The term molar incisor hypomineralization (MIH) was introduced in 2001 to describe the clinical appearance of enamel hypomineralization of systemic origin affecting one or more permanent first molars (PFMs) that are associated frequently with affected incisors. The condition is attributed to disrupted ameloblastic function during the transitional and maturational stages of amelogenesis. This condition is recognized in various terms such as hypomineralized PFMs, idiopathic enamel hypomineralization , dysmineralized PFMs, nonfluoride hypomineralization and cheese molars.
|Molar incisor hypomineralization|
The prevalence data for MIH are limited due to various diagnostic classifications. According to existing data the prevalence ranges from 4% to 25% across different populations. The number of hypomineralized PFMs in an individual can vary from 1 to 4, affecting particularly 2 or more molars including the contralateral tooth, where the teeth are moderately or severely affected. The risk of involvement of the permanent maxillary incisors appears to increase when more PFMs are affected.
Putative factors associated with disrupted amelogenesis of PFMs include systemic conditions and environmental insults influencing natal and early development specially during the child’s first 3 years. The systemic conditions implicated to date include nutritional deficiencies, brain injury and neurologic defects, cystic fibrosis, syndromes of epilepsy and dementia (Kohlschutter-Tonz syndrome), nephrotic syndrome, atopia, lead poisoning, repaired cleft lip and palate, radiation treatment, rubella embryopathy, epidermolysis bullosa, ophthalmic conditions, celiac disease, and gastrointestinal disorders. Conditions common in the first 3 years, such as upper respiratory diseases, asthma, otitis media, tonsillitis, chicken pox, measles, and rubella, are also known to be associated with MIH. Some studies suggest the association of Preterm birth with increased prevalence of enamel defects, including hypomineralization and hypoplasia in the permanent dentition.
Clinical presentation and Diagnosis
Criteria for the diagnosis of demarcated opacities, post-eruption breakdown (PEB), atypical restorations, and extracted PFMs due to MIH were developed by Weerheijm et al. Dentitions with generalized opacities present on all teeth rather than limited to the PFMs and permanent incisors, are not considered to have MIH.
Four PFMs and 8 erupted permanent incisors are examined wet for demarcated opacities (white-cream or yellow-brown in color, of normal thickness with a smooth surface), post eruptive breakdown, and atypical restorations.
The opacities are usually limited to the incisal or cuspal one third of the crown, rarely involving the cervical one third.
Due to the unusual size and shape, restorations may not conform to typical caries patterns and frequently involve the cuspal or incisal one third of the crown.
· Enamel opacities may occur adjacent to restoration margins.
Diagnostic Categories of MIH
· Mild MIH
o Demarcated opacities are in nonstress-bearing areas of the molar
o No enamel loss from fracturing is present in opaque areas
o There is no history of dental hypersensitivity
o There are no caries associated with the affected enamel
o Incisor involvement is usually mild if present
· Moderate MIH
o Atypical restorations can be present
o Demarcated opacities are present on occlusal/incisal third of teeth without posteruptive enamel breakdown
o Posteruptive enamel breakdown/caries are limited to 1 or 2 surfaces without cuspal involvement
o Dental sensitivity is generally reported as normal
· Severe MIH
o Posteruptive enamel breakdown is present
o There is a history of dental sensitivity
o Caries is associated with the affected enamel
o Crown destruction can advance to pulpal involvement
o Defective atypical restoration
o Aesthetic concerns are expressed by the patient or parent
o It can be differentiated from fluorosis as its opacities are demarcated, unlike the diffuse opacities that are typical of fluorosis. Fluorosis is caries resistant and MIH is caries prone and also fluorosis can be related to a period in which the fluoride intake was too high
o Choosing between amelogenesis imperfecta (AI) and MIH: only in very severe MIH cases, the molars are equally affected and mimic the appearance of AI
o In MIH, the appearance of the defects will be more asymmetrical and in AI, the molars may also appear taurodont on radiograph and there is often a family history.
MIH’s clinical management is challenging due to:
1. The sensitivity and rapid development of dental caries in affected PFMs
2. The limited cooperation of a young child
3. Difficulty in achieving anesthesia
4. The repeated marginal breakdown of restorations.
|Management of Molar incisor hypomineralization|