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Molar Incisor Hypomineralization: Review and Recommendations

Abstract
Molar incisor hypomineralization (MIH) describes the clinical picture of hypomineral-
ization of systemic origin affecting one or more first permanent molars (FPMs) that are
associated frequently with affected incisors. Etiological associations with systemic condi-
tions or environmental insults during the child’s first 3 years have been implicated. The
complex care involved in treating affected children must address their behavior and anxiety,
aiming to provide a durable restoration under pain-free conditions. The challenges include
adequate anaesthesia, suitable cavity design, and choice of restorative materials. Restorations
in hypomineralized molars appear to fail frequently; there is little evidence-based literature
to facilitate clinical decisions on cavity design and material choice. A 6-step approach to
management is described: (1) risk identification; (2) early diagnosis; (3) remineralization
and desensitization; (4) prevention of caries and posteruption breakdown; (5) restorations
and extractions; and (6) maintenance. The high prevalence of MIH indicates the need for
research to clarify etiological factors and improve the durability of restorations in affected
teeth. The purpose of this paper was to describe the diagnosis, prevalence, putative etiologi-
cal factors, and features of hypomineralized enamel in molar incisor hypomineralization
and to present a sequential approach to management. (Pediatr Dent 2006;28:224-232)
KEYWORDS: ENAMEL HYPOMINERALIZATION, MOLAR ,
DENTAL HYPOMINERALIZATION, ENAMEL OPACITY

Received July 8, 2005 Revision Accepted January 18, 2006

T
he term molar incisor hypomineralization (MIH) 3. difficulty in achieving anesthesia; and
was introduced in 2001 to describe the clinical ap- 4. the repeated marginal breakdown of restorations.
pearance of enamel hypomineralization of systemic Research on adhesion of restorative materials to hypo-
origin affecting one or more permanent first molars (PFMs) mineralized enamel is limited, and clinical decisions to date
that are associated frequently with affected incisors.1 Also have not been evidence-based. This may reflect a paucity
referred to as “hypomineralized” PFMs, 2 “idiopathic of extracted hypomineralized molars with suitable surfaces
enamel hypomineralization,”3,4 “dysmineralized” PFMs,5 for in vitro studies. A recently developed microshear bond
“nonfluoride hypomineralization,”6,7 and “cheese molars,”8,9 strength test has allowed initial studies of the bond strength
the condition is attributed to disrupted ameloblastic func- of materials to small surface areas of hypomineralized
tion during the transitional and maturational stages of enamel.11
amelogenesis.3,10 The purpose of this paper was to describe the diagnosis,
MIH’s clinical management is challenging due to: prevalence, putative etiological factors, and features of hy-
1. the sensitivity and rapid development of dental caries pomineralized enamel in molar incisor hypomineralization
in affected PFMs; and to present a sequential approach to management.
2. the limited cooperation of a young child;
MIH diagnosis
1
Dr. William is honorary dental officer at the Royal Children’s Hospi- Criteria for the diagnosis of demarcated opacities, post-
tal, Melbourne, Australia, and was a former postgraduate student in eruption breakdown (PEB), atypical restorations, and
Pediatric Dentistry, 2Dr. Messer is the Elsdon Storey Professor of Child extracted PFMs due to MIH were developed by Weerheijm
Dental Health and Director of Graduate Studies, and 3Dr Burrow
is associate professor in Restorative Dentistry and Clinical Dean, all
et al.12 Dentitions with generalized opacities present on all
at the School of Dental Science, University of Melbourne, Victoria, teeth (such as in several forms of amelogenesis imperfecta),
Australia. rather than limited to the PFMs and permanent incisors, are
Correspond with Dr. Messer at [email protected] not considered to have MIH.12 After thorough cleaning, the

224 William et al. Molar Incisor Hypomineralization Pediatric Dentistry – 28:3 2006
4 PFMs and 8 erupted permanent incisors are examined wet pH disrupted crystal growth and proteinase function. This
for demarcated opacities, PEB, and atypical restorations.12 resulted in protein retention and hypomineralization. This
