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Molar-incisor hypomineralisation: narrative review on etiology, epidemiology, diagnostics and treatment decision


Molar-incisor hypomineralisation (MIH) is clinically defined as demarcated structural enamel defects affecting at least one first permanent molar with or without the involvement of incisors. It is foremost a qualitative developmental defect of systemic origin. The prevalence for MIH is estimated at 12.9% with significant differences between countries. Its etiology and pathogenesis are still not completely understood. Several environmental and medical causes have been suggested to alter enamel maturation. The hypomineralised enamel may collapse shortly after eruption and as a consequence caries lesions seem more likely to develop. Besides cavitation, hypersensitivity and/or pain are the hallmarks of clinical symptoms. Both are associated with increased dental anxiety and fear of children suffering from MIH. Consequently, patients’ care and management are challenging and necessitates a large range of non-, micro- and invasive strategies. MIH might be mixed up with three different other types of developmental defects in the enamel: fluorosis, enamel hypoplasia, and amelogenesis imperfecta. Careful diagnostic differentiation should be made before starting any dental treatment. A recent published classification system links the severity of the lesion to a treatment need index. This index is based on four values regarding two key symptoms: hypersensitivity and post-eruptiv enamel breakdown (PEB). Without PEB sealing is strongly recommended in order to prevent caries. For hypersensitive teeth as well as those with PEB use of glass ionomer cement as an intermediate cover, but mainly composite resins are materials of choice. For improvement of aesthetically compromised MIH-incisors, the resin infiltration technique has been proposed.

Accepted for publication:March 18, 2021

Published online: March 24, 2021

The final edited and typeset version of this article will appear in the future.


Developmental defects in the enamel (DDE) derive from disturbances in hard tissue matrices formation and/or mineralization during odontogenesis. These defects can be localized or appear more widespread, affecting single/multiple teeth or groups of teeth (COMMISSION ON ORAL HEALTH, RESEARCH AND EPIDEMIOLOGY, FDI 1992). Examples of DDE are fluorosis (FS), enamel hypoplasia (EH) and amelogenesis imperfecta (AI). Another entity of DDE is the so called “molar-incisor hypomineralisation” (MIH).

Since the early 1970’s dentists have reported a developmental defect primarily located in first molars and incisors in the permanent dentition. Early denominations referred to this clinical condition in a descriptive manner for “which is not”:

1.    non-endemic stained enamel (JACKSON 1961),
2.    idiopathic hypomineralisation of the enamel of the first molars (KOCH ET AL. 1987),
3.    hypomineralisation of the permanent first molars not caused by fluoride (LEPPÄNIEMI ET AL. 2001)
4.    cheese molars (KREULEN ET AL. 1995).

This reflected a poor understanding of its etiology that continues to this date. WEERHEIJM ET AL. baptized this pathology as MIH in 2001 and was adopted as the official denomination at the sixth annual conference of the European Academy of Paediatric Dentistry (EAPD) in 2003 (WEERHEIJM ET AL. 2001). MIH is defined as developmental (systemic) qualitative enamel defects that are present on one or more first permanent molars (FPMs), each possibly with different degrees of severity. The (central) permanent incisors might be affected additionally. If incisors are affected, at least one first molar must also show enamel hypomineralisation to confirm the diagnosis MIH.  

The aim of this review is to summarize the current knowledge on the etiology, prevalence and diagnostics of MIH as well as provide guidance on treatment decision as well as discuss evidence of non- and micro-invasive interventions. A second review by our group will focus on the choice of invasive treatment options.

Prevalence and incidence

Nowadays, MIH is recognized as a global dental problem. In spite of the EAPD criteria cited above, cross-comparisons of the results from various epidemiological studies have been difficult due to the use of various indices and criteria, examination variability, methods of recording and varying age groups (JÄLEVIK 2010). Prevalence is defined by how often a condition is present in a population, and incidence by how many new cases occur each year. The reported prevalence of MIH in children and adolescents varies significantly between studies varying between 2 and 40% (JÄLEVIK 2010). A recent systematic review and meta-regression analysis (SCHWENDICKE ET AL. 2018) estimated a global mean (95% CI) prevalence for MIH of 12.9% (11.7–14.3%) with significant differences between countries. The highest numbers of prevalent cases were found in high-income and heavily populated countries. Another meta-analysis (ZHAO ET AL. 2018) estimated the prevalence of MIH around 14% globally with no statistical difference between sexes, but <10-year-olds had a higher prevalence than older individuals (15% vs 12%). It was also noted that MIH was particularly high in some regions such as South America (18%) and Spain (21%). For Switzerland no representative data have been reported so far.

A study on the distribution and severity of MIH affected molars in four areas in Germany revealed that the majority of children with MIH showed more than one affected molar (only one affected molar in 39.2%, two affected molars in 33.5%, three affected molars in 12.0% and four affected molars in 15.3%) (PETROU 2012). About half showed hypomineralisation in FPMs without additionally affected incisors. Twelve percent of the children with MIH showed hypomineralised defects in at least one of the second primary molars. Furthermore, FPMs were usually more often and more severely affected than permanent incisors. Upper permanent incisors were usually more often affected than lower permanent incisors and, if lower incisors were affected, in most cases hypomineralisation in upper permanent incisors as well as in FPMs were documented (PETROU 2012).

