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Kuhnisch J, Heitmuller D, Thiering E, Brockow I, Hoffmann U, Neumann C Proportion and extent of manifestation of molar-incisor-hypomineralizations according to different phenotypes. J Public Health Dent. 2014; 74:42-49
Elfrink MEC, Schuller AA, Weerheijm KL, Veerkamp JSJ. Hypomineralized second primary molars: prevalence data in Dutch 5-year-olds. Caries Res. 2008; 42:282-285
Elfrink MEC, ten Cate JM, Jaddoe VWV, Hofman A, Moll HA, Veerkamp JSJ. Deciduous molar hypomineralization and molar incisor hypomineralization. J Dent Res. 2012; 91:551-555
Ghanim A, Manton D, Marino R, Morgan M, Bailey D. Prevalence of demarcated hypomineralisation defects in second primary molars in Iraqi children. Int J Paediatr Dent. 2013; 23:48-55
Ghanim A, Elfrink ME, Weerheijm K, Marino R, Manton DJ. A practical method for use in epidemiologic studies on enamel hypomineralisation. Eur Arch Paediatr Dent. 2015; 16:235-246
Jalevik B, Noren JG. Enamel hypomineralization of permanent first molars: a morphological study and survey of possible aetiological factors. Int J Paediatr Dent. 2000; 10:278-289
Costa-Silva D, Cristiane M, Ambrosano G, Jeremias F, Souza D, Juliana F Increase in severity of molar–incisor hypomineralization and its relationship with the colour of enamel opacity: a prospective cohort study. Int J Paediatr Dent. 2011; 21:333-341
Elfrink MEC, Schuller AA, Veerkamp JSJ, Poorterman JHG, Moll HA, Ten Cate BM. Factors increasing the caries risk of second primary molars in 5-year-old Dutch children. Int J Paediatr Dent. 2010; 20:151-157
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Oliver K, Messer LB, Manton DJ, Kan K, Ng F, Olsen C Distribution and severity of molar hypomineralisation: trial of a new severity index. Int J Paediatr Dent. 2014; 24:131-151
da Costa-Silva CM, Jeremias F, de Souza JF, Cordeiro RdCL, Santos-Pinto L, Zuanon ACC. Molar incisor hypomineralization: prevalence, severity and clinical consequences in Brazilian children. Int J Paediatr Dent. 2010; 20:426-434
Ghanim A, Morgan M, Marino R, Bailey D, Manton D. Molar-incisor hypomineralisation: prevalence and defect characteristics in Iraqi children. Int J Paediatr Dent. 2011; 21:413-421
Lygidakis NA, Dimou G, Briseniou E. Molar-incisor-hypomineralisation (MIH). Retrospective clinical study in Greek children. I. Prevalence and defect characteristics. Eur Arch Paediatr Dent. 2008; 9:200-206
Parikh DR, Ganesh M, Bhaskar V. Prevalence and characteristics of Molar Incisor Hypomineralisation (MIH) in the child population residing in Gandhinagar, Gujarat, India. Eur Arch Paediatr Dent. 2012; 13:21-26
Chawla N, Messer EPL, Silva M. Clinical studies on molar-incisor-hypomineralisation part 1: distribution and putative associations. Eur Arch Paediatr Dent. 2008; 9:180-190
Jasulaityte L, Weerheijm KL, Veerkamp JS. Prevalence of molar-incisor-hypomineralisation among children participating in the Dutch National Epidemiological Survey (2003). Eur Arch Paediatr Dent. 2008; 9:218-223
Crombie FA, Manton DJ, Weerheijm KL, Kilpatrick NM. Molar incisor hypomineralization: a survey of members of the Australian and New Zealand Society of Paediatric Dentistry. Aust Dent J. 2008; 53:160-166
Fagrell TG, Lingström P, Olsson S, Steiniger F, Norén JG. Bacterial invasion of dentinal tubules beneath apparently intact but hypomineralized enamel in molar teeth with molar incisor hypomineralization. Int J Paediatr Dent. 2008; 18:333-340
Rodd HD, Boissonade FM, Day PF. Pulpal status of hypomineralized permanent molars. Pediatr Dent. 2007; 29:514-520
Rodd H, Abdul-Karim A, Yesudian G, O'Mahony J, Marshman Z. Seeking children's perspectives in the management of visible enamel defects. Int J Paediatr Dent. 2011; 21:89-95
Lygidakis NA, Wong F, Jalevik B, Vierrou A-M, Alaluusua S, Espelid I. Best Clinical Practice Guidance for clinicians dealing with children presenting with Molar-Incisor-Hypomineralisation (MIH): An EAPD Policy Document. Eur Arch Paediatr Dent. 2010; 11:75-81
Chawla N, Messer EPL, Silva M. Clinical studies on molar-incisor-hypomineralisation part 2: development of a severity index. Eur Arch Paediatr Dent. 2008; 9:191-199
Crombie FA, Manton DJ, Palamara JE, Zalizniak I, Cochrane NJ, Reynolds EC. Characterisation of developmentally hypomineralised human enamel. J Dent. 2013; 41:611-618
Farah RA, Monk BC, Swain MV, Drummond BK. Protein content of molar–incisor hypomineralisation enamel. J Dent. 2010; 38:591-596
