Molar incisor hypomineralisation (MIH) is a type of enamel defect affecting, as the name suggests, the first molars and incisors in the permanent dentition. MIH is considered a worldwide problem with a global prevalence of 12.9% and is usually identified in children under 10 years old. This developmental condition is caused by the lack of mineralisation of enamel during its maturation phase, due to interruption to the function of ameloblasts. Peri- and post-natal factors including premature birth, certain medical conditions, fever and antibiotic use have been found to be associated with development of MIH. Recent studies have suggested the role of genetics and/or epigenetic changes to be contributors of MIH development. However, further studies on the aetiology of MIH are required because it is believed to be multifactorial.
MIH often presents as discolouration of the affected permanent molars and incisors. The enamel of the affected teeth appears yellow, brown, cream or white and thus are sometimes referred to as 'cheese molars'. These teeth are deemed less aesthetically pleasing, potentially causing distress in children with MIH and their parents. Although there is difference in enamel translucency in the affected teeth, there should not be any changes to the enamel thickness, unlike in enamel hypoplasia.
As a consequence, children with MIH are more likely to experience tooth decay compared to those without the condition. Moreover, the development of tooth decay is very rapid due to the less-mineralised enamel. MIH only becomes visible once the permanent molars start to erupt and that is when opacities on the tooth can be observed if it is affected. It is important for the children who are suspected to suffer from MIH to visit their dentist at regular intervals to prevent any further complications affecting their oral health.
Signs and symptoms
The manifestation of the disease in those affected with MIH can vary greatly. It can be common for the enamel of one molar to be affected while the enamel of the contralateral molar is clinically unaffected, or with minor defects only.
Lesions The lesions that appear in teeth affected with MIH can present as opacities that vary from white to yellow-brown. They are usually asymmetrical in appearance, with a sharp demarcation that distinguishes between normal and affected enamel. The lesions usually do not involve the cervical third of affected teeth.
Post-eruptive breakdown Post-eruptive breakdown (PEB) is a clinical feature, often observed in the majority of severely affected cases and requires prompt dental treatment. The rate of PEB may be increased by the loading of masticatory forces on enamel weakened by MIH. The lesions resulting from PEB are irregularly shaped, with rough margins from the shearing of the enamel. PEB is more likely to occur in MIH-affected teeth with yellow or brown opacities rather than those with white opacities, as darker lesions reflect a greater deficit in mineral content.
Atypical caries Teeth affected with MIH are at an increased risk of acquiring atypical dental caries (cavities). This is because the properties of the enamel are altered with increased porosity and decreased hardness. Essentially, the normal balance between mineralisation and demineralisation shifts to favour demineralisation of enamel, giving the tooth less resilience in structure, thereby making it vulnerable to caries.
The poor structural properties of the enamel in teeth with MIH also increase the likelihood of cavitation of any lesion, thereby causing the lesion to progress at a faster rate. Progression of the carious lesion is also more rapid in teeth with MIH as patients may experience tooth sensitivity while carrying out oral hygiene, causing them to avoid doing so and consequentially accelerating the decay.
Hypersensitivity Teeth affected by MIH are often affected by hypersensitivity due to changes in temperature or tooth brushing. A study has suggested that a possible cause of hypersensitivity in MIH is the inflammatory reactions in the pulp due to oral bacteria penetrating through the hypomineralised enamel into the dentinal tubules.
Difficult to anaesthetise It has been reported that MIH-affected teeth were more difficult to anaesthetise. Difficulty achieving adequate anaesthesia in MIH-affected teeth may be caused by the chronic inflammation of the pulp due to the penetration of bacteria as the presence of inflammation can reduce the efficacy of local anaesthetics which may then result in more anaesthetic being given to achieve profound anaesthesia. Undertaking dental treatment without profound local anaesthesia can result in a child becoming more fearful and anxious when receiving dental treatment. This can be especially challenging in paediatric dentistry; thus, additional methods may be needed to provide appropriate treatment for these teeth.
Opacities due to MIH can be quite visible especially on anterior teeth presenting aesthetic problems. Patients frequently claim aesthetic concerns when anterior teeth are involved. The discoloured appearance of the anterior teeth could also have negative effects on a child's psychological development and self-esteem.
Tooth breakdown and restoration problems MIH-affected teeth are more prone to breakdown as they are hypomineralised which weakens the enamel structure. Restorations placed on MIH-affected teeth were found to be more prone to failure due to both loss of tooth structure and material loss. The enamel can also fracture more easily due to chewing forces.
Causes
The exact cause of MIH is unknown but thought to be multifactorial.
It has been found that peri- and post-natal factors play a more important role in development of MIH than prenatal factors.