This was corroborated by other studies showing that the FPMs and incisors are often affected, although there can be considerable differences within a dentition. MIH has also been observed in other teeth of the permanent dentition (second molar, second premolar, canine) as well as in second primary molars and also primary canines (ELFRINK ET AL. 2012; FUCHS 2009). MIH is supposed to affect 878 million individuals, with a global number of incident cases estimated at 16.0 million people in 2016. It is, therefore, imperative to develop appropriate dental healthcare strategies to treat MIH and to identify its etiology in order to prevent.

Etiology and pathogenesis

MIH has been reported to have a negative impact on children’s quality of life and socio-psychological status (DANTAS-NETA ET AL. 2016). Affected teeth are in higher need for dental treatment, especially those with post-eruptive enamel breakdown (PEB). As a consequence, caries lesions develop more easily, leading finally to pulpal inflammation along with hypersensitivity or pain. Thus, it is of great importance to identify the etiology of MIH and to understand its pathogenesis. Despite an augmented interest in MIH and much published research on the subject, its etiology remains, to this day, not completely understood (CROMBIE ET AL. 2009; ALALUUSUA 2010; SILVA ET AL. 2016).

Environmental causes

MIH is considered to establish due to an impaired calcium and phosphate incorporation during enamel matrix formation and enamel maturation. Ameloblasts are sensitive to insults, both indirect and direct. Even the smallest changes in the environment of the ameloblasts may irreversibly disrupt the formation of the enamel matrix and the maturation of the enamel. Another key factor in understanding the etiology of MIH is the chronology of tooth mineralization. The mineralization of enamel in a first permanent molar starts just before birth and is completed in the first year of life (REID & DEAN 2006). Therefore, it seems logical that any possible cause must have occurred during the period from just before birth until the first year of life (Fig. 1, SCHROEDER 2000, DULLA ET AL. 2018). Research on the etiology of MIH have compiled a long list of candidates but failed to prove causality due to low numbers of prospective birth-cohort studies. Nonetheless, ongoing studies have elucidated some risk factors (e.g. “LISA” and “GINIplus”; FLEXEDER et al. 2020). “LISA” (Influence of life-style factors on the development of the immune system and allergies in East and West Germany) and “GINIplus" (German Infant Study on the influence of Nutrition Intervention PLUS environmental and genetic influences on allergy development) are two populated-based German birth cohorts. They aim to describe the natural course of chronic diseases and intermediate phenotypes in childhood and its determinants and to identify potential genetic effect modifications.

Potential environmental causes can be grouped into either being of prenatal, perinatal or postnatal origin (Table I). As indicated in Table I there was little evidence of an association between the most frequently investigated prenatal factors (maternal smoking, illness, medication) and MIH as well as perinatal factors (prematurity, low birth weight, cesarean delivery, birth complications) and MIH. A consistent finding is that early childhood illness, in particular pyrexia, appears to be associated with MIH.

Genetic influence

The amelogenesis phase has been shown to be modulated by genes (FINCHAM ET AL. 1999) and the size, shape, structure and composition of the enamel seem to be influenced by genetic variations. The potential role of genetics or epigenetics in association with MIH has been discussed (VIEIRA & MANTON 2019; HO?EVAR ET AL. 2020). Several genes related to MIH, such as Enam, Ameloblastin, Amelogenin, Bone morphogenetic protein 2 have been investigated (BUSSANELI ET AL. 2019; JEREMIAS ET AL. 2013). In addition to these single gene effects, gene-to-gene interactions may also play a role in MIH (PANG ET AL. 2020). However, data based on twin studies (TEIXEIRA ET AL. 2018) only showed tendencies of an influence of genetics on MIH prevalence, while higher family income and gestational bleeding were strongly positively associated with MIH. Genetic variability may influence the etiology, but seems not to act as the primary cause of MIH. ?

Some intriguing observations

MIH can affect one sibling and not the other(s) and teeth forming at the same period can be affected to varying degrees or not at all. Histological studies reported that MIH lesions extend through the full thickness of enamel, affecting mainly the coronal and not the cervical enamel, and often the buccal surface of the tooth (CROMBIE ET AL. 2013; FAGRELL ET AL. 2013; GAMBETTA-TESSINI ET AL. 2017). VIEIRA & MANTON attempted to address these variables in the clinical presentation of MIH (VIEIRA & MANTON 2019). According to these authors, the reason why only one side of a bilateral structure is affected likely involves differential gene expression between the left and right despite the dentition being mirrored between one side and the other. As for the disturbances of specific areas, and the multiple degrees of the severity, they postulated that this resulting anatomical appearance is a combination of random microenvironment influences (i.e., pressure from surrounding liquid within the connective tissues surrounding the enamel organ) and/or genetic variants (i.e., differential levels of expression at the cellular level and the directionality of molecular signaling).


