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3rd year - module 6 > Paeds > Flashcards

Paeds Flashcards

1
Q

When do we become concerned about bilateral asymmetry (eruption)?

A

after 6 months

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2
Q

How long after eruption do teeth normally reach full length but still have large canals?

A

around 3 years after eruption

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3
Q

What is hypodontia?

A

missing teeth as a result of them failing to develop

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4
Q

What is anodontia?

A

total lack of teeth in one or both dentitions

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5
Q

What is oligodontia?

A

rare condition where more than 6 primary or permanent teeth are absent

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6
Q

What is the prevalence of hypodontia?

A
  • primary dentition <1%
  • permanent dentition 3-6%
  • F:M, 4:1
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7
Q

Which teeth are most commonly missing in hypodontia?

A
  • 8s, lower 5s, upper 2s and then upper 5s
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8
Q

What is the relationship between missing primary teeth and missing permanent teeth?

A

around 50% of patients with missing primary teeth have missing permanent teeth

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9
Q

What is the aetiology of hypodontia?

A
  • unknown/unclear
  • likely genetic - autosomal dominant inheritance pattern in families, mutatuions in MSX1 gene on chromosome 4
  • occasionally environmental insult or combination of both
  • linked to single-gene disorders
  • associated with certain syndromes - trisomy 21 (down syndrome), ectodermal dysplasia
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10
Q

What is ectodermal dysplasia and what are the signs/symptoms?

A

group of inherited conditions
- males (X-linked)
- abnormal development of teeth, nails, skin, thin sparse hair and absence of sweat glands
- difficulty regulating temperature
- early identification crucial
- microdontia (peg laterals especially)
- multiple missing teeth

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11
Q

What are the treatment options for missing upper laterals?

A
  • space closure - bring canine into lateral position
  • space opening - placement of prosthesis
    planning based on eruption of canine and patient’s wishes
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12
Q

Where is the most common site for supernumary teeth?

A

anterior maxilla

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13
Q

What is the prevalence of supernumary teeth in permanent and primary dentitions?

A

permanent = 1.5-3.5%
primary = 0.2-0.8%

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14
Q

What percentage of patients with cleft lip and palate develop supernumaries?

A

40%

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15
Q

What are mesiodens?

A

extra tooth in midline, usually peg or conical shaped

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16
Q

What is a supplemental tooth?

A

extra tooth that looks like a normal tooth

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17
Q

How is a conical supernumary tooth managed?

A
  • if not inverted, good chance of eruption
  • if not impeding other teeth, can be monitored until eruption then extracted
  • if inverted, may migrate superiorly towards nose
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18
Q

What are the issues with tuberculate supernumaries and what do they look like?

A

don’t tend to migrate but do impede eruption of adjacent teeth
more than one cusp or tubercle (barrel shaped)

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19
Q

How are supplemental teeth managed?

A

usually based around extraction/monitoring spontaneous alignment and use of ortho where necessary

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20
Q

What is cleidocranial dystosis and what are the skeletal and dental features of it?

A
  • rare autosomal dominant
  • skeletal features - hypoplasia/aplasia of clavicles, delayed closure of fontanelles, underdevelopment of bones/joints
  • dental features - delayed loss of primary dentition, delayed/failed eruption, supernumary teeth
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21
Q

When taking a radiograph to locate a supernumary, if it travels with the X-ray tube where is it placed?

A

palatally placed

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22
Q

When taking a radiograph to locate a supernumary, if it travels away from the X-ray tube where is it placed?

A

buccally placed

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23
Q

What is the prevalence of microdontia?

A

0.?-0.5% in primary teeth
2.5% in permanent teeth
F>M

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24
Q

Which teeth are most commonly affected by microdontia?

A

lateral incisors, e.g. peg shaped teeth

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25
Q

What are three examples of types of macrodontia?

A
  • double teeth
  • dens in dente (dens invaginatus)
  • talon cusps (evaginatus)
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26
Q

What does fusion mean when referring to a double tooth?

A

abnormal shaped tooth resulting from fusion of two separate tooth germs

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27
Q

What does gemination mean when referring to a double tooth?

A
  • two teeth develop from one tooth germ, look abnormally wide, appear similar clinically and radiographically
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28
Q

What is the term now used to described “fused” and “geminated” teeth?

