| First Author | Fujihara H | Year | 2019 |
| Journal | Cells | Volume | 8 |
| Issue | 10 | PubMed ID | 31569682 |
| Mgi Jnum | J:293301 | Mgi Id | MGI:6452554 |
| Doi | 10.3390/cells8101157 | Citation | Fujihara H, et al. (2019) Spontaneous Development of Dental Dysplasia in Aged Parp-1 Knockout Mice. Cells 8(10):1157 |
| abstractText | 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 Parp-1(-/-) mouse incisors showed more frequent dental dysplasia in both ICR/129Sv mixed background and C57BL/6 strain compared to aged Parp-1(+/+) 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 Parp-1(-/-) mice. The relative calcification levels of Parp-1(-/-) incisors were higher in both enamel and dentin (p < 0.05). Immunohistochemical analysis revealed (1) Parp-1 positivity in ameloblasts and odontoblasts in Parp-1(+/+) incisor, (2) weaker dentin sialoprotein positivity in dentin of Parp-1(-/-) incisor, and (3) bone sialoprotein positivity in dentin of Parp-1(-/-) incisor, suggesting ectopic osteogenic formation in dentin of Parp-1(-/-) 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. |
