Molar Incisor Hypomineralization (MIH): Conservative Treatment Approach  

Dental News Volume XXIV, Number I, 2017

Dr H. Ouertani – Assistant Professor, Department of Dental Medicine, Military Principal Hospital of Instruction, Tunis, Tunisia

Pr S. Marouane – Professor, Department of Dental Medicine, Military Principal Hospital of Instruction, Tunis, Tunisia

Pr L. Bhouri – Professor, Department of Restorative Dentistry and Endodontics, Dental Clinic, Monastir, Tunisia

Pr MB. Khattech – Professor, Department of Dental Medicine, Military Principal Hospital of Instruction, Tunis, Tunisia

Abstract

Molar Incisor Hypomineralization (MIH) is defined as a hypomineralization of systemic origin of one to four permanent first molars, frequently associated with similarly affected permanent incisors. The affected molars are related to major clinical problems in severe cases. Clinically, MIH includes the presence of demarcated enamel opacities, post eruptive breakdown due to soft and porous enamel and atypical restoration. Early diagnosis is very important due to the risk of rapid breakdown of tooth structure.

The early intervention is essential; it includes monitoring, preventive treatment to help in remineralization of the hypomineralized enamel and in some cases restoration with resin composite.

The late or the improper diagnosis can result in mismanagement of the defect, tooth sensitivity to cold air and hot water, rapid development of dental caries, pulpal inflammation, enamel and restoration breakdown and early loss of affected first permanent molars. The high prevalence of MIH indicates the need for more research to clarify etiological factors.

The purpose of this article was to describe the diagnosis information, prevalence, etiological factors of the MIH for a better knowledge of this phenomenon and to illustrate its clinical management.

Molar Incisor Hypomineralization (MIH), Enamel hypomineralization, Tooth abnormalities, Aetiology, Diagnosis, Clinical management

Introduction

In spite of dental caries is strongly influenced by social, economic, cultural, religious and environmental factors, its severity may be increased by structural changes of enamel/dentin such those observed in cases of Molar Incisor Hypomineralization (MIH) (Márcia et al, 2012).

In the literature, MIH is also known as non-fluoride enamel opacities, internal enamel hypoplasia, non-endemic mottling of enamel, opaque spots, idiopathic enamel opacities and idiopathic enamel hypomineralization. ^{10, 17}

This condition is due to disrupted ameloblastic function during the transitional and maturational stages of amelogenesis. ^{11, 13}

MIH was defined in 2001 by Weerheijm; it describes the clinical picture of enamel hypomineralization of systemic origin. Affecting one to four permanent first molars and frequently associated with permanent incisors. ^{1, 2, 3, 4, 11, 12, 13, 16, 17, 21}

Molars are always affected by this phenomenon and often we can find a combination of molars and demarcated opacities of the involved incisors. ¹²

Even though MIH is defined as a chronological and general disturbance, the number of permanent first molars and the degree of hypomineralization varies extensively. (Fagrell, 2011)

We should also notice that if the opacities are only on the incisors, it may indicate another origin of the defect different from MIH. ¹²

MIH is one of the forms of structural abnormalities during tooth development, also referred as tooth dysplasia. (Rossitza et al, 2012)

In the Netherlands, the term of “Cheese Molar” has been used to describe this enamel defect. ¹⁰

The main clinical characteristics of the MIH are: demarcated opacities, posteruptive breakdown and atypical restorations. ¹⁴

Referring to Fagrell in 2011, enamel in teeth affected by MIH exhibits disorganized enamel prisms, a porous structure and loosely packed crystallites.

The European Academy of Paediatric Dentistry (EAPD) organized, in Helsinki in May 2009, an Interim Seminar and Workshop concerning the MIH. It was revealed that there are only a limited number of evidence based research papers on this subject. ⁷

The world prevalence of MIH ranges from 2.4% to 40% (Fragelli et al, 2015). Referring to the European Academy of Paediatric Dentistry (EAPD), the MIH is classified as mild or severe. This classification depends on the extension of the defect and on the complexity of the treatment required. ¹⁴

Treating the MIH has some challenges such as sensitivity, increased risk of plaque accumulation, unexpectedly rapid development and progression of caries, inability to anaesthetize, pulpal inflammation (due to the porosity of the enamel), difficult cooperation of the young patient (dental fear and anxiety), severe discomfort, repeated marginal breakdown of dental restorations and unpredictable behavior of apparently intact opacities. ^{1, 4, 5, 13, 14, 15, 17, 20}

These co-morbidities (dentine hypersensitivity, aesthetic concerns, caries and oral hygiene) are capable of impacting negatively on the quality of life of the children. (Oyedele et al, 2015) Several aetiological factors are mentioned as the cause of MIH and they are frequently associated with childhood diseases or nutritional conditions during the first three years of life. (Márcia et al, 2012)