A

double teeth

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29
Q

What is dens in dente?

A

“tooth within a tooth”
- localised area of crown folded inwards
- can result in area of caries, leading to pulpitis and PA infection
- difficult/impossible to endodontically treat

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30
Q

What is talon cusp?

A

an extra cusp on an anterior tooth which arises as a result of evagination on the surface of a crown before calcification has occurred. May have its own bit of pulp and can be mistaken for supernumary when PE

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31
Q

What is amelogenesis imperfecta?

A

spectrum of hereditary defects in the function of ameloblasts and mineralisation of enamel matrix.
that affects the structure and appearance of the enamel of the teeth

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32
Q

What are the two main types of amelogenesis imperfecta?

A

Hypoplastic type - thin but hard enamel, normal bond strength
Hypomineralised type - full thickness enamel but very soft, impaired bond strength

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33
Q

What is the type of inheritance involved in amelogenesis imperfecta?

A
  • autosomal dominant
  • X-linked
  • autosomal recessive
  • sporadic inheritance patterns
  • sporadic cases
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34
Q

What are the associated dental defects in amelogenesis imperfecta?

A
  • pulp calcification
  • delayed eruption
  • gingival overgrowth
  • taurodontism
  • skeletal anterior open bite (around 50% of pts)
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35
Q

What is the difference between hypoplastic generalised and hypoplastic localised amelogenesis imperfecta?

A
  • generalised = thin, patchy, rough aspect of enamel layer
  • localised = same but limited to a part of the crown
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36
Q

How does hypoplastic amelogenesis imperfecta present radiographically?

A

can be difficult to observe
hypoplasia of enamel layer, more pronounced in coronal 2/3

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37
Q

What are the two sub-types of hypomineralised amelogenesis imperfecta and what is their clinical appearance?

A

1) hypocalcified - after eruption enamel persists only on cervical part
2) hypomature - chalky appearance with orange, brown or white colour

38
Q

What is the radiographic appearance of hypocalcified amelogenesis imperfecta?

A

normal thickness of enamel before eruption, enamel radiolucency similar to dentine

39
Q

What is the radiographic appearance of hypomature amelogenesis imperfecta?

A

normal thickness of enamel, enamel radiolucency slightly higher than dentine

40
Q

What are the diagnostic criteria for amelogenesis imperfecta?

A
  • involves exclusion of extrinsic environmental or other factors
  • correlation with dates of tooth formation to exclude a chronological developmental disturbance
  • establishment of likely inheritance pattern
  • recognition of phenotype (e.g. hypomature)
41
Q

For a differential diagnosis of amelogenesis imperfecta, what other diagnoses must be excluded?

A
  • extrinsic disorders of tooth formation
  • dental fluorosis
  • chronological disorders of tooth formation
  • GI upset such as coeliac disease
  • initiation of anti-leukaemic therapy
  • renal disease
  • localised disorders of tooth formation
  • trauma
  • MIH
42
Q

What is dentinogenesis imperfecta?

A

inherited disorder affecting dentine. Defective dentine formation results in discoloured teeth that are prone to attrition and fracture

43
Q

What type of condition is dentinogenesis imperfecta?

A

autosomal dominant inherited condition

44
Q

What are the sub-types of dentinogenesis imperfecta?

A

Type I - associated with OI
Type II - DI on its own
Type III - “Bradywine isolate”

45
Q

If a dentinogenesis imperfecta patient also has osteogenesis imperfecta, what kind of DI do they have?

A

Type I DI

46
Q

What are the features of type I dentinogenesis imperfecta?

A

associated with osteogenesis imperfecta
- likelihood of skeletal abnormalities
- >70% class III skeletal pattern
- likelihood of bone fractures
- bisphosphonates routinely used in management
- likelihood of cardiac defects

47
Q

How does dentinogenesis imperfecta present in primary dentition?

A
  • colour = amber
  • attrition
  • pulp obliteration
  • spontaneous abscesses
48
Q

How does dentinogenesis imperfecta present in the permanent dentition?

A
  • colour = grey/translucent
  • short roots
  • pulp obliteration
  • spontaneous abscesses
49
Q

What are the 5 main clinical problems in dentinogenesis imperfecta?

A

1) poor aesthetics
2) chipping and attrition of enamel
3) exposure of dentine
4) poor OH, gingivitis, caries
5) pain and infection, pulpal necrosis

50
Q

What are the treatment objectives for dentinogenesis imperfecta in the primary dentition?

