Molar-Incisor-Hypomineralisation (MIH) in Lebanon

4 (80%) 1 vote
banner

Molar-Incisor-Hypomineralisation (MIH) in Lebanon: A preliminary clinical observation

Dr. Mary Antoun, BDS, DU Oral Biol., Department of Esthetic and Restorative Dentistry

Dr. Paul Nahas, BDS, CES Oral Biol., CES Removable Prostho., CES Fixed Prostho., Cert. Immunopathol.,

Dr. Assaad Nasr, BDS, DESS Restorative Dent., Department of Esthetic and Restorative Dentistry

Dr. Hicham Mansour, BDS, DESS Endo., Department of Esthetic and Restorative Dentistry

Lebanese University, School of Dentistry

Journal of the Lebanese Dental Association Volume 49-N#2-December 2014

 

Abstract 

Hypomineralization of Incisors and Molars, known as MIH, is an enamel qualitative defect of systemic origin. Although studies were carried out in various countries, none of them was reported on the Lebanese population. The purpose of this preliminary clinical observation is to increase awareness of this disease within Lebanese and Arab dental communities, and to encourage dentists towards its early diagnosis and contemporary treatments (such as amelioration of oral hygiene, re-mineralization with fluoride, application of calcium and bio-available phosphate, and fissure sealant up to partial or total coverage in case of severe damage of tooth hard tissue).

Introduction 

MIH is a particular anomaly structure that has been described for the first time in the early 70s in Sweden 4. MIH 23,24,25 was defined by Weerheijm (2001) as”hypomineralisation of systemic origin of 1 to 4 permanent first molars, frequently associated with affected incisors”.

In the literature, MIH is also referred as “cheese molar” (Weerheijm et al., 2001), “idiopathic enamel hypomineralisation” (Fearne, Anderson, and Davis, 2004 – Koch et al., 1987), “non fluoride hypomineralisation in permanent first molars” (Leppaniemi, Lukinmaa, and Alaluusua, 2001), and “hypomineralised permanent first molars” (Jälevik and Norén, 2000).

MIH is a disease with uncertain etiology20. Unlike hypoplasia, which is a quantitative defect of enamel, MIH is characterized by a qualitative defect of systemic origin8; it affects one or more first permanent molars that are frequently associated with an affected incisor 15. MIH is responsible for severe dental pain in childhood and for the psychological impact caused by the obvious aesthetic consequences on incisors 8.

The structure abnormality may cause extensive tissue damage in absence of diagnosis and early care16.  Although no difference was reported in the prevalence between male and female genders17, the wide variation in prevalence (2.4% to 40.2%) is due to the difference in recording methods, indicators used, and different age or population investigated. In some countries, caries levels may mask the true prevalence of MIH 17. In order to establish easy comparison between different prevalence studies, the European Academy of Paediatric Dentistry (EAPD) defined criteria for diagnosing MIH, based on clinical observation of dried and cleaned dental tissue 4.

MIH treatment requires a genuine strategy to deal with several problems related to hypomineralization: hypersensitivity, rapid development of caries, difficulties during analgesia, and recurring failure of restorations leading to more limited child cooperation 16.

The majority of publications deal with the diagnosis and epidemiology of this disease; yet, few articles have discussed the protocol of action. The main objective of the treatment is to define a long term follow-up prophylaxis and an adapted restorative therapy for these patients 11.

Prevalence (Table 1) 

Many studies were conducted in various countries to highlight MIH prevalence in their populations. In 2010, Jälevik reviewed several well-documented studies assessing MIH prevalence. This review showed a very wide variation in the disease prevalence, worldwide: it ranged between 2.4% and 40.2%.

In European countries, it varies between 3.6% and 25%, and in East Asia, a single study reported a prevalence of MIH in Hong Kong to be around 2.8% in a sample of 2,635 children, with 12 years as a mean age (Cho, Ki, and Chu – 2008).

An Iraqi study (Ghanim, Morgan, Marino, Bailey, and Manton – 2011) showed a prevalence of 18.6% while a Jordanian one reported a prevalence of 17.6% in Jordanian children aged between 7 and 9 years (Zawaideh, Al-Jundi, and Al-Jaljoli – 2011).

More studies have also shown an increase in the prevalence of MIH over time: in Germany, it increased from 9.7 % in 1999 to 14.3 % in 200312. In Lebanon, no studies have been reported yet to determine its prevalence. Our limited clinical observations have shown variable severity between patients and between different teeth, within the same mouth.

Etiology 

TMIH is a multifactorial disease. Ameloblasts are very sensitive to lack of oxygen during their maturation phase. Hence, a premature infant may run the risk of sustaining amelogenesis process due to the lack of oxygen 11.

