Dental anomalies Flashcards
1
Q
What cells are involved in tooth development and what are the stages?
A
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.
2
Q
How does the tooth develop from the primary epithelial band?
A
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
3
Q
What are the stages of tooth development?
A
- 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.
4
Q
What are the types of anomalies and the aetiology?
A
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.
5
Q
What are some occasional major influences?
A
- 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
6
Q
What does the cellular response to stimuli depend on?
A
- Developmental stage
- Adaptive range
- Stimulus, severity, duration, interaction
- Individuals response capacity
7
Q
What are the anomalies of tooth number?
A
Hypodontia, supernumerary teeth, anodontia and oligodontia (6 or more teeth missing).
8
Q
What is hypodontia and the most common teeth?
A
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.
9
Q
What is the prevalence of hypodontia?
A
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).
10
Q
What is the aetiology of hypodontia?
A
- 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
11
Q
What conditions can be associated with hypodontia?
A
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.
12
Q
What are the types of supernumerary teeth and the prevalence
A
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.
13
Q
What are the associations with supernumerary teeth?
A
- Invaginated teeth
- Palatal clefts
- Syndromes e.g. cleidocranial dysplasia, oral-facial-digital syndrome and gardner syndrome
14
Q
What teeth and gender does micro/megadontia affect?
A
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.
15
Q
What is the prevalence of microdontia and megadontia?
A
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.
16
Q
What is the aetiology of micro/macrodontia?
A
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.
17
Q
What are the anomalies of tooth form/morphology?
A
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.
18
Q
What is the prevalence of double teeth and the management?
A
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.
19
Q
What are the types of accessory cusp?
A
- Carabelli on upper 6’s
- Talon on 1s and 2s
- Buccal cusp (paramolar tubercles) on upper 4s and upper 5s and molars
20
Q
What is an invaginated tooth?
A
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.
21
Q
What is the prevalence of an invaginated tooth?
A
In the permanent dentition it is seen in 1-5% and in maxillary incisors frequently. Male:female is 2:1. Th
22
Q
What is an evaginated tooth?
A
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.
23
Q
What are root size anomalies?
A
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.
24
Q
What are the anomalies of root form?
A
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.
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
What are the types of enamel defect?
- Hypomineralisation
- Hypoplasia
- Discolouration
32
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.
33
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)
34
What can cause localised defects?
- Infections/trauma
| - Cleft lip/palate - surgery for repair can disrupt associated developing teeth
35
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).
36
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.
37
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.
38
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.
39
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.
40
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.
41
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
42
What indices can be used to record enamel defects?
- FDI DDE 1982, 1992
| - EDI 2001
43
What is the prevalence of opacity and hypoplasia in school children in the UK in 1998?
68% opacities and 14.6% hypoplasia. Many patients will have these defects and can have them together.
44
What is amelogenesis imperfecta?
It is hereditary and has a 1:700 to 1:14000 prevalence depending on the population. It affects the structure and appearance of enamel. There are enamel defects not usually associated with systemic abnormality but can be seen with anterior open bite, cone rod dystrophy, hearing impairment, renal calcifications, Heimler syndrome. It can present with hypomineralisation, hypoplasia and different mixed combinations (14-15 types - diverse phenotypes). Both dentitions are affected by most types but permanent teeth tend to be affected worse. There is often bilateral symmetry but not always and the radiographic contrast will be lost. Hypomineralised soft enamel wears away. You can get parts of the crowns affected such as incisal portions of anterior and occlusal portions of poster and this is called snowcapped.
Teeth are small, discoloured and pitted and prone to rapid wear and breakage.
45
What gene mutations can cause amelogenesis imperfecta?
It is caused by single gene mutations in genes that are critical for enamel formation: AMELX gene for amelogenin, ENAM gene for enamelin and PEX1 and PEX6. The inheritance patterns are autosomal dominant, autosomal recessive and X-linked so it it inherited in different ways. There is a variation in expression of the faulty gene. You get different clinical pictures with the same gene defect. There are also environmental influences. There will be variation in expression within families and within individuals: between dentitions, within dentition and within tooth.