A
  • maintain occlusal face height
  • maintain OH
  • address sensitivity/infection/abscesses
  • preserve function, aesthetics and normal growth
51
Q

What are the treatment objectives for dentinogenesis imperfecta in the permanent dentition?

A
  • address aesthetics
  • protect incisors/first permanent molars from wear
  • maintain occlusal face height
  • maintain OH
  • address sensitivity/infection/abscesses
52
Q

What are the treatment options for dentinogenesis imperfecta in the primary dentition?

A
  • monitor wear
  • overdenture
  • SSCs for posteriors, composite crowns for anteriors
  • fluoride applications for sensitivity
  • extractions if abscessed
53
Q

What are the treatment options for dentinogenesis imperfecta in the permanent dentition?

A
  • monitor wear
  • cast restorations on occlusal surfaces of FPMs (and premolars if needed)
  • composite veneers
  • concern about enamel shear with fixed orthodontics, however, can be used with care
54
Q

What are 5 examples of non-hereditary disturbances in formation?

A

1) molar incisor hypomineralisation
2) dental fluorosis
3) Turner’s tooth
4) dilaceration of tooth
5) metabolic disturbances

55
Q

What is MIH?

A

Molar incisor hypomineralisation - developmental defect in enamel structure
altered enamel structure with less mineral content caused by disruption to the maturation/late transitional stage of amelogenesis

56
Q

What teeth are typically affected by MIH?

A

typically primarily first permanent molars and central incisors

57
Q

How common is MIH?

A

very common, up to 20% population

58
Q

Which teeth are typically more affected in MIH, molars or incisors?

A

molars

59
Q

What is the appearance of MIH?

A

demarcated enamel opacities ranging in colour - creamy white to yellow/brown
can appear hypoplastic, normally as a result of post-eruptive breakdown

60
Q

What do patients with MIH present complaining of?

A
  • breakdown of teeth, sensitivity, aesthetic concerns, failed restorations
61
Q

What is the suspected aetiology of MIH?

A
  • ?environmental factors during late pregnancy or first year of life
  • ?genetic component
62
Q

What is hypomineralisation?

A

qualitative defect that presents as clearly identifiable demarcated defects in the translucency of enamel

63
Q

What is different about the enamel form and composition of teeth with MIH?

A
  • greater carbon incorporation and lower Ca and P concentrations
  • different Ca and P ratio compared to normal enamel
64
Q

What does fluorosis occur as a result of and how does it present?

A
  • high F concentrations during amelogenesis
  • irregular enamel opacities, stained if severe
  • unusual in scotland
65
Q

How is MIH managed?

A
  • early identification
  • prevention of caries and post-eruptive breakdown
  • desensitisation and remineralisation
  • long term treatment plan
  • maintenance
66
Q

How is MIH identified early and what should be done?

A
  • when incisors erupt before molars, opacity on incisor is a strong indicator of MIH
  • if diagnosed, “high caries risk” prevention protocols should be followed
  • consider photography
67
Q

What can be done in prevention of caries and post-eruptive breakdown in MIH?

A
  • may need temporisation with restorative material or SS crown
68
Q

How can desensitisation and remineralisation be carried out on a tooth with MIH?

A
  • repeated application of 5% sodium fluoride varnish
  • use of commercially available ‘sensitive toothpastes’
  • use of 0.4% stannous fluoride gels
  • CCP-ACP (topical application containing fluoride)
69
Q

What is the long term treatment plan for a person with MIH?

A

decide and discuss whether to restore teeth definitively or extract
- long term prognosis of affected molar teeth
- occlusion/malocclusion
- aesthetic impact of anterior lesions

70
Q

Why are MIH affected teeth difficult to restore?

A
  • defects vary greatly in size and shape
  • dramatic reduction in hardness of enamel
  • enamel fractures under normal occlusal forces
  • excessive chipping and wear
  • sensitivity and pain = anxiety
  • no typical etching patterm
71
Q

What is a compensating extraction?

A

when a lower first permanent molar is removed, removing the upper molar to prevent its overeruption

72
Q

What is considered a rough guide of planning an extraction of a FPM?

