MIH Flashcards
(40 cards)
What is MIH?
A clinical diagnosis to describe hypomineralisation of systemic origin of one or more of the four permanent first molars frequently associated and affected incisors
What is the prevalence of MIH?
3.6-25%
How does MIH present?
Affecting one or more first permanent molars and/or incisors
Demarcated patches
White-brown, cream
Post-eruptive breakdown
Missing 6’s due to early XLA
Heavily restored/abnormal restorations
Calculus as brushing is not comfortable for these children
Differential diagnosis
Fluorosis - increased F content of water
Amelogenesis imperfecta - family history or sporadic mutation
Chronological hypomineralisation
What age is the diagnosis made?
7-9 years
When does tooth formation begin?
6w iu
When do 1st molars begin to calcify?
4/12 iu and calcify at birth
When do central incisors and lower laterals start forming?
3-4/12 iu
When do upper laterals start forming
10-12/12 iu
How is amelogenesis affected?
Secretory phase
- defines the form of the tooth
- deposition of organic matrix plus small thin crystallites
- incremental growth in thickness
- not a continuous process
Describe enamel hypoplasia
Disruption in secretory phase
Early in developmental process
Small pits and grooves
Gross enamel surface deficits
Describe how the maturation stage is affected?
Establishes quality of the tooth
Degradation of the organic matrix
Further remineralisation
Ameloblasts move Ca and PO4
Process continues post eruption
Apoptosis of the ameloblasts
Underlying causes of MIH
Insult to enamel formation from around 37w to 3y
Transitional and maturation phase of enamel is effected - may be reversible damage to ameloblasts with qualitative disturbances to enamel formation
Protein retention and poor crystal formation
Can be produced experimentally in rats with conditions of low pH and low Ca and phosphate ability
What has been disrupted in maturation phase?
Hypomineralisation - disruption in maturation phase
poor mineralisation of matrix
happens later in development
White/brown opacities
normal thickness but dubious quality of enamel
(altered calcium/phosphate ratio, less distinct enamel rods, bacterial penetration of enamel, lower hardness of enamel)
How does this happen?
Timing of insult
Pyrexia
Hypocalcaemia
Hypoxia of mother/child
(exposure to chemicals, peri-natal/neonatal problems/ common childhood illnesses and medically compromised children)
Common childhood illnesses causing MIH
Rest issues, otitis media
Coeliac, renal disease and CF
Appearance as a challenging factor
Appearance to parents and children
Transition to secondary school
Managing expectations
Challenges - sensitivity
Greter innervations in subodontoblastic pulp horn/regions
increased immune cell density
increased vascularity in sensitive teeth
porous enamel - exposed dentine
activation of A delta fibres
Underlying increase of c-fibre action (peripheral sensitisation)
Restorative factor challenges
Site, colour, bonding, caries devo, poor prognosis, immature dentine, difficult to anaesthetise, crumbly, over-eruption of upper molars
Restorations tend to fail 2x by the age of 9y
Prevention methods
Fluoride, desensitising toothpaste, CPP-ACP products (casein phosphopeptide, amorphous calcium phosphate)
FS
OH
Temporisation methods
GIC
Fill in defects
SSC
Restore or extract?
Depends on extent of damage
Consider structure of enamel
Age
Presence of adjacent teeth
Occlusal/orthodontic factors
Preferable restoration methods
Composite
Gold/CoCr only
THEN SSC
FGC useful in growing years to maintain space and eruption of other teeth
Benefits of SSCs
Good longevity
Easy to fit
Separators
Occlusal dimension settles
Gingival health
Erupting 7s