46
How can amelogenesis imperfecta be classified?
It can be classified based on clinical and radiographic appearance, mode of inheritance, molecular defect and biochemical result. Also classified by the range of different types: hypoplastic, hypomature, hypocalcified and hypomature hypoplastic with taurodontism.
47
What is non-penetrant amelogenesis imperfecta?
When the individual inherits the defective gene but it is not expressed. This is due to modifying effects of other genes.
48
What is lyonisation?
It is only seen in females due to random inactivation of one X-chromosome. You get a striped appearance with bands of normal and abnormal enamel. It is not seen in males (XY). They present with thin enamel which is more severely and uniformly affected. It is seen in amelogenesis imperfecta.
49
What are some other genetic reasons why enamel may not form properly?
Associated with genetic disorders:
- Epidermolysis bullosa
- Tuberous sclerosis
- Vitamin D dependent rickets
- Microdento-osseous syndrome
50
What are the causes of anomalies in dentine?
Genetic and environmental. We don't know as much about dentine anomalies as we cannot readily examine it.
51
What are the genetic anomalies of dentine (which are limited to dentine)?
- Dentinogenesis imperfecta
- (Radicular) dentine dysplasia which is limited to root dentine
- Fibrous dysplasia
52
What generalised disorders are dentine anomalies associated with?
- Osteogenesis imperfecta (with DI type I)
- Ehlers-Danlos syndrome
- Vitamin D dependent and resistant rickets
- Hypophosphatasia
53
What is dentinogenesis imperfecta?
It is hereditary opalescent dentine which appears glassy. It is the commonest form. It has a prevalence of 1:6000/8000. It is autosomal dominant and caused by a defect in the DSPP gene. This causes a defect in non-collagenous dentine matrix proteins (DSP, DPP and DGP 10% of proteins). There is a variability in expression and severity so reclassified.
The teeth appear opalescent on transillumination and they can have a blue or brown hue colour. It affects all teeth in both dentitions but the primary teeth are more severely affected. The severity varies between and within families. You get very bulbous crowns and short thin roots. The pulpal chamber can be obliterated by excess abnormal dentine. The ADJ is often flattened and not scalloped like normal. This means normal enamel can chip away and the soft dentine is exposed and can wear away. The dentine is abnormal: less tubules and irregular, cellular inclusions from pulp, gradual pulp obliteration.
54
What are the other variants of DI?
There is a continuum of expression. You can get thistle or flame shaped pulps so pulp is bigger than normal as the enamel and dentine are thin. You can get shell teeth which is rare, seen in primary dentition and in severely affected cases. There is a large pulp chamber, thin dentine and enamel. Isolated population in USA.
55
What is DI type I?
It is associated with osteogenesis imperfecta which is a group of connective tissue disorders (type I collagen). It is caused by a mutation in collagen type I genes. There is bone fragility and deformity, lax joints, blue sclera, opalescent dentine (collagenous protein is affected which is 90% of proteins). Primary teeth resemble DI and secondary teeth have a better prognosis.
56
What is dentine dysplasia?
It is genetically caused and called radicular dentine dysplasia. It affects the roots dentine. Normal bluish or brown colour. It affects both dentitions. Radiographically there is normal crown morphology and crown dentine but the roots appear short and blunt and the teeth are mobile. It is rare.
57
What is fibrous dysplasia of dentine?
This is the third genetic type. There are lots of lacunae within dentine and cellular inclusions (cells which shouldn't be there). It is seen more in the permanent dentition but it is rare.
58
What are environmental dentine defects?
Dentine formation starts before enamel formation. Environmental factors can affect the dentine formation:
- Local trauma
- Nutritional deficiencies
- Drugs
This can lead to:
- Interglobular dentine forming (holly shape in dentine which isn't mineralised), predentine and osteoid (unmineralised bone)
59
What are the clinical, histological and radiographic features of dentinogenesis imperfecta?