Mangum JE, Crombie FA, Kilpatrick N, Manton DJ, Hubbard MJ. Surface integrity governs the proteome of hypomineralized enamel. J Dent Res. 2010; 89:1160-1165
Mahoney EK, Rohanizadeh R, Ismail F, Kilpatrick N, Swain M. Mechanical properties and microstructure of hypomineralised enamel of permanent teeth. Biomaterials. 2004; 25:5091-5100
Jalevik B. Prevalence and diagnosis of molar-incisor-hypomineralisation (MIH): a systematic review. Eur Arch Paediatr Dent. 2010; 11:59-64
Mittal N, Sharma B. Hypomineralised second primary molars: prevalence, defect characteristics and possible association with Molar Incisor Hypomineralisation in Indian children. Eur Arch Paediatr Dent. 2015; 16:441-447
Jedeon K, De la Dure-Molla M, Brookes SJ, Loiodice S, Marciano C, Kirkham J Enamel defects reflect perinatal exposure to bisphenol A. Am J Pathol. 2013; 183:108-118
Laisi S, Ess A, Sahlberg C, Arvio P, Lukinmaa PL, Alaluusua S. Amoxicillin may cause molar incisor hypomineralization. J Dent Res. 2009; 88:132-136
Alaluusua S, Lukinmaa PL, Koskimies M, Pirinen S, Hölttä P, Kallio M Developmental dental defects associated with long breast feeding. Eur J Oral Sci. 1996; 104:493-497
Laisi S, Kiviranta H, Lukinmaa PL, Vartiainen T, Alaluusua S. Molar-incisor-hypomineralisation and dioxins: new findings. Eur Arch Paediatr Dent. 2008; 9:224-227
Lygidakis NA, Dimou G, Marinou D. Molar-incisor-hypomineralisation (MIH). A retrospective clinical study in Greek children. II. Possible medical aetiological factors. Eur Arch Paediatr Dent. 2008; 9:207-217
Alaluusua S. Aetiology of molar-incisor hypomineralisation: a systematic review. Eur Arch Paediatr Dent. 2010; 11:53-58
Crombie F, Manton D, Kilpatrick N. Aetiology of molar-incisor hypomineralization: a critical review. Int J Paediatr Dent. 2009; 19:73-83
Jeremias F, Koruyucu M, Küchler EC, Bayram M, Tuna EB, Deeley K Genes expressed in dental enamel development are associated with molar-incisor hypomineralization. Arch Oral Biol. 2013; 58:1434-1442
Kühnisch J, Thiering E, Heitmüller D, Tiesler CM, Grallert H, Heinrich-Weltzien R Genome-wide association study (GWAS) for molar–incisor hypomineralization (MIH). Clin Oral Investig. 2014; 18:677-682
Silva MJ, Scurrah KJ, Craig JM, Manton DJ, Kilpatrick N. Etiology of Molar Incisor Hypomineralization – a systematic review. Community Dent Oral Epidemiol. 2016; 44:342-353
Jalevik B, Klingberg GA. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralization of their permanent first molars. Int J Paediatr Dent. 2002; 12:24-32
Chay PL, Manton DJ, Palamara JE. The effect of resin infiltration and oxidative pre-treatment on microshear bond strength of resin composite to hypomineralised enamel. Int J Paediatr Dent. 2014; 24:252-267
William V, Burrow MF, Palamara JE, Messer LB. Microshear bond strength of resin composite to teeth affected by molar hypomineralization using 2 adhesive systems. Pediatr Dent. 2006; 28:233-241
Lygidakis NA. Treatment modalities in children with teeth affected by molar-incisor enamel hypomineralisation (MIH): a systematic review. Eur Arch Paediatr Dent. 2010; 11:65-74
William V, Messer LB, Burrow MF. Molar incisor hypomineralization: review and recommendations for clinical management. Pediatr Dent. 2006; 28:224-232
Baroni C, Marchionni S. MIH supplementation strategies prospective clinical and laboratory trial. J Dent Res. 2011; 90:371-376
Crombie F, Cochrane N, Manton D, Palamara J, Reynolds E. Mineralisation of developmentally hypomineralised human enamel in vitro. Caries Res. 2013; 47:259-263
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Lygidakis N, Dimou G, Stamataki E. Retention of fissure sealants using two different methods of application in teeth with hypomineralised molars (MIH): a 4 year clinical study. Eur Arch Paediatr Dent. 2009; 10:223-226
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Zagdwon A, Fayle S, Pollard M. A prospective clinical trial comparing preformed metal crowns and cast restorations for defective first permanent molars. Eur J Paediatr Dent. 2003; 4:138-142
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What's new in molar incisor hypomineralization? Mihiri J Silva Nicky Kilpatrick Felicity Crombie Aghareed Ghanim David Manton Dental Update 2024 44:2, 707-709.
Authors
Mihiri JSilva
BDSc, MDSc, DCD, PhD Candidate
Department of Paediatrics, University of Melbourne and Murdoch Children's Research Institute, Institute, Melbourne, Australia (mjsilva@student.unimelb.edu.au)