There are also environmental pollutants (“digoxin”) and contaminants that induce toxic effects and that are involved in the development and growth of embryo. Tooth would probably be an excellent model for the study of toxic effects because odontogenesis is very sensitive to environmental changes and may be at the origin of MIH20. A lack in vitamin D, calcium, a phosphocalcic metabolism disorder, many childhood diseases (mumps, German measles = rubella, bronchitis, asthma…), chronic renal failure, chronic digestive infection, malabsorption, and malnutrition can cause the appearance of MIH 20,22.

In addition, there may be a positive correlation between high fever and the development of MIH 11.

 

Differential diagnosis

MIH can be confused with many other dental diseases and it is essential to properly make our observation in order to correctly diagnose 11.
Diagnostic criteria 24 of MIH, set by the European Academy of Pediatric Dentistry -EAPD- (2003), are the following:

1- Presence of demarcated opacity
2- Post-eruptive enamel breakdown
3- Atypical restoration
4- Extraction of molar due to MIH
5- Delayed eruption of a molar or incisor.

Screen Shot 2017-02-20 at 5.30.38 PM

Differential diagnosis of MIH is made with the following dental pathologies:

Differential diagnosis of MIH is made with the following dental pathologies:

1. Amelogenesis imperfecta

Is a hereditary quantitative defect of enamel affecting all teeth (temporary and permanent dentitions). It is sometimes associated with a qualitative defect. This condition is characterized by impairment of enamel, which modifies the shape and volume of teeth. Early attrition leads to the following consequences: incisors and canines lose their edges, while molars lose their cusps 20.

According to Weerheijm (2004), amelogenesis imperfecta differs from MIH by:

•   Diffuse and symmetrical opacities;

•   Higher number of affected teeth;

• Possible radiographic pre-eruptive detection through taurodontism* (for certain forms of amelogenesis imperfecta) 3,20.

2. Dentinogenesis imperfecta

Is a hereditary pathology of dentin, not enamel, which constitutes the main difference with the MIH. It affects temporary and permanent teeth.

All teeth are opalescent, ranging from blue to brown. Teeth often have constriction marking the corono-radicular junction, and radiographically, roots are thin, with an obliteration of pulp chamber. Teeth are relatively resistant to decay 5,19,20.

* Taurodontism = a developmental anomaly characterized by a vertical enlargement of pulp chamber and a shortening of roots (taurodontism is mostly observed in human molars).

3. Regional odontodysplasia 20

It is a non-hereditary anomaly of dental hard tissue characterized clinically by radioopacites affecting dentitions of maxilla and mandible. Radiographically, the contrast of enamel and dentine is decreased (less radiopaque than normallly). Histologically, areas of hypocalcification are combined with irregular direction of enamel prisms, as well as fibrotic dentin 7.

4. Hypoplastic enamel

This condition is common and comes in the form of macroscopic defects reaching a more or less extended surface of the tooth. It affects both dentitions, with higher frequency in permanent teeth. In case of general disorder, hypoplastic enamel symmetrically affects with hypoplasia all teeth of the same group.

Hypoplastic enamel differs from the MIH by:

– regular edges;

– symmetrical dental damage

– at least two teeth are affected

– possibly affects both dentitions.

5. Dental fluorosis (“mottled enamel”)

Chronic fluoride poisoning (dental fluorosis), reflects the effect of excessive ingestion during the first years of life.

Fluorosis differs from the MIH by:

– White flecks, or yellow, or brown spots or areas, scattered irregularly on the surface of the tooth

– the resistance of teeth against caries process

(initial stages).

6. Turner’s hypoplasia

Turner’s Hypoplasia presents with a thin enamel on permanent teeth. In extreme cases, enamel is almost absent. Turner’s tooth can be observed on incisors, canines, and premolars.
Enamel’s hypoplasia is the main feature, with sometimes a yellow deposit on cementum. It is thought to be caused by congenital syphilis, hypocalcemia, vitamin D deficiency, pre-term birth, and nutritional deficiencies.

7. Other non-hereditary or acquired disorders to be differentiated from MIH, include accidental trauma: due to accidental trauma that occurrs during temporary dentition, teeth deformation generally appears at the level of incisors, showing a deficit of mineralization and non-symmetrical but well-defined boundaries.
Teeth could be opaque, or even strongly marked by hypoplasia 11,20.

 

Therapy

A six step approach 25 to MIH management is suggested:

1- risk identificarion,

2- early diagnosis,

3- remineralization and desensitization,

4- prevention of caries and post-eruption breakdown,

5- restorations and extractions,

6- maintenance.

