No abstract

Background: The aetiology of molar incisor hypomineralisation (MIH) is unclear. The asymmetric distribution of MIH in the dentition may indicate that an insult of short duration that affects ameloblasts at a vulnerable stage could be a causative factor. Apgar ≤ 5 at 5 min may indicate asphyxia (hypoxic-ischemic insult) during birth. It was hypnotised that low Apgar score during birth may cause MIH. The present study aimed to examine a possible association between Apgar ≤ 5 at 5 min and the occurrence of MIH. Method: Two study groups were selected for examination. The cases comprised 67 children aged 8-10 years born with Apgar score equal to or below 5 after 5 min. The control group comprised 157 age-matched healthy children. First permanent molars, second primary molars and all permanent incisors were examined in all children. Clinical examination was undertaken by two calibrated examiners and intraoral close-up photographs of the teeth were later evaluated by three calibrated and blinded clinicians. Demarcated opacities, post-eruptive breakdown, atypical restorations and extractions due to MIH, according to the criteria of the European Association of Paediatric Dentistry, were assessed. Results: The prevalence of MIH did not differ between the two groups. A chi-square test failed to confirm any statistically significant relationship between 5-min Apgar scores and MIH occurrence. In addition, there was no statistically significant relationship between the number of affected first permanent molars in cases and controls. Conclusion: There was no association between Apgar ≤ 5 at 5 min and the occurrence of MIH.

The aim of this study was to investigate the effect of hypoxic conditions on the expression of enamel genes and on the secretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), cytokines, and interleukins by an ameloblast-derived cell line. Murine ameloblast-derived cells (LS-8 cells) were exposed to 1% oxygen for 24 and 48 h and harvested after 1, 2, 3, and 7 d. The effect of culture in hypoxic conditions on the expression of structural enamel matrix genes and on the secretion of cytokines and interleukins, as well as ALP and LDH, into the cell-culture medium was calculated relative to the expression and secretion of these factors by untreated cells (controls) at each time point. Hypoxia increased expression of the structural enamel matrix genes amelogenin (Amelx), ameloblastin (Ambn), and enamelin (Enam), and the enamel protease matrix metalloproteinase-20 (Mmp20). Expression of hypoxia-inducible factor 1-alpha (Hif1α), and secretion of several vascularization factors and pro-inflammatory factors, were increased after 24 and 48 h of hypoxia. The ALP activity was reduced after 24 and 48 h of hypoxia, whereas the LDH level in the cell-culture medium was higher after 24 h of hypoxic conditions compared with 48 h. In conclusion, hypoxic exposure may disrupt the controlled fine-tuned expression and processing of enamel genes, and promote the secretion of pro-inflammatory factors.