Biomedical researchers investigate multiple aspects of periodontitis etiology

After examining the latest research findings dealing with periodontitis and the periodontal ligament in mouse models, the Department of Biomedical Sciences at Texas A&M University Baylor College of Dentistry recently published papers in two professional journals.

TAMBCD faculty contributed to the cover article of the March 2015 International Journal of Biological Sciences, which explains how osterix, a growth factor needed to transmit DNA information as bones form, impacts cementum, the thin layer of mineralized tissue essential for anchoring teeth to bone. The cementum cells, known as cementoblasts, proliferate and differentiate when the presence of osterix maintains low levels of the protein DKK1 and the signaling pathway Wnt-β-catenin. Understanding the mechanism involved in this process has applications in tissue reconstruction for periodontitis patients.

In other findings published in The Journal of the Federation of American Societies for Experimental Biology, TAMBCD researchers showed that removing a gene known as sclerostin or blocking its function significantly restores bone and periodontal ligament defects. This research is part of continued efforts to understand the makeup of the periodontal ligament in an attempt to develop an effective treatment for bone and ligament damage resulting from periodontitis.

As is evident from these findings, scientific breakthroughs don’t happen overnight. It takes many steps involving testing and retesting to discover what causes diseases and how they can be cured. In this case, further experimentation will be necessary to learn more about periodontitis and how it can be prevented.

Citation: Cao Z, Liu R, Zhang H, Liao H, Zhang Y, Hinton R, Feng J. Osterix controls cementoblast differentiation through downregulation of Wnt-signaling via enhancing DKK1 expression. International Journal of Biological Sciences 2015 March; 11(3): 335-344.

Citation: Ren Y, Han X, Ho S, Harris S, Cao Z, Economides A, Qin C, Ke H, Liu M, Feng J. Removal of SOST or blocking its product sclerostin rescues defects in the periodontitis mouse model. The Journal of the Federation of American Societies for Experimental Biology 2015 June; 29(6): 1-10.