title: Nfic gene disruption inhibits differentiation of odontoblasts responsible for root formation and results in formation of short and abnormal roots in mice.
abstract: BACKGROUND
  Nuclear factor I genes play an important role in the development of the brain, lung, and roots of teeth. We had reported that Nfic-deficient mice form normal crowns, but abnormal roots of molar teeth. However, the mechanism by which the disruption of Nfic gene causes abnormal root formation remains unknown.
  
  
  METHODS
  To understand this mechanism, the root formation in Nfic-deficient mice was examined and compared to that of wild-type mice by morphological, immunohistochemical, and in situ hybridization analyses.
  
  
  RESULTS
  Nfic-deficient mice formed normal Hertwig's epithelial root sheath (HERS) but severely disrupted odontoblast differentiation, leading to the formation of aberrant odontoblasts in the early stage of root formation. They became dissociated and polygonal in shape, lost their orientation and polarity, and did not express dentin sialophosphoprotein. The abnormal roots contained trapped aberrant odontoblasts, thereby resembling osteodentin in overall morphology. No osteoclasts were associated with abnormal roots. Further, the abnormal roots exhibited a decreased number of cementoblasts and cementum formation on the root surface.
  
  
  CONCLUSIONS
  The loss of Nfic did not interfere with the formation of HERS, but it caused disrupted odontoblast differentiation, which resulted in the formation of short and abnormal roots, and decreased cementum. This finding suggests that root dentin is required for normal cementum formation. Therefore, Nfic may be a key regulator of root odontoblast differentiation and root formation.
authors.affiliation: Department of Oral Histology and Anatomy, College of Dentistry, Chosun University, Gwang-Ju, Korea. jcapark@chosun.ac.kr
authors.forename: Joo-Cheol
authors.initials: JC
authors.lastname: Park
authors.forename: Yeek
authors.initials: Y
authors.lastname: Herr
authors.forename: Heung-Joong
authors.initials: HJ
authors.lastname: Kim
authors.forename: Richard M
authors.initials: RM
authors.lastname: Gronostajski
authors.forename: Moon-Il
authors.initials: MI
authors.lastname: Cho
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D048430:Cell Shape; D025021:Cementogenesis / Q000235:genetics*; D003810:Dentinogenesis / Q000235:genetics; D004847:Epithelial Cells / Q000166:cytology; D016326:Extracellular Matrix Proteins; D018507:Gene Expression Regulation, Developmental; D050437:Genes, Developmental / Q000502:physiology; D007124:Immunoenzyme Techniques; D017403:In Situ Hybridization; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D023421:Models, Animal; D051839:NFI Transcription Factors / Q000235:genetics* / Q000502:physiology*; D009804:Odontoblasts / Q000473:pathology*; D010750:Phosphoproteins; D011498:Protein Precursors / Q000096:biosynthesis; D012795:Sialoglycoproteins; D014092:Tooth Root / Q000002:abnormalities*; D000099311:Dentin Sialophosphoprotein
chemical_list: D016326:Extracellular Matrix Proteins; D051839:NFI Transcription Factors; D010750:Phosphoproteins; D011498:Protein Precursors; D012795:Sialoglycoproteins; D000099311:Dentin Sialophosphoprotein; C497648:Nfic protein, mouse