website: 86th General Session & Exhibition of the IADR

ABSTRACT: 2941  

Craniofacial bone and tooth morphogenesis of mecp2 null mice

K. TAKAMORI, Meiki University, Tokyo, Japan, M. ITOH, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan, and S. WATANABE, Meikai University, Saitama, Japan

Objective: Rett syndrome (RTT) is an inherited neurodevelopmental disorder that occurs heterozygous by a mutation in the methlyl-CpG-binding protein 2 (MeCP2), a well known protein that binds to methylated site in genomic DNA and resulting in gene silencing. The mecp2-null mutation mice have been reported to show the same behavior and symptoms at RTT.

Therefore, RTT patients frequently experience bruxism in as many as 85 to 90% of patients. We hypothesized that MeCP2 or their regulate gene‚“ induce or coordinate of RTT bruxism. However, the details of the craniofacial bone and tooth morphogenesis of mecp2 null mice are not well documented. The aim of this study was to evaluate the craniofacial bone and tooth morphogenesis of mecp2 null mice.

Methods: We analysed craniofacial bone and tooth morphologies by using micro focus X-ray CT on mice the same number (n=5) of weeks in age in both the mecp2 null and wild type mice.

Results: Mecp2-null mice have been seen to have smaller size of craniofacial bone and high calcification of their calvarial sutures, and are seen to have deep bite occlusion compared with the wild type, however were not showing deformity or misalignment in either jaw.

On the other hand, uniformity wear of their incisors and severe attrition of molars have been observed.

Conclusions: These results suggested that Mecp2-null mice have irregular abrasion of their incisors and molars, it possibilities was leaded to over movement and activity of jaw e.g. bruxism.

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