Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals 2021! > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Prevalence of TDIs in the Permanent Dentition of Children

A

12% of 12yr olds & 10% of 15yr olds have sustained visible injury to 1(+) permanent incisors.
Decline over last 40yrs.
Peak incidence 8-10yrs.
M:F = 2:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Prevalence of TDIs in the Primary Dentition of Children

A 
Boys = 31-40%
Girls = 16-30%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aetiology of TDIs in Children (5)

A
  1. Falls & collisions.
  2. Contact sports.
  3. General playing around.
  4. Assault.
  5. Non-accidental injury.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Predisposing Factors of TDIs in Children (8)

A
  1. Increased OJ (2x risk if OJ > 6mm).
  2. Poor lip coverage.
  3. Previous trauma (increased risk of 4-30%).
  4. Epilepsy (poorly controlled).
  5. Poor motor control.
  6. Obesity.
  7. Poor life circumstances.
  8. Attention deficit and hyperactivity disorder.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prevention of TDIs in Children (5)

A
  1. Mouthguards for sports.
  2. Seatbelts.
  3. Safety straps in wheelchairs.
  4. Early ortho intervention.
  5. Playground design.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Classification of TDIs (4)

A
  1. Enamel infraction.
  2. Enamel fracture (uncomplicated).
  3. Enamel-dentine fracture; uncomplicated or complicated (involving the pulp).
  4. Root fracture; apical, middle or coronal 1/3, may be oblique or horizontal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Classification of Dentoalveolar Injuries (4)

A
  1. Concussion.
  2. Subluxation.
  3. Luxation; intrusion, extrusion, lateral or avulsion.
  4. Alveolar Injuries; crushing/compression of alveolar wall, # alveolar socket wall, # alveolar process, # of maxilla +/- mandible.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Definition of Concussion (1)

A

Injury to tooth supporting structures withOUT abnromal loosening or displacement of the tooth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Definition of Subluxation (1)

A

Injury to tooth supporting tissues WITH abnormal loosening, but without displacement of the tooth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the types of hypodontia? (3)

A

Mild (<2), moderate (3-5) and severe/oligodontia (>6) -missing permanent teeth excluding 8s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of hypodontia?

A

Obscure aetiology.
Polygenic + intrauterine systemic factor, incl. LBW, multiple births & increased maternal age.
Single gene mainly for Upper 2s; PAX9 or MSX1.
Hypodontia associated with down syndrome, rubella, thalidomide embryopathy & CLP.
Severe hypodontia & micodontia related to anhidrotic ectodermal dysplasia, X-linked hypohidroic ED and AR chondrocectodermal dysplasia (Ellis-van-Creveld syndrome).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical presentation of hypodontia

A

Poor aesthetics
Compromised function
Loss of VD (look prematurely aged).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which teeth are most commonly affected by hypodontia in the primary dentition?

A

Upper Bs most commonly affected.
Maxilla > Mandible
F = M
0.1-0.9% caucasian.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which teeth are most commonly affected by hypodontia in the permanent dentition?

A

8s>5s>Upper 2s>4s -tends to be the last tooth in a series missing.
F:M 4:1
Prevalence of 3.5-6.5% (9-37% if incl. absence of 8s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of Hypodontia

A 
MDT approach; ortho, paeds & restorative.
Maintain dentition -prevention.
Ortho management of spacing.
Partial dentures.
Adhesive dentistry.
Implants when 18/19/20.
Genetic test if pt has ED.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Problems with management of hypodontia pts

A 
Pt compliance
Small crowns
Lack of undercuts
Lack of alveolar bone 
Loss of OVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What conditions are supernumerary teeth/hyperdontia associated with?

A 
Cleidocranial dysostosis; features are extra teeth & missing or diminutive clavicles.
Oral-facial-digital syndrome.
Gardener syndrome (multiple osteomas).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the different names for supernumerary teeth?

A

Supplemental -normal series.
Accessory -atypical form.
Location -mesiodens (adj to midline suture)
Other names incl. conical, tuberculate, odontome, paramolar, distomolar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where is the most common region for supernumeraries to occur?

A

Premaxilla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What percentage of supernumeraries don’t erupt?

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the prevalence of supernumeraries in the primary dentition?

A

0.2-0.8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the prevalence of supernumeraries in the permanent dentition?

A

1.5-3.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Prevalence of supernumaries in males vs. females

A

M:F, 2:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Prevalence of supernumaries in the maxilla vs. mandible

A

Max:mand
5:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What percentage of primary supernumeraries in the premaxilla are followed by a permanent supernumerary?