General diagnostic criteria and a simple classification system were set by the EAPD to facilitate the diagnosis of MIH (WEERHEIJM ET AL. 2003). It can be summarized by the following:

•    The visual aspect of the lesion is opaque, clearly demarcated from the healthy enamel, varies in colour (white, yellow, brownish) and size. The darker opacity indicates more hypomineralised (softer) enamel.
•    The enamel thickness is normal, but its breakdown appears after the eruption of the affected tooth (PEB).
•    When restorations are present, these extend in most cases to the buccal and palatal/lingual surfaces with an opacity at the margin of the restoration.  
•    For incisors, these restorations are not related to a history of trauma.
•    A missing FPM, in an otherwise sound dentition, can be an indication of a history of MIH.  
•    In some cases, eruption difficulties of FPMs due to enamel roughness have been proposed (ALMUALLEM & BUSUTTIL-NAUDI 2018).

Several descriptive classifications have been proposed; e.g. LEPPÄNIEMI ET AL. 2001 rated the severity of MIH within three categories:

1.    Mild: opacities without PEB;
2.    Moderate: opacities with PEB limited to enamel;
3.    Severe: PEB with dentin involvement, atypical restorations and tooth extraction due to MIH.

Another simple classification system, also based on the severity of MIH, proposed distinction between mild and severe cases (LYGIDAKIS ET AL. 2010):

1.    In mild cases, the demarcated opacities do not exhibit a PEB, but can present occasional sensitivity to external stimulus with less aesthetic concerns.
2.    In severe cases, the demarcated enamel is associated with PEB, hypersensitivity (HS) and high aesthetic demands.

In an attempt to standardize MIH diagnostic criteria and treatment needs, conceived a classification system that links the severity of the lesion to a treatment need index (TNI) (STEFFEN ET AL. 2017). This index is based on four values (Fig. 2) regarding two key symptoms that are considered the most important ones with respect to MIH: HS and PEB. The highest value is recorded for each sextant by the use of good light and drying with an air syringe.

Teeth affected by MIH show various characteristics (Figs. 3-8). HS is a common symptom in MIH teeth that might impair oral hygiene, limit dietary habits, cause chronic pain and trigger dental anxiety. Its intensity depends on the severity of the lesion. A recent study (RAPOSO ET AL. 2019) concluded that mild cases of MIH are associated with HS of a low intensity, while severe cases showed more frequently higher degrees of HS. Severely hypomineralised teeth are at higher risk of developing caries, which could increase HS considerably. The cause of this HS appears to be chronic pulp inflammation due to repeated triggers, whether thermal, mechanical, or bacterial (FAGRELL ET AL. 2008). PEBs occur due to the severe porosity of the hypomineralised opaque areas that fracture when subjected to masticatory forces, resulting in unprotected dentin being more prone to external triggers (GARG ET AL. 2012). Interestingly, whitish discolored MIH teeth seem to be at ca. 33% lower risk for PEB than yellowish/brownish ones (CABRAL ET AL. 2016). ?

Clinical examination

With the complete eruption of all first molars and incisors at ca. eight years of age hypomineralised enamel of relevant teeth can be preferably detected and MIH be diagnosed (LYGIDAKIS ET AL. 2010). Nonetheless, MIH might be diagnosed during the eruption of the FPM. An early diagnosis may limit the degree and size of PEB and the high risk of subsequent HS and dental caries (GARG ET AL. 2012).

FPMs are first screened for MIH and then for caries. Teeth should be cleaned with a toothbrush and fluoride toothpaste and examined in wet condition using a mirror and probe. The tooth surface can also be gently cleaned with a cotton roll but should preferably not be dried. Intraoral photography is a great tool to better examine and assess the damaged tooth on a computer monitor (CHEN ET AL. 2013). Subsequently, the tooth is dried using air jet or, if not possible with cotton rolls, to examine for caries and to evaluate possible HS.

Differential diagnosis

MIH might be mixed up with three different other types of DDE: FS, EH, and AI. It can be helpful that MIH is the most prevalent type. It is a well-demarcated qualitative “chalky” defect (contrary to EH), non-symmetrical (contrary to FS, AI), limited to one or more FPM (contrary to AI, FS), with or without central permanent incisors implication (contrary to FS, AI), caries prone (contrary to FS), generally but not always hypersensitive (contrary to FS), with no history of trauma on the affected tooth (WEERHEIJM 2004; COMMISSION ON ORAL HEALTH, RESEARCH AND EPIDEMIOLOGY, FDI 1992; ELCOCK ET AL. 2006; CRAWFORD ET AL. 2007) (Table II). Furthermore, traumatic injury as well as prolonged periapical inflammation process of a primary tooth may affect the development or maturation of the permanent successor and lead to a so-called Turner’s tooth / Turner’s hypoplastic tooth, which is one example for EH.

Pain control & therapy

For the affected and suffering quite young child, visiting a dentist is often accompanied with a great portion of anxiety and reluctance. In order to rebuild the bridge of trust between the child and the dentist, a painless first examination is absolutely essential. Thermal stimuli such as air syringe, cold water, or cold instruments should be avoided. Any subsequent dental treatment should be performed under a very effective pain control protocol (JÄLEVIK & KLINGBERG 2002).

