Molar-incisor hypomineralisation (MIH) Flashcards

1
Q

MIH definition

A

hypomineralisation of a systemic origin - presenting itself as demarcated, qualitative defects of enamel of 1-4 first permanent molars, frequently associated with affected incisors also

Must be present on molar teeth

No change in enamel thickness only mineralisation and enamel hardness

not fluoride related

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2
Q

MIH visual presentation

A

Spectrum

White, cream yellow or brown opacities (not translucent like normal enamel)

May be diffuse or well demarcated

Post eruptive breakdown - due to low mineralisation

If more molars are affected - higher chance of incisor involvement

Mild speckling

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3
Q

Other clinical features of MIH

A

Atypical restorations

Caries on cusp tips

Asymmetric distribution

Canine tip involvement

Primary teeth are unaffected

may affect 2nd molars

risk of hypodontia - lower 5s

Ectopic 1st perm molars - more mesial (early loss of upper second primary molars)

Primary molar infraocclusion

macrodont and microdont teeth

DHS

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4
Q

How to distinguish MIH from caries?

A

MIH lesions may be present occlusally, buccally or palatally - not just in areas of stagnations such as fissure pattern and mesial/distal

Fissure caries - small break in enamel with white deminerlisation around it - spread is more in dentine

Cuspal breakdown occurs in severe cases and teeth can appear shallow looking

atypical restorations (shallow) are seen - cuspal breakdown around restoration

caries will be seen spreading into dentine (cone shaped lesions RG) - areas of stagnation –> fissures and interproximally

can get caries on MIH

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5
Q

Aetiology of MIH

A

Cause is unclear

Localised and asymmetrical legions = systemic

disruption in amelogenesis process during the early maturation stage or late secretory stage (tooth doesn’t reach required mineralisation only correct thickness)

systemic factors during last gestational trimester and 1st 3 years of life (Pre, peri and post natal)

more teeth seem to be affected/more marked lesions if the disturbance occurred prenatally

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6
Q

Possible causes of MIH to deduce from medical history

A

SYSTEMIC INSULTS
Previous history of

-Upper resp tract infections
-Use of antibiotics
-Perinatal complications (jaundice, feeding issues)
-Dioxins (pollutant)
-Low birth weight
-Oxygen Starvation
-Calcium and Phosphate metabolic disorders
-Frequent childhood diseases - 1st 3 years of life
-Genetic (do parents or siblings have it)

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7
Q

Clinical problems associated with MIH

A

Post eruptive enamel breakdown - pulp involvement

Prone to caries on top - pulp involvement

Tooth sensitivity - poor OH. Teeth have similar nerve state to those with caries induced chronic pulp inflammation
- not a PC as not known any different (Ask if avoid hot or cold)

May make anaesthesia difficult -consider articaine buccal infiltration

Behavioural management issues

Aesthetics (anterior teeth) - dont rush into restorative cycle - teeth tend to mature and improve

Tooth loss - extractions :( in hypodontia cases

Multiple appts - time of school, parents, financial pressure to attend appts, transport, cooperation etc

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8
Q

Treatment of MIH with products

A

Enhanced prevention of caries (high risk)/desensitisation/remineralisation:

fluoride

CPP ACP tooth mousse - makes teeth less sensitive and prevents wear of outer enamel. Apply with clean finger or cotton bud after brushing

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9
Q

Treating anterior teeth for MIH

A

Bleaching - to even out whiteness, not allowed below age of 18

Microabrasion- 3 cycles of phosphoric etch applied to brown lesions under rubber dam. Removes 100 micron of tooth tissue. May be followed by comp veneer - CARE with sensitivity

Etch bleach, seal- Etch tooth, bleach with NaOCl, seal with clear resin

Infiltration with ICON resin - works well on well demarcated white lesions

Composite restorations / veneers
*CONSIDERATION: you can remove brown discolourations with handpiece instead of etch BUT if intense then lots of removal required and also bulk fill of composite after - neither ideal

Porcelain veneers (when older and gingival margins are fully developed?)

