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 P 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.
Raffaelli, L., Serini, S., Piccioni, E., Manicone, P. F., Berardi, D., Perfetti, G., Calviello, G., n-3 polyunsaturated fatty acid effect in periodontal disease: state of art, future perspectives and possible mechanisms involved, <<INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY>>, 2008; (21): 261-266. [doi:10.1177/039463200802100202] [http://hdl.handle.net/10807/20974]
n-3 polyunsaturated fatty acid effect in periodontal disease: state of art, future perspectives and possible mechanisms involved
Raffaelli, Luca;Serini, Simona;Piccioni, Elisabetta;Manicone, Paolo Francesco;Calviello, Gabriella
2008
Abstract
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 P 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.