A novel autosomal‐recessive mutation, <i>whitish chalk‐like teeth</i>, resembling amelogenesis imperfecta, maps to rat chromosome 14 corresponding to human 4q21

Masuyama, Taku; Miyajima, Katsuhiro; Ohshima, Hayato; Osawa, Masaru; Yokoi, Norihide; Oikawa, Toshihiro; Taniguchi, Kazuyuki

doi:10.1111/j.1600-0722.2005.00254.x

Cited by 4 publications

(7 citation statements)

References 29 publications

(49 reference statements)

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“…The aberration of this process is considered to be attributed to white, chalk-like abnormal incisors in the wct homozygous mutation (Masuyama et al 2005). Since the ameloblasts contained ferritin in their cytoplasm in the pigmentation stage, the secretory pathway of ferritin as well as enamel proteins may be disturbed in the ameloblasts throughout the maturation stage of amelogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…nbrp.jp). The heredity of this trait and the genetic background were described in detail in our previous report (Masuyama et al 2005). Twenty heterozygous (+/wct) and homozygous (wct/wct) male rats (30 days old) were used in this study.…”

Section: Animalsmentioning

confidence: 99%

“…Recently, we reported a rat mutant, whitish chalk-like teeth (wct), with white, chalk-like abnormal incisors, among an outbred colony of Sprague-Dawley (Crj : CD(SD)IGS) rats (Masuyama et al 2005). The homozygous mutant rats (wct/wct) showed tooth enamel defects similar to those of human AI: the wct homozygous mutation was found to disturb the morphological transition of ameloblasts from secretory to maturation stages, resulting in cyst formation in addition to the disturbance of iron transfer to the enamel surface.…”

Section: Introductionmentioning

confidence: 99%

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Rat wct mutation prevents differentiation of maturation-stage ameloblasts resulting in hypo-mineralization in incisor teeth

Osawa

Kenmotsu

Masuyama

et al. 2007

Histochem Cell Biol

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A recent study provided genetic and morphological evidence that rat autosomal-recessive mutation, whitish chalk-like teeth (wct), induced tooth enamel defects resembling those of human amelogenesis imperfecta (AI). The wct locus maps to a specific interval of rat chromosome 14 corresponding to human chromosome 4q21 where the ameloblastin and enamelin genes exist, although these genes are not included in the wct locus. The effect of the wct gene mutation on the enamel matrix synthesis and calcification remains to be elucidated. This study clarifies how the wct gene mutation influences the synthesis of enamel matrix and its calcification by immunocytochemistry for amelogenin, ameloblastin and enamelin, and by electron probe micro-analysis (EPMA). The immunoreactivity for enamel proteins such as amelogenin, ameloblastin, and enamelin in the ameloblasts in the homozygous teeth was the same as that in the heterozygous teeth from secretory to transitional stages, although the homozygous ameloblasts became detached from the enamel matrix in the transitional stage. The flattened ameloblasts in the maturation stage of the homozygous samples contained enamel proteins in their cytoplasm. Thus, the wct mutation was found to prevent the morphological transition of ameloblasts from secretory to maturation stages without disturbing the synthesis of enamel matrix proteins, resulting in the hypo-mineralization of incisor enamel and cyst formation between the enamel organ and matrix. This mutation also prevents the transfer of iron into the enamel.

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Section: Discussionmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Rat wct mutation prevents differentiation of maturation-stage ameloblasts resulting in hypo-mineralization in incisor teeth

Osawa

Kenmotsu

Masuyama

et al. 2007

Histochem Cell Biol

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“…kyoto-u.ac.jp/nbr/) founded by MEXT in Japan (http:// www.nbrp.jp). The heredity of this trait and the genetic background are described in detail in our previous study (Masuyama et al 2005). Thirty male rats (Sprague Dawley; postnatal 4-to 30-day-old wild-types and wct homozygous mutants) were used in this study.…”

Section: Animalsmentioning

confidence: 99%

“…We have reported a rat autosomal-recessive mutant, whitish chalk-like teeth (wct), with white chalk-like abnormal incisors, among an outbred colony of Sprague Dawley (Crj:CD(SD)IGS) rats (Masuyama et al 2005). The wct homozygous mutants (wct/wct) exhibit tooth enamel defects similar to those of human AI.…”

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confidence: 93%

Rat wct mutation induces a hypo-mineralization form of amelogenesis imperfecta and cyst formation in molar teeth

et al. 2007

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Our previous findings have demonstrated that the rat autosomal-recessive mutation, whitish chalk-like teeth (wct), induces enamel defects resembling those of human amelogenesis imperfecta (AI) in continuously growing incisor teeth. The present study clarifies the effect of the wct mutation on the morphogenesis and calcification of rat molar teeth. Formalin-fixed maxillae obtained from animals aged 4-30 days were examined by electron probe micro-analysis (EPMA) and by immunocytochemistry for amelogenin, ameloblastin, and enamelin. There were no distinct differences in the calcium and phosphorous contents and the amount of enamel between homozygous mutant and wild-type teeth during postnatal days 4-11. Although the mineral density in the enamel matrix considerably increased in the wild-type teeth until day 15, no changes occurred in mutant teeth during days 11-30. The immunoreactivity for enamel proteins in the secretory-stage ameloblasts in mutant teeth was similar to that in the wild-type teeth, and subsequently mutant maturation-stage ameloblasts became detached from the enamel surface, resulting in odontogenic cyst formation between the enamel organ and matrix until day 7 and the expansion of the cyst around the whole tooth crown on day 15. On day 30, the erupted mutant teeth presented morphological changes such as enamel destruction and tertiary dentin formation in addition to low mineral density in the enamel. Thus, the wct mutation prevents mineral transport without disturbing the synthesis of enamel proteins in molar teeth because of the absence of maturation-stage ameloblasts, in addition to the occurrence of odontogenic cysts.

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Positional and ultrastructural changes in peripheral pulp capillaries correlate with the active phase of dentin deposition and mineralization in rat molars

Seino

Takano

Ohshima

2017

Journal of Oral Biosciences

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A novel autosomal‐recessive mutation, whitish chalk‐like teeth, resembling amelogenesis imperfecta, maps to rat chromosome 14 corresponding to human 4q21

Cited by 4 publications

References 29 publications

Rat wct mutation prevents differentiation of maturation-stage ameloblasts resulting in hypo-mineralization in incisor teeth

Rat wct mutation prevents differentiation of maturation-stage ameloblasts resulting in hypo-mineralization in incisor teeth

Rat wct mutation induces a hypo-mineralization form of amelogenesis imperfecta and cyst formation in molar teeth

Positional and ultrastructural changes in peripheral pulp capillaries correlate with the active phase of dentin deposition and mineralization in rat molars

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