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10
Q

Treatment of posterior teeth with MIH

A

Restorations, crowns, onlays:

Temporary stabilisation:
- GIC (uncooperative sensitive lesion, stabilise tooth before extraction?) , GIC may bond better to hypomineralised enamel than composite.

–Preformed metal crowns (hall technique - minimal prep)- full coverage, stabilises and reduces sensitivity to preserve tooth for longer for def restorations later. If the molar has not fully erupted, trim the crown down

Definitive tx:
Composite (occlusal surfaces is ideal, minimal lesions, remove brown hypomineralised tissue for good bonding)

Indirect onlays - metal, gold, tooth-coloured, require cooperation (older), shallow defects as only 3/4 crown and prep on unaffected enamel
CONSIDER when past point of extractions and only one or two teeth affected

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11
Q

Tx plan for an MIH patient

A

Emergency -
Skip unless patient is in pain or sensitivity –> temporary restoration

Stabilisation-
Temporary restorations on molars - GIC will be able to better cover areas of exposed dentine

SSC - immediate first step too until definitive restoration

Fluoride varnish

Desensitising toothpaste/tooth mousse - CPP ACP
Prevention-
Plaque scores, PMPR, interdental cleaning

Fluoride:
-Duraphat toothpaste - 2800 ppm

-Topical FV

-Daily fluoride rinse

Diet chart

Fissure seal PE molars/premolars - GIC if resin does not work

Restorative-
Anterior:
-Microabrasion followed by ICON infiltration concept (clean, etch, dry and then icon resin infiltrate (dry)) (no LA required, just rubber dam and light cure)
-composite veneers (buildup) - use handpiece to remove discolouration and create space for composite - composite masking not 100% if opacity intense –> either have to remove lots of tooth tissue or bulk fill composite - neither ideal

Posterior:

-planned XLAs of 6s poor prognosis and wait for orthodontics timing (OPG to see development - 7s to replace them)- temporise with GIC/PMC to buy time
(if 12 years or above, 7s may be past bifurcation but still XLA and fixed appliance option viable)

Crown/ metal onlay/ restoration

Maintenance-
MIH patients are high risk, see every 3 months with 6 monthly bws. Fluoride varnish 4 times a year.
OHI
Plaque scores
Check FS and restorations and SSCs
PMPR
Bitewings - 6 mos

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12
Q

What to consider when extracting 6s?

A

May be necessary if prognosis is poor

Consider the prognosis of the remaining 6s

Which teeth are present and what is the developmental status of the rest of the dentition?

Is there malocclusion present?

Lower molars have less predictable space closure than uppers

Compensating > balancing as more evidence

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13
Q

Timing the extraction of lower 6s

A

Why? - less predictable space closure than uppers - so cant do late extractions

To be timed between ages of 8-10

Upper 2’s erupted/5s not yet erupted

Consider whether the bifurcation of the 7s has formed and whether there is bone overlying the occlusal surface

Position of the 5s - in the bifurcation of E’s

Have the 8s started to develop? May not start to develop until the age of 14. Big factor in whether there will be spontaneous space closure.

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14
Q

What to do about the 6 in a patient with class 1 molar relationship who is unlikely to need orthodontics with extractions

Poor prognosis 6, TPM present

A

If 6 is of poor prognosis -

Extract between the age of 8-10 before the 7 erupts

Compensate for lower 6 extraction to prevent over-eruption of the upper tooth

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15
Q

What to do about the 6 in a patient that may need possible orthodontic tx with extractions (class II or class III) (poor prognosis, TPM present)

A

If 6 poor prognosis and TPM present, malocclusion:

-Interceptive extraction over restoration
-Extract 6’s and any other teeth needing removal at time specified by orthodontist (consult)

NOTE:
-Maintain until 7s erupted
As ortho tx w/ extractions is creating space to relieve crowding and align SO e.g.