Demarcated opacities are defects of altered enamel translu- supported rat studies where hypomineralization followed
cency; the defective enamel is white-cream or yellow-brown altered pH after respiratory acidosis.19 Speculatively, such
in color, of normal thickness with a smooth surface, and has conditions affecting matrix pH during enamel maturation
a distinct boundary adjacent to normal enamel.2,13 may predispose MIH.18
The opacities are usually limited to the incisal or cuspal Lack of calcium phosphate may also contribute to the
one third of the crown, rarely involving the cervical one formation of hypomineralized enamel.8 Using secondary
third.2 The intact enamel surface is typically hard, smooth, ion mass spectrometry and X-ray microanalysis, increas-
and often hypermineralized following post-eruptive matu- ing severity of hypomineralization correlated positively
ration; the subsurface enamel is soft and porous.2 Having with increasing carbon concentration and decreasing con-
unusual size and shape, restorations may not conform to centrations of calcium and phosphorus. This resulted in
typical caries patterns and frequently involve the cuspal or significantly lowered calcium/phosphorous ratios in the
incisal one third of the crown.12 Enamel opacities may occur enamel.20 This also supported other studies where cystic
adjacent to restoration margins. Where one or more PFMs fibrosis transmembrane regulator knockout mice had
have been extracted, teeth in an otherwise sound dentition decreased levels of calcium and calcium/phosphorus ratios
should be examined for possible causes (eg, opacities) and in hypomineralized enamel when compared to normal
the child’s history should be assessed for putative etiologi- enamel.21 Thus, impaired calcium metabolism may have a
cal factors. role in the development of hypomineralized enamel.20,21
Teeth with developmental defects of enamel may pres- The color of hypomineralized enamel defects may reflect
ent similarly, regardless of etiology, and the development differences in hardness, porosity, and mineral content. Yel-
defects of enamel hypoplasia may be confused with MIH. low-brown defects have lower Knoop hardness values and
Enamel hypoplasia (EH) is a quantitative defect associated greater porosity than white defects and normal enamel.2,22
with a reduced localized thickness of enamel, following dis- Nano-indentation studies have shown significantly lower
ruption of the secretory phase of amelogenesis. The enamel values for hardness and modulus of elasticity than seen in to
may be translucent or opaque, with single or multiple pits or unaffected enamel.23 Under scanning electron microscopy,
grooves and partial or complete absence of enamel over sig- the defects showed increased porosity and disorganized rod
nificant areas of dentin.2,13 The EH defects tend to occur in structure of fractured surfaces.23
the incisal or cuspal one third of the crown. Diagnostically, Clinically, PFMs can differ in defect severity in an
MIH and EH can be difficult to differentiate when affected individual where all 4 molar germs appear to have been
molars have PEB due to caries or masticatory trauma. In subjected to the same systemic disorder.3,24 Concurrently
a child with a high caries rate, MIH can be masked by ex- mineralizing PFMs may show randomly distributed opaci-
tensive caries or restorations. Also, EH and MIH can occur ties in single or several molars in the same individual.2,3 The
together, particularly at a histological level.13,14 gradient of mineral content of these opacities decreases from
the dentoenamel junction to the subsurface enamel (the
Hypomineralized enamel characteristics reverse of normal enamel); usually the surface layer becomes
Enamel is a highly mineralized tissue of ectodermal origin, hypermineralized with post-eruptive maturation.3 Zones of
secreted from ameloblasts that differentiate from the inter- apparently sound enamel in hypomineralized molars show
nal dental epithelium. Hypomineralization is thought to an overall reduction in mineral concentration (of about 5%)
follow deposition of the full thickness of enamel matrix. and lower calcium/phosphorus ratios, indicating that the
The transitional ameloblast is considered most vulnerable. entire crown is affected to some extent.3,20 Clinical examples
When these cells do not undergo complete maturation, of affected PFMs are shown in Figures 1a to 1d.