Molar Incisor Hypomineralization (MIH) poses a significant challenge to clinicians worldwide. Since its description in 2001, extensive research has provided some insight into the condition, its aetiology, natural history and management. An appreciation of the unique clinical features and management considerations of MIH is essential to maximize patient outcomes. Early diagnosis is the first of several key steps in developing an appropriate management plan, which must account for short- and long-term needs of the patient. While traditional caries preventive approaches are important, more proactive restorative strategies may also be useful.
CPD/Clinical Relevance: This review provides clinicians with an update of the recent literature and discusses the contemporary management of MIH.
Article
It has been over a decade since the term Molar Incisor Hypomineralization (MIH) was first proposed by Weerheijm et al to describe demarcated, qualitative enamel defects of systemic origin affecting one or more first permanent molars with or without incisor involvement.1 This unifying definition and subsequent publication of assessment criteria pre-empted a considerable, worldwide research effort to understand the condition better.2 While many questions, principally in relation to aetiology, remain unanswered, the growing understanding of MIH has translated into clinical gains, particularly relating to diagnosis and management.
Demarcated opacities of non-index teeth
MIH is unique amongst developmental defects of systemic origin in that only the first permanent molars (FPMs), and sometimes the incisors, are affected. However, this definition has recently been the subject of some debate, as similar lesions have been reported in other primary and permanent teeth.3,4 The term ‘hypomineralized second primary molars’ (HSPM) is now used to describe similar lesions in the second primary molars, with the condition being considered a risk factor for MIH.5,6,7
Despite being remarkably similar in clinical presentation, lesions in teeth such as the permanent canines and second molars are currently considered beyond the scope of the definition. Inclusion of these teeth as part of a spectrum may develop as our knowledge of the condition and, in particular, its aetiology continues to evolve.8
Clinical features
Lesion description
Teeth affected by MIH present with demarcated enamel opacities, ranging in colour from creamy white (Figure 1) to yellow/brown (Figure 2).1 The cervical third of affected teeth is rarely involved.9
Post-eruptive breakdown
Upon loading with masticatory forces, MIH-affected enamel is susceptible to breakdown, resulting in irregularly shaped post-eruptive breakdown (PEB) lesions (Figure 3).10 These lesions have in the past been incorrectly described as hypoplasia but can be distinguished by several features. Rough margins surrounding these lesions suggest shearing of the enamel, as opposed to the developmental absence of enamel seen in hypoplastic lesions. Furthermore, the presence of opacities in the adjacent enamel of the same tooth and/or opacities in other FPMs or incisors are also key points of difference between the two.8 Distinguishing hypoplasia from hypomineralization has important clinical implications because hypoplastic enamel is generally normally mineralized and therefore does not pose the same clinical challenges in relation to adhesion of restorative materials. Furthermore, there is a greater risk of PEB in MIH-affected teeth with yellow or brown opacities as compared with those that are associated with white opacities. This difference is reflective of the greater mineral deficit in the darker lesions.10
Atypical caries
There is mounting evidence that MIH is a risk factor for dental caries with the association being more apparent in countries with low caries rates (Figure 4).11 MIH-affected teeth may be more susceptible to dental caries due to altered properties of enamel, such as increased porosity and decreased hardness. These are likely to mean that the balance between remineralization and demineralization is more easily shifted to favour demineralization leading to the development of carious lesions as the structure of enamel is less resilient. In addition, the poor mechanical properties of MIH-affected enamel may increase the likelihood of cavitation and therefore rapid progression of carious lesions. The avoidance of effective oral hygiene measures due to tooth sensitivity is likely to facilitate the progression of dental caries further.