*class II - aim is to reduce overjet so extraction of 6s not ideal
*class III - dont want to extract at all, espesh lower molars
6s arent good extraction teeth for creating space in ortho

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16
Q

What to do about a patient with good short term prognosis 6, long term prognosis uncertain, TPM absent

A

Restoration better than extraction

17
Q

Other dental defects

A

Fluorosis

Amelogenesis imperfecta

Dentinogenesis Imperfecta/ Dentine dysplasia

Chronological hypoplasia

18
Q

Chronological hypoplasia and tx

A

Linear defect which develops at the time of the environmental systemic insult

Reduced quantity of enamel - enamel is well mineralised but reduced in thickness and little pits.

Most common cause is Vit D deficiency

May pick up brown staining

Easily filled with composite - polish and microabrasion of staining beforehand

19
Q

Fluorosis

A

Hypomineralisation of enamel resulting in white opaque appearance

Chronic exposure to fluoride in drinking water greater than 1.5 ppm

Brown staining of hypomineralised areas can occur

Treat with veneers and composite bonding (white/bleach shade)

-microabrasion of front teeth not helpful as hard to blend white shades - more for brown discolouration

20
Q

Amelogenesis imperfecta main features

A

Effects ALL teeth (primary and permanent)

7-8 years - only got incisors and molars so cant distinguish w/ MIH

Hypoplastic enamel - reduced thickness

Hypomineralised - poorly calcified

Hypomature - mineral not laid down at all - chipping of cusp tips
(more similar to MIH - non linear, asymmetric and localised)

21
Q

Associated features of Amelogenesis imperfecta

A

Taurodontism - enlarged pulp chamber and shorter roots, more apical bifurcation

delayed eruption

anterior open bite

pre-eruptive resorption - enamel resorbed before teeth erupt

periodontal disease, teeth are rough and difficult to keep clean

22
Q

Hypoplastic AI

A

Teeth are thin and rough - reduced enamel thickness

Poor appearance

Conical shaped, pointy canines

Incisal edges are very thin

Can be built up with composite and full coverage composite crowns

Consider yellow - calculus build up - difficult to keep clean

23
Q

Hypomineralised AI

A

Teeth have thickness but the enamel is poor quality and weak

Teeth chip easily as they are erupting

Difficult to keep clean - plaque and calculus

Yellow and sensitive teeth

Symmetrical lesions affecting ALL teeth whereas MIH well demarcated incisors and molars - LINEAR

Anterior open bites common

24
Q

Hypomature AI

A

looks most like MIH

Diffuse opacities - not completely linear/symmetrical

Need to wait and see premolars and canines when they erupt to make diagnosis (over MIH)

Teeth are completely affected, no normal enamel on entire incisor = AI (not MIH)

Not much tx -
Treat with microabrasion for appearance and possible restorations etc

25
Q

Clinical presentation of dentinogenesis imperfecta

A

DI-I - standard
DI-II - brandy wine ice look

Primary and/or permanent dentitions (mild)

Teeth are amber, brown, blue in colour - the dentine is discoloured but the enamel is relatively normal (more prominent in primary dentition as enamel thinner

Enamel wear - at EDJ

26
Q

Radiographic appearance of Dentinogenesis imperfecta

A

Bulbous crowns that look like flowers

Small or obliterated pulp chambers (stones)

Narrow/thin spindly roots with small or obliterated root canals - interrupted root development

Primary teeth wear away very quickly - pulp involvement

27
Q

Classification of dentinogenesis imperfecta and dentine dysplasia

A

Genetic disorder - disruption in the DSPP gene (dentine silophospho protein)

Based on phenotype

DI-I
DI-II
DD-I –> normal teeth, little root development on RG
DD-II –> pulp stones, thistle shaped PC

DI may be present in osteogenesis imperfecta patients - short stature, blue sclera.