| First Author | Wu Y | Year | 2019 |
| Journal | Bone | Volume | 122 |
| Pages | 176-183 | PubMed ID | 30408613 |
| Mgi Jnum | J:273273 | Mgi Id | MGI:6286788 |
| Doi | 10.1016/j.bone.2018.10.023 | Citation | Wu Y, et al. (2019) Aberrantly elevated Wnt signaling is responsible for cementum overgrowth and dental ankylosis. Bone 122:176-183 |
| abstractText | Vertebrate teeth are attached to the jawbones using a variety of methods but in mammals, a fibrous connection is the norm. This fibrous periodontal ligament (PDL) allows teeth to move in the jawbones in response to natural eruptive forces, mastication, and orthodontic tooth movement. In some disease states the PDL either calcifies or is replaced by a mineralized tissue and the result is ankylosis, where the tooth is fused to the alveolar bone. To understand how the PDL maintains this fibrous state, we examined a strain of mice in which tooth movement is arrested. Dabetacat(Ot) mice express a stabilized form of beta-catenin in DMP1-positive alveolar bone osteocytes and cementocytes, which results in elevated Wnt signaling throughout the periodontium. As a consequence, there is an accrual of massive amounts of cellular cementum and alveolar bone, the PDL itself calcifies and teeth become ankylosed. These data suggest that to maintain its fibrous nature, Wnt signaling must normally be repressed in the PDL space. |