Pain is a subjective experience especially when it overlaps with anxiety and fear. The fear of having pain can be overwhelming for a child especially in case of previous traumatic dental experiences. A prerequisite for any pain control protocol to be effective is to ensure a proper emotional management of the suffering child otherwise, the protocol is doomed to failure. This behavioral and emotional management is the standard in pediatric dentistry (MCNEIL ET AL. 2006). A combination of three techniques i.e. analgesic, anesthetic and sedation is often necessary in pain management of MIH teeth.

Systemic analgesic premedication

The use of an analgesic premedication can be helpful in the treatment of hypersensitive MIH molars. The choice of the drug can be paracetamol or non-steroidal anti-inflammatory drugs NSAID (Ibuprofen or Metamizole). STEFFEN & VAN WAES described a treatment protocol based on patients suffering from chronic back pain. The protocol recommends the ingestion of a very high but short-term dosage (24-48h). The anti-inflammatory effect of NSAIDs is desirable especially in chronically inflamed MIH teeth. In order to influence chronic pain, medication should be taken > 24 hours before the dental treatment. The four doses are distributed as follows: > 24h, 12h, 6-8h before dental treatment and the last dose shortly before the procedure (STEFFEN & VAN WAES 2011).


Treatment of MIH affected teeth in young patients is challenging due to chronic pulpal inflammation caused by porous enamel and exposed dentin. Failure in achieving profound and sufficient anesthesia may lead to behavior problems and affect the quality of restorations. The clinician might reach the maximum anesthetic dose (limited by weight and age) and the tooth remains hypersensitive. Type and dose of the anesthetic are not as important as the accessory techniques employed to achieve anesthesia (DISCEPOLO & BAKER 2011). For lower FPM, inferior alveolar nerve block adjunct to buccal infiltration is commonly used. Periodontal ligament injections can help in the establishment of anesthesia although its safety is constantly debated. Intraosseous injection technique used in endodontics, is also proven to be effective and provides profound anesthesia of long duration (60 minutes or greater) (NUSSTEIN ET AL. 2005). Crestal intraosseous local anesthesia by the use of a computer-assisted injection system is an effective and safe technique to achieve profound anesthesia in MIH-affected hypersensitive teeth. This technique could be beneficial when treating an MIH tooth with a pulpitis (DIXIT & JOSHI 2018; DISCEPOLO & BAKER 2011; FOUAD & LEVIN 2006). ?


While anesthesia helps to reduce pain, sedation helps tremendously in removing the emotional context of fear and anxiety accompanying the dental treatment. Drug sedation can be used especially in very young children. However, whenever the child maintains nasal breathing, inhalation sedation (nitrous oxide / oxygen mixture) is the medication of choice especially in treating MIH cases (ESCH 2009; STEFFEN & LANGERWEGER 2018; STEFFEN 2018). If the child shows no cooperation at all, general anesthesia remains the only option.

Treatment decision

Fortunately, not all MIH affected teeth need immediate treatment. In any case, an intensive prophylactic protocol should be administered as early as MIH is diagnosed. The purpose is to delay enamel breakdown and prevent the development of dental caries. Based on the MIH-TNI, BEKES ET AL. have developed two therapy schemes for patients with either low or high caries risk. Prophylaxis is based on a self-applied “home” and a professional “in office” part. The former comprises mainly the home-use of fluoride toothpaste, but also other preventive measures (e.g. CPP-ACP mousse) haven been proposed, but no conclusive evidence of increased beneficial effects exists. It should be combined with regular professional application of fluoride varnishes (BEKES ET AL. 2016; FÜTTERER ET AL. 2020). Nonetheless all of these recommendations are mainly based on clinical studies regarding caries prevention, since no distinct non-invasive intervention has yet been proven to be more efficacious than another with respect to PEB prevention and/or HS reduction in teeth affected by MIH.

Indication and choice of treatment is driven by local factors (HS with or without PEB) and general factors (mainly patient age). For a FPM affected by MIH without PEB with or without HS, sealing therapy with a resin-based fissure sealant is the method of choice in addition to intensive home-based preventive measures. In a high caries risk patient with partially erupted FPM, the application of a flowable glass ionomer cement (GIC) is recommended as an intermediate protection. In order to stabilize the porous structure of hypomineralised molars, resin infiltration seem to prevent from enamel breakdown to a greater extent when compared with fluoride varnish (NOGUEIRA ET AL. 2020). If HS persists after the application of a sealant, a direct or indirect restoration should be chosen.

The presence of PEB (with or without HS) will result in an invasive, mostly restorative treatment. The extent of it will determine whether the tooth is restorable or not. The treatment of a FPM with PEB but without HS is determined by the localization and the size of the defect. If the loss of substance is not in the fissure and includes less than 1/3 of the tooth surface, the application of a sealant is recommended. However, if there is substance loss located in the fissure or defect size is more than 1/3 of the tooth or the defect is close to the pulp, then short-term temporary restoration using GIC with or without an orthodontic band should be the therapy of choice. After the tooth has matured, the temporary filling can be replaced by a definitive restauration. Alternatively, a temporary long-term restoration in form of a steel crown can also be an option.

