Molar-incisor hypomineralization and the association with childhood illnesses and antibiotics in a group of Finnish children.

Objective: Molar-incisor hypomineralization (MIH) is a developmental enamel defect affecting 1-4 first permanent molars (FPMs) and often also incisors. The aim of this study was to assess whether childhood illnesses or medication are associated with MIH.

Material And Methods: FPMs and incisors of 287 Finnish children were examined for MIH in line with the criteria of the EAPD.

Background factors of molar-incisor hypomineralization in a group of Finnish children.

Objective: Molar-Incisor Hypomineralization (MIH) is a common developmental enamel defect characterized by demarcated opacities in permanent molars and incisors. Its etiology still remains unclear. The aim of this retrospective cohort study was to assess if the socioeconomic environment of the child is associated with MIH.

Combined effect of amoxicillin and sodium fluoride on the structure of developing mouse enamel in vitro.

Objective: Excess fluoride intake during tooth development is known to cause dental fluorosis. It has also been suggested that amoxicillin use in early childhood is associated with enamel hypomineralization. The aim was to investigate separate and combined effects of sodium fluoride (NaF) and amoxicillin on enamel formation in vitro.

Tributyltin alters osteocalcin, matrix metalloproteinase 20 and dentin sialophosphoprotein gene expression in mineralizing mouse embryonic tooth in vitro.

We showed in a previous in vitro study that tributyltin (TBT) arrests dentin mineralization and enamel formation in developing mouse tooth. The present aim was to investigate the effect of TBT on the expression of genes associated with mineralization of dental hard tissues. Embryonic day 18 mouse mandibular first molars were cultured for 3, 5 or 7 days and exposed to 1.

Combined effect of fluoride and 2,3,7,8-tetrachlorodibenzo-p-dioxin on mouse dental hard tissue formation in vitro.

Fluoride interferes with enamel matrix secretion and mineralization and dentin mineralization. The most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), also impairs dental hard tissue formation and mineralization in vitro and in vivo. Our aim was to investigate in vitro whether the combined effect of sodium fluoride (NaF) and TCDD on dental hard tissue formation is potentiative.

Tributyltin impairs dentin mineralization and enamel formation in cultured mouse embryonic molar teeth.

Tributyltin (TBT), earlier used as an antifouling agent in marine paints, causes damage to the aquatic ecosystem, for example, impaired shell calcification in oysters. TBT affects hard tissue mineralization even in mammals: delayed bone mineralization has been observed in rodents exposed to TBT in utero. To see if TBT interferes with tooth development, especially dental hard tissue formation, we exposed mouse E18 mandibular first and second molars to 0.