Human chemokine-like receptor 1 regulates the resolution of acute inflammation and ligature-induced periodontitis in transgenic mice

PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.Thesis (D.Sc.)--Boston University, Henry M. Goldman School of Dental Medicine, 2007 (Periodontology and Oral Biology).Periodontitis is a bacterially induced inflammatory disease resulting in the destruction of tooth-supporting tissues, including the periodontal ligament and the alveolar bone. We have compared two classic experimental models of periodontal disease, molar ligation and Porphyromonas gingivalis oral inoculation, and found that ligation results in a more rapid and more profound alveolar bone loss than P. gingivalis inoculation. Similarly to dental calculus, the ligature not only serves as a reservoir for oral bacteria but it also exerts mechanical pressure on the gingiva, thus interfering with gingival microcirculation. Removal of the ligature resulted in regrowth of the alveolar bone, indicating the reversibility of the tissue damage in this model. Acute inflammation is comprised of proinflammatory and resolution phases, both regulated by a diverse range of endogenous mediators. The resolution phase of inflammation is now recognized as an active process mediated by formation and activation of local lipid mediators and termination of pro-resolving signals, aimed at tissue restoration. Novel lipid mediators such as lipoxins, resolvins, and protectins have been identified and characterized to possess anti-inflammatory and/or pro-resolving properties, In our study, we have analyzed the actions of resolvin E1 and its receptor, ChemR23 on acute inflammation and periodontitis. [TRUNCATED