Distinguishing a carious lesion associated with HSPM from early childhood caries or, in the case of the permanent dentition, MIH from a carious lesion due to traditional risk factors, is important to determine caries risk and prompt appropriate treatment planning and patient counselling. Patients with atypical caries due to MIH may not have the most common risk factors of frequent dietary sugar consumption or poor oral hygiene. In addition, some restorative options may be less successful in MIH-affected teeth.12,13
MIH distribution
The number of affected teeth may range from one molar to all four first permanent molars, as well as the permanent incisors. Incisor involvement, however, is less frequent and is thought to occur in more severe cases of MIH.3,14 There is conflicting evidence about whether maxillary or mandibular teeth are more susceptible to MIH and HSPM.15,16,17,18
White opacities are the most common clinical presentation of both MIH and HSPM, followed by yellow/brown opacities and then post-eruptive breakdown.15,16 Most lesions on incisors are white and PEB is rare. Increasing numbers of affected molars and involvement of the incisors are indicative of increasing severity of MIH.19 Findings from several studies indicate that, with increasing involvement of molar teeth, the chance of post-eruptive breakdown and incisor involvement increases.7,19,20
Symptoms
Teeth with MIH have been reported to be hypersensitive, particularly to cold stimuli, but even spontaneously in severe cases.1 In addition, clinicians frequently report that it is difficult to gain adequate anaesthesia when trying to restore some MIH-affected teeth.21 A greater density of nerves in the sub-odontoblastic layer coupled with increased permeability of hypomineralized enamel allowing bacterial entry, even when the surface appears macroscopically sound, may account for these symptoms.22,23
The aesthetic problems resulting from MIH lesions on incisors are another significant challenge reported, with affected children being more likely to suffer from unpleasant comments from peers, impacting on confidence and willingness to smile.21,24
Severity
Several factors can be used to determine severity of MIH, including lesion colour and size, presence of enamel loss, sensitivity, quality of life and treatment required. Generally, teeth with demarcated opacities with only occasional sensitivity have been considered mild.25 Severe lesions are likely to have enamel breakdown, persistent sensitivity and be associated with significant aesthetic concerns. The Molar Hypomineralization Severity Index (MHSI) is a recently described, systematic method for determining the severity of MIH in a dentition, which also factors in the number of teeth as well as the sites affected.26
Differential diagnoses
Other than dental caries and enamel hypoplasia, fluorosis and amelogenesis imperfecta (AI) are possible differential diagnoses. Specific to MIH are the distinct margins of the demarcated opacities which differ markedly from the diffuse opacities associated with fluorosis, for which a history of excessive fluoride exposure is also required. AI can be distinguished by its distribution, as all teeth (primary and permanent) are generally affected and there is often a familial history. In addition, all teeth in AI are similarly affected and present with a much more consistent clinical appearance, compared to MIH which often affects the different FPMs with a striking inconsistency such that, within the individual, one FPM may appear sound and yet another may have substantial PEB.8
Structural and ultra-structural changes in MIH-affected teeth
The structural and ultra-structural changes in hypomineralized enamel can explain many of the clinical challenges associated with MIH.9 The enamel in MIH has been found to be abnormal in terms of mineral quantity, with reductions of up to 45% reported, and quality, due to the incorporation of carbonate.27 The protein content in hypomineralized enamel is significantly higher than in normal enamel and comprises exogenous proteins such as serum albumin and antitrypsin.28,29 In addition, ultra-structural abnormalities such as poor crystal organization and surface defects have been reported.30 The culmination of these abnormalities result in enamel with increased porosity, decreased hardness and lower modulus of elasticity.9,27,30
