Holistic treatment planning for children with molar incisor hypomineralisation Flashcards
Definition of MIH (2)
A clinical diagnosis to describe: “hypomineralisation of systemic origin of one to four first permanent molars, frequently associated with affected incisors” 'Idiopathic hypomineralisation' 'Cheese molars' 'Popcorn molars'
Hypomineralisation vs hyploplasia
Hypomineralisation: qualitative disturbance in enamel formation
Hypoplasia; quantitative disturbance in enamel formation
Clinical presentation of MIH (6)
Affected molars present with well-demarcated white/yellow or brown/yellow enamel opacities
1-4 FPMs may be affected, conflicting data as to whether maxillary or mandibular teeth more at risk
In severe cases, defective enamel is lost soon after eruption to expose underlying dentine
Affected incisors also present with well-demarcated white/yellow or brown/yellow enamel opacities
Post-eruptive enamel loss is not usually a feature
Increased risk of hypomineralised incisors where molars are more severely affected
World wide prevalence of MIH (2)
Meta-analysis published 2018 found a global prevalence of 13% (Schwendicke et al)
Pre-natal aetiology of MIH (9% of MIH cases) (6)
Maternal pyrexia Medication (antibiotics) Prolonged vomiting Maternal diabetes Vitamin D deficiency In vitro fertilisation
Peri-natal factors in aetiology of MIH (34% of MIH cases) (4)
Caesarean section
Prolonged/complicated delivery
Prematurity/low birth weight
Twins
Post-natal factors in aetiology of MIH (34% of MIH cases) (6)
Ear/nose/throat infections Respiratory problems Pyrexia Seizures Urinary infections Antibiotics
Aetiology of MIH (4)
Most ‘causes’ seem to be associated with hypocalcaemia and hypoxia
May also involve a genetic susceptibility?
No obvious causes in 10-24% of MIH patients (Jalevik & Noren, 2000)
Conflicting findings regarding role of environmental pollutants such as dioxins (Laisi et al., 2008)
MIH: underlying mechanisms (5)
Insult to enamel formation from around 37 weeks to 3 years
Transitional and maturation phase of enamel affected
reversible or irreversible damage to ameloblasts with qualitative disturbance to enamel formation
Protein retention and poor hydroxyapetite crystal formation
Low content of calcium and phosphate ions
MIH lab studies: enamel (3)
Porous
Weak
Poor etch pattern
MIH lab studies: dentine (2)
Sparse reparative dentine and irregular globular dentine
Influx of bacteria in dentine tubules
MIH lab studies: pulp (3)
Underlying chronic pulpal inflammation
Increased immune cells, vascularity and neural density
MIH clinical challenges: pt related factors (4)
Extreme tooth sensitivity
Aesthetic concerns
Anxious about dental treatment (Jalevik and Klingberg, 2002)
Need for long-term interventions (financial burden)
MIH clinical challenges: clinical related factors (4)
Difficulty in achieving adequate level of analgesia for restorative treatment
High failure rate for adhesive restorations and sealants (poor shear bond strength)
Tooth tissue loss
High caries experience
MIH: holistic care for children (4)
I. Prevention, remineralisation, alleviation of symptoms
II. Treatment planning for first permanent molars
III. Improvement of incisor aesthetics
IV. Incorporating a child-centred approach