A

in a class 1, uncrowded occlusion, the FPMs of poor long term prognosis should be extracted when the calcification bifurcation of the second permanent molars can be seen radiographically

73
Q

What is fluorosis?

A
  • result from ingestion of high F concentrations during amelogenesis
  • irregular shaped opacities, stained if severe
  • only affects teeth being formed during time of excessive fluoride (chronological)
74
Q

What is Turner’s tooth?

A

affects successional tooth (often 2nd premolars)
- allegedly hypoplastic enamel following infection around the interradicular area of a primary tooth
- Enamel Hypoplasia reduces the tooth’s enamel thickness, increases tooth sensitivity, leaves the affected tooth more susceptible to decay

75
Q

Why is carious tissue removed?

A

bacterially contaminated/demineralised tissues close to the pulp do not need to be removed, to not agitate pulp.
carious tissue is only removed to create conditions for long-lasting restorations

76
Q

What is the average size of hall crown used?

A

4
if not, most likely 3 or 5

77
Q

What is a D5 hall crown used for?

A

size 5, tooth D

78
Q

What should a correctly sized hall crown feel like?

A

do NOT seat on try-in
should cover all cusps with feeling of “spring back”

79
Q

Which way does the writing on a hall crown always face?

A

buccal

80
Q

How do you place a hall crown?

A
  • dry crown
  • fill with GI luting cement (aquasem), ensuring crown well-filled (2/3)
  • dry tooth
  • place crown over tooth and partially seat
  • remove finger and encourage child to bite or fully seat with finger pressure alone
  • child open wide and clean excess cement away quickly (bad taste)
  • once excess cleaned, but cement still soft, get child to bite down on cotton wool for 1-2mins, more cement will flow out
  • clean cement away, allow set, check and floss contact points
  • blanching of gingivae follows, indicator of good fit
81
Q

What should you tell the parent/patient about placement of hall crown?

A
  • crown supposed to fit tightly and gum will adjust
  • child will get used to feeling within 24hrs
  • occlusion tends to adjust within a few weeks
82
Q

What are the requirements for a hall crown?

A
  • band of ‘normal’ looking dentine visible between pulp chamber and cavity on radiograph
  • teeth should be visualised on bitewings
  • tooth must be asymptomatic (or at worst reversible pulpitis)
83
Q

What are the contraindications for a hall crown?

A
  • irreversible pulpitis or abscess/infection
  • clinical or radiographic caries reached the pulp, pulp exposure or apical pathology
  • badly broken down tooth
  • no clear band of ‘normal’ looking dentine
  • teeth with arrested caries
84
Q

What is SDF?

A

silver diamine fluoride
- clear, odourless, metallic-taste liquid that will stain most oxidisable surfaces black upon exposure to light due to formation of silver oxide layer (skin, tissues, carious lesions, clinic surfaces etc)

85
Q

What is the mechanism of action of SDF?

A

Ag+ - effects on bacteria, hydroxyapatite doping, collagen degradation inhibition
F - mineral formation, collagen degradation inhibition

86
Q

What are the indications for use of SDF?

A
  • pts at high risk of developing caries - xerostomia, severe early childhood caries
  • pre-cooperative pt
  • treatment challenged by behavioural or medical conditions
  • patient with several carious lesions that may not all be treated in one visit
  • difficult to treat carious lesions
  • patients without access to dental care
87
Q

What are the contraindications for the use of SDF?

A
  • silver allergy
  • pain - irreversible pulpitis or PA periodontitis - spontaneous, severe, constant pain or wakening the child at night
  • infection - swelling of tissues, abscesses or fistula
  • patient refusing treatment or unable to cope
  • unable to isolate tooth and maintain control over oral environment
88
Q

How is SDF applied?

A
  • isolation with cotton wool rolls, dry tooth with air
  • dispense a minimal amount of SDF into dish
  • using microbrush, apply SDF to carious lesion and agitate for 1 min
  • remove excess SDF following procedure completion
89
Q

How should you prepare for the placement of SDF?

A
  • ensure pt knows that lesion will go black
  • ensure child has safety glasses and apron on
  • warn nurse it will stain anything it touches
90
Q

How often should SDF be used on a lesion?

A

twice per year

91
Q

What concentration of SDF should be used?

A

38%

92
Q

What can SDF be effective at?

A

arresting carious lesions

3rd year - module 6 (14 decks)

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