Clinical features:
- Enamel usually fractures off early due to lack of dentine support
- Soft exposed dentine then quickly wears away
- Affected teeth have a brown discolouration often with a distinctly amber translucency.
Histology:
- Irregularly formed and poorly mineralised dentine
Radiographic features
- Bulbous crowns, short thin, blunt roots, obliteration of root canal
60
What would a treatment plan be for a case of DI?
- OHI and prophylaxis
- Composite build-up of anterior teeth with an increase in OVD
- Following lab preview (diagnostic wax up) construct direct/indirect composite onlays, construct gold onlays
- Consultant orthodontic opinion
Opaquers can be used to mask dentine discolouration under composite
61
What would the clinical considerations be for a case of DI?
- Masking of underlying discolouration - opaquers used in this case
- Reduced shear bond strength of resin composites in patients with DI so full crown coverage may be used to maximise bonding surface area
- Orthodontic management
- Life-long maintenance of restorative interventions
62
What is the prevalence and most common site for a talon cusp?
It is uncommon and increased in some racial groups (7.7% Northern Indian population, 0.17% American population, 0.06% Mexican population). It is increased in males 2:1 and is more common in maxillary teeth. It is 3 times more common in the permanent dentition than the primary dentition. The maxillary lateral incisor is the most frequently affected tooth. The labial surface of teeth may also (uncommonly) be affected.
63
What is a talon cusp caused by and what syndromes/conditions is it associated with?
It is caused by a multifactorial (polygenetic and environmental factors involved) disturbance of tooth formation. There are familial associations. There is increased prevalence in patients with consanguineous parents. There is increased prevalence in some syndromes e.g. Ellis Van Creveld, Rubinstein Taybi, Sturge Weber. It may be associated with other dental anomalies e.g. supernumerary teeth, dens invaginatus, microdent lateral incisors, shovel shaped lateral incisors, bifid cingulum, enlarged cusps of carabelli so look out for these.
64
What are the clinical problems with a talon cusp?
- Occlusal interference which may lead to displaced teeth, TMJ dysfunction, acute apical periodontitis
- Caries
- Poor aesthetics
- Tongue irritation
- Attrition or fracture of cusp with pulpal exposure and ensuing pulp necrosis
65
Can you be sure if there is pulp tissue in a talon cusp?
You cannot be sure and histological studies have shown some talon cusps do contain pulpal extensions and others do not. Radiographs are of little diagnostic help. Large talon cusps that project away from the tooth surface are the most likely to contain pulp tissue.
66
What is the treatment for talon cusps?
There can be caries prevention so early use of fissure sealants or composite to occlude caries prone fissures between talon cusp and tooth surfaces. Give appropriate OHI also. You can treat with cusp reduction but be aware of the possibility of pulp exposure. The objective is to undertake gradual cusp reduction with reparative dentine formation and pulpal recession. The literature suggests time intervals of 4, 6, 8 weeks and 4 months. 1-1.5mm of tooth tissue reduction is recommended at each visit. There should be placement of fluoride varnish after each visit to desensitise exposed dentine. This should be done after root formation is complete.
67
What are the treatment options for double teeth?
- Accept
- Section, remove portion, restore, realign
- Extraction and partial denture with appropriate sized tooth
68
What are the types of abnormality of tooth colour?
- Tetracycline staining
- Opacities (enamel defects)
- Congenital hepatic disorder
- Non-vital teeth
- Dentinogenesis imperfecta
- Caries-post-orthorontic demineralised lesions
It can be intrinsic or extrinsic staining. It may be part of a generalised abnormality of tooth development.
69
What is the management of tooth staining?
- Tetracycline staining is usually resistant to bleaching attempts, may have to resort to veneers
- Microabrasion is the first line of treatment for most superficial intrinsic enamel staining
- Tooth whitening with commercial products (carbamide peroxide)
- Resin infiltration (ICON)
- veneers - direct/indirect composite with opaquers
70
What condition is hyperplasia associated with?
Cleidocranial dysostosis.
71
What is the clinical rationale for treatment for hypodontia?