Hypoxia, caesarean section, and premature birth are among perinatal factors that have been associated with development of MIH. Additionally, postnatal factors such as urinary tract infection, otitis media, measles, kidney disease, pneumonia, asthma, antibiotic use, and fever have all been associated with MIH.
Prenatal risks such as infection, maternal psychological stress and frequent exposure to ultrasonic scans were all correlated with increased risks of MIH.
During the perinatal stage, Pitiphat found that cesarean section and complications during vaginal delivery could contribute to an increased chance of MIH. Children born preterm and those with poor general health or systemic conditions in their first three years of development also run a higher risk of developing MIH. It has also been proposed that developmental dental defects were associated with long-term breastfeeding due to exposure to dioxin. However, a recent meta-analysis has reported prolonged breastfeeding to not be associated with MIH.
More recent evidence has suggested a relationship between respiratory diseases and oxygen shortage of the ameloblasts and MIH. Lastly, oxygen shortage combined with low birth weight is suspected to be a contributing factor
Diagnosis Differential diagnosis It is essential to exclude other causes of enamel opacities, differentiating MIH from them, to ensure an appropriate treatment plan is made. These conditions include: Dental caries, which is the most common cause of destruction of dental hard tissues. This is more unlikely in a patient with a previously intact primary dentition. White spot lesions are also uncommon on incisors, hence ruling out dental caries. Fluorosis, which can result from an intake of a high fluoride concentration while the tooth is still undergoing mineralisation. Fluorosis presents as irregular, diffuse enamel opacities which affect more than one tooth, in contrast to the well-demarcated borders of hypomineralised enamel seen in MIH. Amelogenesis imperfecta, a genetic condition; thus, there may be a history of similar defects in other family members. This condition affects both the primary and permanent dentition, and all surfaces tend to be equally affected, differentiating it from MIH. Trauma to primary incisors resulting in discolouration of permanent incisors. Administration of tetracycline during pregnancy and to children under six resulting in tooth staining (grey or yellow). Enamel hypoplasia, caused by defective enamel matrix formation, is a quantitative defect which presents as a localised reduction in enamel thickness. This differs from hypomineralisation, which is a qualitative defect affecting the translucency of enamel.
Classification
MIH examination should be carried out on clean, moist teeth. The ideal age for examination is when the child is eight years old – the age where all permanent first molars and most of the incisors are erupted. The permanent first molar will also still be in a comparatively sound condition without excessive post-eruption breakdown. Judgements of each individual tooth should be recorded, aiding the correct diagnosis of the condition.
There is currently a lack of standardisation in the scoring system and severity indices used to record the diagnosis of MIH. Various systems commonly employed in studies include: Modified Defect of Dental Enamel (DDE) Index: This set of criteria allows for enamel defects to be detected, enabling a distinction between demarcated and diffused opacities. European Academy of Paediatric Dentistry (EAPD) judgement criteria: This set of criteria was developed in 2003 to standardise classifications for use in epidemiological studies. However, while it allows the categorisation of the enamel condition, it does not address the severity of the enamel condition. Molar Hypomineralisation Severity Index (MHSI): This set of criteria has been developed to address deficiencies in indices concerning the severity of hypomineralisation. It is based on both the clinical characteristics of hypomineralised defects and the EAPD judgement criteria. It was found to be effective in guiding the clinical management of children by predicting treatment undertaken for affected permanent first molars. Ghanim et al index: The index combines principles of the EAPD judgement criteria and DDE index in order to grade the clinical status, amount of tooth surface area affected, and other enamel defects comparable to MIH. The index has been validated and a training manual was developed to assist researchers in implementing the index in a standardised manner.
Prevention Prevention is of prior importance at an early developmental age as the defective tooth is more likely to have caries and post-eruptive breakdown due to its increased porosity. Appropriate dietary advice and toothpaste with a fluoride level of at least 1,000 ppm F should be recommended. For treating spontaneous hypersensitivity professional applications of fluoride varnish (e.g. Duraphat 22,600ppm F) or 0.4% stannous fluoride gel may be helpful.
Casein Phosphopepetide-Amorphus Calcium Phosphate (CPP-ACP) provides a supersaturated environment of calcium and phosphate on the enamel surface to enhance remineralisation in the form of toothpaste or sugar free chewing gum. Its clinical effectiveness is still debatable but may benefit those patients who complain of mild pain to external stimuli.
Treatment The frequency of first permanent molar treatment for children with MIH is nearly 10 times greater compared to children without MIH. 27.4% of MIH-affected teeth will need treatment due to pain, sensitivity or post-eruptive breakdown. The available treatment modalities for MIH is extensive but the decision on which treatment should be used is complex and multifactorial. Factors may include condition severity, the patient's dental age, the child and parent's social background and expectations. There are treatment modalities available to manage children affected by MIH; however, the evidence supporting these modalities are still weak.
Anterior teeth
Etch-bleach-seal technique