full-thickness hypomineralization occurs.3 Enamel matura-
tion involves:
1. the removal of acid-labile mineral; Putative factors associated with
2. replacement with more acid-resistant apatite; and molar incisor hypomineralization
3. an influx of calcium and phosphate ions, increasing Putative factors associated with disrupted amelogenesis
the crystal width and thickness.15 of PFMs include systemic conditions and environmental
Hypomineralization is thought to be due to disturbed insults influencing natal and early development.8,25,26 A
resorptive potential of ameloblasts and proteolytic enzyme recent study in Greece of 151 MIH children reported that
inhibition, leading to protein retention (particularly am- 78% had experienced medical problems: (1) prenatally
elogenin) and interference with crystal growth and enamel (19%); (2) perinatally (44%); and (3) neonatally (22%).27
maturation.10,14,16,17 Regulation of pH during mineralization Only 15% of the children did not appear to have a putative
is considered necessary for normal apatite deposition and etiological factor in their history.27
crystallite growth.18 Investigating the relationship between Causal relationships, however, cannot be assigned de-
enamel matrix pH during the maturation phase in cystic finitively from studies relying on parental recall of medical
fibrosis mice, Sui et al18 reported that reduced enamel matrix and dental events in their child’s first 3 years.1,3 Determina-

Pediatric Dentistry – 28:3 2006 Molar Incisor Hypomineralization William et al. 225
tion of etiological factors is also complicated when a child hyperbilirubinaemia, metabolic disturbances including
has more than one medical problem in this time period. hypocalcemia and hypoglycemia, haematological disorders,
Although a number of etiological factors may contribute patent ductus arteriosus, and intracranial hemorrhage.38
to MIH, the threshold level needed to cause enamel defects A study of 32 Finnish children 9 to 11 years old found
at sensitive stages of amelogenesis is unknown.28 While enamel defects in 36% of children born fullterm and 84%
systemic illnesses may not produce a developmental defect of children born preterm.36 A study of 40 children born
of enamel when experienced singly, 2 or more concurrent preterm with very low birthweight (<1,500 gm) in Bris-
conditions may act synergistically to produce a defect.2,28 bane, Australia showed a significantly higher percentage
This is illustrated in a study of 53 Swedish children with of enamel defects in their PFMs (17%) than in a matched
22q11 microdeletion syndrome.29 Phenotypically, this mul- sample of normal birthweight children (8%).35 The enamel
tiple anomaly has a characteristic facies, and may include defect severity increased with decreasing gestational age and
congenital heart defects, velopharyngeal insufficiency with lower birthweight.35
or without cleft palate, immune problems, feeding dif- Associations have been made between the presence of
ficulties, hypocalcemia, learning disabilities, behavioural polychlorinated dibenzo-p-dioxins (PCDDs) in breast
problems, and skeletal, neurologic, and gastrointestinal milk and enamel hypomineralization in both clinical and
abnormalities.29 Of 47 affected children, 3 (6%) had EH laboratory studies.39-41 The PCDDs belong to a class of en-
in the permanent dentition and 16 (34%) had hypomin- vironmental pollutants known as polyhalogenated aromatic
eralized permanent teeth. Computerized inductive analyses hydrocarbons.39 Persistence and accumulation of PCDDs
showed that the EH of permanent and primary teeth corre- in tissue lipids and in the food chain may result in chronic
lated with prematurity and heart defects (30%) and enamel low-level exposure in humans.42 In studies of Finnish chil-
hypomineralization correlated with frequent preschool age dren examined for hypomineralization of PFMs, increases in
infections and heart defects (43%).29 severity and numbers of defects were seen in those exposed
Conditions common in the first 3 years, such as up- to higher amounts of PCDD and furan via their mother’s
per respiratory diseases, asthma, otitis media, tonsillitis, breast milk compared to those less exposed.39,40
chicken pox, measles, and rubella, appear to be associated Although other clinical studies have not found asso-
with MIH.2,8,26 In a retrospective study of 21 Dutch MIH ciations between dioxin compounds in breast milk and
children, 67% had suffered from bron-
chitis, asthmatic bronchitis, pneumonia,
and upper respiratory tract infections.8
Antibiotic usage has also been implicated.
Due to the concurrence of disease and
antibiotic therapy, however, it is difficult
to ascertain whether the MIH was associ-
ated with the disease or the antibiotic.26
Children with poor general health and
systemic conditions are more likely to have
developmental defects of enamel.30,31 The
systemic conditions implicated to date
include nutritional deficiencies, brain
injury and neurologic defects, cystic fibro-
sis, syndromes of epilepsy and dementia
(Kohlschutter-Tonz syndrome), nephrotic
syndrome, atopia, lead poisoning, repaired
cleft lip and palate, radiation treatment,
rubella embryopathy, epidermolysis bul-
losa, ophthalmic conditions, celiac disease,
and gastrointestinal disorders.30,32-34
Preterm birth has been associated with
increased prevalence of enamel defects, Figure 1a. Clinical case of right and left permanent first molars severely affected by molar
including hypomineralization and hypo- incisor hypomineralization.
plasia in the permanent dentition.33,35-37 Figure 1b. Permanent first molar showing yellow-brown demarcated opacity of enamel.