In general, cervical enamel is rarely affected by MIH and has the same structure and properties as normal enamel.9 Enamel that appears clinically sound in MIH-affected teeth appears to have similar porosity, hardness and mineral content as sound enamel in patients unaffected by MIH.27 In affected enamel, the outer half is often much more abnormal. In addition, a thin surface layer with reduced porosity and increased mineral content, which develops post-eruptively, has been found overlying affected enamel both in intact and PEB lesions.27
Although MIH is primarily a defect of enamel, changes in dentine and pulp have also been reported. Dentine under hypomineralized enamel has been found to have variable mineral content and hardness, which is suspected to be a post-eruptive consequence of the increased porosity of overlying enamel.31 The pulp of MIH teeth appears to show signs consistent with chronic inflammation, including increased innervation, accumulation of immune cells and increased vascularity. These may exacerbate the hypersensitivity that is triggered by fluid movement within dentinal tubules exposed through the porous MIH-affected enamel.23
Prevalence
Prevalence rates for MIH from around the world range from 2.4%–40.2%.32 This variation may indicate the true geographic distribution of the condition or may be reflective of inconsistent diagnostic criteria and research methods. The limited studies of HSPM indicate that it is less common than MIH, with rates of 4.9%–6.9%, although a more recent unpublished study of a low caries risk population in Melbourne found a prevalence of 16%.5,7,33,34 Despite a long-standing perception that the incidence of MIH has been increasing, there is currently insufficient evidence to support this. It is, however, possible that, as caries experience declines, MIH has become more easily and hence more frequently diagnosed.
Aetiological factors
There have been a number of observational as well as laboratory studies investigating the aetiology of MIH. The presence of exogenous serum proteins, such as albumin, which can inhibit crystal growth and impair protein degradation, has led some investigators to suggest that MIH may result from bleeding into the enamel organ as a result of localized haemorrhage.28,29 High carbonate content in hypomineralized enamel has led to suggestions that a metabolic insult may impair ameloblast function and subsequent mineralization.27 While animal studies have shown that exposure to toxins such as Bisphenol A and amoxicillin can disrupt enamel formation in a similar fashion to that seen in MIH, these are, as yet, unsupported by human studies.35,36 There is, however, consensus that the condition arises from a disruption to the maturation/late transitional stage of amelogenesis.9,7,28
As such, environmental factors during the third trimester of pregnancy through to the first few years of life may be important factors in the development of MIH. Breastfeeding, environmental toxins, pre- and perinatal complications and childhood illness have been variously implicated and dismissed over the years.37,38,39 Two systematic reviews in 2009 and 2010 cited a lack of evidence to support any clear conclusion regarding possible aetiological factors.40,41 Recently, the role of genetics in MIH has been explored and genes important in enamel development have been found to be associated with the condition.42,43 However, further studies are needed to understand better the role of both genetics and epigenetics.
Although no one specific aetiological factor has been identified, the theme of early childhood illness seems to be consistently reported in the literature.44 Ultimately, the aetiology of MIH is likely to be complex and multifactorial, with some degree of genetic or epigenetic involvement.
Management
By 9 years of age, the frequency of treatment of the FPM for children with MIH is nearly 10 times that of children without MIH.45 The irregular shape of the PEB cavities, poor bond strengths to adhesive restorative materials, the young age of patients and difficulty obtaining adequate anaesthesia combine to impede successful outcomes using traditional approaches.21,46,47 Although a number of guidelines for the management of MIH are available, the evidence for such recommendations is weak.48 However, several novel ways of improving treatment outcomes for patients with MIH have been investigated, in particular regarding preventive and minimally invasive therapies. Although the treatment option for each MIH-affected tooth is mostly determined by severity and the patient's ability to manage treatment, clinicians should employ a holistic approach that considers the entire dentition, the child and his/her family. Conservative treatment may be preferred in young patients, with more complex options becoming suitable as the child and dentition matures.
