Dental Anomalies Flashcards
In tooth formation, what are the interacting tissues at initiation?
The interaction between the epithelium and the ectomesenchyme
The tooth germ is organised into 3 parts - what are these 3 parts and what do they each produce?
Enamel organ - ameloblasts, root sheath
Dental papilla - odontoblasts, pulp
Follicle - cementoblasts, osteoblasts, fibroblasts
When does the process of tooth formation start?
Week 5 of embryonic life
When does the dental lamina form?
Week 6 of embryonic life
When does the primary tooth germ form?
Week 8 of embryonic life
When does the permanent tooth germ form?
Week 14 of embryonic life
What are the 3 phases of enamel formation?
- Pre-secretory - shape of the crown determined, ameloblasts develop and prepare to secrete organic matrix
- Secretory - ameloblasts lay down organic matrix
- Maturation - ameloblasts transport specific ions to mineralise the matrix
When does dentine/enamel formation of primary teeth start to occur?
Week 18 of embryonic life
When does dentine/enamel formation of permanent 1st molars start to begin?
32 weeks of embryonic life
When does the mineralisation of primary teeth begin?
14-18 weeks of embryonic life
When do crowns of first permanent molars begin mineralisation?
7-8 months gestation
When do permanent incisors begin mineralisation?
Within the 1st year of life
At what point should all permanent teeth (excluding 8s) have begun mineralisation?
Before 6 years old
What are 2 quantitative developmental anomalies?
Hypodontia
Supernumeraries - cleidocranial dysplasia
What is the term used to describe a total lack of teeth in one or both dentitions?
Anodontia
What is the name of a rare condition that involves >6 primary or permanent missing teeth ?
Oligodontia
In order state the 4 most commonly missing teeth?
- 8s
- Lower 5s
- Upper 2s
- Upper 5s
Which syndromes might Hypodontia be associated with?
Trisomy 21 (Down syndrome)
Ectodermal dysplasia
Autosomal dominant inheritance pattern in some families
Mutations in the MSX1 gene on chromosome 4
List some common features of ectodermal dysplasia
Males (X-linked)
Thin, sparse hair
Absence of sweat glands - Heat intolerance
Multiple missing teeth
Microdontia (peg laterals especially)
How might you treat multiple missing teeth?
Detection
Refer as necessary - multidisciplinary input
Maintain excellent dental health
Undertake restorative treatment as necessary
How might you treat missing upper laterals?
Treatment planning based around the eruption of canine and patient’s wishes
2 treatment options:
- Space closure – bring canine into lateral position
- Space opening – placement of prosthesis.
Often a staged treatment plan, with temporary space maintenance (aesthetic considerations!) until full maturity
Will usually require a joint orthodontic/restorative opinion
What are a type of supernumerary teeth that are found in the midline and usually peg-shaped known as?
Mesiodens
What are supplemental teeth?
A type of supernumerary tooth that looks like a normal tooth
What might happen if conical supernumaries are inverted?
They may migrate superiorly towards the nose
What can happen with tuberculate supernumaries?
They can impede eruption of adjacent teeth
What is cleidocranial dysplasia/dysostosis?
A rare autosomal dominant condition
What are the skeletal features of cleidocranial dysplasia?
Hypoplasia/aplasia of clavicles
Delayed closure of the frontanelles
Underdevelopment of bones and joints
What are the dental features of cleidocranial dysplasia?
Delayed loss of primary teeth
Delayed/failed eruption
Supernumerary teeth
How do you manage supernumerary teeth?
Usually based around extraction/monitoring, spontaneous alignment, and use of orthodontics where necessary
Determining which teeth to take out can sometimes be difficult if supplemental (look identical)
Liaison with orthodontics
List 5 different abnormalities that affect the size/form of the teeth?
Microdontia
Macrodontia
Double teeth
Dens in dente
Talon cusps
What are 2 old terms that have been used to classify double teeth?
Fusion - an abnormal shaped tooth resulting from the fusion of 2 separate tooth germs, normal number of crowns
Germination - 2 teeth develop from one tooth germ, look abnormally wide, extra crown (count the number of crowns
What is dens in dente/dens invaginatus?
A tooth within a tooth
Localised area of the crown folded inwards
What are the complications associated with dens in dente?
Can result in an area of caries, leading to pulpitis and PA infection - often difficult/impossible to treat endodontically
Why should you NOT shave down a talon cusp?
As it may contain its own bit of pulp
List 2 different hereditary disturbances of tooth structure
- Amelogenesis Imperfecta
- Dentinogenesis imperfecta
What is Amelogenesis Imperfecta?
A spectrum of hereditary defects in the function of ameloblasts and mineralisation of enamel matrix
Affects both primary and permanent dentition
What is the prevalence of Amelogenesis Imperfecta?
1:700-4,000
How might you classify Amelogenesis imperfecta?
By inheritance or phenotype
What are the 2 different phenotypic classifications of Amelogenesis Imperfecta?
- Hypoplastic type
- affects the quantity of enamel
- thin, hard enamel, normal bond strength
- teeth affected before eruption - Hypomineralised type
- affects the quality of enamel
- teeth affected after eruption
- full-thickness enamel but very soft, impaired bond strength
- can be sub-categorised into hypocalcified and hypomature
What is the most common inheritance pattern seen in Amelogenesis Imperfecta?
