Molar Incisor Hypomineralisation












Management ofDental Emergencies inChildren andAdolescents, First Edition.
Editedby Klaus W.Neuhaus andAdrianLussi.
© 2019 John Wiley & Sons Ltd. Published 2019 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/neuhaus/dental_emergencies
257
Introduction
Whilst caries in children and adolescents
has been steadily decreasing in incidence in
recent decades, a marked increase in devel-
opmental defects in the permanent teeth has
been reported. Molar–incisor hypominerali-
sation (MIH) is the most common manifes-
tation of this condition. According to national
and international epidemiological trials,
prevalence rates for MIH in children and
adolescents range from 10 to 30% (Kühnisch
et al., 2014a). Analyses of the dentition at
the tooth level reveals that ~90% of all teeth
affected by MIH have enamel opacities without
enamel breakdown (Kühnisch etal., 2014a).
Only about 10% of affected teeth (mainly
posterior teeth) have enamel breakdown
requiring extensive treatment.
With regard to clinical practice, two points
should be emphasised: first, enamel defects
have a heterogeneous appearance (Figures
7.1.1–7.1.5), and second, factors such as
endodontic complications, the state of dental
development and the child’s ability to coop-
erate have a significantly influence on the
treatment strategy. The aim of this chapter is
to describe and assess critically treatment
options for patients with MIH, and to derive
recommendations for clinical practice.
Diagnosis ofMIH
MIH is the diagnosis of developmental
defects characterised by qualitative enamel
mineralisation changes. MIH defects range
from white to yellowish or brownish opacities
of the enamel. If defects can be demarcated
from the healthy enamel, the disturbance is
classified as MIH. Since demarcated opacities
might also be caused by dental trauma or
as sequence of apical inflammations of the
deciduous teeth, differential diagnosis is
needed. Diffuse opacities, on the other hand,
are frequently discussed as a cause of high
fluoride exposure (dental fluorosis) and
should not be misclassified as MIH.
Quantitative enamel defects (hypoplasia)
are characterised by a reduction in the normal
enamel thickness. In the case of MIH, pre‐
eruptive enamel breakdown or less‐devel-
oped hypoplastic and hypomineralised enamel
can be diagnosed in a distinct number of cases.
Post‐eruptive enamel breakdown, on the
other hand, only occurs in association with
functional loading. The occlusal surfaces of
the (first) permanent molars are predisposed
to post‐eruptive enamel breakdown and may
show signs of disintegration immediately
after tooth eruption. Clinically, differentia-
tion between mild (Figure 7.1.2), moderate
7.1
Molar–Incisor Hypomineralisation
Jan Kühnisch
1
and Roswitha HeinrichWeltzien
2
1
Department of Conservative Dentistry and Periodontology, LudwigMaximiliansUniversity, Munich, Germany
2
Department of Preventive and Paediatric Dentistry, Jena University Hospital, Jena, Germany

7.1 Molar–Incisor Hypomineralisation
258
(Figure7.1.3) and severe (Figure7.1.4) enamel
defects with dentin exposure is possible. The
main clinical sign is hypersensitivity of the
affected teeth to thermal, chemical and
mechanical stimuli (Jälevik and Klingberg,
2002; Weerheijm, 2004). Hypersensitivity
often makes adequate daily oral hygiene of
hypomineralised teeth difficult, leading to an
increased risk of caries in these teeth and
these patients.
Different definitions are used for the
diagnosis of MIH today. The most common
one, favoured by the European Academy of
Paediatric Dentistry (EAPD), involves the
use of index teeth (Weerheijm et al., 2003;
Lygidakis etal., 2010). At least one first per-
manent molar must be affected by hypomin-
eralisation in order to establish the diagnosis
of MIH. However, this definition has been
criticised for various reasons. First, it is based
(a) (b)
Figure 7.1.1 Hypomineralisation on (a) an occlusal and (b) a smooth surface without enamel breakdowns.