Remineralization and fissure sealants
Minimally invasive dentistry has an important role to play in the management of MIH, particularly whilst teeth are erupting, where the goals of treatment are to provide relief from sensitivity, facilitate oral hygiene and increase the resistance of the enamel to breakdown.25 Placement of intermediate fissure sealants using glass-ionomer cement is an effective interim dressing during, or immediately after, eruption when moisture control may be challenging.48 In addition, the use of remineralizing agents such as fluoride varnish and CPP-ACP has been recommended to improve mineral content and reduce sensitivity.49 Evidence for this approach has been emerging, with recent clinical and in vitro studies showing an improvement in mineral content and reduction in porosity.50,51 The possibility of ‘maturing’ hypomineralized enamel with such agents has exciting potential for a ‘medical management’ whereby MIH-affected teeth are spared the restorative cycle of increasingly destructive treatment. Further, in cases where restorative treatment is needed, such as in teeth with PEB, it is much more likely to succeed if the enamel is of better quality. However, the success of remineralization is dependent on application as early as possible, as the effectiveness of remineralizing agents may be impaired by the highly mineralized surface layer which forms post-eruptively.51
Fully erupted FPM with mild MIH defects would benefit from resin-based fissure sealants. Unfortunately, the retention of such sealants is often dependent upon the degree of hypomineralization.52,53 The bond strength of resin composite fissure sealants to hypomineralized FPM may be improved by pre-treating with 5% sodium hypochlorite for one minute after etching, as well as use of a bonding agent, although evidence from clinical studies of MIH-affected teeth is still lacking.54,55
Posterior teeth
Direct restorations
Resin composite has been shown to be successful as a direct restorative material for moderately MIH-affected FPMs.56 However, the design of cavity preparations for such restorations is controversial. In the case of more severely affected teeth with large areas of yellow/brown opacities or post-eruptive breakdown, conservative restorations are likely to fail due to cohesive failure of the hypomineralized enamel or failure of the enamel bond.47 Restoration longevity is much more likely to improve if cavity margins are placed on sound enamel. However, not only can it be difficult to determine the health of the surrounding enamel, but such a strategy may come with a significant biological cost.49
More recently, techniques have been described to improve bonding of resin composite to hypomineralized enamel, which offers hope of improving restoration longevity without excessive destruction of tooth structure. Pre-treating hypomineralized enamel with 5% sodium hypochlorite has had mixed results in vitro, with some studies reporting bond strengths to hypomineralized enamel almost equal to those to unaffected enamel, while others show no improvement.46,54 The application of sodium hypochlorite after etching appears to be slightly more successful, which may be because pre-etching allows sodium hypochlorite to penetrate the enamel better and, therefore, more effectively break down the proteins that impair the bond to resin composite.46 If sodium hypochlorite is to be used, rubber dam is imperative.
Alternatively, a technique that enables resin infiltrant to enter the porosities of carious white spots lesions of enamel has been shown to improve mechanical properties and seal pathways of mineral dissolution. However, resin infiltration techniques on hypomineralized teeth do not appear to be as consistent as they are for carious lesions and so are not currently recommended.57
Indirect restorations
The use of conventional pre-formed metal crowns (PMCs), otherwise known as stainless steel crowns, minimizes the risk of marginal breakdown and leakage and has good longevity.58 However, the need for removal of sound tooth structure to accommodate a conventional PMC can be a disincentive to its frequent use and therefore it is only recommended for restoration of moderate to severely affected teeth.25 The use of separators to reduce approximal tooth preparation, which has been recommended in other developmental dental defects such as X-linked hypophosphatemic rickets, can also be useful in the restoration of MIH-affected teeth to minimize destruction of tooth structure.59 Placing PMC on MIH-affected FPM without tooth preparation, with conservative removal of tooth tissue when possible, will avoid the need for excessive destruction of tooth structure. However, the clinical applicability of such a technique may be limited in some cases because some FPMs still require a degree of preparation to enable a good fit. Although evidence suggests that PMCs are well accepted, a minority of children and parents report concerns about the metallic appearance.60 Most importantly, PMCs are interim options and require replacement with definitive restorations in adolescence to prevent periodontal complications.61
Cast adhesive copings, such as nickel chrome alloys, have also been suggested in various guidelines.25 Although these may be more conservative of tooth structure and provide longer-term options than PMCs, problems regarding aesthetics and cost, and the need for two-stage treatment, limit their clinical applicability, as well as the issue of where to finish the preparation – on remnant hypomineralized enamel or sound enamel.
