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Nicotinamide Improves Delayed Tooth Eruption in Runx2 Mice.

H Yoon¹, H J Kim¹, H R Shin¹

¹Department of Molecular Genetics and Pharmacology, School of Dentistry and Dental Research Institute, BK21 Program, Seoul National University, Seoul, Republic of Korea.

Journal of Dental Research

|November 4, 2020

Summary

This summary is machine-generated.

Nicotinamide, a vitamin B3, effectively treats delayed tooth eruption in a mouse model of cleidocranial dysplasia (CCD). This vitamin B3 derivative restores osteoclastogenesis, offering a potential therapeutic for dental issues in CCD patients.

Keywords:

bone biology bone remodeling/regeneration mineralized tissue/development osteoblast osteoclast posttranslational modifications

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Area of Science:

Genetics and Molecular Biology
Developmental Biology
Pharmacology

Background:

Cleidocranial dysplasia (CCD) causes severe dental anomalies, including delayed tooth eruption.
Current treatments involve invasive surgical and orthodontic interventions due to a lack of medication.
The RUNX2 gene is crucial for bone and tooth development, and its mutations lead to CCD.

Purpose of the Study:

To investigate the therapeutic potential of nicotinamide for delayed tooth eruption in a mouse model of CCD.
To elucidate the molecular mechanisms by which nicotinamide affects osteoclastogenesis and tooth eruption.
To identify nicotinamide as a potential drug candidate for dental abnormalities in CCD.

Main Methods:

Utilized the Runx2-deficient (Runx2-/-) mouse model, a standard model for CCD.
Administered nicotinamide to assess its effects on delayed tooth eruption and osteoclastogenesis.
Analyzed gene and protein expression levels of key factors including RUNX2, CSF1, RANKL, and OPG.
Investigated the regulatory role of RUNX2 in Csf1 gene expression and the impact of nicotinamide on RUNX2 activity.

Main Results:

Nicotinamide significantly improved delayed tooth eruption in Runx2-/- mice.
Treatment with nicotinamide restored osteoclastogenesis by increasing RUNX2 and CSF1 expression and the RANKL/OPG ratio.
RUNX2 was found to directly regulate Csf1 gene expression.
Nicotinamide enhanced RUNX2 protein levels and activity through Sirt2 inhibition.

Conclusions:

Nicotinamide demonstrates significant therapeutic potential for treating delayed tooth eruption in CCD.
The study reveals the underlying molecular mechanism involving the restoration of osteoclastogenesis via RUNX2 and CSF1 regulation.
Nicotinamide is proposed as a promising candidate drug for addressing dental abnormalities associated with cleidocranial dysplasia.