If a FPM shows substance loss and HS, the treatment follows the same stages as in MIH-TNI 2 (BEKES ET AL. 2016). It should be noted that restorative recommendations are only based on a low scientific evidence level (see second paper regarding MIH of our group; WEBER ET AL. 2021). If future extraction is indicated, orthodontic treatment should follow. The aim is to allow the second permanent molar to erupt naturally as a substitute of the lost FPM. Thus, the timing of the extraction (ca. 8-11 years of age depending on the status of tooth development) is of great importance.

Therapy of MIH affected incisors

For improvement of aesthetically compromised MIH-incisors, the resin infiltration technique originally developed to arrest and mask caries lesions, has been proposed. However, in contrast to caries lesions and fluorotic teeth, MIH is not always completely masked by resin infiltration only. A higher degree of surface removal (etching) prior to the application of the infiltrating resin has been proposed for better aesthetic results. Still, in non-satisfying cases, as well as when hypoplastic areas are apparent from the beginning, composite on top of deeply infiltrated areas are necessary to achieve optimal results (MEYER-LÜCKEL ET AL. 2017; MEYER-LÜCKEL ET AL. 2020).


•    The reported prevalence of MIH in children and adolescents varies significantly between studies varying between 2.4 to 40.2% (JÄLEVIK 2010). Globally a mean (95% CI) prevalence for MIH of 12.9% (11.7–14.3%), with significant differences between countries, has been estimated (SCHWENDICKE ET AL. 2018).
•    FPMs are usually more often and more severely affected than permanent incisors. Upper permanent incisors are more often affected than lower permanent incisors (PETROU 2012).
•    Despite an augmented interest in MIH and much published research on the subject, its etiology is still not completely understood (CROMBIE ET AL. 2009; ALALUUSUA 2010; SILVA ET AL. 2016). The current evidence suggests that multiple, most presumably environmental and medical risk factors trigger MIH during enamel formation and maturation.  
•    MIH might be mixed up with three different other types of DDE: FS, EH, and AI. Careful diagnostic differentiation should be made before starting any dental treatment.
•    In an attempt to standardize MIH diagnostics and treatment a new classification system that links the severity of the lesion to a TNI has been proposed (STEFFEN ET AL. 2017). The index is based on two most important key symptoms with respect to MIH: HS and PEB.
•    Without PEB sealing is strongly recommended in order to prevent caries. For hypersensitive teeth as well as those with PEB use of GIC as an intermediate cover, but mainly composite resins are materials of choice. Resin infiltration might be a suitable additional option in particular for aesthetic improvement in visible teeth. It should be noted that restorative recommendations are only based on a low scientific evidence level (WEBER ET AL. 2021).

Conflicts of interest

JAD declares no conflicts of interest, real or perceived, financial or nonfinancial. HML is appointed as inventor for patents of an infiltration technique for dental caries lesions, held by Charité-Universitätsmedizin Berlin, and receives royalties from DMG, the manufacturer of Icon.


ALALUUSUA S: Aetiology of Molar-Incisor Hypomineralisation: A systematic review. Eur Arch Paediatr Dent 11: 53-8 (2010)

ALALUUSUA S, LUKINMAA PL, KOSKIMIES M, PIRINEN S, HÖLTTÄ P, KALLIO M, HOLTTINEN T, SALMENPERÄ L: Developmental dental defects associated with long breast feeding. Eur J Oral Sci 104: 493-7 (1996) (a)

ALALUUSUA S, LUKINMAA PL, VARTIAINEN T, PARTANEN M, TORPPA J, TUOMISTO J: Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother's milk may cause developmental defects in the child's teeth. Environ Toxicol Pharmacol 1: 193-7 (1996) (b)

ALLAZZAM SM, ALAKI SM, EL MELIGY OA: Molar incisor hypomineralization, prevalence, and etiology. Int J Dent (2014)

ALMUALLEM Z, BUSUTTIL-NAUDI A: Molar incisor hypomineralisation (MIH) – an overview. Br Dent J (2018)

ARROW P: Risk factors in the occurrence of enamel defects of the first permanent molars among schoolchildren in Western Australia. Community Dent Oral Epidemiol 37: 405-15 (2009)

BEENTJES VE, WEERHEIJM KL, GROEN HJ: Factors involved in the aetiology of molar-incisor hypomineralisation (MIH). Eur J Paediatr Dent 3: 9-13 (2002)

BEKES K, KRÄMER N, VAN WAES H, STEFFEN R: Das Würzburger MIH-Konzept Teil 2. Der Therapieplan. Oralprophylaxe Kinderzahnheilkd 38: 171–175 (2016)

BROGÅRDH-ROTH S, MATSSON L, KLINGBERG G: Molar-incisor hypomineralization and oral hygiene in 10- to-12-yr-old Swedish children born preterm. Eur J Oral Sci 119: 33-9 (2011)

BUSSANELI DG, RESTREPO M, FRAGELLI CMB, SANTOS-PINTO L, JEREMIAS F, CORDEIRO RCL, BEZAMAT M, VIEIRA AR, SCAREL-CAMINAGA RM: Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization. Caries Res 53: 217-227 (2019)