As the PFM commences mineralization Figure 1c: Mandibular permanent first molar affected by molar incisor hypomineral-
soon after birth, a persistent systemic de- ization, extensive post-eruptive breakdown, and marginal breakdown surrounding a
rangement postnatally may affect enamel restoration.
mineralization.35 Preterm birth can be Figure 1d. Maxillary permanent first molar affected by molar incisor hypomineralization,
associated with respiratory difficulties, extensive post-eruptive breakdown, and marginal breakdown surrounding a restoration.

226 William et al. Molar Incisor Hypomineralization Pediatric Dentistry – 28:3 2006
 Table 1. Recent Studies Reporting Prevalence of Molar Table 2. A Clinical Management Approach for Permanent
Incisor Hypomineralization (MIH) First Molars Affected by Molar Incisor Hypomineralization
First permanent molar Steps Recommended procedures
Study and year
Study sample (PFM) prevalences
of publication Assess medical history for putative
reported Risk identification
etiological factors
2,226 Swedish 4%-15% children had
Koch et al Examine at-risk molars on radiographs
children born “idiopathic hypominer-
(1987)4 Early diagnosis if available
1966-1974 alization” of PFMs
102 Finnish Monitor these teeth during eruption
Alaluusua et al 17% of children had
children 6-7 Remineralization Apply localized topical fluoride
(1996)39 hypomineralized PFMs
ys old and desensitization
97 Finnish Institute thorough oral hygiene home
children 12 Prevention of care program
ys old with dental caries and
Alaluusua et al 25% children had PFM Reduce cariogenicity and
a history of post-eruption
(1996)40 hypomineralization erosivity of diet
extensive and breakdown (PEB)
prolonged Place pit and fissure sealants
breast-feeding
Place intracoronal (resin composite)
18% children had bonded with a self-etching primer
516 Swedish MIH; affected children adhesive or extracoronal restorations
Jalevik et al Restorations or
children 7-8 averaged 3.2 hypomin- (stainless steel crowns)
(2001)43 extractions
ys old eralized teeth, of which
2.4 were PFMs Consider orthodontic outcomes
post-extraction
488 Finnish 19% of children had
Leppaniemi et Monitor margins of restorations for PEB
children 7-13 “nonfluoride hypomin-
al (2001)7
ys old eralizations” of PFMs Maintenance Consider full coronal coverage
10% of children restorations in the long term
497 Dutch had “cheese molars
Weerheijm et children 11 ys (idiopathic enamel
al (2001)9 old and born disturbances)”; 79% of were born preterm or who were exposed to certain environ-
in 1988 affected children had 2 mental contaminants may be at risk for MIH.
or more affected PFMs
2,408 German 6% of children had Prevalence of molar incisor
Dietrich et al
children 10- MIH; affected children hypomineralization
17 ys old and averaged 4.8 hypomin- The limited prevalence data for MIH reflects several diag-
(2003)45
born 1985- eralized teeth, of which
1992 2.2 were PFMs nostic classifications. Using the criteria of Weerheijm et al,12
the prevalence ranges from 4% to 25%.24 Recent studies
2,640 Greek
children at- reporting prevalences from several countries are shown
Lygidakis et al tending a in Table 1. The number of hypomineralized PFMs in an
6% children had MIH
(2004)27 children’s individual can vary from 1 to 4, affecting particularly 2 or
community more molars including the contralateral tooth, where the
health center
teeth are moderately or severely affected.9,39,43-46 The risk of
2,339 Slovenian 14% of children had at involvement of the permanent maxillary incisors appears
Kosem et al
adolescents least 1 PFM with
(2004)44 to increase when more PFMs are affected.1,43,47
12-18 ys old “demarcated opacity”
Australian
children Risk identification, remineralization, and
Chawla et al
attending a Of 182 MIH children, preventive management
large pediatric 70% had ≥1 affected MIH children often experience PFM pain and sensitivity
(2004)46
dental special- PFMs
ist referral
and aesthetic concerns when their incisors are affected.
practice A 6-step management approach is proposed (Table 2).
