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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;

View larger version (26K): [in this window] [in a new window]   Figure 1. Lipid mediators derived from arachidonic acid in inflammation. Prostaglandins and leukotrienes generated by cyclooxygenase (COX) and the 5, 12, and 15 lipoxygenases amplify inflammation. Lipoxins are generated through transcellular biosynthetic routes through the action of two lipoxygenases on the same arachidonic acid molecule to act as endogenous stop signals in inflammation. NSAID: Non-steroidal anti-inflammatory drug.

View larger version (28K): [in this window] [in a new window]   Figure 2A. Local and regional lipoxin biosynthesis by vascular and mucosal routes.

View larger version (20K): [in this window] [in a new window]   Figure 2B. Lipoxin biosynthetic regulators.

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