(a) (b)
Figure 7.1.2 Mild, small‐sized enamel breakdown on (a) a hypomineralised occlusal surface and (b) a smooth surface.

Diagnosis ofMIH
259
solely on an empirical assumption that has
yet to be validated (Weerheijm etal., 2001).
Second, the occurrence of enamel defect is
related to the exposure time, which can be
variable. The implications for clinical practice
are that, ultimately, all teeth of both denti-
tions can be affected, and index tooth‐based
diagnosis leads to underestimation of the
true prevalence of MIH. Therefore, a shift
from using index teeth to tooth‐ and tooth‐
surface‐related registration of demarcated
opacities, enamel breakdowns, atypical resto-
rations and tooth extractions due to MIH is
recommended (Kühnisch etal., 2014a). This
methodological approach is comparable to
the well‐accepted dmf/DMF index.
(a) (b)
Figure 7.1.3 Moderate, medium‐sized enamel breakdown on (a) a hypomineralised occlusal surface and
(b) a smooth surface.
(a) (b)
Figure 7.1.4 Severe enamel breakdown on (a) a hypomineralised occlusal surface and (b) a smooth surface.
Due to the extensive disintegration of hard tissue, dentin is exposed.

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Management ofDental Emergencies inChildren andAdolescents, First Edition. Editedby Klaus W.Neuhaus andAdrianLussi. © 2019 John Wiley & Sons Ltd. Published 2019 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/neuhaus/dental_emergencies257 IntroductionWhilst caries in children and adolescents has been steadily decreasing in incidence in recent decades, a marked increase in devel-opmental defects in the permanent teeth has been reported. Molar–incisor hypominerali-sation (MIH) is the most common manifes-tation of this condition. According to national and international epidemiological trials, prevalence rates for MIH in children and adolescents range from 10 to 30% (Kühnisch et al., 2014a). Analyses of the dentition at the tooth level reveals that ~90% of all teeth affected by MIH have enamel opacities without enamel breakdown (Kühnisch etal., 2014a). Only about 10% of affected teeth (mainly posterior teeth) have enamel breakdown requiring extensive treatment.With regard to clinical practice, two points should be emphasised: first, enamel defects have a heterogeneous appearance (Figures 7.1.1–7.1.5), and second, factors such as endodontic complications, the state of dental development and the child’s ability to coop-erate have a significantly influence on the treatment strategy. The aim of this chapter is to describe and assess critically treatment options for patients with MIH, and to derive recommendations for clinical practice. Diagnosis ofMIHMIH is the diagnosis of developmental defects characterised by qualitative enamel mineralisation changes. MIH defects range from white to yellowish or brownish opacities of the enamel. If defects can be demarcated from the healthy enamel, the disturbance is classified as MIH. Since demarcated opacities might also be caused by dental trauma or as sequence of apical inflammations of the deciduous teeth, differential diagnosis is needed. Diffuse opacities, on the other hand, are frequently discussed as a cause of high fluoride exposure (dental fluorosis) and should not be misclassified as MIH.Quantitative enamel defects (hypoplasia) are characterised by a reduction in the normal enamel thickness. In the case of MIH, pre‐eruptive enamel breakdown or less‐devel-oped hypoplastic and hypomineralised enamel can be diagnosed in a distinct number of cases. Post‐eruptive enamel breakdown, on the other hand, only occurs in association with functional loading. The occlusal surfaces of the (first) permanent molars are predisposed to post‐eruptive enamel breakdown and may show signs of disintegration immediately after tooth eruption. Clinically, differentia-tion between mild (Figure 7.1.2), moderate 7.1Molar–Incisor HypomineralisationJan Kühnisch1 and Roswitha HeinrichWeltzien21 Department of Conservative Dentistry and Periodontology, LudwigMaximiliansUniversity, Munich, Germany2 Department of Preventive and Paediatric Dentistry, Jena University Hospital, Jena, Germany 7.1 Molar–Incisor Hypomineralisation258(Figure7.1.3) and severe (Figure7.1.4) enamel defects with dentin exposure is possible. The main clinical sign is hypersensitivity of the affected teeth to thermal, chemical and mechanical stimuli (Jälevik