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ICP > Dental anomolies/abnormalities > Flashcards

Dental anomolies/abnormalities Flashcards

1
Q

4 Stages of tooth development

A
  1. Initiation - correct number of teeth in the right jaw
  2. Morphodifferentiation - teeth shape
  3. Cytodifferentiation - different tissues formed
  4. Tooth formation
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2
Q

Aetiology of developmental abnormalities

A 
Genetic
- Part of a disorder e.g. Down's, Ectodermal dysplasia
- Specific gene mutation e.g. DSPP in DI
Environmental
- Local
- Systemic/generalised
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3
Q

Types of tooth development abnormalities (general) [6]

A 
Tooth number
Tooth shape
Tooth size
Tooth eruption
Tooth tissues
Root abnormalities
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4
Q

Tooth number abnormalities [7]

A 
Hypodontia
- Oligodontia (6+ missing teeth)
- Adontia
Hyperdontia/supernumeraries
- Accessory = atypical
- Supplemental = normal
- Mesiodens in midline
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5
Q

Aetiology of hypodontia and associated factors

A

Environmental e.g. low birth weight, multiple births, old mother
Associated with Dwarfism, ectodermal dysplasia and Down’s syndromes (+microdontia)
Single gene mutations e.g. PAX9 - U2s
More common in females

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6
Q

Hyperdontia associated factors [6]

A

More common in males
Associated with cleft palate, invaginated teeth and syndromes e.g. Gardner’s syndrome, Cleidocranial dysplasia, orofacial digital syndrome
Can affect the eruption of teeth
Primary hyperdontia is associated with secondary teeth hyperdontia

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7
Q

Abnormalities of tooth size

A

Microdontia

  • More common in females
  • Generalised e.g. Down’s, ectodermal dysplasia

Megadontia

  • More common in males
  • Generalised e.g. pituitary gigantism, facial hyperplasia

Can be specific to one tooth, generalised, affecting crown, root or whole tooth.

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8
Q

Developmental abnormalities in tooth shape [4]

A

Double teeth
Invaginated tooth (dens-in-dente)
Evaginated tooth
Accessory cusps

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9
Q

Invaginated teeth [4]

A

Enamel epithelium grows into dental papilla
Invagination can be into enamel, dentine or pulp
Caries spreads v quickly into the pulp and can be difficult to treat
Most commonly affecting maxillary incisors, and bilateral
AKA dens-in-dente

Diagnose early and prevention (FS, OHE) bc RCT can be difficult w abnormal pulps.

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10
Q

Accessory cusps and problems associated [4] [5]

A

Evaginations - an outgrowth of dental tissues or focal hyperplasia of ectomesenchyme
Accessory cusps e.g. cusp of carabelli, talon cusps on incisors
Can cause wear on opposing teeth, altered occlusion, plaque retention, fractures, irritated tongue.

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11
Q

Double teeth [4]

A

Can be 1 tooth germ splitting, or 2 fusing
Can share pulp chambers/canals - more difficult to manage
More common in primary dentition
Can cause eruption problems bc takes longer to resorb the root

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12
Q

Conscrescence

A

Excess cementum causes teeth to fuse after they’ve formed

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13
Q

Developmental abnormalities of roots
[4]
[3]

A 
Taurodontism
Short or large roots
Fused/pyramidal roots
Extra roots/growths e.g. enamel pearls.
Dentine dysplasia and irradiation therapy can affect root formation and cause short roots
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14
Q

Taurodontism [5]

A

Crown elongated at the expense of roots
No CEJ/neck of the tooth is lost
Large pulp space
Caused by problems to Hertwig’s root sheath and associated w syndromes e.g. AI

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15
Q

Dental eruption developmental abnormalities
[3]
[4]

A

Premature eruption

  • If tooth germ developed too close to epithelium/in the wrong place
  • Need to XLA bc these can be mobile, risk of inhalation, get caries, cause trauma, problems feeding
  • Found in large birth weight babies or hormonal problems like excessive growth hormone or thyroid hormone

Delayed eruption

  • Impacted or ectopic
  • Slow development, low birth weight babies, pre-term
  • Hormonal abnormalities e.g. hypopituitary or hypothyroid
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16
Q