• Treatment approach of MIH depends on some factors: ^{5, 9}

– Extension and severity of the defect

– Degree of tooth eruption

– Occlusion

– Child’s compliance

– Oral hygiene /Motivation

– Extent of treatment recommended

– Prognosis of the teeth affected

– Financial cost

– Diet habits …

• Management options of MIH: ⁸

– Early diagnosis +++

– Caries risk management,

– Remineralization therapy,

-Restorations (composite restorations, crowns…)

– Veneers for anterior teeth…

Strategies for correct diagnosis, treatment plan and possible prevention attitude are recommended. ¹²

MIH Diagnosis

First of all, for an appropriate clinical evaluation, we should clean carefully the four first permanent molars and the eight erupted permanent incisors. They should be wet for an accurate examination (opacities…). ^{1, 5}

The age of eight years is considered the appropriate age for diagnosing MIH because all permanent first molars and majority of permanent incisors are erupted at this age. ^{5, 11, 13, 19}

To diagnose MIH, at least one first permanent molar has to be affected (Lygidakis et al, 2010).

Clinical characteristics of MIH are:  demarcated opacities (altered enamel translucency, variable in degree) of different colour, post-eruption breakdown, atypical restorations, and extracted first permanent molars due to MIH. ^{1, 12, 14, 17} The porous opacity of the hypomineralized enamel can be white, yellow or even brown. ^{2, 4, 5, 12, 11, 17, 20, 22}

The borders of opacity are well-defined and different from healthy and adjacent enamel.  ^{2, 3, 6}

Most of the time, opacities are limited to the incisal or cuspal one third than the cervical one third. ¹

In general, the enamel defects in the incisors are milder than in molars due to the absence of chewing forces. ^{3, 10, 17} Frequently, in the affected molars restorations are extended to the buccal or palatal smooth surface. ^12,17

Enamel opacities may occur adjacent to restoration margins. (William et al, 2006) The hypomineralized enamel looks soft, porous and has the appearance of discolored chalk or Old Dutch cheese. ^{3, 4, 11, 17, 21}

The breakdown of teeth affected by MIH can occur just after eruption in case of significant porosity of the opacity ^{2, 3}. The loss of porous and brittle enamel can be the result of masticatory forces. ^{3, 4}

Consequences are dentin exposure, tooth sensitivity and an unexpectedly rapid caries development.^2,5

Tooth hypersensitivity is a common problem resulting from MIH, leading to poor oral hygiene, eating difficulty and compromising the affected teeth. ⁹

The yellow and brown opacities present as microscopically porous, with a higher clinical risk of breakdown than that of the white opacities. (Fragelli et al, 2015)

The creamy-white opacities are present in the internal part of the enamel. ¹⁰

The severity of the defect can be clinically evaluated through the stained degree of MIH enamel. ⁵

The young patient history should be investigated to determine possible etiological factors. ¹

There is a difference in the severity of the MIH between patients and even in the same mouth since not all the permanent first molars can be affected with the same degree of extension. ³

Within one patient, intact opacities can be found on one molar; while in another molar large parts of the enamel break down soon after eruption. (Weerheijm et al, 2004)

Where there are more molars and incisors affected the more severe is the defect. (Lygidakis et al, 2010)

The risk of affected upper incisors is increased with more affected first permanent molars. ^{4, 10, 11, 17}

The absence of first permanent molars in a healthy dentition associated to the presence of demarcated opacities on the incisors is suspected for MIH. ^{12, 17}

Young patients may complain about the unesthetic appearance of their affected incisors.⁵

The bonding to enamel is difficult and risky in such case, because of the prismatic morphology in the porous enamel is altered; as a result the loss of the defective restoration and frequent re-treatments. ^{17, 20}

There are two forms of severity of MIH that should be recorded by the clinician to help for the clinical management.In the mild form, we find demarcated enamel opacities, absence of enamel breakdown, presence of occasional tooth sensitivity and mild aesthetic concerns on discoloration of the incisors. ^{7, 14}

The characteristics of the severe form are: demarcated enamel opacities with post-eruptive enamel or enamel and dentine breakdown, caries, persistent/spontaneous hypersensitivity, restorations with atypical shape, extension or even extractions and strong aesthetic concerns. ^{7, 14}

It is imperative to identify the early diagnosis, associated problems to MIH and to explain them to the parents and the young patient. ³

Differential diagnosis

There are different enamel abnormalities that can be confused with MIH.

quantitative defect (deficient enamel matrix formation) due to disruption of the secretory phase during ameloblast function. In such case, the thickness of the enamel is reduced. ^1,3                                                                                                                       Referring to Márcia et al. in 2012, in case of enamel hypoplasia, the enamel can be partially present or totally absent, presence of white colored lesions that are symmetrical or isolated, presence of vertical or horizontal grooves and deep fissures, presence of smooth edges associated to adjacent normal enamel.

