MIH Flashcards
What is MIH?
Molar Incisor Hypomineralisation (MIH) = a qualititive demarcated enamel defect affecting permanant molars and sometimes permanant incisors.
It results from disrupted enamel mineralisation during tooth development
Put more simply as…
…lesions of hypomineralisation >1mm (w/w out incisor involvement)
Note: risk of incisor defects increase the more molars are affected
Describe the opacities present in MIH
Colour: white, cream, yellow, brown
Mottled
Diffuse or well demarcated
What are the other clinical features of MIH? (6)
Primary teeth usually unaffected
Opaque enamel(white, yellow, or brown discoloration)
Soft, porous enamel, leading to rapid breakdown
Increased sensitivityto temperature and brushing
Higher risk of cavities& post-eruptive breakdown
Prominent canine tips (+/- opacity)
What are MIH pts at increased risk of?
○ hypodontia (most commonly lower second premolars)
○ ectopic first permanent molars
○ primary molar infraocclusion
○ macrodont & microdont teeth
Explain the difference between caries & MIH
Location:
- MIH lesions in O, B & /or P
- Carious lesions in fissures or M / D contact points
Appearance:
- MIH can present as post-eruptive breakdown (+/- cusp breakdown if severe) w/w out atypical restorations
- caries appears as triangles in dentine on x-ray
What is the classification of MIH (EAPD 2021)
EAPD 2021
1) Mild MIH
- Demarcated opacities in non-stress bearing areas of molars
- No caries
- No hypersensitivity
- Mild or no incisor involvement
2) Moderate MIH
- Demarcated opacities on molars & incisors
- Post-eruptive enamel breakdown limited to 1 or 2 surfaces w/out cuspal involvement
- Normal sensitivity
3) Severe MIH
- Post-eruptive enamel breakdown
- Crown destruction
- Caries
- Hx of sensitivity
- Pulpitis symptoms
- Aesthetic concerns
Possible causes of MIH (7)
1 - Prenatal or perinatal complications
2 - low birth weight
3 - Childhood illnesses (high fever e.g.measles, influenza & chicken pox; GI infections e.g. Helicobacter pylori & rotavirus; respiratory e.g. pneumonia & asthma, esp if frequent)
4 - Antibiotic use (e.g. amoxicillinstrongly assoc. w/ MIH,macrolides (erythromycin, azithromycin)+tetracyclinesalso assoc. Why?
These antibiotics candisrupt ameloblast function(cells responsible for enamel formation), leading tohypo-mineralized enamelin developing teeth.)
5 - Environmental toxins (e.g., dioxins, pollutants)
6 - O2 starvation
7 - Calcium & phosphate metabolic disorders
How do infections contribute to MIH?
1) High fever→ Disrupts ameloblast activity, leading to weak enamel.
2) Inflammation→ Alters calcium and phosphate metabolism needed for mineralization.
3) Antibiotic use→ Amoxicillin and other antibiotics may interfere with enamel formation.
4) Nutritional deficits→ Illnesses causing malabsorption or dehydration can affect tooth development
How can you diagnose MIH?
Visual examination, looking for opacities or enamel breakdown inat least one first permanent molar (6s) w/w out incisor involvement.
(canine tips sometimes affected, primary teeth unaffected, some cases second primary molars affected 6s)
what are the problems dentists face when treating MIH?
- Post-eruptie enamel breakdown (→
dentine exposure →
risks pulpal involvement)- Tooth sensitivity (→ poor OH → increases caires risk)
- LA problems (chronic pulp inflammation? Recommended to tx w inhalation sedation)
- Dental anxiety (triggered by many uncomfortable apts at the dentist)
- Aesthetic concerns in anterior
- Tooth loss
- Negative impact of child’s school performance due to absences at school to attend dentist
- Financial concern for families
What are differentials for MIH?