Dental exfoliation developmental abnormalities
[2]
[2]

A

Premature exfoliation

  • Cementum hypoplasia/aplasia stops PDL from inserting into teeth so they become mobile and fall out
  • Nutritional or immune deficiencies destroy PDL

Delayed exfoliation

  • No successor tooth
  • Submerged/ankylosed
  • XLA and maintain space
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17
Q

Abnormalities in tooth tissue structure - environmental aetiology [4] and examples [8]

A

Environmental

  • All or some tissues can be affected
  • Depends on timing/severity of insult and what part of the tooth was developing at the time
  • Can show as chronological
  • Can be localised or generalised
  • E.g. chemo, trauma, fluoride, tetracycline, bilirubin, measles, neonatal complications, nutritional deficiencies
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18
Q

Developmental enamel abnormalities

[4]

A

AI
Hypomineralisation
Hypoplastic enamel
Discoloured

19
Q

Amelogenesis imperfecta

A

Autosomal dominant/recessive and X-linked inherited
Gene mutations = AMELX, ENAM, MMP20
4 types:
- Hypomature enamel (hypomineralised)
- Hypocalcified enamel (hypomineralised)
- Hypoplastic enamel
- All + taurodontism
Affects primary and secondary teeth but 2 worse
Associated w AOB, eye and hearing problems

Lots of post-eruptive breakdown bc enamel is weak, poor quality or pitting/grooves/areas of absences
Opacities or brown staining

X-linked - in females, if they have 1 normal copy and 1 mutated, then ameloblasts will be 1 normal, 1 mutated and have a banding pattern on the enamel where some abnormal and then some normal etc. = lyonisation

20
Q

Enamel Hypomineralisation

A

Less mineralised = weaker porous enamel, opacities, white/brown/staining.
Can be generalised, localised, have a clear boundary or be diffuse.
Can be fluoride-induced
Teeth get post-eruptive breakdown

21
Q

Enamel hypoplasia

A

Less enamel = pitting, grooves, areas of absence
Can be localised, generalised, chronological
Can be due to trauma to the primary tooth which affects the underlying tooth germ (Turner tooth)

22
Q

Enamel discolouration causes

A

Intrinsic - fluoride, enamel hypomineralisation or hypoplastic, tetracycline staining (grey/brown), bilirubin into teeth if pt has a hepatic disorder during tooth development (green staining)

23
Q

Developmental

dentine abnormalities

A

DI
Fibrous dysplasia affecting dentine (hollows and spaces in the dentine)
Radicular dentine dysplasia
- OI, Ehler’s Danlos affect collagen formation so affect the dentine too (90% collagenous proteins)

24
Q

Cementum aplasia/hypoplasia

A

Stops PDL attaching to tooth so teeth get mobile and fall out

25
Q

Dentinogenesis Imperfecta

A

Autosomal dominant
Defective DSPP gene
3 types
- with OI (lots of broken bones)
- without OI but has hearing loss/impairment
- Without OI
Primary and secondary teeth affected but primary affected more

Dentine proteins affected (non-collageneous =10%, or with OI, collageneous proteins affected too = 90%)
Makes dentine softer, weaker

Shiny, smooth, opalescent, grey/blue enamel
Discoloured tooth
Bulbous crown and short roots, the pulp chamber is filled in.
+/- shell teeth - large pulp chamber with a thin layer of dentine around it.
Flat ADJ and weak soft dentine so enamel shears off or wears down quickly = post-eruptive breakdown and caries

26
Q

Radicular dentine dysplasia

A 
Discoloured crowns (blue/grey) but normal coronal dentine.
Abnormal root dentine = short blunt rounded roots and mobile teeth
27
Q

General management of children with dental anomolies

A

Prevention

  • OHE
  • Fissure seal if the enamel quality is good enough for bonding
  • Tooth mousse releases calcium (topical or in a tray)
  • High F toothpaste
  • Diet advice

Full coverage crowns or PMC
Preventive restorative work
Coordinate w ortho before any XLA
Maintain space (between teeth and OVD)

Manage sensitivity
Aesthetic concerns

28
Q

management of children with DI

A

Prevention

  • OHE, diet
  • Fluoride supplements and tooth mousse

Dentine and enamel wear down quickly

  • Sensitivity/symptoms management - fluoride, cover teeth
  • PMC, full-coverage crowns, restorations as early as possible to protect the tooth and preserve OVD
  • Ortho and enamel bonding is difficult bc enamel shears off and wears quickly - Fuji triage doesn’t need acid etch or air.