CABRAL RN, SOVIERO VM, NYVAD B, LEAL SC: Colour of MIH defects as a predictor of enamel breakdown: A logitudinal 24-month study. Caries Res 50: 235 (2016)

CHEN Y, LEE W, FERRETTI GA, SLAYTON RL, NELSON S: Agreement between photographic and clinical examinations in detecting developmental defects of enamel in infants. J Public Health Dent 73: 204-9 (2013)

COMMISSION ON ORAL HEALTH, RESEARCH AND EPIDEMIOLOGY: A review of the developmental defects of enamel index (DDE Index). Report of an FDI working group. Int Dent J 42: 411-426 (1992)

CRAWFORD P, ALDRED M, BLOCH-ZUPAN A: Amelogenesis imperfecta. Orphanet J Rare Dis 2: 17 (2007)

CROMBIE FA, MANTON DJ, PALAMARA JE, ZALIZNIAK I, COCHRANE NJ, REYNOLDS EC: Characterization of developmentally hypomineralised human enamel. J Dent 41: 611-8 (2013)

CROMBIE F, MANTON D, KILPATRICK N: Aetiology of molar-incisor hypomineralization: a critical review. Int J Paediatr Dent 19: 73-83 (2009)

DANTAS-NETA NB, MOURA LF, CRUZ PF, MOURA MS, PAIVA SM, MARTINS CC, LIMA MD: Impact of molar-incisor hypomineralization on oral health-related quality of life in schoolchildren. Braz Oral Res 30: 117 (2016)

DISCEPOLO K, BAKER S: Adjuncts to traditional local anesthesia techniques in instance to hypomineralized teeth. N Y State Dent J 1: 22–6 (2011)

DIXIT UB, JOSHI AV: Efficacy of Intraosseous Local Anesthesia for Restorative Procedures in Molar Incisor Hypomineralization-Affected Teeth in Children. Contemp Clin Dent 9 Suppl 2: 272-277 (2018)

DULLA J, SCHAFFNER M, LUSSI A: Molaren-Inzisiven-Hypomineralisation. Swiss Dent J 128: 7-8 (2018)

DURMUS B, ABBASOGLU Z, PEKER S, KARGUL B: Possible medical aetiological factors and characteristics of molar incisor hypomineralisation in a group of turkish children. Acta Stomatol Croat 47: 297–305 (2013)

of methods for measurement of hypoplastic lesions. Eur J Oral Sci 114 Suppl 1: 365-9 (2006)

ELFRINK ME, TEN CATE JM, JADDOE VW, HOFMAN A, MOLL HA, VEERKAMP JS: Deciduous molar hypomineralization and molar incisor hypomineralization. J Dent Res 91: 551-555 (2012)

ESCH J: Anxiolyse und Sedierung mit Lachgas in der Kinderzahnheilkunde. Quintessenz 60: 1215–23 (2009)

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 18: 333-40 (2008)

FAGRELL TG, LUDVIGSSON J, ULLBRO C, LUNDIN SA, KOCH G: Aetiology of severe demarcated enamel opacities--an evaluation based on prospective medical and social data from 17,000 children. Swed Dent J 35: 57-67 (2011)

FAGRELL TG, SALMON P, MELIN L, NORÉN JG: Onset of molar incisor hypomineralization (MIH). Swed Dent J 37: 61-70 (2013)

FINCHAM AG, MORADIAN-OLDAK J, SIMMER JP: The structural biology of the developing dental enamel matrix. J Struct Biol 126: 270-99 (1999)

FLEXEDER C, KABARY HASSAN L, STANDL M, SCHULZ H, KÜHNISCH J: Is There an Association between Asthma and Dental Caries and Molar Incisor Hypomineralisation? Caries Res 54:87-95 (2020)

FOUAD A, LEVIN L: Pulpal reactions to caries and dental procedures. In: Cohen S, Hargreaves KM, editors. In: Pathways of the pulp. 9th ed. St. Louis, Mo.: Elsevier Mosby (2006)

FUCHS C, BUSKE G, KRÄMER N: Schmelzbildungsstörungen – Fallbericht einer generalisierten Schmelzbildungsstörung in der 1. Dentition (Enamel malformations – Case report of a generalised enamel malformation in the primary dentition). Oral Prophyl 31: 178–186 (2009)

FÜTTERER J, EBEL M, BEKES K, KLODE C, HIRSCH C: Influence of customized therapy for molar incisor hypomineralization on children's oral hygiene and quality of life. Clin Exp Dent Res 6: 33-43 (2020)

GAMBETTA-TESSINI K, MARIÑO R, GHANIM A, ADAMS GG, MANTON DJ: Validation of quantitative light-induced fluorescence-digital in the quantification of demarcated hypomineralized lesions of enamel. J Investig Clin Dent 8 (2017)

GARG N, JAIN AK, SAHA S, SINGH J: Essentiality of early diagnosis of molar incisor hypomineralization in children and review of its clinical presentation, etiology and management. Int J Clin Pediatr Dent 5: 190-6 (2012)

