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A common feature of seasonal colds and other infections is painful joints. This is due to an acute reactive inflammatory arthritis which almost always resolves. Unfortunately, for some people the inflammation never completely resolves but rather precedes progression to chronic inflammatory arthritis. The existing dogma that accounts for why chronic inflammatory joint disease persists is that it is due to an excess of pro-inflammatory signals and that resolution occurs by pro-inflammatory mediator catabolism. Recent discoveries have supported a new paradigm which proposes that the resolution of inflammation is an active process with genetic, molecular and cellular programs that promote catabasis. By seeking to understand the mechanisms behind the spontaneous resolution of inflammation, we can gain insight into why inflammation sometimes fails to resolve. This review seeks to highlight the mechanisms behind the resolution of joint inflammation and how endogenous pro-resolving mediators could be used to treat chronic persistent inflammatory joint disease.

Original publication




Journal article


Semin immunol

Publication Date





194 - 199


Arthritis, Inflammation, Resolution, Anti-Inflammatory Agents, Non-Steroidal, Arthritis, Aspirin, Docosahexaenoic Acids, Humans, Inflammation, Inflammation Mediators, Joints, Lipid Metabolism, Signal Transduction