Severity of MIH lesions varies from one patient to another, and even in the same patient, from one tooth to another. Time, intensity, and duration of the disorder are responsible for the location and the severity of the disease 15.

Diagnosis should be done as early as possible because of the fragility of tooth hard tissues. This allows a rapid establishment of therapy before the evolution of decay 16.

Depending on the severity of hypomineralisation, different treatments may be implemented.

A- In case of minor damage, various treatments can delay the progression of the disease:

a. dietary precautions: food questionnaire allows to intercept harmful habits (nibbling, acids, sugars) and provide appropriate recommendations20;

b. good oral hygiene: in case of uncontrolled plaque acculmulation, new recommendations for oral hygiene should be established regarding the technique and the frequency of teeth brushing 16;

c. re-mineralization by brushing with a fluoride gel (~ 1%)6 or by an application of gel or fluorinated varnish in dental office 21,22;

(a, b and c are considered to be general recommendations).

d. application of calcium and bio-available phosphate that interacts with fluoride ions to create amorphous calcium-phosphate (CPP-ACP) on the surface of teeth, which releases calcium ions, fluorine, and phosphate for the re-mineralization creating more acido-resistant fluorapatites. The efficacy of this product remains uncertain and it should be confirmed by a wider panel of studies 20. CPP-ACP exists in different forms: topical cream for teeth with the tricalcium phosphate (3M ESPE, St. Paul, MN, USA), tooth mousse® (GC, Tokyo, Japan), and sugar free chewing gum (Recaldent®) 12. Studies from Bologna-Italy, published in March 2011, showed that calcium and phosphate casein improves mineralization, shape, and porosity of MIH affected teeth 1,4,8;

e. fissure sealing: using high viscosity glass ionomer (GC Fuji Triage® of Alsip, IL, USA, = a high -Fluoride- releasing glass ionomer, and, Riva Protect®, SDI, Southern Dental Industries of Australia = a glass ionomer fissure and tooth protector) can effectively seal the fissures and pits. In addition to its natural adhesion to dental tissues, it has a re-mineralizing action. On hypo-mineralized molars, the use of adhesive system promotes the retention of a resin for fissure sealant 20.

B- In case of moderate damage, hypo-mineralized tooth can be restored by taking into account the following factors:

• challenges of analgesia;

• reduction of child anxiety;

• determination of the quantity of affected enamel that will be cut and the borders of future restoration.

To manage analgesia difficulties, dentists should not hesitate to use loco-regional analgesia, especially for mandibular molars in anxious and difficult children.

Tooth restoration involves placing:

a. amalgam (unsuitable for MIH) 16,20

b. glass ionomer cement (GIC) 11,16:

GIC is interesting for dentinal alternatives or for transitional restorations (natural adhesion to enamel and dentin, leaching of fluorine). Addition of resin improves resistance to wear and fracture. GIC is not indicated for occlusal surfaces of hypo-mineralized molars 20.

Fillings of great extent, carried out with GIC, should be often replaced in a second phase with composite materials 14.

c. composite resin:

Composite resins are the material of choice for hypo-mineralized teeth, especially when preparation borders are supra-gingival, located on healthy or slightly porous enamel, and when restoration is affecting only one to two sides of the affected tooth. In all cases, etching time must be reduced and placing rubber dam is essential.

Among adhesive systems, self-etching systems are recommended 16,20.

 

Cases of MIH in Lebanon

Case 1: Moderate hypo-mineralization

Fig.1b. Spot of hypo-mineralizationat cusp level of a Maxillary molar (tooth 16).

 

Fig.2. Spots of hypo-mineralization on maxillary and mandibular incisors (teeth 21 and 41).

Fig.3. Old composite restorations on central incisors.

Case 2: Restorable severe Hypo-mineralization with decay

Fig.4. Buccal view of a mandibular molar (tooth 46).

Fig.5: Occlusal view of a maxillary molar with an open pulp chamber (tooth 26).

Fig.6a: Occlusal view of the right mandibular molar with x-ray (tooth 46).

Fig.6b: Occlusal view of the left mandibular molar with x-ray (tooth 36).

Fig.6c: Occlusal view of the left maxillary molar (tooth 26).

Fig.6d: Occlusal view of the right maxillary molar with arrested decay (tooth 16).

Fig.7: Severe MIH of the incisors with plaque and decay

C- In case of severe hypo-mineralization, advanced treatment is required with the pedodontic preformed caps (PPC) 11,16, or inlays/onlays and prosthetic rehabilitation for the final extraction of affected tooth 16. These extractions must be done before the age of 8-10 years, always in collaboration with the pediatric dentist: they allow a proper repositioning of the unaffected second permanent molar. The choice of therapy, however, depends not only on the extent of hypo-mineralization of incisors and molars, but also on Angle’s Class and space available 14. Severely affected molars can receive endodontic treatment, instead of extraction 18.

