The ‘mysterious aetiology’ of molar incisor hypomineralisation

Zameer, Mohammed; Birajdar, Sameen Badiujjama

doi:10.1007/s40368-022-00743-5

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…Recently, the analysis of the MIH enamel identified serum albumin and other blood proteins ( Perez et al, 2020 ; Farah et al, 2010 , Mangum et al, 2010 ), proposing albumin as an impediment to the growth of enamel crystals and attainment of normal mineral content ( Hubbard et al, 2021 ). However, cellular events of the pathophysiology are still unknown, and the need for understanding the pathways leading to opaque, demarcated enamel lesions has been pointed out ( Zameer and Birajdar, 2022 ). Animal models induced opaque hypomineralized enamel with bisphenol A and amoxicillin in rats ( Jedeon et al, 2013 ; Duman et al, 2022 ); demarcated lesions were induced by infections with parasites in sheep ( Suckling et al, 1983 ; Suckling et al, 1986 ).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel

Chun,

Tan,

Villanueva

et al. 2024

Front. Physiol.

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Introduction: Developmental defects of the enamel manifest before tooth eruption and include amelogenesis imperfecta, a rare disease of underlying gene mutations, and molar–incisor hypomineralization (MIH), a prevalent disease in children originating from environmental and epigenetic factors. MIH enamel presents as the abnormal enamel marked by loss of translucency, demarcation between the healthy and affected enamel, and reduced mineral content. The pathophysiology of opaque, demarcated enamel lesions is not understood; however, the retention of enamel proteins in the matrix has been suggested. Ameloblastin (Ambn) is an enamel protein of the secreted calcium-binding phosphoproteins (SCPPs) critical for enamel formation. When the Ambn gene is mutated or deleted, teeth are affected by hypoplastic amelogenesis imperfecta.Methods: In this study, enamel formation in mice was analyzed when transgenic Ambn was overexpressed from the amelogenin promoter encoding full-length Ambn. Ambn was under- and overexpressed at six increasing concentrations in separate mouse lines.Results: Mice overexpressing Ambn displayed opaque enamel at low concentrations and demarcated lesions at high concentrations. The severity of enamel lesions increased starting from the inner enamel close to the dentino-enamel junction (DEJ) to span the entire width of the enamel layer in demarcated areas. Associated with the opaque enamel were 17-kDa Ambn cleavage products, a prolonged secretory stage, and a thin basement membrane in the maturation stage. Ambn accumulations found in the innermost enamel close to the DEJ and the mineralization front correlated with reduced mineral content. Demarcated enamel lesions were associated with Ambn species of 17 kDa and higher, prolonged secretory and transition stages, a thin basement membrane, and shortened maturation stages. Hypomineralized opacities were delineated against the surrounding mineralized enamel and adjacent to ameloblasts detached from the enamel surface. Inefficient Ambn cleavage, loss of contact between ameloblasts, and the altered basement membrane curtailed the endocytic activity; thus, enamel proteins remained unresorbed in the matrix. Ameloblasts have the ability to distinguish between Ambn concentration and Ambn cleavage products through finely tuned feedback mechanisms. The under- or overexpression of Ambn in murine secretory ameloblasts results in either hypoplastic amelogenesis imperfecta or hypomineralization with opaque or sharply demarcated boundaries of lesions, similar to MIH.

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Section: Introductionmentioning

confidence: 99%

Overexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel

Chun,

Tan,

Villanueva

et al. 2024

Front. Physiol.

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Molar incisor hypomineralization: Prevalence, severity and associated aetiological factors in children seeking dental care at Armed Forces Hospital Jazan, Saudi Arabia

Zameer,

Wali Peeran,

Nahid Basheer

et al. 2024

The Saudi Dental Journal

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Analysis of enamel hypoplasia causes and risk factors in children

Karpova,

Tkachenko,

Savushkina

et al. 2023

jour

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Relevance. Enamel hypoplasia is one of the most common defects of a child's hard dental tissue. Molar incisor hypomineralization (MIH) is one of the systemic hypoplasia forms. MIH is defined as a qualitative defect of enamel development in children and adolescents affecting at least one permanent molar with or without the involvement of the incisors. As for the causes, MIH, as a form of enamel hypoplasia, proved to be a multifactorial disease.Material and methods. Conducted in dental clinics of St. Petersburg, an empirical study surveyed 90 respondents with the anonymous original questionnaire developed by us. The report summarized the results of descriptive statistics on measurements related to the data of the three groups on existing disorders of the hard dental tissues in children.Results. The average age of women whose children are not diagnosed with caries and enamel hypoplasia was 35.52 years, while the average age of mothers of children with MIH was 40.17 years. The study of the number of previous pregnancies and childbirths revealed no signs of MIH and pitting enamel hypoplasia (PET) in children of the first pregnancy. The analysis of the past medical history impact in women during pregnancy on the development of enamel defects provided statistically significant results for such illnesses as URTI and VURTI, as well as chronic endocrine diseases. According to the data obtained, influenza, past respiratory diseases and antibiotic intake during the first year of a child's life led to the development of various types of enamel hypoplasia.

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The ‘mysterious aetiology’ of molar incisor hypomineralisation

Cited by 3 publications

References 14 publications

Overexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel

Overexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel

Molar incisor hypomineralization: Prevalence, severity and associated aetiological factors in children seeking dental care at Armed Forces Hospital Jazan, Saudi Arabia

Analysis of enamel hypoplasia causes and risk factors in children

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