Long term monitoring, reviews - risk of burnout in these patients

29
Q

management of children with AI

A

Prevention

  • OHE, diet
  • Fluoride supplements and tooth mousse

Poor enamel quality so can’t get good bond - use full-coverage crowns, PMCs, fuji-triage to protect the tooth and reduce sensitivity
Ortho/bonded brackets are not possible bc the risk of enamel coming off

Long term monitoring, reviews - risk of burnout in these patients

30
Q

management of talon cusps/evaginated teeth

A

FS

Slowly reduce over time - allow time for tertiary dentine to form to reduce risk of exposure

31
Q

Management of double teeth

A

If separate pulp canals/chambers then can split into 2

Or reduce and use restorative techniques to disguise it

32
Q

Intrinsic tooth discolouration management options [5]

A 
Teeth whitening
Teeth bleaching
Microabrasion
Resin infiltrate
Veneers/composite masking
33
Q

management of children with hypodontia

A

Preserve space and OVD
Protect remaining teeth (prevention)
Use ortho and restorative work

34
Q

management of children with hyperdontia

A

Diagnose early
XLA if causing problems and if unerupted (can cause infection, cysts, resorption of other roots, impaction of other teeth)

35
Q

management of children with impacted first molars

A

If impacted on E’s - if left it will cause decay in the E (= XLA, and problems w 5s erupting), possible overeruption of opposing tooth.
Use ortho to align or if going to XLA needs to be planned early before the 7s have completed root formation

36
Q

management of children with infraoccluded teeth

A

Diagnose early - can cause overeruption and tilting of surrounding teeth, caries, periodontal disease.
XLA and maintain space

37
Q

MIH - what is it [5]

A

Systemic hypo-mineralisation of 6’s and incisors.
Causes porous/weaker enamel, with staining (white, brown)
post-eruptive breakdown and sensitivity.
6’s affected worse than incisors

38
Q

MIH - risk factors [4]

A

Pre-natal - mother pyrexia/illness, diabetes, Vit D deficiency, neonatal illness, antibiotics
Peri-natal - Birthing complication e.g. low birth weight, twins, C-section)
Post-natal - severe illness e.g. measles, ENT or respiratory infections, antibiotics
Anything that can cause hypoxia or hypocalcaemia during tooth development

39
Q

MIH - tooth structure [5]

A

Enamel has high protein content and low mineral content, porous.
Dentine tubules have bacteria in them
Chronic low-grade inflammation of the pulp (from bacteria and sensitivity), hypervascular and hyper-innervated pulp

40
Q

MIH - clinical challenges [5]

A

Sensitivity
Poor enamel quality = post-eruptive breakdown, caries, can’t get a good bond, failing restorations
Hyper-innervated and inflamed pulp = harder to get LA
Aesthetic problems

41
Q

Management of MIH

A

Prevention
Aesthetic management
Sensitivity management
PMC/full coverage crowns on 6s (indirect only after occlusion has stabilised 12/13yrs)
Or if decide to XLA needs to be before 7’s complete root formation.
- GIC and fuji triage for cons/FS

42
Q

Micro-abrasion for aesthetic management

A

Use HCL slurry with particulates on staining - don’t overdo or you will remove too much enamel
POI - avoid dark stained foods
- Only for surface stains e.g. no DI or tetracycline staining. Doesn’t work great on MIH

43
Q

Resin infiltration for aesthetic management

A

Isolate
Clean surface
Special acid etch (HCL)
Infiltrate with flowable/low viscosity resin
Light cure
- But can’t whiten this resin in the future

44
Q

Gardner’s syndrome

A

Odontomes, supernumerary teeth, osteomas (small, well-defined radiolucency by root apices

ICP (7 decks)

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