and Klingberg, 2002; Weerheijm, 2004). Hypersensitivity often makes adequate daily oral hygiene of hypomineralised teeth difficult, leading to an increased risk of caries in these teeth and these patients.Different definitions are used for the diagnosis of MIH today. The most common one, favoured by the European Academy of Paediatric Dentistry (EAPD), involves the use of index teeth (Weerheijm et al., 2003; Lygidakis etal., 2010). At least one first per-manent molar must be affected by hypomin-eralisation in order to establish the diagnosis of MIH. However, this definition has been criticised for various reasons. First, it is based (a) (b)Figure 7.1.1 Hypomineralisation on (a) an occlusal and (b) a smooth surface without enamel breakdowns.(a) (b)Figure 7.1.2 Mild, small‐sized enamel breakdown on (a) a hypomineralised occlusal surface and (b) a smooth surface. Diagnosis ofMIH259solely on an empirical assumption that has yet to be validated (Weerheijm etal., 2001). Second, the occurrence of enamel defect is related to the exposure time, which can be variable. The implications for clinical practice are that, ultimately, all teeth of both denti-tions can be affected, and index tooth‐based diagnosis leads to underestimation of the true prevalence of MIH. Therefore, a shift from using index teeth to tooth‐ and tooth‐surface‐related registration of demarcated opacities, enamel breakdowns, atypical resto-rations and tooth extractions due to MIH is recommended (Kühnisch etal., 2014a). This methodological approach is comparable to the well‐accepted dmf/DMF index.(a) (b)Figure 7.1.3 Moderate, medium‐sized enamel breakdown on (a) a hypomineralised occlusal surface and (b) a smooth surface.(a) (b)Figure 7.1.4 Severe enamel breakdown on (a) a hypomineralised occlusal surface and (b) a smooth surface. Due to the extensive disintegration of hard tissue, dentin is exposed. 7.1 Molar–Incisor Hypomineralisation260 Aetiology ofMIHBoth systemic and local factors seem to play a key role in the development of MIH or hypoplasia (Crombie etal., 2009; Alaluusua, 2010). There is consensus that systemic damage of the ameloblast cells must occur during tooth development. Various factors are discussed in the literature. These include exposure to the environmental contaminants bisphenol A (BPA) and dioxin, early child-hood infections, antibiotic medications in early childhood, oxygen deficiency during childbirth, decreased serum vitamin D levels (Kühnisch et al., 2015), and disorders of calcium or phosphate metabolism. However, the exact etiologic chain of MIH is still unknown (Crombie et al., 2009; Alaluusua, 2010; Kühnisch etal., 2014b). Prevention ofMIHIn view of the lack of an evidence‐based proof of the aetiological chain of MIH, there is currently no effective approach to its prevention. This underscores the need for further efforts to identify the causes of this enamel disorder. Noninvasive Dental Care ofMIH‐Affected TeethIn clinical practice, the most common feature of MIH is off‐white to yellowish brown areas of hypomineralisation/opacity without enamel breakdown (Figure7.1.1), associated with a varying degree of hypersensitivity. These teeth generally require no restorative treatment and should receive “classical” caries prevention measures, such as topical fluoride (Hellwig et al., 2013) and fissure sealant application (Kühnisch etal., 2017). The aim of topical fluoride application is to (re)mineral-ise hypomineralised tooth surfaces. Fluorides also help to counteract the problem of hyper-sensitivity. Sealants are applied to protect pits and fissures on molars affected by MIH. Recently, the use of (nano)hydroxylapatite products to stabilise enamel surfaces and MIH-related enamel/dentin breakdownDentin-Pulp complex& Endodontic therapyPatient’ s cooperation& AnalgesiaOperativedental careVital pulpCooperativeRestorableUncooperativeLocal anaesthesiaUnrestorableIndirect restorationExtractionSedationGeneral anaesthesiaOutpatient dental careMinimal invasive dental careDirect restorationReversible pulpitisIrreversible pulpitis NecrosisPulp protectionPulpotomyRoot canal treatmentFigure 7.1.5 Influencing factors and possible treatment options in MIH‐related tooth defects. Restorative Dental Care261reduce hypersensitivity in teeth with MIH defects has been suggested. However, scien-tific studies of this approach are lacking. In regard to casein