N-3 polyunsaturated fatty acid effect in periodontal disease: state of art and possible mechanisms involved.
Anti-inflammatory properties have been widely reported for n-3 polyunsaturated fatty acids (PUFAs) and some studies have been focalized on their possible role in the modulation of gingivitis and alveolar bone resorption in periodontal disease (PD). Increased formation of arachidonic acid-derived inflammatory eicosanoids and augmented oxidative stress are two molecular mechanisms pathogenetically involved in the progression of PD and known to be inhibited by n-3 PUFAs in PD setting. The present review will focus also on other molecular pathways and factors known to be altered in the development of PD and known to be subject to n-3 PUFA modulation in other pathological settings different from PD. Overall, the available findings strongly encourage further experimental studies on animals subject to experimental PD and treated with n-3 PUFAs, long term n-3 PUFA intervention studies on PD patients and molecular studies to identify additional potential molecular routes of n-3 PUFA action in PD.
Institute of Clinical Dentistry, Catholic University, Largo F. Vito 1, Rome, Italy.
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D000818:Animals; D015815:Cell Adhesion Molecules; D015777:Eicosanoids / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000627:therapeutic use*; D006801:Humans; D045726:Metalloproteases / Q000096:biosynthesis; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D010510:Periodontal Diseases / Q000503:physiopathology / Q000517:prevention & control*; D053245:RANK Ligand / Q000378:metabolism
D015815:Cell Adhesion Molecules; D015777:Eicosanoids; D015525:Fatty Acids, Omega-3; D016328:NF-kappa B; D053245:RANK Ligand; D020928:Mitogen-Activated Protein Kinases; D045726:Metalloproteases