Spontaneous Development of Dental Dysplasia in Aged Parp-1 Knockout Mice

摘要

Poly(ADP-ribose) polymerase (Parp)-1 catalyzes polyADP-ribosylation using NAD and is involved in the DNA damage response, genome stability, and transcription. In this study, we demonstrated that aged mouse incisors showed more frequent dental dysplasia in both ICR/129Sv mixed background and C57BL/6 strain compared to aged incisors, suggesting that Parp-1 deficiency could be involved in development of dental dysplasia at an advanced age. Computed tomography images confirmed that dental dysplasia was observed at significantly higher incidences in mice. The relative calcification levels of incisors were higher in both enamel and dentin ( < 0.05). Immunohistochemical analysis revealed (1) Parp-1 positivity in ameloblasts and odontoblasts in incisor, (2) weaker dentin sialoprotein positivity in dentin of incisor, and (3) bone sialoprotein positivity in dentin of incisor, suggesting ectopic osteogenic formation in dentin of incisor. These results indicate that Parp-1 deficiency promotes odontogenic failure in incisors at an advanced age. Parp-1 deficiency did not affect dentinogenesis during the development of mice, suggesting that Parp-1 is not essential in dentinogenesis during development but is possibly involved in the regulation of continuous dentinogenesis in the incisors at an advanced age.