Children at risk for MIH should be identified prior to
hypomineralized enamel,6,26 a positive association was dem- PFM eruption, based upon a relevant history of putative
onstrated when 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin was etiological factors in the first 3 years and from careful study
administered to lactating rats. The arrested degradation and under magnification of the unerupted molar crowns on any
removal of matrix proteins resulted in protein retention and available radiographs.
hypomineralized enamel.42 Future studies should elucidate During PFM eruption, the hypomineralized surface
if children exposed to such environmental pollutants may is very susceptible to caries and erosion. The cariogenic-
be at risk for MIH. Although the etiology may be unclear, ity and erosivity of the child’s diet should be assessed and
children with poor general health in the first 3 years who appropriate recommendations made for dietary modifica-

Pediatric Dentistry – 28:3 2006 Molar Incisor Hypomineralization William et al. 227
tion. Thorough oral hygiene should be instituted; this 3. apply a low concentration fluoride treatment gel regu-
could include a desensitizing toothpaste. Remineralization larly using a cotton bud.
therapy should commence as soon as the defective surface As remineralization and desensitization of the affected
is accessible, aiming to produce a hypermineralized surface molars occurs, regular oral hygiene strategies can be insti-
layer and to desensitize the tooth.3,48 Remineralization and tuted.
desensitization may be accomplished with casein phospho- For partially erupted PFMs where moisture control is
peptide-amorphous calcium phosphate (CPP-ACP) oral suboptimal, glass ionomer cement sealants can provide car-
care products. The CPP-ACP can interact with fluoride ies protection and reduce surface permeability. Retention is
ions, producing an amorphous calcium phosphate stabilized poor, however, and such sealants may need rebuilding later
by CPP at the tooth surface and providing soluble calcium, with a resin-based sealant when optimal moisture control
fluoride, and phosphate ions to promote remineraliza- is possible.52,53 Without preventive care, hypomineralized
tion with fluorapatite that is more acid resistant.49 Three PFMs are at risk of PEB in the acidic and masticatory
CPP-ACP oral care products are commercially available in challenges of the oral cavity. When PEB occurs, the porous
Australia, the United States, Europe, and Japan: subsurface enamel or dentin is exposed, resulting in teeth
1. a topical tooth crème (Tooth Mousse or MI Paste, GC sensitive to cold air, warm water, and tooth-brushing.1 Poor
Corporation, Tokyo, Japan); oral hygiene favors plaque retention and promotes rapid
2. a sugar-free chewing gum (Recaldent Pty Ltd, Mel- caries development.7,28,54
bourne, Australia); and
3. lozenges (Adams/Cadbury Schweppes, Morris Plains, Restoring hypomineralized
NJ) containing CPP-ACP as Recaldent (Recaldent Pty first permanent molars
Ltd, Melbourne, Australia).49 Restoring affected PFMs is complicated frequently by:
These products enhance remineralization by creating a 1. difficulties in achieving anesthesia;
state of supersaturation followed by deposition of calcium 2. managing the child’s behaviour;
and phosphate ions at the enamel surface.49 While clinical 3. determining how much affected enamel to remove; and
protocols for CPP-ACP oral care products await develop- 4. selecting a suitable restorative material.1
ment, anecdotal reports describe surface hardening and The porous exposed subsurface enamel or dentin may
reduction in tooth sensitivity from daily home use.50 promote chronic inflammation of the pulp, complicating
Topical fluoride, delivered as concentrated varnishes anaesthesia.48,55,56 The adjunctive use of nitrous oxide-
or gels, can remineralize enamel, reduce sensitivity, and oxygen analgesia may alleviate anxiety and reduce dental
enhance resistance to demineralization by providing a pain, or general anesthesia may be required for restorative
reservoir of fluoride ions for redeposition as fluorapatite treatment. In determining cavity margin placement, 2 ap-
during remineralization.51 Anecdotal reports ascribe con- proaches are described:
siderable clinical benefit to topical application of fluoride 1. All defective enamel is removed.
