Aims: To determine the available evidence in the literature for whether hypoxia-reperfusion injury plays a role in the pathogenesis of joint diseases in general and of osteoarthritis (OA) of the temporomandibular joint (TMJ) in particular. Methods: The electronic databases CENTRAL, PubMed, and EMBASE were systematically searched. The search strategy combined thesaurus terms “reperfusion injury” and “joints” and excluded “tourniquet,” which possibly induces iatrogenic reperfusion injury. Inclusion and exclusion criteria were applied, data were extracted, and quality was assessed. Results: Four studies could be included, investigating four different aspects of the hypoxia-reperfusion mechanism in joints. All studies investigated several arthritides in the knee or shoulder joint and were observational studies, except for one section of one of the studies, which was a randomized controlled trial. These studies do not provide any evidence to support or reject the hypothesis that hypoxia reperfusion occurs in TMJ OA. Positive but weak evidence is provided to support the hypothesis that hypoxia-reperfusion injury occurs in OA of the knee joint. Furthermore, some results of the included studies suggest differences between OA and other types of arthritis in relation to the hypoxia-reperfusion mechanism. Conclusion: There is no evidence to support or reject the hypothesis that hypoxia reperfusion occurs in TMJ OA, and limited evidence is provided to support that hypoxia-reperfusion injury occurs in OA of the knee joint. Since the studies suggest differences between OA and other types of arthritis in relation to hypoxia-reperfusion mechanisms, further research in this field needs to distinguish OA from other types of arthritis. J OROFAC PAIN 2012;26:233–239

Key words: free radicals, osteoarthritis, reperfusion injury, temporomandibular joint