OBJECTIVE: The objective of this study was to assess the strength of evidence for the aetiology of molar-incisor hypomineralization (MIH), often as approximated by demarcated defects. METHOD: A systematic search of online medical databases was conducted with assessment of titles, abstracts, and finally full articles for selection purposes. The level and quality of evidence were then assessed for each article according to Australian national guidelines. RESULTS: Of 1123 articles identified by the database search, 53 were selected for review. These covered a variety of potential aetiological factors, some of which were grouped together for convenience. The level of evidence provided by the majority of papers was low and most did not specifically investigate MIH. There was moderate evidence that polychlorinated biphenyl/dioxin exposure is involved in the aetiology of MIH; weak evidence for the role of nutrition, birth and neonatal factors, and acute or chronic childhood illness/treatment; and very weak evidence to implicate fluoride or breastfeeding. CONCLUSION: There is currently insufficient evidence in the literature to establish aetiological factor/s relevant for MIH. Improvements in study design, as well as standardization of diagnostic and examination protocols, would improve the level and strength of evidence.
OBJECTIVE: The objective of this study was to assess the strength of evidence for the aetiology of molar-incisor hypomineralization (MIH), often as approximated by demarcated defects. METHOD: A systematic search of online medical databases was conducted with assessment of titles, abstracts, and finally full articles for selection purposes. The level and quality of evidence were then assessed for each article according to Australian national guidelines. RESULTS: Of 1123 articles identified by the database search, 53 were selected for review. These covered a variety of potential aetiological factors, some of which were grouped together for convenience. The level of evidence provided by the majority of papers was low and most did not specifically investigate MIH. There was moderate evidence that polychlorinated biphenyl/dioxin exposure is involved in the aetiology of MIH; weak evidence for the role of nutrition, birth and neonatal factors, and acute or chronic childhood illness/treatment; and very weak evidence to implicate fluoride or breastfeeding. CONCLUSION: There is currently insufficient evidence in the literature to establish aetiological factor/s relevant for MIH. Improvements in study design, as well as standardization of diagnostic and examination protocols, would improve the level and strength of evidence.