- Poor aesthetics
- Compromised function
- Loss of vertical dimension
72
What is the management of hypodontia?
- Multidisciplinary approach - orthodontic, paediatric dentistry and restorative input
- Maintain dentition - prevention
- Orthodontic management of spacing
- Partial dentures
- Adhesive dentistry
- Implants
73
What are the problems of management of hypodontia?
- Patient compliance
- Small crowns
- Lack of undercuts
- Lack of alveolar bone
- Loss of vertical dimension
74
What is the clinical rational for treatment of hyperdontia?
- Poor aesthetics
- Malocclusion - impediment to tooth eruption
- Pathology associated with unerupted teeth - resorption of adjacent teeth, follicular changes
75
What are the principles of management of hyperdontia?
- Early diagnosis - appropriate radiographs
- Orthodontic opinion re supplemental teeth
- Referral for surgical removal if necessary
- Space maintenance where necessary
- Review of unerupted teeth
76
What is the clinical rationale for treatment of infraocclusion?
Malocclusion and caries/periodontal disease
77
What are the principles of management?
- Early diagnosis - regular review, photos, study models, usually only monitoring when necessary
- Orthodontic opinion where successor is absent
- Space maintenance where necessary, composite onlay, GIC, PMC, overdenture
- Early extraction to avoid need for more complex surgery, care with ankylosis
78
What is molar incisor hypomineralisation?
It is hypomineralisation of systemic origin of one to four first permanent molars frequently associated with affected incisors. It can also be called idiopathic hypomineralisation and 'cheese/popcorn' molars.
79
What is the difference between hypomineralisation and hypoplasia?
Hypomineralisation is qualitative disturbance in enamel formation. It is when you have the right amount of enamel but it is porous, high protein content and not mineralised. You get post-eruptive breakdown which can make it look like hypoplasia.
Hypoplasia is a quantitative disturbance in enamel formation. The enamel is mineralised and strong but there is not enough of it.
80
What is the clinical presentation of MIH?
Affected molars present with well-demarcated white/yellow or brown/yellow enamel opacities. 1-4 first permanent molars may be affected and there is conflicting data as to whether maxillary or mandibular teeth are more at risk. In severe cases defective enamel is lost soon after eruption which exposes underlying dentine. Affected incisors are also present with well-demarcated white/yellow or brown/yellow opacities. Post-eruptive enamel loss is not usually a feature. There is increased risk of hypomineralised incisors where molars are more severely affected. Hypomineralisation is usually seen on the lower third of incisors.
81
What is the prevalence of MIH and the cause?
The global prevalence is 13% (Schwendicke et al). We don't know the cause but we know risk factors. Most causes seem to be associated with hypocalcaemia and hypoxia. It may also involve a genetic susceptibility. There are no obvious causes in 10-24% of MIH patients and conflicting findings regarding the role of environmental pollutants such as dioxins.
82
What are the pre-natal risk factors?
9% of MIH cases
- Maternal pyrexia
- Medication (antibiotics)
- Prolonged vomiting
- Maternal diabetes
- Vitamin D deficiency
- In vitro fertilisation
83
What are the peri-natal risk factors
34% of MIH cases
- Caesarean section
- Prolonged/complicated delivery
- Prematurity/low birth weight
- Twins
84
What are the post-natal risk factors?
34% of MIH cases
- Ear/throat/nose infections
- Respiratory problems
- Pyrexia
- Seizures
- Urinary infections
- Antibiotics
85
What are the MIH underlying mechanisms?
- Insult to enamel formation from around 37 weeks to 3 years
- Transitional and maturation phase of enamel affected
- Reversible or irreversible damage to ameloblasts with qualitative disturbance to enamel formation
- Protein retention and poor hydroxyapatite crystal formation
- Low content of calcium and phosphate ions
86
What do MIH laboratory studies show about the enamel, dentine and pulp?
The enamel is porous, weak and poor etch pattern.
The dentine shows sparse reparative dentine and irregular globular dentine. There is an influx of bacteria in dentine tubules.
