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Related Experiment Video

Updated: Sep 12, 2025

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Genetic Variants in KIF7 May Contribute to Supernumerary Tooth Formation.

Phohathai Chainaphaphorn1, Chumpol Ngamphiw2, Sissades Tongsima2

  • 1Center of Excellence in Medical Genetics Research, Chiang Mai University, Chiang Mai, Thailand; Division of Pediatric Dentistry, Department of Orthodontics and Pediatric Dentistry, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand.

International Dental Journal
|August 7, 2025
PubMed
Summary
This summary is machine-generated.

Genetic variants in Kinesin Family Member 7 (KIF7) may contribute to supernumerary teeth formation. This study identified novel KIF7 variants associated with various dental anomalies, including extra teeth.

Keywords:
CiliopathyMesiodensOdontomaSHH signallingSupernumerary teethWNT signalling

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Area of Science:

  • Genetics
  • Developmental Biology
  • Oral Biology

Background:

  • Kinesin Family Member 7 (KIF7) is crucial for maintaining ciliary integrity.
  • Cilia-mediated sonic hedgehog signaling influences tooth development, including number, position, and morphology.
  • Disruptions in these pathways can lead to dental anomalies.

Purpose of the Study:

  • To investigate the potential role of KIF7 gene variants in the etiology of supernumerary teeth.
  • To identify specific KIF7 mutations associated with dental abnormalities.

Main Methods:

  • Whole-exome sequencing was conducted on 153 individuals from 130 families presenting with isolated supernumerary tooth types.
  • Immunohistochemistry was used to examine Kif7 expression during mouse embryonic odontogenesis.
  • Computational modeling was employed to analyze the impact of identified KIF7 variants on protein structure and function.

Main Results:

  • Six KIF7 variants (4 rare missense, 1 novel missense, 1 insertion) were identified in patients with supernumerary teeth, including mesiodens, supernumerary molars, and compound odontomas.
  • Variants in the KIF7 motor domain (p.His54Tyr, p.Val59Met) are predicted to impair tubulin interaction and disrupt ciliary localization.
  • Other variants (p.Arg851Cys, p.Glu628Lys, p.Glu630_Glu631dup, p.Pro655Arg) are predicted to affect protein structure and charge balance.

Conclusions:

  • This study provides the first evidence linking KIF7 variants to supernumerary tooth phenotypes.
  • KIF7 mutations represent a potential genetic factor contributing to the development of extra teeth.
  • Further research is warranted to fully elucidate the mechanisms by which KIF7 dysfunction leads to dental anomalies.