GHANIM A, MANTON D, BAILEY D, MARIÑO R, MORGAN M: Risk factors in the occurrence of molar-incisor hypomineralization amongst a group of Iraqi children. Int J Paediatr Dent 23: 197-206 (2013)

HO?EVAR L, KOVA? J, PODKRAJŠEK KT, BATTELINO S, PAVLI? A: Dataset on amelogenesis-related genes variants (<i>ENAM</i> and <i>ENAM</i> interacting genes) and on human leukocyte antigen alleles (DQ2 and DQ8) distribution in children with and without molar-incisor hypomineralisation (MIH). Data Brief 32: 106224 (2020)

JACKSON D: A clinical study of non-endemic mottling of enamel. Arch Oral Biol 5: 212-23 (1961)

JÄLEVIK B: Prevalence and Diagnosis of Molar-Incisor- Hypomineralisation (MIH): A systematic review. Eur Arch Paediatr Dent 11: 59-64 (2010)

JÄLEVIK B, KLINGBERG GA: Dental treatment, dental fear and behavior management problems in children with severe enamel hypomineralization of their permanent first molars. Int J Paediatr Dent 12: 24-32 (2002)

JÄLEVIK B, NORÉN JG, KLINGBERG G, BARREGÅRD L: Etiologic factors influencing the prevalence of demarcated opacities in permanent first molars in a group of Swedish children. Eur J Oral Sci 109: 230-4 (2001)

JEREMIAS F, KORUYUCU M, KÜCHLER EC, BAYRAM M, TUNA EB, DEELEY K, PIERRI RA, SOUZA JF, FRAGELLI CM, PASCHOAL MA, GENCAY K, SEYMEN F, CAMINAGA RM, DOS SANTOS-PINTO L, VIEIRA AR: Genes expressed in dental enamel development are associated with molar-incisor hypomineralization. Arch Oral Biol 58: 1434-42 (2013)

KOCH G, GALLONSTEN AL, LUDVIGSSON N, HANSSON BO, HOLST A, ULLBRO C: Epidemiologic study of idiopathic enamel hypomineralization in permanent teeth of Swedish children. Community Dent Oral Epidemiol 15: 279-85 (1987)

KREULEN CM, VAN AMERONGEN WE, AKERBOOM HB, BORGMEIJER PJ: Two-year results with box-only resin composite restorations. ASDC J Dent Child 62: 395-400 (1995)

KÜHNISCH J, MACH D, THIERING E, BROCKOW I, HOFFMANN U, NEUMANN C, HEINRICH-WELTZIEN R, BAUER CP, BERDEL D, VON BERG A, KOLETZKO S, GARCIA-GODOY F, HICKEL R, HEINRICH J: GINI Plus 10 Study Group. Respiratory diseases are associated with molar-incisor hypomineralizations. Swiss Dent J 124: 286-93 (2014)

KUSCU OO, CAGLAR E, ASLAN S, DURMUSOGLU E, KARADEMIR A, SANDALLI N: The prevalence of molar incisor hypomineralization (MIH) in a group of children in a highly polluted urban region and a windfarm-green energy island. Int J Paediatr Dent 19: 176-85 (2009)

LAISI S, ESS A, SAHLBERG C, ARVIO P, LUKINMAA PL, ALALUUSUA S: Amoxicillin may cause molar incisor hypomineralization. J Dent Res 88: 132-6 (2009)

LAISI S, KIVIRANTA H, LUKINMAA PL, VARTIAINEN T, ALALUUSUA S: Molar-incisor- hypomineralisation and dioxins: new findings. Eur Arch Paediatr Dent 9: 224-7 (2008)

LEPPÄNIEMI A, LUKINMAA PL, ALALUUSUA S: Nonfluoride hypomineralizations in the permanent first molars and their impact on the treatment need. Caries Res: 35: 36-40 (2001)

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 9: 207-17 (2008)

LYGIDAKIS NA, WONG F, JALEVIK B, VIERROU AM, 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 11: 75-81 (2010)


MEYER-LÜCKEL H, PARIS S, SCHULT A: Update Kariesinfiltration; Zahnmedizin up2date, Thieme, Heft 3, pp 267–290 (2017)

MEYER-LÜCKEL H, SCHMIDT C, PARIS S, SCHULT A: Zehn Jahre Kariesinfiltration - Erfolgreich auch bei Fluorose und MIH. Zm 110: 286-9 (2020)

NUSSTEIN J, WOOD M, READER A, BECK M, WEAVER J: Comparison of the degree of pulpal anesthesia achieved with the intraosseous injection and infiltration injection using 2% lidocaine with 1:100,000 epinephrine. Gen Dent 53: 50-3 (2005)

NOGUEIRA VKC, MENDES SOARES IP, FRAGELLI CMB, BOLDIERI T, MANTON DJ, BUSSANELI DG, CORDEIRO RCL: Structural integrity of MIH-affected teeth after treatment with fluoride varnish or resin infiltration: An 18-Month randomized clinical trial. J Dent 29: 105: 103570 (2020)

PANG L, LI X, WANG K, TAO Y, CUI T, XU Q, LIN H: Interactions with the aquaporin 5 gene increase the susceptibility to molar-incisor hypomineralization. Arch Oral Biol 111: 104637 (2020)