The pulp shows underlying chronic pulp inflammation. It also shows increased immune cells, vascularity and neural density.
87
What are the clinical challenges of MIH? (patient related and clinical related)
Patient related factors:
- Extreme tooth sensitivity
- Aesthetic concerns
- Anxious about dental treatment
- Need for long term interventions (financial burden)
Clinical related factors:
- Difficulty in achieving adequate level of analgesia for restorative treatments
- High failure rate for adhesive restorations and sealants (poor shear bond strength)
- Tooth tissue loss
- High caries experience
88
What does the EAPD policy document recommend for the holistic care of children with MIH?
- I - prevention, remineralisation, alleviation of symptoms, improve oral hygiene and diet, reduction in caries risk
- II - Treatment planning for first permanent molars
- III - improvement of incisor aesthetics (if this is what the child wants
- IV - incorporating a child-centred approach
89
What is tooth mousse?
It is a water based, sugar free dental topical cream containing casein phosphopeptide-amorphous calcium phosphate. It has been marketed for remineralisation of enamel since 1996. It is a delivery system for bio-available calcium and phosphate ions. There needs to be patient application daily in trays or locally to the affected tooth. It may improve sensitivity symptoms, appearance and structure of DDE (developmental defects of enamel). The evidence is not very strong.
90
Are fissure sealants used for MIH and how should they be placed?
They are recommended but have high failure rates in hypomineralised enamel (only 25% survival at 4 years). Pre-use of 5% sodium hypochlorite to remove protein content has been recommended. Clinical tips are the use of warm water and cotton pledgets to remove etch and avoid aspirators and use of light cured glass ionomer sealants (fuji triage).
91
What are the treatment options for developmental defects of enamel?
- Review (only if minor) and prevention including topical fluoride application, tooth mousse and fissure sealants
- Restore (short, mid or long term) - adhesive restorations, preformed metal crowns, laboratory formed crowns
- Extract -LA/IS/GA, need for compensating extractions, ortho considerations - may need to consider timing of extractions if child likely to need ortho in future.
The big decision is whether to extract or restore first permanent molars. There needs to be early assessment of long-term prognosis of first permanent molars and orthodontic status. The aim of restoration is to reduce sensitivity and protect hard tissues.
92
What are the ortho considerations in MIH?
In class II cases try to maintain upper first permanent molars until the 8s are erupted. In class III cases try to restore. If you extract the 6 too early then the 5 will drift distally. If it is extracted too late then the 7s will tilt mesially. First definitely seek an orthodontic opinion for class II, II, hypodontia cases and severe crowding cases.
93
What are the choices for restoration of teeth with MIH?
- RMGIC
- Composite resin
- Amalgam (not for under 15s and enamel chips around it)
- Preformed metal crowns
- Cast onlays/crowns
94
How can adhesive restorations be used for MIH?
GICs are useful as a short term restoration prior to definitive restoration or extraction e.g. fuji triage, GC America Inc. Composite resins are only indicated for mildly affected teeth with no cuspal involvement. The margins of the restoration should extend beyond visibly affected enamel.
95
When may hall crowns be placed and how long will they last?
They can be done if the orthodontist recommends that the tooth needs to be retained for a few years. They are a mid-term restoration (2-5 years). The use of elastic separators may obviate the need for interproximal tooth preparation (Hall technique).
96
What are the advantages and disadvantages of preformed metal crowns?
Advantages:
- Prevent further tooth deterioration/caries
- Controls tooth sensitivity
- Establish correct interproximal contacts and occlusal relationships
- Not as technique sensitive or costly as cast restorations
- Quick
Disadvantages:
- Adverse reactions in patients with a nickel allergy
- Production of anterior open bite if not fitted correctly
- Gingival inflammation
- Not a permanent restoration
97
How can cast restorations be used for MIH?