phosphopeptide (CPP)‐ and amorphous calcium phosphate (ACP)‐containing products (GC Toothmousse, GC Europe, Leuven, Belgium), Baroni and Marchionni (2011) reported that their use led to clinical improvement of the enamel struc-ture and clinical symptoms of MIH. The use of a product containing calcium carbonate and arginine (Elmex Sensitive Professional, CP GABA, Hamburg, Germany) also led to a decrease in hypersensitivity (Bekes et al., 2017). However, the effects of topical products can only be expected on the outer enamel sur-face, and complete repair of hypomineralised enamel is still not possible. Another empirical observation in this context is that the initial hypersensitivity after tooth eruption decreases over the course of dentin maturation and tooth development in many cases.Another aspect is that, when the vestibu-lar surfaces of permanent anterior teeth are affected, patients frequently complain of impaired aesthetics (Fayle, 2003; Lygidakis, 2010; Lygidakis etal., 2010). A micro‐inva-sive infiltration technology (ICON, DMG America, Hamburg, Germany) has been pro-posed as a treatment option for these cases. However, the success rates achieved in the few studies conducted to date are heteroge-neous (Crombie et al., 2014; Kumar et al., 2017), meaning that infiltration treatments for MIH do not always result in satisfactory aesthetic results. Therefore, a restrictive approach to establishing the indication for these treatments is currently recommended. Restorative Dental CareIf enamel breakdown has occurred, restora-tive treatment measures may be indicated (Lygidakis et al., 2003, 2010; Mejare et al., 2005). Whilst monitoring of teeth with mini-mal enamel defects is recommended, direct fillings are indicated for those with moderate to severe enamel breakdown. Indirect restora-tions are a treatment option, particularly in posterior teeth with extensive enamel defects. Adhesively bonded restorations are prefer-entially used in all cases. Restorability and the absence of pulpitis symptoms are crucial to preserving hypomineralised teeth via the direct‐filling technique. Direct restorations are also indicated in patients with extensive dentin exposure, associated with hypersensi-tivity and pain during chewing or the perfor-mance of daily tooth brushing. In these cases, the treatment goals are to preserve chewing function, prevent endodontic complications and promote the healing of any reversible pulpitis. However, in making the decision to restore, the dentist must meet the require-ments for long‐lasting, high‐quality dental restorations, which is necessary to avoid costly and time‐consuming repeat treatments and maintain the child’s ability to cooperate. From the perspective of materials science, the use of adhesively bonded composite materials is preferred. Because these cavities do not offer much retentiveness but are occlusion‐ bearing, the use of amalgam and glass ionomer cements (GICs) should be restricted.There are clinical limitations on the direct restorability of multisurface enamel defects with composite materials, especially in the posterior region. Although the placement of multisurface, occlusion‐bearing composite fillings is technically possible, it must be borne in mind that the probability of partial or complete loss increases with increasing restoration size. Therefore, indirect restora-tions represent a functional and long‐lasting treatment alternative in cases with complete (or near‐complete) involvement of the occlusal surface (Manhart etal., 2004). The strategic importance of the (first) permanent molars to dentition development and masti-catory function justifies this approach. Today, indirect restorations are recommended for the treatment of hypomineralised molars (Koch and García‐Godoy, 2000; Feierabend etal., 2012). The main advantages of placing indirect restorations are that tooth prepara-tion can be performed (congruent to the margins of hypomineralised defects in an enamel‐preserving manner) and no additional retention is needed. 