Figure 1a displays a moderate MIH of a mandibular molar (tooth 36); while Figure 1b exhibits a moderate MIH of a maxillary molar (tooth 16); both were treated with resin composite while keeping the slightly hypo-mineralized cusp untouched. A follow-up with fluorinated gel, combined with patient’s good motivation for dental hygiene, can delay the progression of the disease. Similar treatment can be achieved for hypo-mineralized incisors (displayed in figure 2). Composite restorations can preserve healthy hard tissue for long time and reduce the psychological impact of MIH unaesthetic brown spots on anterior incisors (Figure 3).

Figures 4 and 5 display mandibular and maxillary molars with severe hypo-mineralization involvement (endodontic therapy, followed by a crown restoration, are needed).

Figures 6a-b-c and d exhibit unrestorable first molars of a 12-year old patient, indicating the amount of tooth damage and the rapidity of the disease, while incisors can still be conserved using composite restorations (in figure 7).

Conclusion

Early recognition of MIH is essential since damage of dental hard tissues can be fast. Impairment should be anticipated with the appropriate treatment. Patients in Lebanon aren’t safeguarded against MIH and dentists should be aware and ready to implement a diagnosis and a treatment in order to stop disease progression and limit hard tissue’s damage.

Our paper is only a preliminary clinical observation. We have no comparison group: consequently, we cannot draw conclusions about MIH and its pathophysiology. However, cohort studies and randomized controlled trials (RCTs) on MIH are warranted in order to further elucidate various aspects of this dental disease.

 

References 

1. Angelillo IF, Romano F, Fortunato L, Montanaro D. Prevalence of dental cariesand enamel defectsin children livingin areaswith differentwater fluoride concentrations. CommunityDentHealth 1990;7:229-236.
2. ArrowP. Prevalence of developmental enamel defectsof the firstpermanentmolarsamongschool children in Western Australia. AustDentJ. 2008;53:250-259.
3. BeslotA., Villette F. Prise en charge précoce de l’amélogenèse imparfaite. L’information dentaire 2010:4-2;12-19.
4. Bimboire J. La première molaire permanente immature : Mise à jour desconnaissancesactuelles, Université Bordeaux Segalen 2013.
5. Cameron A., Widmer R. Dental Anomalies.Handbook of pediatricdentistry. Parkinson M., TaylorA., LaingA., third edition. Edinburgh, London, NewYork, 2008.
6. Fteita D, Ali A, Alaluusua S. Molar-incisor hypomineralization (MIH) in a group of school-aged children in Benghazi, Libya. Eur Arch Paediatr Dent2006;7:92-95.
7. Gündüz K, Zengin Z, Celenk P, Ozden B, KurtM, Gunhan O. Regional odontodysplasia of the deciduousand permanentteeth associated with eruption disorders: Acase report. Med Oral Patol Oral Cir Bucal 2008;13:E563-566.
8. HébertS. L’hypominéralisation desmolairesetdesincisives. 12esJournéesde Santé Dentaire Publique du Québec, St- Jean-sur-Richelieu, 14 juin 2013.
9. Jasulaityte L, Veerkamp JS, Weerheijm KL. Molar incisor hypomineralization: reviewand prevalence data from the studyof primaryschool children in Kaunas/Lithuania. Eur Arch Paediatr Dent2007;8:87-94.
10. Jasulaityte L, Weerheijm KL, Veerkamp JS. Prevalence of molar-incisor-hypomineralisation amongchildren participatingin the Dutch National Epidemiological Survey(2003). Eur Arch Paediatr Dent2008;9:218 223.
11. Kellerhoff N.M., Lussi A. L’hypominélarisation desmolaires-incisives. MensSuisse Odontostomatol 2004;114:250-253.
12. Kukleva MP, Petrova SG, Kondeva VK, Nihtyanova TI. Molar incisor hypomineralisation in 7-to-14-year old children in Plovdiv, Bulgaria-an epidemiologicstudy. Folia Med (Plovdiv) 2008;50:71-75.
13. Kusku OO, Caglar E, Sandalli N. The prevalence and aetiologyof molar-incisor hypomineralisation in a group of children in Istanbul. Eur J Paediatr Dent2008;9:139-144.

 

Republished with permission of the Lebanese Dental Association 

© JLDA 2016


Comments are closed.

Loading...
Dental News Menu