Arrest of Rat Molar Tooth Development by Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Lukinmaa, Pirjo‐Liisa; Sahlberg, Carin; Leppäniemi, Anu; Partanen, Anna-Maija; Kovero, Outi; Pohjanvirta, Raimo; Tuomisto, Jouko; Alaluusua, Satu

doi:10.1006/taap.2001.9155

Cited by 42 publications

(31 citation statements)

References 47 publications

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“…considerable size reduction), developmental delays, root anomalies and calcification defects and the teeth that are affected depend on the age when the treatment is given. Increased prevalence of tooth agenesis was reported among people exposed to dioxin in Seveso, Italy, and dioxin also disturbs tooth development in experimental animals (Lukinmaa et al, 2001;Alaluusua et al, 2004;Yasuda et al, 2005). Although cancer therapy and dioxin accidents represent rare circumstances, tooth size reduction has been described in association with maternal tobacco smoking, maternal systemic diseases and alteration of birth weight (Heikkinen et al,'94; reviewed by Paulsson et al, 2004).…”

Section: Etiology Of Tooth Agenesismentioning

confidence: 95%

Genetic basis of tooth agenesis

Nieminen¹

2009

J Exp Zool Pt B

225

215

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Tooth agenesis or hypodontia, failure to develop all normally developing teeth, is one of the most common developmental anomalies in man. Common forms, including third molar agenesis and hypodontia of one or more of the incisors and premolars, constitute the great majority of cases. They typically affect those teeth that develop latest in each tooth class and these teeth are also most commonly affected in more severe and rare types of tooth agenesis. Specific vulnerability of the last developing teeth suggests that agenesis reflects quantitative defects during dental development. So far molecular genetics has revealed the genetic background of only rare forms of tooth agenesis. Mutations in MSX1, PAX9, AXIN2 and EDA have been identified in familial severe agenesis (oligodontia) and mutations in many other genes have been identified in syndromes in which tooth agenesis is a regular feature. Heterozygous loss of function mutations in many genes reduce the gene dose, whereas e.g. in hypohidrotic ectodermal dysplasia (EDA) the complete inactivation of the partially redundant signaling pathway reduces the signaling centers. Although these mechanisms involve quantitative disturbances, the phenotypes associated with mutations in different genes indicate that in addition to an overall reduction of odontogenic potential, tooth class-specific and more complex mechanisms are also involved. Although several of the genes so far identified in rare forms of tooth agenesis are being studied as candidate genes of common third molar agenesis and incisor and premolar hypodontia, it is plausible that novel genes that contribute to these phenotypes will also become identified.

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Section: Etiology Of Tooth Agenesismentioning

confidence: 95%

Genetic basis of tooth agenesis

Nieminen¹

2009

J Exp Zool Pt B

225

215

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“…This result differs from those of other studies, which show that lactating pups frequently lacked third molars when administered a single dose of 50 or 1000 mg/kg TCDD at PND1 or when pregnant dams were exposed to 1 mg/kg TCDD on gestation day 15. 22,7 We suggest two reasons to explain the difference between these studies and ours as follows: First, TCDD administered at 5 mg/kg may be insufficient to arrest the development of the third molar. Second, TCDD was administered too late to induce molar agenesis.…”

Section: Discussionmentioning

confidence: 52%

“…5 A single high dose of TCDD administered to healthy adult rats or lactating pups causes chronic defects in erupting incisors and blocks the development of third molars of offspring. 6,7 During pregnancy, TCDD exposure interferes with tooth morphogenesis, cell differentiation, and root development, which leads to tooth malformation in the offspring. [8][9][10] TCDD mediates numerous adverse biological effects, mainly through the aryl hydrocarbon receptor (AHR).…”

mentioning

confidence: 99%

Exposure to a continuous low dose of tetrachlorodibenzo-p-dioxin impairs the development of the tooth root in lactational rats and alters the function of apical papilla-derived stem cells

Guo¹,

Zhang²,

Wei³

et al. 2015

Archives of Oral Biology

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“…We have earlier shown that exposure of cultured mouse tooth germs to TCDD, representing the most toxic dioxin congener, during the formation of dental hard tissues impairs dentin mineralization and arrests enamel formation [Partanen et al, 1998]. TCDD exposure of rat pups via lactation also arrested the deposition of dentin and enamel matrices [Lukinmaa et al, 2001], delayed the degradation of enamel matrix during enamel maturation and impaired dentin mineralization in developing molar teeth [Gao et al, 2004]. TCDD was not found to alter Mmp-20 expression in ameloblasts of cultured mouse embryonic teeth, but in odontoblasts, the expression was slightly decreased [Kiukkonen et al, 2006].…”

Section: Discussionmentioning

confidence: 99%

Tributyltin Alters Osteocalcin, Matrix Metalloproteinase 20 and Dentin Sialophosphoprotein Gene Expression in Mineralizing Mouse Embryonic Tooth in vitro

Salmela

Alaluusua²,

Sahlberg³

et al. 2011

Cells Tissues Organs

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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 1.0 µM TBT and studied by real-time quantitative polymerase chain reaction (RT-QPCR) for the expressions of osteocalcin (Ocn), alkaline phosphatase (Alpl), dentin matrix protein 1 (Dmp1), dentin sialophosphoprotein (Dspp) and matrix metalloproteinase 20 (Mmp-20).Ocn, Mmp-20 and Dspp, whose expressions showed changes in RT- QPCR, were further analyzed by in situ hybridization of tissue sections. In situ hybridization showed that TBT decreased Ocn expression in odontoblasts but increased the expression in the epithelial tooth compartment. In QPCR assays, the net effect in the whole tooth was increased expression. TBT also reduced Mmp-20 expression in ameloblasts and odontoblasts. Dspp expression varied but both QPCR assays and in situ hybridization showed a decreasing trend. TBT exposure had no clear effect on Alpl and Dmp1 expressions. Increased Ocn expression by epithelial enamel organ may inhibit dentin mineralization and enamel formation. Decreased Ocn, Mmp-20 and Dspp expressions in odontoblasts may indicate delayed cell differentiation, or TBT may specifically decrease the expression of genes involved in dentin mineralization. While decreased Mmp-20 expression by TBT in ameloblasts may impair enamel mineralization, the coincident reduction in Mmp-20 and Dspp expressions in odontoblasts may potentiate the delay of dentin mineralization.

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Arrest of Rat Molar Tooth Development by Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Cited by 42 publications

References 47 publications

Genetic basis of tooth agenesis

Genetic basis of tooth agenesis

Exposure to a continuous low dose of tetrachlorodibenzo-p-dioxin impairs the development of the tooth root in lactational rats and alters the function of apical papilla-derived stem cells

Tributyltin Alters Osteocalcin, Matrix Metalloproteinase 20 and Dentin Sialophosphoprotein Gene Expression in Mineralizing Mouse Embryonic Tooth in vitro

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