Resolution of inflammation in periodontitis - PubMed (original) (raw)

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Resolution of inflammation in periodontitis

Alpdogan Kantarci et al. J Periodontol. 2005 Nov.

Abstract

Chronic inflammatory illnesses such as diabetes, arthritis, and heart disease are now seen as problems that might have impacts on the periodontium, and reciprocal effects of periodontal diseases are being considered as factors potentially affecting the progression of these diseases. Successful management of the inflammatory disorders in the human body depends on the identification of common pathways that would lead to a better understanding of the disease processes and development of novel treatment strategies. In this review, our objective is to identify the inflammatory basis of periodontal disease and common inflammatory mechanisms underlying several disorders elsewhere in the body, with an emphasis on how the potential extrinsic and intrinsic control methods could be used to prevent or treat the harmful effects linked to inflammation.

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Figures

Figure 1

Figure 1

Mediators of arachidonic acid metabolism lead to generation of prostaglandins (PG) and leukotrienes (LT) through cyclooxygenase (COX) and lipoxygenase (LO) pathways.

Figure 2

Figure 2

Sequential events in inflammation. PMN-mediated inflammation is the first step in host response against infection. This phase is followed by monocyte-dominated events during which granulation tissue formation occurs. Stop signals of LX and RvE prevent excessive PMN-mediated tissue response to stimuli.

Figure 3

Figure 3

Biosynthesis of resolvins. Omega-3 polyunsaturated fatty acids (ω-3 PUFA) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are metabolized by the acetyl salisilic acid (aspirin) acetylation of cyclooxygenase (COX)-2 into resolvins. Human PMN through the action of COX-2 converts DHA into 13-hydroxy-DHA, which is switched to 17R-HDHA through aspirin. This molecule is transformed into two compounds via 5-lipoxygenation that are each rapidly transformed into two intermediates. These two novel epoxide intermediates open to bioactive trihydroxy-containing products denoted 17R series Resolvin D-1, Resolvin D-2, Resolvin D-3, and Resolvin D-4. Meanwhile, endothelial cells that express COX-2 will convert EPA into 18R-H(p)EPE in the presence of aspirin, and this line of molecules will give rise to Resolvin-E1.

Figure 4

Figure 4

15-LO transgenic rabbits exhibited no evidence of periodontitis.

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