7.1 Molar–Incisor Hypomineralisation262The clinical and laboratory effort required for indirect restoration is high, however, and often exceeds the paediatric or adolescent patient’s ability to cooperate. The availability of chairside dental CAD/CAM technologies that enable the rapid production of indirect res-torations in a single appointment (Wittneben et al., 2009) is increasingly challenging the dogma that indirect restoration is contraindi-cated in children and adolescents. As with the treatment of adults, it requires good cooperation on the part of the patient or the use of general anaesthesia (Pfisterer et al., 2016). Although long‐term data on the pro-posed treatment in children and adolescents are currently unavailable, the clinical experi-ence gained in similar case studies suggests that it has a good long‐term prognosis (Millet etal., 2015; Zimmermann etal., 2016).From our point of view, prefabricated stain-less‐steel crowns, which are commonly used in paediatric dentistry, should no longer be a treatment option in MIH‐affected molars. Although easy to perform, non‐technique‐sensitive, long‐lasting and protective against further enamel fractures and defects (Zagdwon etal., 2003; Kotsanos etal., 2005), this approach has major disadvantages when it comes to performing later indirect restoration. Whilst teeth need to be prepared tangentially for stainless‐steel crowns, the preparation margins usually run subgingival to the interproximal surfaces. This substantially restricts the adhesive placement of definite indirect resto-rations. Therefore, we believe that placement of prefabricated crowns should only be per-formed on permanent teeth without any circumferential preparation, which increases the risk of overhanging crown margins. Periodontal complications due to non‐indi-vidualised crown margins have also been described (Guelmann etal., 1988). Overhanging crown margins might possibly impede the eruption of adjacent teeth. Moreover, many patients (and their parents/guardians) find the aesthetic unsatisfactory. Because of these disadvantages, prefabricated crowns for res-toration of the permanent dentition should be used in a restrictive manner. Cavity PreparationThe issue of whether and to what extent the removal of structurally damaged enamel is necessary is a matter of discussion. The answer will depend on the size of the defect and the cooperation of the paediatric patient. In many cases, hypomineralised enamel is stable enough to withstand the mechanical forces of mastication in spite of its defects. This means that it is not necessary to remove all of the hypomineralised enamel, and a defect‐related approach should be routinely used, particularly in paediatric patients. Therefore, small to medium‐sized defects can often be treated using a non‐ or minimally invasive cavity preparation followed by adhe-sive restoration management. When treating larger defects with dentin involvement, it is important to design a sufficiently contoured cavity in order to reduce the risk of partial or total losses. From the clinical perspective, both the removal of hypomineralised hard tissue and the location of the cavity margins in sound enamel play an important role. If an indirect restoration is to be used, strict adher-ence to the aforementioned preparation prin-ciples is crucial. Treatment oftheDentin–Pulp ComplexExtensive enamel loss on dentin exposure due to MIH may be comparable to (deep) dentinal caries where microbial infection and dentinal destruction occur, leading to similar responses of the dentin–pulp complex (Rodd et al., 2007). Moreover, the risk of pulpitis increases as infectious processes progresses towards the pulp. Clinical key features are thermal hypersensitivity of the teeth and pain during food intake. Whilst reversible inflammation signs dominate in the initial stages, the risk of an irreversible pulpitis or pulp necrosis increases as the disease spreads, or where it is located near the pulp. Spontaneous and nocturnal complaints are clinical key markers of an irreversible Treatment oftheDentin–Pulp Complex263inflammatory process. This must be distin-guished from teeth with percussion and biting sensitivity, which are associated with apical periodontitis.Regarding the diagnostic spectrum of the disease, two treatment strategies should be discussed (Figure7.1.6). In case of reversible inflammation, protection of the dentin–pulp (a) (b)(c)(d)(e)(f)Figure 7.1.6 Clinical management of a moderate enamel breakdown on an occlusal surface over an observation period of 13 years. Just after (a) tooth eruption, (b) an enamel disintegration was diagnosed, which was covered with (c) an adhesively bonded flowable composite restoration. Nearly 1 year later, the restoration was(d) worn and had to be (e) repaired. The clinical situation at the ages of (f) 11, (g) 12, (h) 13, (i) 14 and (j)19 years was basically stable. Nevertheless, the composite restoration was renewed at the age of 14 (i). 