Indirect gold onlays are the restoration of choice for moderate or severe hypomineralisation where the maintenance of first permanent molars is indicated in the long term. Placement is usually considered in the late mixed or early permanent dentition. There are no significant differences in successful outcome of cast metal crowns vs preformed metal crowns in children with enamel defects. Caution with conventional full crowns. Immature teeth have short crowns, large pulps and the procedure is highly destructive to tooth tissue.
98
What are the options for clinical (aesthetic) management of anterior teeth with MIH?
- Tooth whitening
- Composite resin (direct/indirect)
- Resin infiltration (ICON)
- Microabrasion
99
What can visible enamel defects have an effect on?
We treat due to psychological impacts. Visible enamel defects may have negative impacts on quality of life and well-being:
- Social interactions and functioning
- Self-esteem
- Peer and adult social judgement
100
What should you do before treating MIH?
- Ask the child to indicate exactly what concerns them (are their expectations realistic)
- Assess colour, tooth tissue loss and sensitivity
- Take good clinical photos and shade pre and post treatment
- Obtain written consent/assent for treatment
101
How does tooth whitening work, what are the methods and how can it be used for MIH?
It is based on the action of hydrogen peroxide or precursor carbamide peroxide. Worldwide there is the use of between 10-40% carbamide peroxide gel. The two main approaches are a home based technique or in-office technique using photo activation. There is a complex action where free radicals diffuse into hard tissues and react with coloured organic pigments to create less pigmented molecules which reflect less colour 'whitening effect'. There is a debate as to whether enamel structure (roughness) is affected or not. The main complication is post-operative sensitivity.
102
What is the current GDC guidance on tooth bleaching?
A dentist must:
- Act in the best interests of patients in providing a high standard of care
- Obtain fully informed consent for treatment which they must be competent to carry out
- Obtain a medical history of the patient before starting treatment
- Give necessary explanations about benefits and risks
- Check with their own defence organisation or other (local) indemnity provider
In June 2014 the GDC changed its position on bleaching for under 18s. Products containing or releasing between 0.1-6% hydrogen peroxide cannot be used on any person under 18 years of age except where such use is intended wholly for the purpose of treating or preventing disease. This is unclear.
103
What is the approach for tooth bleaching in CCDH?
Use of 10% carbamide peroxide gel (ultradent) used nightly in custom made trays (trimmed away from gums) which could include reservoirs around selected teeth. It degrades to release around 3.6% hydrogem peroxide. It is used for approximately 2-4 weeks and then review. Provide written child friendly information and obtain written consent/assent. For one tooth you can get a bleaching tray with a single tooth reservoir.
104
What is microabrasion?
It is a technique first described in 1989. It involves chemical (acid) and mechanical removal of intrinsic and superficial enamel staining (50-250 microns). It is safe, effective, conservative, simple and economical. It works well on superficial enamel opacities not for tetracycline staining or dentinogenesis imperfecta. We use Opalustre by Ultradent which is a 6.6% HCL slurry with silicon carbamide microparticles. 1 minute, wash, check repeat and up to 10 cycles. After 3 or 4 if it is not working then stop. It tends to be the most effective on brown marks. If the patient has orange food or acidic food then the teeth will turn orange so leave for a couple of days.
105
How does resin infiltration using ICON work?
Isolate using rubber dam, apply ICON etch (15% hydrochloric acid) for 2 mins, remove etch and rinse for 2 minutes. Apply ICON dry for 30 seconds (repeat etch and icon dry cycles for 3-4 times until opacity disappears), apply ICON infiltrant for 3 minutes, remove excess, light cure for 40 secondary, repeat infiltrant if necessary and polish. You need to warn patients that tooth whitening is no longer effective after ICON.
106
When are composite resin restorations used?
They are indicated to camouflage residual discolouration (hypomineralised tooth) or to replace missing enamel (hypoplastic tooth). There can be direct or indirect composite veneers. Microabrasion, tooth bleaching or resin infiltration may be performed initially. Refrain from treating surface with fluoride if restoring immediately after microabrasion. The use of opaquer (or dentine shades) may then still be required. There is a high risk of failure with DDE. Can use cellulose acetate crowns.
