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Year : 2014  |  Volume : 5  |  Issue : 4  |  Page : 248-252

Molar incisor hypomineralisation: A review of its current concepts and management

1 Department of Pedodontics and Preventive Dentistry, Ariyanoor, Salem, Tamil Nadu, India
2 Department of Oral Pathology, VMSDC, Ariyanoor, Salem, Tamil Nadu, India

Date of Web Publication20-Nov-2014

Correspondence Address:
Ramesh Krishnan
Professor, Department of Pedodontics and Preventive Dentistry, VMSDC, NH 47 Sankari Main Road, Ariyanoor, Salem - 636 308, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0976-433X.145129

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Over the past two decades, there is an increasing number of congenital defects affecting enamel mineralisation referred to as "molar incisor hypomineralisation" (MIH). This defect usually involves one to four permanent first molars and permanent incisors. Clinically, the defect presents as opaque lesions varying in colour from white to yellow or brown, with a sharp demarcation between the affected and sound enamel to posteruptive enamel breakdown. The destruction of enamel is so rapid and clinically, it presents as if the enamel has not formed at all. It has been postulated that MIH is a consequence of a variety of environmental factors acting systemically, which disturb the ameloblasts during amelogenesis. However, the possibility of a genetic component in the development of MIH cannot be excluded. Management of MIH always pose a big problem to the clinicians, as well as for the child due to severe sensitivity caused by the defective enamel.

Keywords: Aetiology, molar incisor hypomineralisation defects, molar incisor hypomineralisation prevalence, molar incisor hypomineralisation, permanent first molars, permanent incisors

How to cite this article:
Krishnan R, Ramesh M. Molar incisor hypomineralisation: A review of its current concepts and management. SRM J Res Dent Sci 2014;5:248-52

How to cite this URL:
Krishnan R, Ramesh M. Molar incisor hypomineralisation: A review of its current concepts and management. SRM J Res Dent Sci [serial online] 2014 [cited 2023 Jan 29];5:248-52. Available from:

  Introduction Top

Developmental defects of teeth are caused by complex interactions between genetic and environmental factors during tooth development. Enamel is a unique hard tissue which does not undergo remodelling like bone and as a result the structure of enamel is affected during its formation permanently. The changes induced during amelogenesis can be correlated with the timing and the nature of adverse biological events occurred. One such developmental defect of enamel occurring due to changes in the environment, causing permanent damage is molar incisor hypomineralisation (MIH). Historically, MIH has been suggested to be first seen as early as the 17 th -18 th century archaeological extracts of sub-adult samples of a London cemetery. [1]

In 1992 Fédération dentaire internationale Commission on Oral Health, Research and Epidemiology classified the developmental defects of enamel into two distinct categories. [2],[3]

  1. Hypomineralised enamel or enamel opacities which is a qualitative defect of enamel.
  2. Enamel hypoplasia which is a quantitative defect.

Different terminologies were used for developmental defects of enamel in molars, with or without association of post-eruptive breakdown of enamel as nonfluoride enamel opacities, internal enamel hypoplasia, nonendemic mottling of enamel, opaque spots, idiopathic enamel opacities, enamel opacities or cheese molars. [4],[5]

In 2001, the term MIH was first cited by Weerheijm et al. [6] and he defined MIH as the clinical appearance of morphological enamel defects involving the occlusal and/or incisal third of one or more permanent molars or incisors as result of hypomineralisation of systemic origin. [7],[8]

  Prevalence of molar incisor hypomineralisation Top

Koch et al. [4] called these as cheese molars after carrying out the first epidemiological study. Weerheijm and Mejàre [9] reported a prevalence rate ranging from 3.6% to 25% after carrying out studies in European countries. Later, a systematic review by Jälevik [10] showed a wide variation in the prevalence of MIH between 2.4% and 40.2%. A nonsystematic online search and screening in the PubMed data base using the terms: European Academy of Pediatric Dentistry (EAPD); MIH; after the year 2003 showed prevalence of MIH ranging from 3.5% to 40.2%. [11]

  Aetiological considerations Top

Molar incisor hypomineralisation has no hypoplastic defects as there is no discernable reduction in enamel thickness. Any reduction in enamel thickness seen clinically is indicative of posteruption disintegration of enamel. The insult affects the developing tooth after the enamel secretion is completed and it affects the maturation phase of the mineralization process in a localized area of enamel. [12],[13] MIH is a qualitative defect in enamel classified as hypomineralised type that follows the natural incremental lines of enamel formation, from cusp tip to cemento enamel junction. [12] Aetiological factors causing changes in organic/inorganic composition of MIH affected teeth are still unknown. [14],[15] MIH is caused due to multifactorial aetiology, with a genetic predisposition associated with one or more of a range of systemic insults occurring at a susceptible stage during tooth formation. Thus it confirms the manner, where several teeth are severely affected while their antimeres are unaffected. [16] The multifactorial aetiology is further tabulated in [Table 1].
Table 1: Various etiological factors of MIH

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  Molar incisor hypomineralisation and amelogenesis Top

Amelogenesis takes place in three stages:

  1. Matrix formation during which proteins involved in amelogenesis are produced;
  2. Calcification during which mineral content is acquired and the proteins are removed;
  3. Maturation during which the enamel is calcified and the remaining proteins are removed.