A

30-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Management of supernumeraries/hyperdontia

A

Early diagnosis -appropriate radiographs.
Ortho opinion re. supplemental teeth.
Referral for surgical removal if necessary.
Space maintenance if necess.
Review of unerupted teeth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is anodontia?

A

The total absence of one or both dentitions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is microdontia?

A

Smaller teeth, unusual form, tapering (peg shaped).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of microdontia

A

Multifactorial; polygenic and environment.
Single gene inheritance described.
Assoc. with Down’s syndrome & ectodermal dysplasia.
F>M.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Prevalence of microdontia in primary dentition

A

0.2-0.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prevalence of microdontia in permanent dentition

A

2.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is megadont/macrodont

A

Larger teeth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What causes generalised mega/macrodonts?

A

Pituitary gigantism

Unilateral facial hyperplasia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes isolated megadonts?

A

Hereditary gingival hyperplasia

Hypertrichosis (XS hairgrowth).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the prevalence of megadonts in the permanent dentition?

A

1.1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which teeth are most likely to be megadonts?

A

Upper 1s or 5s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is hypomineralisation?

A

Hypomineralisation is the qualitative disturbance in enamel formation (laid down in right thickness but porous, high protein content, different translucency –> post eruptive breakdown).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Clinical presentation of Hypomineralisation

A 
Opaque patches (White/cream, yellow/brown).
Altered translucency, altered texture.
Demarcated or diffuse boundary.
Localised or generalised.
Symmetrical or asymmetrical.
Post-eruptive breakdown (enamel loss).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the presentation of fluorosis?

A

Brown opacities, enamel loss (PEB), primary and permanent (more often in permanent teeth), posterior & anterior, dose dependent (greater = worse) & symmetrical distribution.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is enamel hypoplasia?

A

Quantitative disturbance in enamel formation (missing or thin enamel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the clinical presentation of enamel hypoplasia?

A

Pits, grooves, areas.
Chronological; ‘matching’ regions of teeth affected.
Localised; ‘Turner tooth’ -affects 1-5 only (commonly 4s & 5s) due to trauma or infection of primary predecessor –> damage to underlying developing permanent tooth germ. May also exhibit hypomin.

42
Q

What causes discolouration/variation in tooth colour?

A

Changes in tooth thickness &/or structure (hypomin or hypoplasia) or incorporation of circulating substances/pigment deposits (e.g. circulating bilirubin or Tetracycline).

43
Q

What are the acquired causes of tooth discolouration?

A

Incorporation of pulp products (loss of vitality and infection)
Exogeneous agenets, e.g. bacterial, medication or cultural/diet.

44
Q

Management of Tetracycline staining

A

Resistant to bleaching -may have to resort to veneers

45
Q

Treatment of intrinsic enamel staining

A

Microabrasion = first line of Tx for the most superficial intrinsic enamel staining.
Tooth whitening w/ commercial products.
Resin infiltration (ICON).
Veneers -direct/indirect composite with opaquers (used to give tooth its basic shade).

46
Q

Causes of abnormalities in root size

A

Irradiation –> shortened roots.
Racial variation.
Small roots due to dentine dysplasias -roots predominantly made up of dentine therefore abnormalities means may not get full root formation.

47
Q

Which tooth is likely to have the largest root and what is the M:F?

A

Upper 3s.

M>F; 5:1

48
Q

What is taurodontism?

A

Crown elongated coron-apically, ACJ constriction absent, bull like appearance in silhouette.

49
Q

What causes taurodontism?

A

Due to syndromes & polygenic inheritance. Caused by an abnormality in Hertwig’s root sheath as root is forming.

50
Q

What are accessory roots?

A

Carabelli tubercle, paramolar tubercle, enamel pearls

51
Q

What causes accessory roots?

A

May be traumatic or genetic in origin.

52
Q

What are pyramidal roots?

A

Multi-rooted (fused), about 40% of 7s and 8s have their roots fused together -implications for root Tx and XLA.

53
Q

What is amelogenesis imperfecta (AI)?

A

A congenital disorder which presents with a rare abnormal formation of enamel, unrelated to any systemic or generalised conditions.

54
Q

What causes AI?

A

Hereditary; AD or AR (X-linked).
Single gene mutations; amelogenin (AMELX) or enamelin (ENAM), PEX1 and 6.
Can be associated with other generalised disorders; epidermolysis bullosa, tuberous sclerosis, Vit D-dependnet rickets & microdento-osseous syndrome.