AI is defined as clinically and genetically heterogeneous group of condition, affecting the appearance and the structure of the enamel of all or approximately all dentition.  It is  sometimes associated  with other dental, oral and extraoral tissues.  The degree of severity is different in the same mouth. ²³ In case of AI, the pathology affects all dentition, the family history is usually involved and the radiographic examination can reveal taurodont teeth. ¹¹ All teeth are affected with the generalized opacities. ⁵ The permanent first molars are equally affected and imitative of appearance of Amelogenesis imperfecta only in severe cases of MIH. ^{4, 11}

Dental fluorosis is a development disturbance of enamel that is characterized by increased porosity and lower mineral content. It is caused by the repeated exposure of the patient to important concentrations of fluoride during tooth development.²⁴ The fluorosis is considered as caries resistant due to the structure of enamel and opacities are diffuse. However, in MIH opacities are well demarcated and caries prone. ^{4, 11}

The number of teeth affected with fluorosis is related to the time of exposure. ¹¹

White spot lesions represent areas of demineralized dental enamel and it is usually due to prolonged plaque accumulation and colonization of aciduric bacteria. Any tooth surface can be involved especially when the microbial biofilm can develop and remain a long period such as during orthodontic therapy. ²⁵ The absence of treatment of white spot lesions will lead to the development of cavitated caries. ²⁵

Prevalence of Molar Incisor Hypomineralization (MIH)

Referring to the literature, the prevalence figures range from 3.6 % to 25%. ^{3, 4, 5, 6, 21}

Márcia et al in 2012 indicated that according to the results of recent studies the prevalence of the defect is between 3.5 % and 40.2%.

Most of the epidemiological studies about MIH were conducted in European countries. ^{3, 5, 20, 21}

In Jeddah, the prevalence of MIH in 8–12-year-old patients was 8.6%. ¹⁷

In Ankara Turkey, the prevalence of MIH in a group of 4,018 children was 7.7% and researchers also find that severity of lesions increased with age. ¹⁹

A study of Ahmadi et al in 2012, showed a prevalence of 12.7% for MIH in a group of Iranian children. ²⁰

The prevalence of MIH was 20.4% among Brazilian schoolchildren aged 8 and 9 years. ¹⁸

It gives the impression to differ between countries, birth cohorts, criteria used in the diagnosis and methodological differences. ^{4, 18, 21}

For the same patient, the number of affected first permanent molars varies from 1 to 4, involving especially 2 or more molars including the controlateral tooth. ¹

The more first permanent molars affected, the higher risk of affected permanent incisors. ^{4, 10, 11, 17}

Etiological factors associated to MIH :

Although MIH causes are still unclear and difficult to identify, some factors have been associated with this enamel defect.

The causative factors suggested by some authors are systemic conditions and environmental insults that influence natal and early post natal development. ^{1, 11}

There is a relationship between health problems occurring during pregnancy, environmental factors and MIH. ² During the perinatal period, factors that can contribute to MIH are hypoxia, hypocalcaemia and preterm birth. ^{15, 16}

Children with poor general health in the first years of life are believed to be more likely to be affected by more severe MIH. ^{6, 19}

When the young patient had more than one medical problem in his childhood, it would be very difficult to determine the etiological factors. ¹

Referring to Allazzam et al. in 2014, higher percentage of children with MIH had histories of illnesses during the first four years of their childhood.

Referring to William et al. in 2006, conditions common in the first 3 years, such as upper respiratory diseases, asthma, otitis media, tonsillitis, chicken pox, measles, and rubella, appear to be associated with MIH.
The use of antibiotic is also suggested to be involved in this disease. ^{1, 3, 4, 7, 10, 14, 16, 19, 20} There is about a 2-fold increase in risk of MIH if amoxicillin is used in the first year of life. (Lygidakis et al. 2010)

Other possible causes suggested are: environmental conditions, premature birth, perinatal complications, exposure to dioxine by prolonged breast-feeding, respiratory diseases and oxygen shortage of the ameloblasts, calcium and phosphate metabolic troubles, oxygen starvation associated to low birth weight and febrile childhood diseases. ^{3, 4, 9, 10}

Vaccines administrated in an early age can be a cause of MIH. ⁴ An underlying genetic predisposition is mentioned to contribute to MIH development. ⁶ Actually, there is no evidence of relationship between genetic component and MIH. ⁷ Knowledge on causative factors can contribute to the identification of children who are more prone to this pathology and facilitate to establish a preventive treatment plan.

