Elsevier

Bone

Volume 122, May 2019, Pages 176-183
Bone

Full Length Article
Aberrantly elevated Wnt signaling is responsible for cementum overgrowth and dental ankylosis

https://doi.org/10.1016/j.bone.2018.10.023Get rights and content
Under a Creative Commons license
open access

Highlights

  • Stabilize β-catenin in DMP1 cells increases Wnt signaling in periodontium.

  • Increased Wnt signaling in periodontium causes tooth eruption defect.

  • Eruption required bone resorption remains unchanged after increasing Wnt signaling.

  • Increased Wnt signaling causes ankylosis by enhancing osteogenic differentiation.

Abstract

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. DaβcatOt mice express a stabilized form of β-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.

Keywords

Periodontium
Ankylosis
Dental
Tooth eruption
Cementum

Cited by (0)

1

Shared first authors.