55
Q

What is the clinical presentation of AI?

A

Thin/no enamel.
Issues with sensitivity, appearance and loss of tooth structure.
Permanent teeth more severely affected than primary teeth.
Bilateral symmetry (but not always).
Variation in expression -within fams, individuals & environmental factors.

56
Q

What is the prevalence of AI?

A

1:700 to 1:14,000

57
Q

What percentage of pts with AI have an AOB?

A

25-50%

58
Q

What is lyonisation?

A

Bands of normal and abnormal enamel, seen in females due to random inactivation of one X chromosome (not seen in males, they present with thin enamel which is more severely and uniformly affected).

59
Q

What is the radiographic presentation of AI?

A

Shows no enamel formation (contrast lost!)

60
Q

Management of AI

A

OHI
Desensitising agents (tooth mousse or duraphat t/p in trays).
Protect the teeth (composites, PMCs).
Those with AOB require complex MDT approach.

61
Q

What are the types of AI?

A

Hypoplastic.
Hypomature.
Hypocalcifed and hypomature.
Hypoplastic w/ taurodontism.

62
Q

What is dentinogenesis imperfecta (DI)?

A

A genetic disorder of tooth development; a type of dentine dysplasia.

63
Q

What causes DI?

A

Usually AD inheritance, caused by fault in DSPP gene.
Defect in non-collagenous dentine matrix proteins (DSP, DPP and DGP).
Variability in expression and severity.

64
Q

What is the prevalence of DI?

A

1:6000-8000

65
Q

What is the clinical presentation of DI?

A

Loss of enamel with brown/yellow/blue opalescent dentine (looks like marble, sim. to tetracycline staining) which wears rapidly.
Primary and permanent dentitions affected -primary MORE severely affected.
Enamel usually #s off early due to lack of dentine support.
Flatted ADJ -scalloping lost –> PEB –> soft dentine exposure (hypomin) & wears away.

66
Q

What is the radiographic appearance of DI?

A

Bulbous crowns.
Short thin blunt roots.
Obliteration of root canal (not sens!)

67
Q

What is the histological appearance of DI?

A

Irregularly formed and poorly mineralised dentine, tubules decrease & irregular, cellular inclusions from pulp and gradual pulp obliteration.

68
Q

Management of DI

A

OHI

Protect the teeth (likely to require full crown coverage).

69
Q

What is dens-in-dente/dens invaginatus?

A

When the enamel folds into the dentine during tooth development.

70
Q

What are the causes of dens invaginatus?

A

Permanent (1-5%) maxillary incisors; enamel epithelium in-grows down into dental papilla –> deep cingulum pit (due to ingrowth of cells) –> gross distortion of crown & roots of teeth.

71
Q

Where are dens invaginatus most common?

A

Most commonly in upper anterior region, usually conical lateral incisors.

72
Q

What is the M:F ratio of dens invaginatus?

A

2:1

73
Q

What is the clinical presentation of dens invaginatus?

A 
Bilateral symmetry (+ supernumeraries).
Enamel can be complete or incomplete (exposed dentine = sens!!)
Dentine may be missing therefore bacteria can get straight into the pulp from the oral cavity! -pt present with acute alveolar abscess shortly after eruption of the tooth.
74
Q

Management of dens invaginatus

A

Early diagnosis; subsequent RCT is difficult (enamel inside pulp cavity, risk of perforations), therefore aim to FS/occlude communicating channels or caries-prone sites.

75
Q

What is dens evaginatus + talon cusp?

A

Accessory cusp consisting of enamel, dentine +/- pulp; outgrowth of tooth tissue.
Enamel epithelium or focal hyperplasia of ectomesenchyme growing outwards.

76
Q

What causes dens evaginatus?

A

Multifactorial; polygenetic and environment.
Increased prevalence in pts with consanguineous parents.
Increased prevalence in some syndromes (e.g. Sturge-Weber or Ellis-van Creveld).
May be associated with other dental anomalies, e.g. supernumeraries, dens invaginatus, microdent lateral incisors etc.

77
Q

What is the prevalence of dens evaginatus?

A

Uncommon, increased in some racial grps (e.g. North Indian population = 7.7%)
M:F 2:1

78
Q

Which teeth/dentition is more likely to be have dens evaginatus?

