with cleft lip/palate.
What are the types of supernumerary teeth and the prevalence
They can be supplemental (normal series) and accessory (atypical form). Sometimes teeth are named by location such as mesiodens which is an extra tooth in the midline suture. Other types are conical, tuberculate, odontoma, paramolar and distomolar. 75% do not erupt so are chance findings. They may prevent eruption e.g. mesiodens. The premaxilla is the most common region. In the primary dentition the prevalence is 0.2-0.8% and in the permanent dentition it is 1.5-3.5% unilateral. Male: female is 2:1 and the maxilla: mandible is 5:1. 30-50% of primary supernumerary teeth in the premaxilla are followed by permanent supernumerary.
What are the associations with supernumerary teeth?
- Invaginated teeth
- Palatal clefts
- Syndromes e.g. cleidocranial dysplasia, oral-facial-digital syndrome and gardner syndrome
What teeth and gender does micro/megadontia affect?
Microdontia is small teeth and megadontia is large teeth. Females usually have smaller teeth than males. More females are affected by microdontia and hypodontia than males. More males are affected by megadontia and supernumeraries. Large teeth often affect the upper central incisor and 5. It may affect the whole tooth, crown or root. It may affect isolated teeth, multiple, uni or bilateral. There can be unusual form and tapering.
What is the prevalence of microdontia and megadontia?
Microdontia is uncommon in the primary dentition (0.2-0.5%). In the permanent dentition it is 2.5%. Megadontia/macrodontia prevalence is 1.1% in the permanent dentition.
What is the aetiology of micro/macrodontia?
It is multifactorial. For microdontia it can be single gene inheritance associated with down syndrome or ectodermal dysplasia.
Macrodontia can be generalised, seen in pituitary gigantism and unilateral facial hyperplasia. Isolated megadontia can be seen in hereditary gingival hyperplasia and hypertrichosis.
What are the anomalies of tooth form/morphology?
There can be double teeth which may be due to fusion or gemination. It can range from a minor notch to almost separate crowns. It can be with/without the common pulp space and root canal. There can be delayed eruption due to retarded root resorption.
There can also be accessory cusps.
There is dens in dente/dens invaginatus, dens evaginatus, talon cusp and microdontia (peg/conical lateral incisors).
Concrescences are excess cementum uniting teeth occurring after tooth development and this is different.
What is the prevalence of double teeth and the management?
The labial segment in the mandible is affected more in the primary dentition. The incisors are more affected in the permanent dentition. It occurs more in the primary dentition (0.5-1.6%). Female and male is equal. The mode of development is unclear and may be genetic. Permanent anomalies follow double primary teeth in 30-50% Caucasian and 70% Japanese.
Management is very complex, seek orthodontic opinon (assessment) and management is dependent on pulp morphology.
What are the types of accessory cusp?
- Carabelli on upper 6’s
- Talon on 1s and 2s
- Buccal cusp (paramolar tubercles) on upper 4s and upper 5s and molars
What is an invaginated tooth?
The enamel epithelium ingrows into the dental papilla underneath and invaginates. It is also known as dens in dente or invaginated odontome. This can result in a deep cingulum pit. There can be bilateral symmetry (plus supernumeraries). Enamel can be complete or incomplete in the invagination part. If incomplete this would mean exposed dentine. The dentine can be missing so bacteria can get straight to the pulp. This would result in an acute alveolar abscess soon after the tooth erupts. Early diagnosis of dens-in-dente is important as subsequent RCT is difficult. You would aim to fissue sealant/occlude communicating channels or caries prone sites.
What is the prevalence of an invaginated tooth?
In the permanent dentition it is seen in 1-5% and in maxillary incisors frequently. Male:female is 2:1. Th
What is an evaginated tooth?
It occurs in premolars. It is an outgrowth of tooth tissue. Enamel epithelium grows outwards or focal hyperplasia of ectomesenchyme. It is rare in Caucasians. Pulp extensions.
What are root size anomalies?
Roots can be large often seen in upper 3s. This is more common in males 5:1. They can be small which is seen in primary and permanent dentition. This is seen in dentine dysplasias. It may be due to irradiation (shortened roots) or racial variation.
What are the anomalies of root form?
Taurodontism is an abnormality seen in multirooted teeth. There is a very long crown and short roots. The crown is elongated corono-apically. ACJ constriction (cervix) is absent. It is seen in syndromes and polygenic inheritance.
There can be accessory roots often seen if carabelli tubercle, paramolar tubercle, enamel pearls or trauma or genetic.
Pyramidal roots are seen when multi-rooted teeth are fused.
Why might there be premature tooth eruption?
It can be seen in the primary and permanent dentition. Primary eruption can be natal/neonatal. Natal refers to the period of birth and neonatal is the first 30 days of life so the baby can be born with a tooth. We would not expect to see teeth until 6 months of age. Natal/neonatal teeth will be ectopic and have incomplete root formation so will be very wobbly. This causes problems with feeding, risk of trauma and aspiration. Natal teeth are usually extracted. The toothgerm is in a superficial and ectopic position. Eruption can also be premature in high birth weight babies and if there are hormonal abnormalities.
When can there be delayed eruption?