7.1 Molar–Incisor Hypomineralisation264complex is the primary focus of clinical attention. This is achieved by removing the bacterial biofilm and sealing the cavity with a restoration (Kidd, 2004). The range of treatment options may also include direct pulp capping or pulpotomy, particularly in teeth with incomplete root growth. If the history and clinical examination show signs of irreversible pulpitis, pulpal necrosis or apical periodontitis, trepanation, cleaning, irrigation, disinfection, shaping and tempo-rary or permanent filling of the root canal system is indicated. Especially in such cases, tooth extraction followed by orthodontic space closure may be justified from a prag-matic point of view, as the prognosis of the tooth is difficult to assess in children and adolescents. Extraction andOrthodontic Space ClosureExtraction followed by orthodontic space closure is a further treatment option for MIH‐affected molars (Jälevik and Möller, 2007). In the authors’ opinion, extraction should be limited to individual cases, since it is always associated with extensive follow‐up measures, which may require general anaesthesia in pae-diatric patients and pose additional challenges to the patient’s family, dentist and ortho-dontist. Indications for extraction include molars with extensive destruction and endo-dontic complications like apical periodontitis. Orthodontic aspects (e.g. dental crowding) and the age of the patient also play a role in the indi-cation for extraction. Ideally, a first permanent (g) (h)(i)(j)Figure 7.1.6 (Continued) References265molar should not be extracted until immedi-ately before the eruption of the second perma-nent molar, in order to prevent possible growth inhibition associated with early extraction (Eichenberger et al., 2015). This approach allows physical mesial migration of the second permanent molar. For these reasons, the cor-rect timing of tooth extraction can significantly promote the orthodontic space‐closure proce-dure. However, this strategy generally requires temporarily preservation of the affected tooth until the time of extraction. In routine clinical practice, this means that patients must receive adequate restorative treatment and probably even temporary endodontic care between the ages of 6 and 11 years. Interim Management until Adolescence or AdulthoodWhen children of early school age first present with MIH, tooth‐related problems such as hypersensitivity and marked enamel defects are at the forefront of treatment. Both factors affect the ability to cooperate during restorative treatment (Jälevik and Klingberg, 2002). In cases with a correctly established treatment indication and prognosis, experi-ence has shown that simple measures are more successful. More invasive and challeng-ing treatments can then be postponed until adolescence, when the patient is better able to cooperate. Coverage of enamel defects with universal adhesive and (flowable) com-posite without tooth preparation is an effec-tive simple measure to achieve defect sealing and hypersensitivity reduction. These resto-rations may be more prone to wear, which is a disadvantage of the simplified procedure. As a rule of thumb, it can be said that the risk of repeated restoration increases proportionally with the defect size and occlusal stress. Based on clinical experience, early definitive treat-ment seems more advisable in case of children and adolescents with extensive or multisur-face enamel defects, and compromise treat-ments consisting in temporary solutions are not recommended. This is supported by the observation that repeated dental treatments exhaust the patient’s ability to cooperate, so that, ultimately, rehabilitation can only be achieved under general anaesthesia. Thus, providing adequate pain relief and establish-ing a treatment plan that takes into account the patient’s cooperation are important facets of patient management during early dental treatment (Figure7.1.6). Implications forDental PracticeThe concepts presented in this chapter illus-trate the challenges and limitations of the available treatment options for the manage-ment of children and adolescents with MIH (Figure7.1.6). Since effective local anaesthesia is often difficult to achieve, sedation or general anaesthesia is required in order to perform extensive invasive treatment procedures in paediatric patients with limited ability to coop-erate. Direct adhesive restoration is the tooth‐conserving treatment of choice for teeth with mild to moderate enamel breakdown. In cases of hypomineralisation with severe enamel and dentin defects, the dentist may choose between an adhesive and an indirect restoration. The latter can help lengthen restoration cycles and improve the cooperation and quality of life of affected children and adolescents. The extrac-tion of MIH‐affected molars with subsequent orthodontic space closure is reserved for teeth with extensive destruction of the clinical crown and is relatively rarely indicated. ReferencesAlaluusua, S. 2010. Aetiology of molar‐incisor hypomineralisation: a systematic review. European Archives of Paediatric Dentistry, 11, 53–8.Baroni, C., Marchionni, S. 2011. MIH supplementation strategies: prospective clinical and laboratory trial. Journal of Dental Research, 90, 371–6. 7.1 Molar–Incisor Hypomineralisation266Bekes, K., Heinzelmann, K., Lettner, S., Schaller, H. G. 2017. Efficacy of desensitizing products containing 8% arginine and calcium carbonate for hypersensitivity relief in MIH‐affected molars: an 8‐week clinical study. Clinical Oral Investigations, 21(7), 2311–17.Crombie, F., Manton, D., Kilpatrick, N. 2009. Aetiology of molar‐incisor hypomineralization: a critical review. International Journal of Paediatric Dentistry, 19, 73–83.Crombie, F., Manton, D., Palamara, J., Reynolds, E. 2014. Resin infiltration of developmentally hypomineralised enamel. International Journal of Paediatric Dentistry, 24, 51–5.Eichenberger, M., Erb, J., Zwahlen, M., Schätzle, M. 2016. The timing of extraction of non‐restorable first permanent molars: a systematic review. European Journal of Paediatric Dentistry, 16, 272–8.Fayle, S. A. 2003. Molar incisor hypomineralisation: restorative management. European Journal of Paediatric Dentistry, 4, 121–6.Feierabend, S., Halbleib, K., Klaiber, B., Hellwig, E. 2012. Laboratory‐made composite resin restorations in children and adolescents with hypoplasia or hypomineralization of teeth. Quintessence International, 43, 305–11.Guelmann, M., Matsson, L., Bimstein, E. 1988. Periodontal health at first permanent molars adjacent to primary molar stainless steel crowns. Journal of Clinical Periodontology, 15, 531–3.Hellwig, E., Schiffner, U., Schulte, A. 2013. S2k‐Leitlinie: Fluoridierungsmaßnahmen zur Kariesprophylaxe. Available from http://www.awmf.org/leitlinien/detail/ll/083‐001.html (last accessed 30 January 2019).Jälevik, B., Klingberg, G. A. 2002. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralization of their permanent first molars. International Journal of Paediatric Dentistry, 12, 24–32.Jälevik, B., Möller, M. 2007. Evaluation of spontaneous space closure and development of permanent dentition after extraction of hypomineralized permanent first molars. International Journal of Paediatric Dentistry, 17, 328–35.Kidd, E. A. M. 2004. How “clean” must a cavity be before restoration? Caries Research, 38, 305–13.Koch, M. J., García‐Godoy, F. 2000. The clinical performance of laboratory‐fabricated crowns placed on first permanent molars with developmental defects. Journal of the American Dental Association, 131, 1285–90.Kotsanos, N., Kaklamanos, E. G., Arapostathis, K. 2005. Treatment management of first permanent molars in children with molar‐incisor hypomineralisation. European Journal of Paediatric Dentistry, 6, 179–84.Kühnisch, J., Heitmüller, D., Thiering, E., Brockow, I., Hoffmann, U., Neumann, C., etal. 2014a. Proportions and extent of manifestation of molar‐incisor‐hypomineralisations according to different phenotypes. Journal of Public Health Dentistry, 74, 42–9.Kühnisch, J., Mach, D., Thiering, E., Brockow, I., Hoffmann, U., Neumann, C., etal. 2014b. Respiratory diseases are associated with molar‐incisor hypomineralizations. Swiss Dental Journal, 124, 286–93.Kühnisch, J., Thiering, E., Kratzsch, J., Heinrich‐Weltzien, R., Hickel, R., Heinrich, J., etal. 2015. Elevated serum 25(OH)‐vitamin D levels are negatively correlated with MIH. Journal of Dental Research, 94, 381–7.Kühnisch, J., Reichl, F. 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