Autosomal dominant, X-linked
What are the other associated dental defects of Amelogenesis imperfecta?
Pulp calcification
Taurodontism
Delayed eruption
Gingival overgrowth
Skeletal anterior open bite (~50% of patients)
How would you manage amelogenesis imperfecta?
Composite restorations on anteriors
- can be added to as teeth further erupt
- bonding can be an issue
If hypoplastic consider if there enough enamel to bond onto.
If hypomature – pre-treatment with sodium hypochlorite is required to remove proteins and aid bond
If hypocalcified – dentine bonding where enamel has broken down
In the posterior dentition full coverage restorations are often required - particularly hypocalcified where further breakdown likely
What is dentinogenesis imperfecta?
Autosomal dominant inherited condition
What is the prevalence of dentinogenesis imperfecta?
1:80,000
What are the 3 different types of dentinogenesis imperfecta?
Type I - associated with osteogenesis imperfecta (OI)
Type II - dentinogenesis imperfecta on its own
Type III - “Brandywine isolate”
What are common findings associated with Dentinogenesis type 1?
Osteogenesis imperfecta
Likelihood of skeletal abnormalities, bone fractures, cardiac defects
>70% class III skeletal pattern
Bisphosphonates routinely used in management
What are the characteristics associated with dentinogenesis imperfecta in primary dentition?
Colour - amber
Attrition
Pulp obliteration
Spontaneous abscesses
What are the characteristics associated with dentinogenesis imperfecta in permanent dentition?
Colour - grey/translucent
Short roots
Pulp obliteration
Spontaneous abscesses
What are the 4 main clinical problems associated with dentinogenesis imperfecta?
Poor aesthetics
Chipping and attrition of enamel
Exposure of dentine
Poor OH, gingivitis, caries
What are the general treatment objectives for dentinogenesis imperfecta?
Maintain occlusal face height
Maintain OH
Address sensitivity/infection/abscesses
Preserve function, aesthetics and normal growth
Protect incisors/first permanent molars from wear
What are the treatment options for dentinogenesis imperfecta (primary and permanent teeth) ?
Primary dentition:
- Monitor wear
- Overdenture
- SSCs for posteriors, composite crowns for anteriors
- Fluoride applications for sensitivity
- Extractions if abscessed
Permanent dentition:
- Monitor wear
- Cast restorations on occlusal surfaces of 1st permanent molars (and premolars if required)
- Composite veneers
- Orthodontics - with care
List 3 non-hereditary disturbances in fomration?
MIH
Turners tooth
Fluorosis
What is MIH?
Qualitative developmental defect in enamel structure - altered enamel structure with less mineral content
- caused by disruption to the maturation/late transitional stage of amelogenesis
Which teeth are most frequently affected by MIH?
Typically 1st permanent molars and central incisors
What are the clinical findings that you may observe in MIH?
Demarcated enamel opacities, ranging in colour - creamy white to yellow/brown
Can appear hypoplastic (patchy enamel), normally as a result of post-eruptive breakdown
Patients can present c/o breakdown off teeth, sensitivity, aesthetic concerns, failed restorations
How do you treat MIH?
Prevention of caries and post-eruptive breakdown
May need temporisation with restorative material or SS crown
Child anxiety and pain during tx. has to balance against restoration type
Desensitisation and remineralisation:
- Repeated application of 5% sodium fluoride varnish
- Use of commercially available ‘sensitive toothpastes’
- Use of 0.4% stannous fluoride gels
- CPP-ACP
Long-term treatment plan:
- Decide (and discuss with the child/parent) whether to restore the teeth definitively or extract them
- Long-term prognosis of the affected molar teeth
- Occlusion/ malocclusion
- Aesthetic impact of any anterior lesions
Maintenance
What are the complications of MIH?
More susceptible to caries, tend to be hypersensitive – may increase dental anxiety
Defects vary in size and shape
Dramatic transition between hard normal enamel and defective enamel (opacities)
Defective enamel fractures under normal occlusal forces - result in excessive chipping/wear of these areas leading to sensitivity/pain
No typical etching pattern achieved
Crown form often compromised in terms of both the quantity and the quality of the remaining tooth tissue, which makes defining an appropriate cavity form very difficult
Anxiety - due to need for lot of treatment/repeat treatment, increased sensitivity, young age, ineffective LA
Poor mechanical and physical properties - therefore difficult teeth to restore long term
In a class 1, uncrowded occlusion, when would you extract a 1st permanent molar of poor prognosis, with MIH, in the absence of pain/infection?
Should be extracted when the calcification of the bifurcation of the second permanent molars can be seen radiographically
What is fluorosis and how is it caused?
Irregular enamel opacities, stained if severe
It results from ingestion of high F concentrations during amelogenesis
Only affects teeth that are developing during time of excessive fluoride (chronological)
What is turners tooth and which teeth are affected by it?
Hypoplastic enamel following infection around the inter radicular area of a primary tooth
Affects the permanent successors (often secondary premolar)