PETROU MA: Prevalence of Molar?Incisor?Hypomineralisation (MIH) among German school children at four cities in Germany: An epidemiological study. Dissertation Universität Greifswald (2012)

PITIPHAT W, LUANGCHAICHAWENG S, PUNGCHANCHAIKUL P, ANGWARAVONG O, CHANSAMAK N: Factors associated with molar incisor hypomineralization in Thai children. Eur J Oral Sci 122: 265-70 (2014)

RAPOSO F, DE CARVALHO RODRIGUES AC, LIA ÉN, LEAL SC : Prevalence of Hypersensitivity in Teeth Affected by Molar-Incisor Hypomineralization (MIH). Caries Res 53: 424-430 (2019)

REID DJ, DEAN MC: Variation in modern human enamel formation times. J Hum Evol 50: 329-46 (2006)

SCHROEDER HE: Orale Strukturbiologie Entwicklungsgeschichte, Struktur und Funktion normaler Hart- und Weichgewebe der Mundhöhle und des Kiefergelenks. 5. Aufl., Thieme, Stuttgart (2000)

SCHWENDICKE F, ELHENNAWY K, REDA S, BEKES K, MANTON DJ, KROIS J: Global burden of molar incisor hypomineralization. J Dent 68: 10-18 (2018)

SILVA MJ, SCURRAH KJ, CRAIG JM, MANTON DJ, KILPATRICK N: Etiology of molar incisor hypomineralization - A systematic review. Community Dent Oral Epidemiol 44: 342-53 (2016)

SÖNMEZ H, YILDIRIM G, BEZGIN T: Putative factors associated with molar incisor hypomineralisation: an epidemiological study. Eur Arch Paediatr Dent 14: 375-80 (2013)

SOUZA JF, COSTA-SILVA CM, JEREMIAS F, SANTOS-PINTO L, ZUANON AC, CORDEIRO RC: Molar incisor hypomineralisation: possible aetiological factors in children from urban and rural areas. Eur Arch Paediatr Dent 13:164-70 (2012)

STEFFEN R: Einsatz von Lachgas in der Kinderzahnmedizin: Der aktuelle Stand bei der Lachgassedierung Bayerisches Zahnärzte Blatt. BZB 5: 66–9 (2018)

STEFFEN R, KRÄMER N, BEKES K: The Würzburg MIH concept: the MIH treatment need index (MIH TNI): A new index to assess and plan treatment in patients with molar incisior hypomineralisation (MIH). Eur Arch Paediatr Dent 18: 355-361 (2017)

STEFFEN R, LANGERWEGER C: Die Lachgassedation: ein klinischer Leitfaden. Version 4.5, SVK Weiterbildungsmanual fu?r den SVK Fähigkeitsausweis. Zu?rich: SVK Druck (2018)

STEFFEN R, VAN WAES H: Die Behandlung von Kindern mit Molaren-Inzisiven-Hypomineralisation. Eine Herausforderung bei der Schmerzkontrolle und Verhaltenssteuerung. Quintessenz 62 (2011)

TEIXEIRA RJPB, ANDRADE NS, QUEIROZ LCC, MENDES FM, MOURA MS, MOURA LFAD, LIMA MDM: Exploring the association between genetic and environmental factors and molar incisor hypomineralization: evidence from a twin study. Int J Paediatr Dent 28: 198-206 (2018)

VIEIRA AR, MANTON DJ: On the Variable Clinical Presentation of Molar-Incisor Hypomineralization. Caries Res 53: 482-488 (2019)

WEBER KR, WIERICHS RJ, MEYER-LUECKEL H, FLURY S: Restoration of teeth affected by molar-incisor hypomineralisation: a systematic review. Swiss Dent J (2021) (accepted)

WEERHEIJM KL. Molar incisor hypomineralization (MIH): clinical presentation, aetiology and management. Dent Update 31: 9-12 (2004)

WEERHEIJM KL, DUGGAL M, MEJÀRE I, PAPAGIANNOULIS L, KOCH G, MARTENS LC, HALLONSTEN AL: Judgement criteria for molar incisor hypomineralisation (MIH) in epidemiologic studies: a summary of the European meeting on MIH held in Athens, 2003. Eur J Paediatr Dent 4: 110-3 (2003)

WEERHEIJM KL, JÄLEVIK B, ALALUUSUA S: Molar-incisor hypomineralisation. Caries Res 35: 390-1 (2001)

WHATLING R, FEARNE JM: Molar incisor hypomineralization: a study of aetiological factors in a group of UK children. Int J Paediatr Dent 18: 155-62 (2008)

WOGELIUS P, HAUBEK D, NECHIFOR A, NØRGAARD M, TVEDEBRINK T, POULSEN S.: Association between use of asthma drugs and prevalence of demarcated opacities in permanent first molars in 6-to-8-year-old Danish children. Community Dent Oral Epidemiol 38:145-51 (2010)

ZHAO D, DONG B, YU D, REN Q, SUN Y: The prevalence of molar incisor hypomineralization: evidence from 70 studies. Int J Paediatr Dent 28: 170-179 (2018)


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