Extraction
Ultimately, timely extractions are often the preferred mode of treatment of severely affected and symptomatic FPM. Facilitating the eruption of a healthy, unaffected second permanent molar into the space of the FPM eliminates the burden of ongoing restorative treatment.13 Studies suggest that, if planned appropriately, a favourable occlusion may be achieved without fixed orthodontic appliance therapy.13,62 Nevertheless, a full discussion of possible orthodontic sequelae and treatment needed is of utmost importance.63
A range of considerations, including the severity of MIH, patients' aesthetic expectations and suitability for orthodontic treatment, other orthodontic concerns including crowding and facial profile, missing or supernumerary teeth and the presence of third molars all influence the final decision on whether to restore and retain or extract MIH-affected molars. It is critical that clinicians recommending extraction of FPM in the mixed dentition also warn patients and families about the risk that other, as yet, unerupted teeth (such as the second permanent molar) may also be affected by MIH-like lesions that may compromise the long-term viability of those teeth. A recent unpublished study has revealed that 13% of children in an orthodontic cohort had MIH–like lesions in both the FPMs and the second permanent molars.4 In addition, management of children with MIH should be based on a careful assessment of the risks and benefits of retaining MIH-affected teeth and the implications for the future.
Extraction of the FPMs between 8 and 10 years of age, when crown formation of the second permanent molar is complete and the bifurcation has commenced mineralization, may result in the eruption of the adjacent tooth into a favourable position.62 Extraction of the mandibular FPM before 8 years increases the risk of distal drift of the unerupted second permanent premolar, whereas extraction after 10 years is less likely to result in mesial migration of the second permanent molar (Figure 5).64 Consideration should be given to the need for a compensating extraction of the opposing, maxillary FPM when a mandibular FPM is indicated for extraction in order to prevent super-eruption of the maxillary FPM, which could interfere with the mesial migration of the mandibular second permanent molar into a favourable position. The timing of maxillary extractions appears to be less critical, although tilting and rotation of the second permanent molar around the palatal root can occur if the extraction of the FPM occurs after eruption of the second permanent molar.65
In patients with a Class II incisor malocclusion, the extraction of an asymptomatic but poor prognosis FPM may be delayed until after the second permanent molar has erupted. The space resulting from the extraction of the FPM can then be used to correct the Class II malocclusion.65
Anterior teeth
Simple non-invasive treatments can improve the aesthetics of MIH-affected incisors and lead to significant improvements in affected children's satisfaction.24 One such technique is the etch-bleach-seal technique, which involves repeated cycles of etching with 37% phosphoric acid and application of 5% sodium hypochlorite until the discoloration improves66 (Figures 6 a, b). The lesion is sealed with a clear resin composite, or a resin infiltrant.67 In some cases, bleaching may be so effective that further invasive treatment is not required. Microabrasion has also been recommended but may be less likely to succeed as the opacities tend to extend through the full thickness of enamel.68 Even if the opacity cannot be eliminated completely through bleaching, the use of direct and indirect composite veneers may provide an effective medium term means of improving aesthetics with minimal biologic cost.69 More aggressive options, such as ceramic veneers, should be delayed due to the risk of complications such as short clinical crown height, risk of irritation of the pulp of immature teeth and instability of gingival margins as the teeth erupt.25
Advanced behaviour guidance
The high rates of dental anxiety amongst children with MIH has been attributed, in part, to difficulties in achieving adequate local anaesthesia during the treatment of MIH-affected teeth.45 Consideration of patient comfort and perception during treatment is important because past negative experiences are a major risk factor for future dental anxiety and onset can occur in childhood.12,70,71 In addition, lack of patient co-operation is likely to impair the ability of a clinician to provide good quality treatment, increasing the prospect of treatment failure.
Due to the difficulty obtaining effective anaesthesia, high treatment burden of MIH and young age of patients, use of appropriate behaviour management techniques is a key component of an effective management strategy. The use of nitrous oxide sedation and general anaesthesia may be indicated where restorative treatment or extractions are to be undertaken. However, in addition to the benefits associated with moisture control, the routine use of rubber dam when restoring MIH-affected teeth can also improve patient comfort by protecting other teeth from water spray.
Conclusion
As the understanding of MIH improves, it is becoming increasingly clear that the condition provides unique clinical challenges and demands careful interdisciplinary treatment planning. Issues such as increased tooth sensitivity, poor treatment outcomes and long-term treatment burden need to be considered when agreeing on management options. Although significant restorative treatment is often required, particularly in more severe cases, early diagnosis and preventive techniques are rapidly emerging as a promising option for ensuring better outcomes for patients.