MIH differentials:
- fluorosis,
- enamel hypoplasia,
- amelogenesis imperfecta,
- white spot lesion,
- traumatic hypomineralisation
- chronological hypomineralisation
What is amelogenesis imperfecta
= Generalised hypomineralisation &/or hypoplasia of enamel affecting all teeth (incl primary teeth)
Often assoc w ant open bite
2 types of AI:
- HYPOPLASTIC (sharp pointy rough teeth)
- HYPOMINERALISED (teeth shape appear normal but yellow, rough & sensitive)**
General management of MIH (7)
Enhanced prevention
Micro abrasion (0.1mm)
Regional whitening/bleaching
Etch, bleach & seal
ICON resin infiltration
Restorations & PMCs
XLA
What do you do in enhanced prevention? (8)
1) Thorough OHI
2) Diet advice
3) 1450ppmF toothpaste
4) 0.05% NaF mouth rinse (if 8+ yr old)
5) 2.2% FV >2x a year
6) FS
7) Pi free score
8) Long term use of CPP-ACP Tooth Mousse (+/- CPP-ACP containing surgar free gum & lozenges)
CPP-ACP = casein phosphopeptide-amorphous calcium phosphate
How do you treat MIH in incisors? (6)
EAPD 2021
MICROABRASION (0.1mm), indication: discolouration limited to outer surface of enamel (effective in eliminating brown mottling), process: 18% HCl or 37% H3PO4 w pumice
TOOTH BLEACHING (camouflage white opacities) for adolescents, 10% carbamide peroxide gel into custom fitted trays in combo w CPP-ACP Tooth Mousse in 1:6 ratio to 3:4 ratio depending on opacity response to bleaching agent.
CPP-ACP protects tooth structure & remineralises MIH opacities during bleaching process
ETCH-BLEACH-SEAL technique (purpose: removes yellow-brown stains), process: 37% H3PO4 for 60 secs, then continuously apply 5% NaOCl as bleaching agent for 5-10 mins, re-etch & cover tooth w clear fissure sealant or composite bonding agent → white mottled appearance (mor acceptable than prev brown one)
RESIN INFILTRATOIN (improves enamel translucency as refractive index of resin infiltrate is close to healthy enamel) but Inappropriate for mild MIH cases as resin cannot infiltrate is milder porous enamel, instead: ‘DEEP RESIN INFILTRATION TECHNIQUE’ = sandblasting, resin infiltration (+/- composite, ensure it is well polished otherwise can discolour)
COMP RESTOS, STRIP CROWNS OR VENEERS (indicated in large enamel defects that require tx due to exposed dentine or chip), process: removal of defective enamel, etch, pre-tx w 5% NaOCl for 1 min, prime, bond & composite build up using opaque composite to not remove tooth much dark tooth tissue
PORCELAIN VENEERS (for 18+ after gingival margin has matured), option for when other tx above ave been attempted & produced unsatisfactory results
How do you treat MIH in molars? (5)
EAPD 2021
FISSURE SEALANTS
RESIN INFILTRATION (ICON), penetrates into the porous enamel (prevents further post-eruptive breakdown), hence not suitable for mild MIH (defect beneath superficial 2/3rd enamel)
RESTORATION:
○ GIC or RMGIC as temporary
○ COMPOSITE as permanent (for 1-3 surface restorations & pre-tx w 5% NaOCl to improve bond strength)
FULL OR PARTIAL COVERAGE:
○ PMCs in severe MIH (prevents further post-eruptive breakdown, no/little tooth prep & 1-visit)
○ INDIECT ONLAY (non-precious metal, gold or tooth-coloured) option for older children but time-consuming, expensive & technique sensitive
XLA for poor prognosis 6s (aged 8-10 years)
○ Timing for MAXILLARY molars (94%): before eruption of 2nd maxillary molar
○ Timing for MANDIBULAR molars (66%): after eruption of lateral incisors, before eruption of 7, presence of the 8 AND engagement of the 5 into the roots of the E (as 5 might slip into the 6 area)
When is the right time to XLA poor prognosis 6s?
RCS
Maxillary 6s = before eruption of 2nd maxillary molar
(94% success rate for spontaneous space closure)
Mandibular 6s = age 8-10, after eruption of lateral incisor & before eruption on 2nd mandibular molar, presence of the 8s & engagement of the 5 into the roots of the E
(66% success rate for spontaneous space closure)
What is the effect of early loss of 6s?
(6 marks)
Mesial drift & rotation of 7
Distal drift & tip of 5 (may be ectopic)
Poor contact between 5 & 7
Over-eruption of opposing teeth
Non-working side interfaces
Retroclination of the labial segment (+ increased OB)
What is the effect of late XLA of 6s?
(1 mark)
Mesial tilting of 7
ie not full bodily movement & therefore poor space closure)
Would you compensate XLA of molars?
Lower molars consider compensating,
upper molars don’t
