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Resolution of Inflammation: A New Paradigm for the Pathogenesis of Periodontal Diseases

¹ Department of Periodontology and Oral Biology, Boston University, Goldman School of Dental Medicine, 100 East Newton Street, Boston, MA 02118; and
² Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;

Correspondence: *corresponding author, tvandyke{at}bu.edu

The periodontal diseases are infectious diseases caused by predominantly Gram-negative bacteria. However, as our understanding of the pathogenesis of the periodontal diseases grows, it is becoming clear that most of the tissue damage that characterizes periodontal disease is caused by the host response to infection, not by the infectious agent directly. Investigation into the mechanism of action of host-mediated tissue injury has revealed that the neutrophil plays an important role in destruction of host tissues. In this paper, we review the biochemical pathways and molecular mediators that are responsible for regulation of the inflammatory response in diseases such as periodontitis, with a focus on lipid mediators of inflammation. Pro-inflammatory mediators, such as prostaglandins and leukotrienes, are balanced by counter-regulatory signals provided by a class of molecules called lipoxins. The role of lipoxins in the control and resolution of inflammation is discussed, as is the possibility of the development of new therapeutic strategies for the control and prevention of neutrophil-mediated tissue injury in inflammatory diseases like periodontitis.

Key Words: lipid mediators of inflammation • lipoxins • neutrophils • periodontal disease

Journal of Dental Research, Vol. 82, No. 2, 82-90 (2003)
DOI: 10.1177/154405910308200202


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