INVESTIGATING THE ROLE OF DKK3 IN TEMPOROMANDIBULAR JOINT HOMEOSTASIS IN THE MURINE MODEL

Abstract

The temporomandibular joint (TMJ), also known as the jaw joint, is essential to daily human function. Without proper jaw function, necessary activities like eating, drinking, and speaking can become painful and impaired [1]. In studying the TMJ, both histologically and molecularly, our understanding of how disorders of the jaw joint develop can be furthered. Controlling the canonical Wnt (cWnt) signaling pathway has been thought to have essential function in the maintenance of the TMJ. Preventing cWnt signaling in putative progenitor cell populations may allow for these cells to differentiate into necessary fibrocartilage for the TMJ articulating surfaces [2]. One likely inhibitor of cWnt, which has been less thoroughly researched in vivo, is Dkk3. To study the role of Dkk3 in TMJ homeostasis in vivo, the Dkk3 gene was deleted in transgenic mice and compared to Dkk3 wild type. Then, the TMJs of these mice were studied through H&E histology, fluorescent reporters tagging Wnt signaling activity, and micro-CT. Our findings suggest that Dkk3 is indeed important in vivo to the maintenance of putative stem progenitor populations in the TMJ condyle and fossa, and in the absence of Dkk3 these populations may be depleted and differentiated into bone by excessive Wnt signaling, causing abnormal TMJ features, particularly in the fossa.