A

More common in maxillary teeth.
3x more common in permanent dentition than primary dentition.
Maxillary lateral incisor most frequently affected.
Premolars are commonly affected.
Labial surface of teeth maybe affected (uncommon).

79
Q

What type of talon cusps are most likely to contain pulp extensions?

A

Large talon cusps that project away from the tooth surface are the MOST likely to contain pulp tissue.

80
Q

Probs with dens evaginatus?

A

Occlusal interference, caries, poor aesthetics, tongue irritation, attrition or # with pulpal exposure –> pulp necrosis.

81
Q

Treatment of dens evaginatus

A

Caries prevention; FS, composite to occlude caries-prone fissures between talon cusp, OHI.
Cusp reduction; wait until root apex mature (10-11), aim for gradual cusp reduction w/ reactionary dentine formation & pulp recession; 1-1.5mm tooth tissue reduction every 3 months & placement of F- varnish after each visit to desensitise exposed dentine.

82
Q

What is fusion?

A

Two teeth fused together at the crown with separate roots (fusion of two tooth germs).

83
Q

What is gemination?

A

One tooth that’s folded in on itself with a single root (one tooth germ that geminates/splits into two)

84
Q

How wide can double teeth be?

A

14mm

85
Q

Where are double teeth most common?

A

Labial segment mandible ? maxilla (primary.
Incisors frequent (permanent).
Primary > permanent (0.5-1.6%)
M = F.

86
Q

Clinical presentation of double teeth

A

Vary from minor notch to almost separate crowns +/- common pulp space, root canal (either share RC &/or pulp chamber OR have separate roto canals &/or pulp chamber).

87
Q

Prevalence of permanent anomalies following double primary teeth

A

30-50% in Caucasians.

70% in Japaense.

88
Q

Impact of double teeth

A

Delayed erupted due to retarded root resorption.

89
Q

Causes of double teeth

A

Mode of development unclear

?genetic

90
Q

Management of double teeth

A

Radiograph -determine root morphology.
MDT
Tx options; accept, section restore realign or XLA and RPD.

91
Q

What are accessory cusps on upper 6s and the prevalence?

A

Cusp of carabelli, extra mesiopalatal cusp on upper 6s.
60% have this.
Extra fissure subject to plaque trapping.

92
Q

What is the name of the accessory buccal cusp and which teeth tend to have them?

A

Paramolar tubercles, upper 4s, 5s and molars.

93
Q

What is infraocclusion?

A

Malocclusion 1mm+ below occlusal plane.

Usually affects primary molars -if permanent tooth present 97% will fall out normally.

94
Q

Management of infraoccluded primary molars

A

Early diagnosis -regular review, photos, study models, usualyl only monitoring is necessary (RG to see if permanent successor is present).
Ortho option where successor is absent.
Space maintenance where necessary; composite onlay, GIC, PMC, overdenture or XLA and space maintainer.
Early extraction to avoid need for more complex surgery -care with ankylosis.

95
Q

What is primary failure of eruption?

A

Rare non-syndromic condition where the erupted posterior teeth are submerged in the absence of mechanical obstruction –> posterior open bite.

96
Q

Management of primary failure of eruption

A

Teeth do NOT respond to ortho therefore prosthetic rehab is only viable option.

97
Q

What is ectopic or failed eruption?

A

Commonly see max 6s impacting on the back of Es (due to SDA –> resorption of Es).

98
Q

Management of ectopic/failed eruption of maxillary 6s

A

Can get stuck HOLD -tooth not coming through, caries risk 6, cleaning, risk of Es getting abscess; remove E to allow 6 to erupt.
Sometimes will correct itself -JUMP disengage itself

99
Q

Reasons for premature eruption

A

Natal/neonatal -usually because tooth germ is in superficial/ectopic position, incomplete root formation -very wobbly!
High BW
Hormonal abnormalities (XS growth hormone or XS thyroid)

100
Q

Reasons for delayed eruption

A 
LBW/premature babies
Syndromes (e.g. Down's syndrome or Turner's syndrome) or endocrinopathies (e.g. hypoparathyroidisim or hypopitutarism).
Impaction.
Supernumerary.
Early XLA of primary teeth.
101
Q

Reasons for premature exfoliation (primary dent)

A

Trauma
Extraction
Immune (e.g. cyclic neutropenia or cementum deficiencies).

102
Q

Reasons for delayed exfoliation

A

Infraocclusion -can become ankylosed to bone.
Ectopic successors
Double primary (double amount of tooth tissue to be resorbed)
Hypodontia

Finals 2021! (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions