Alveolar bone turnover and periodontal ligament width are controlled by Wnt

The molecular signals responsible for maintaining homeostatic control over the periodontal ligament (PDL) are unknown. The purpose of this study is to investigate the role of Wnt signaling in this process using gain- and loss-of-function approaches.

The function of endogenous Wnt signal in the PDL was evaluated in Lrp5(ACT) mice in which a mutation in the low-density lipoprotein receptor-related protein 5 Wnt coreceptor causes constitutive activation of Wnt signaling, and in adenovirus Dkk1-treated mice in which overexpression of the Wnt inhibitor Dkk1 causes transient Wnt signal inhibition. PDL in both animal models was examined using histology and immunohistochemical analyses for osteopontin, runt-related transcription factor 2 (Runx2), fibromodulin, osterix, ki67, receptor activator of nuclear factor-κB ligand (RANKL), and alkaline phosphatase activity.

Lrp5(ACT) mice exhibited a significant narrowing of the PDL space caused by an increase in osteogenic gene expression, a reduction in RANKL expression and osteoclast activity, and an increase in alveolar bone formation. Conversely, adenovirus Dkk1-treated mice showed decreased expression of osteogenic markers, coupled with an increase in osteoclast activity, which resulted in a slight increase in PDL width.

The Wnt pathway is involved in the homeostatic control of the PDL, and conditions that elevate or repress Wnt signaling alter the expression of osteogenic genes within the PDL space, which in turn affects its overall width.