Management  Approach of MIH

The MIH may contribute to a large treatment need and the difference in treatment requirement is largely related to the affected teeth. ⁴ The treatment plan of MIH is composed of three levels (Preventive, Restorative and Rehabilitation) (Fig. 1)

The decision on which therapy should be used is difficult and is dependent upon on a number of factors such as the severity of the condition, patient’s dental age, the child/parent’s social background and expectation. ⁷

Dentist must explain the MIH pathology and the treatment options to the parent and child.

The prevention plan has a large importance in early post-eruptive stage when the affected tooth is further vulnerable to breakdown and caries attack. ⁷

When restorative treatment is indicated, the proper local anesthesia is obligatory and in some cases, it is difficult to obtain properly anaesthetized molars. ⁴

Cast restorations can be full coverage crown, tooth-colored crown, porcelains or veneers. And they are not advisable in early post-eruptive stage (large pulp size, short crown height…). ⁵

Restorative options include glass ionomer cements (GIC), resin-modified glass ionomer cements (RMGIC), polyacid modified resin composites (PMRC), resin composites (RC), amalgam, stainless steel crowns (SSCs), and indirect adhesive or cast onlays or crowns. (William et al, 2006) Concerning adhesive and fissure sealant for the posterior teeth that are important before breakdown occurs, Lygidakis et al. in 2010 suggested that higher retention rates could be achieved if a 5th generation bonding adhesive is applied prior to fissure sealant application. Composite restorations should be reviewed very frequently. Because more breakdown of the affected enamel can happen at the restoration margins. ⁹

In some cases, extraction of the severely affected molars with a poor long-term prospect, combined with orthodontic therapy, should be considered as an alternative treatment. ⁴

If the orthodontic condition were favorable, the ideal dental age for extracting the defective FPM would be 8.5-9 years of age so as to enable the second permanent molars to drift into the FPM position establishing an adequate occlusion. ⁷

The maintenance is very important. Dentist must monitor margins of restorations for post eruptive breakdown and should consider full coronal coverage restorations in the long term. ¹

Fig. 1: Flow chart illustrated by the authors of clinical management of MIH Children with a history of putative aetiological factors in the first 3 years should be screening at risk for MIH (Alaluusua, 2010, Crombie et al., 2009, Fagrell et al., 2011, Márcia et al., 2012) 5

A twenty two year old patient, who was unsatisfied with the appearance of his anterior teeth, was examined at the service of Dental Medicine and diagnosed with Molar Incisor Hypomineralization. Defined white non-transparent spots on the vestibular surfaces of the maxillary and mandibular incisors were clearly visible.

(Fig.2: a,b,c) The first permanent molars were restored with glass ionomer cements (GIC). (Fig.3: a,b,c)

The treatment plan was:  Microabrasion and restoration with resin composites (RC) of the maxillary and mandibular incisors. Concerning the first permanent molars, full coverage crowns were programmed. (Fig.4, Fig.5, Fig.6, Fig.7, Fig.8, Fig.9)

The maintenance was also programmed.

Fig. 4: Microabrasion of upper incisors. Fig. 5: Microabrasion of lower incisors.

Fig. 6: Result after Microabrasion procedure.

Fig. 7: Phosphoric acid etching (37%) of upper incisors.

Fig. 8: Phosphoric acid etching (37%) of lower incisors.

Fig. 9: Final aspect of the restorations (Patient’s teeth immediately after finishing and polishing procedures).

Case Report N°2:

Fig. 10: Initial view of the patient’s anterior teeth.

Fig. 11: Affected first permanent molars.

Fig. 12: Superficial elimination of the white stains with a diamond burr.

Fig. 13: Acid etching with 37% phosphoric acid.

Fig. 14: With a disposable brush, a resin adhesive is applied according to manufacturer’s instructions.

Fig. 15: Final aspect of the restorations.

Fig. 16: Initial patient’s smile. Fig. 17: Close view of the discolored anterior teeth (21, 32)

Fig. 20: Elimination of the yellow opacity of the tooth 21 by a Diamond Flame Burr.

Fig. 21: Aspect of the tooth 21 after the preparation.

Fig. 22: Elimination of the yellow opacity of the tooth 32 with the same diamond bur.

Fig. 23: Aspect of the tooth 32 after the preparation.

Fig. 24: Final aspect after restoration of the teeth 21 and 32 with Nanohybrid resin composite.

Fig. 25: Restoration of the tooth 36 with glass ionomer cements (GIC).