on hypomineralized molars, resulting in surface hardening 2. Only the very porous enamel is removed, until good
of demineralized enamel prior to restoration.48 One such resistance of the bur to enamel is felt.48
varnish (Duraphat, Colgate Oral Care, Sydney, Australia) The former approach may avoid premature restoration
containing 50 mg NaF/mL (2.26% F, 22,600 ppm F) binds failure, but sacrifices tooth structure; the latter approach
to enamel and plaque, acting as a slow-release fluoride res- is conservative, but places restorations at risk of marginal
ervoir. A less concentrated treatment gel (Gelkam, Colgate breakdown. Removal of all defective enamel is recom-
Oral Care, Sydney, Australia) containing 0.4% SnF (3,000 mended when bonding resin composite restorations to
ppm Sn and 1,000 ppm F) can be applied as a single drop hypomineralized PFMs due to the poor bond strength of
on a cotton bud by the parent (told to “paint on the molar resin adhesives to hypomineralized enamel.57
like nail polish”) several times per week after brushing and MIH children receive much more dental treatment than
flossing. The parent must be very responsible and fully unaffected children.7,55,58 A retrospective Swedish study of
compliant in undertaking this task, as regular swallowing 32 MIH children and 41 control children showed that
of this product prior to eruption of the permanent incisors by age 9, those with MIH had undergone treatment of
could promote anterior fluorosis.51 their PFMs nearly 10 times more frequently than control
In summary, the oral hygiene strategies that could be children; on average, each defective molar had been treated
given to parents or patients in cases where tooth-brushing twice due to restoration failure, PEB, or recurrent caries.55
is difficult due to sensitive, poorly mineralized surfaces of In the control group, no molars were retreated and local
affected molars are as follows: anaesthesia was often unnecessary.55 Consequently, it is not
1. brush affected molars gently with a desensitizing surprising that a MIH child who has had pain, difficulties
toothpaste (preferably containing fluoride) on a soft with anaesthesia, and retreatment develops poor behaviour
toothbrush; and dental anxiety.55 The complex care involved in treat-
2. apply a CPP-ACP topical crème daily using a cotton ing such a child must address their behaviour and anxiety,
bud; and aiming to provide a durable restoration under pain-free
conditions.

228 William et al. Molar Incisor Hypomineralization Pediatric Dentistry – 28:3 2006
 The choice of materials will depend on the defect severity Others report little improvement with acid/pumice micro-
and the age and cooperation of the child.48,54 Restorative op- abrasion used alone, but esthetic improvement was achieved
tions include glass ionomer cements (GIC), resin-modified when the enamel reduction was combined with opaque
glass ionomer cements (RMGIC), polyacid modified resin resins then direct RC veneering.24,48,65 Porcelain veneers are
composites (PMRC), resin composites (RC), amalgam, typically delayed until late adolescence when the teeth have
stainless steel crowns (SSCs), and indirect adhesive or cast fully erupted and the gingival architecture has stabilized.64
onlays or crowns. Amalgam is the least durable due to:
1. poor retention in shallow cavity preparations; and Adhesion to hypomineralized enamel
2. the inability to protect remaining tooth structure, The limited literature on adhesion of dental materials to
which is likely to result in restoration failure.48 hypomineralized enamel has focused on case reports of
Adhesive materials are usually chosen due to the atypi- amelogenesis imperfecta (AI). Hypomineralization appears
cal cavity outlines following removal of hypomineralized most severe in the hypocalcified and hypomaturation types
enamel.54 For dentin replacement or as an interim res- of AI, where the decreased mineral content and increased
toration, GIC provides: (1) placement ease; (2) fluoride protein content of the enamel limit effective etching and
release; and (3) chemical bonding.54,56,59 The RMGICs bonding.64,66,67 Enamel pretreatment with 5% sodium hy-
offer similar advantages to GIC; the incorporation of resin pochlorite to remove protein encasing the hydroxyapatite
and photoinitiators improves: (1) handling; (2) wear resis- has been suggested.64,68 Removal of all hypomineralized
tance; (3) fracture toughness; and (4) fracture resistance.60 enamel prior to placing RC restorations has been recom-
Restorations of GIC or RMGIC are not recommended in mended.47,57,69-71 Literature on bonding to hypomineralized
stress-bearing areas, such as occlusal surfaces of hypominer- enamel is limited, perhaps reflecting the paucity of extracted
alized molars, but may suffice until a definitive restoration hypomineralized teeth with suitable surfaces for bond
is achievable.54,56,59,60 strength testing.