Systemic factors that disturb the ameloblasts during the secretory stage cause restrictions of crystal elongation and result in pathologically thin, or hypoplastic enamel. On the other hand, disturbances during the transitional and/or maturation stage of amelogenesis result in pathologically soft (hypomaturated, hypomineralised) enamel of normal thicknesses. [17]

The principal proteins secreted during amelogenesis are: [16]

  1. Amelogenins (the major protein-90% secreted into the enamel matrix) is a group of heterogeneous proteins (20-30 kDa) that are hydrophobic and rich in proline, histidine and glutamine and they are thought to play a role in the organization and regulation of crystal growth;
  2. Ameloblastins (amelin, sheathelin) constitutes 5-10% of the enamel matrix. It is thought to promote mineralization and crystal elongation; and
  3. Enamelins (60-80 kDa) are a heterogeneous group of proteins that may be involved in crystal nucleation.

Enamel formation as a whole takes approximately 1000 days. [18] Two-thirds of this time is devoted to the maturation stage of amelogenesis. The most critical period for enamel defects of first permanent molars and incisors is during the 1 st year of life coinciding with their early maturation. [18] Ameloblasts are highly sensitive to various environmental disturbances during this period. In first molars enamel maturation takes a longer period to cause hypomineralisation. [19]

Molar incisor hypomineralisation a hypocalcified subtype of enamel defect with reduced mineral content, low residual content of amelogenins containing more than 16 types of proteins in affected teeth, 13 of which are found in saliva and crevicular fluid [15],[20] and others namely hemoglobin, albumin, complement C3 are components of blood. It was also observed that the protein composition of MIH enamel varies with severity of enamel defect. [21]

  Molar incisor hypomineralisation and dentin pulp complex Top

When the Ca:P ratio of dentin below hypomineralised was evaluated, it was almost identical to that of normal enamel, but when the Ca:C ratio was assessed, it was found to be low in dentin with an elevated level of C. The levels of O and P in dentin of normal teeth were found to be higher, but in hypomineralised teeth, dentin showed higher levels of N. [22]

Patients with MIH affected teeth suffer from dentine sensitivity to various thermal, mechanical and osmo-chemical stimuli [23] due to the porous nature of enamel sometimes, exposing the dentin. This can favor ingress of bacterial contaminants [24] thereby resulting in chronic inflammation of the pulp [25] leading to a variety of morphological and cytochemical neuronal changes, with an overexpressed dentin sensitivity.

  Clinical picture of molar incisor hypomineralisation affected teeth Top

Molar incisor hypomineralisation is a qualitative defect of enamel classified as hypomineralised type that follows the natural incremental lines of enamel formation extending from cuspal to cemento-enamel junction. [12],[13] Mostly cervical enamel is sound with no evidence of defective structure. At a more occlusal level, the defect is confined to the inner enamel while the outer enamel does not appear to be affected. In the occlusal region, the hypomineralisation is more evident eventually spreading to the entire thickness of the enamel. The defects usually did not involve the cusp tips; the involvement of margin caused reduction in the height. [12]

Microstructural analysis of sound and hypomineralised enamel showed two marked changes [27]

  1. Less dense prism structure with loosely packed apatite crystals.
  2. Wider sheath regions.

These may be responsible for the marked reduction in hardness and elastic modulus of the affected enamel. [28]

Semi-quantitative analysis by energy dispersive X-ray spectrometry of extracted MIH affected teeth showed low mineral composition of enamel [29] and the average mineral density is about 19% lower than that of sound enamel [12],[30],[31] with a reduction in the Ca:P ratio and with an relative increase in the C content. [13],[29],[31],[32],[33]

The characteristic distinguishing feature of MIH from hypomaturation defects like amelogenesis imperfecta or fluorosis is that, these two contain high residual amelogenin protein. [23],[34],[35] Pathogenically this points to a preeruptive disturbance of mineralization involving overabundance of albumin, interfering with mineralisation.

An indicator of the severity of MIH affected teeth is the actual organic content of its enamel [12] whereas brown enamel, the most severe form of MIH, has the highest protein content (15-21-fold greater), whilst the protein content of white/opaque and yellow enamel are both markedly higher (eight-fold greater) than sound enamel. [12]

These microstructural changes in hypomineralised enamel improve the understanding of some of the problems associated with the clinical management of these teeth like the frequent occurrence of enamel fractures and inadequate retention of adhesive materials, both of which are recognized as significant clinical challenges. The presence of increased amounts of organic matter in the hypomineralised enamel, may inhibit the creation of an adequate etch profile which in turn compromises the adhesion between resin based restorative materials and the defective enamel. [36]

According to EAPD placed in Athens in 2003. [7] The scoring of MIH ranges from 0 to 10 as given below in [Table 2],[Table 3] (Ghanim et al., 2011). [37] Examination for MIH should be performed on wet teeth after removing debris with cotton roll.
Table 2: Definition of the MIH-severity-index according the EAPD criteria (2010) Lygidakis et al.[26]

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Table 3: EAPD scoring criteria for MIH (Ghanim et al., 2011)[37]

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  Clinical management of molar incisor hypomineralisation Top

  Conclusion Top

Hypomineralised enamel defects (MIH) are one of the common clinical problems and should be regarded as a public health problem which brings painful consequences, poor aesthetics and a negative impact on the quality of life.

Molar incisor hypomineralisation is as a result of synergistic action of environmental factors and genetic expressions causing disturbances of enamel.

Good understanding about the etiology, early diagnosis by differentiating from other enamel defects and appropriate treatment are essential for the management of MIH.

The identification of new genes and novel proteins such as amelotin and apin produced by ameloblasts, during the stage of maturation will aid to manipulate genetic and environmental factors and to treat MIH in future.

  References Top

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  [Table 1], [Table 2], [Table 3]

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