It can occur in low birth weight and premature babies. It can occur in some syndromes such as Downs and Turners and endocrinopathies such as hypoparathyroidism where there will be delayed tooth eruption. Local causes of delayed eruption in individual teeth can be impaction and supernumerary teeth. Early extraction of primary teeth can cause a delay in the eruption of their permanent successor.
What are the normal differences in tooth eruption dates?
Jaws so lower teeth erupt before upper and race and gender as female teeth erupt before males.
When can teeth be lost early?
This can be due to trauma or extraction. Primary teeth can be lost early due to immune/cementum deficiencies. Immune deficiencies include cyclic neutropenia which affects periodontal tissues. Cementum deficiencies includes hypophosphatasia leading to hypoplasia or aplasia of cementum. Cementum is the thin hard tissue which surrounds the roots of teeth which the periodontal fibres insert into to hold the tooth in the alveolar socket.
What can cause delayed eruption?
It can be caused by infraocclusion so they fall below the occlusal level. When teeth become infraoccluded they can become ankylosed to the bone which is due to an imbalance between normal resorption and bone deposition and the tooth becomes fused to the bone. Infraoccluded teeth are often seen in hypodontia. Infraocclusion can also be seen in permanent teeth but it is more common in primary teeth. It is likely to have a genetic aetiology. It is commonly seen when there are no permanent successors e.g. 4 and 5 absent.
You can also see delayed eruption if successors are ectopic. Also if there are double primary teeth so twice as much root tissue to be resorbed. Hypodontia is also a cause.
What is odontodysplasia?
It is when all the elements of the tooth germ are affected. Radiographically you can’t see a proper tooth and this is often referred to as a ghost tooth. This can be caused by environmental insults such as chemotherapy, radiotherapy, trauma and acute infection.
What are the types of enamel defect?
- Hypomineralisation
- Hypoplasia
- Discolouration
What are the causes of enamel defects?
There are many different causes, about 100. Although there are multiple causes they often give the same clinical appearance. The aetiology can be genetic (polygenic), environmental or multifactorial determination which is a combination of both. The genetic cause primarily involving enamel is amelogenesis imperfecta. It is associated with generalised disorders and syndromes. Genetic factors give non-chronological presentations and affect both dentitions to a variable extent. Environmentally determined may be systemic/chronological, local or timing (development/insult). Ameloblasts are very sensitive to oxygen levels so this can disrupt their function. Environmental factors can be chronological e.g. trauma, infection, systemic illness. It can be non-chronological if the environment insult is very prolonged e.g. prolonged fluoride exposure.
What systemic effects can cause enamel defects?
- Maternal/foetal conditions e.g. rubella - primary teeth
- Pre-term/low birth weight/neonatal
- Fluoride
- Severe/chronic childhood illness (fevers, measles, chicken pox, tetracyclines)
What can cause localised defects?
- Infections/trauma
- Cleft lip/palate - surgery for repair can disrupt associated developing teeth
What is the idiopathic cause?
This is of no known cause. Molar-incisor hypomineralisation MIH wouldn’t be called idiopathic anymore. There are cheese molars (popcorn teeth).
What is hypomineralisation?
It is when enamel is less mineralised (normally 96%) and is an effect on the quality of the enamel. Normal enamel is smooth, white and translucent and has a known thickness/amount. Where there are hypomineralised defects there will be opacities which are porous and have more protein. Opacities have a range of colours and can be white/cream or yellow/brown. The boundaries of the opacities can be different and can be demarcated or diffuse. There is altered translucency and altered texture. The distribution can vary, it can be localised/generalised or symmetrical/asymmetrical. It is due to a disruption to mineralisation at maturation stage leading to porosity (subsurface/surface). It is somtimes called hypocalcified/hypomature.
What can the opacities/poorly mineralised zones affect?
- Full enamel thickness (maturation permanently interrupted)
- Surface unaffected (ameloblasts returned to normal maturation, deeper defect)
The enamel won’t be as hard in both cases therefore over time with mastication and toothbrushing enamel can be lost and this is called PEB post-eruptive breakdown.
What are fluoride induced opacities?
The opacities are brown and due to enamel loss. They can affect primary or permanent teeth and posterior or anterior. It is dose dependent (variety of appearances) and has a symmetrical distribution.
What is hypoplasia?
There is deficient matrix production leading to thin enamel. It is a quantitative defect and there is less enamel. There can be pits grooves, areas and absence. There is variation in thickness. Can be localised or generalised. It can be chronological so there will be matching teeth affected e.g. systemic effect/upset. It can be seen in localised teeth and this is called a turner tooth. If it is a turner tooth it will affect 1-5 only and commonly 4s and 5s. It is due to trauma or infection of primary teeth leading to damage or underlying developing permanent tooth germ. The teeth may also exhibit hypomineralisation.
What is discolouration?
Intrinsic is within the enamel tissue. As enamel is deposited there is discolouration within this tissue as the tooth is forming. Can be localised or generalised.
What can a variation in tooth colour be due to?
- Changes in tooth thickness and/or structure i.e. hypoplasia or hypomineralisation
- Incorporation of circulating substances/pigment deposits e.g. in metabolic disorders - circulating bilirubin, tetracycline - during development
- Incorporation of pulp products e.g. loss of vitality and infection, not development
- Exogenous agents i.e. extrinsic, not developmental e.g. bacterial, dietary
What indices can be used to record enamel defects?
- FDI DDE 1982, 1992
- EDI 2001