With physical properties superior to GIC and RMGIC, Bond strengths of RC to hypomineralized enamel of
the RCs are esthetic materials with high wear resistance and PFMs affected with MIH are significantly less than bond
adhesion when used with resin-based adhesives; they can strengths to normal enamel for both single-bottle total etch
be used solely or in a sandwich technique following previ- and self-etching primer adhesives.57 A recent laboratory
ous temporization with GIC. RCs are technique sensitive, study by the present authors showed the mean microshear
however, requiring good moisture control under rubber bond strengths (MPa) of resin composite bonded to hypo-
dam and long placement time.61 The RCs are materials of mineralized enamel was significantly lower than for control
choice in MIH where defective enamel is well demarcated enamel (3M ESPE Single Bond, St Paul, Minn: 7.08±4.90
and confined to 1 or 2 surfaces with supragingival margins vs 16.27±10.04; Clearfil SE Bond, Kuraray Medical Inc,
and without cuspal involvement.48 Restoring affected PFMs Tokyo, Japan: 10.39±7.56 vs 19.63±7.42; P=.001).57 After
with RC was clinically successful over 4 years when all defec- phosphoric acid etching, scanning electron microscopy of
tive enamel was removed.47 The PMRCs: hypomineralized enamel showed interprismatic spaces and
1. have good handling characteristics; very little intercrystal porosity within the enamel prisms, al-
2. release and take up fluoride; and lowing limited microtag formation (important for bonding
3. have tensile and flexural strength properties supe- effectiveness of single-bottle, total-etch adhesive systems)
rior to GIC and RMGIC, but inferior to that of RC.62 and weaknesses that could lead to crack propagation within
The use of PMRCs in permanent teeth is restricted to the enamel.57 In restoring molar surfaces with limited
nonstress-bearing areas with limited application in hypo- involvement, RC is recommended. After removing all
mineralized PFMs.61,63 discolored hypomineralized enamel, cavity margins should
be placed on apparently sound enamel and RC should be
Restoring hypomineralized bonded with a self-etching primer adhesive. Marginal place-
permanent incisors ment should be located on apparently sound enamel due to
Hypomineralized incisors in MIH may present esthetic the poor adhesion of RC to hypomineralized enamel.57
concerns to children and their parents.10,48 Microabrasion
can be an effective treatment in shallow defects, but the Full coronal coverage restorations
defects usually extend through the full enamel thickness.48 When PFMs have moderate to severe PEB, preformed SSCs
A conservative approach in managing yellow-brown hypo- are the treatment of choice.48,54,56,72 These crowns:
mineralized enamel involves: 1. prevent further tooth deterioration;
1. etching the lesion with 37% phosphoric acid; 2. control tooth sensitivity;
2. bleaching with 5% sodium hypochlorite; and then 3. establish correct interproximal contacts and proper
3. re-etching the enamel prior to placing a sealant over occlusal relationships;
the surface to occlude porosities and prevent restain- 4. are not as technique sensitive or costly as cast restora-
ing.64 tions; and
One report of this approach described clinical success 5. require little time to prepare and insert.54,73,74
with little or no staining up to 5 years post-treatment.64

Pediatric Dentistry – 28:3 2006 Molar Incisor Hypomineralization William et al. 229
 If not adapted properly, however, SSCs may produce aiming to provide durable restorations under pain-free con-
an open bite, gingivitis, or both.75 Properly placed, SSCs ditions. Restoration of surfaces with limited involvement
can preserve PFMs with MIH until cast restorations are with resin composite is recommended following:
feasible.71,72 1. removal of all discolored hypomineralized enamel;
Partial and full coverage indirect adhesive or cast crowns 2. placement of cavity margins on apparently normal
and onlays may be considered for MIH in the late mixed enamel; and
and permanent dentitions.54,71,76 Such restorations are rarely 3. bonding with a self-etching primer adhesive.
indicated for PFMs in young children due to placement dif- Extensively affected molars may require extracoronal
ficulties associated with: (1) short crowns; (2) large pulps; restorations or extraction. Research is needed to clarify
(3) long treatment time and high cost; and (4) the child’s etiological factors and improve the durability of restorations
limited cooperation.48,75 The use of laboratory-fabricated in affected teeth.
crowns of cast gold, indirect composite, and ceramic placed
in 6- to 8-year-old children, however, has been described References
as clinically very successful over a 2- to 5-year follow-up.75 1. Weerheijm KL, Jalevik B, Alaluusua S. Molar-incisor
Compared to SSCs, cast restorations: hypomineralization. Caries Res 2001;35:390-391.
1. require minimal tooth reduction; 2. Jalevik B, Noren JG. Enamel hypomineralization of
2. minimize pulpal trauma; permanent first molars: A morphological study and
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232 William et al. Molar Incisor Hypomineralization Pediatric Dentistry – 28:3 2006