The analgesic and therapeutic effects of NSAIDs are achieved by COX-2 inhibition [4]. It is likely that COX inhibition by NSAIDs is detrimental to the bone healing process, given the favourable actions of PG on this process [4]. Osteoblasts have the capacity to produce PGs, where PGE2 is most abundant, through the COX pathway though the evidence asserting that PGs have a direct role in bone healing is inconclusive [1, 23]. Furthermore, there is insufficient evidence in the current literature to explicitly conclude that there is a relationship between the use of NSAIDs and early implant failure. However, osseointegration does not appear to be negatively affected by NSAIDs in the human clinical studies, which contrasts with the experimental in vitro and in vivo animal studies. Furthermore, there are no human clinical studies that have investigated the effect of a selective COX-2 NSAID on osseointegration. Therefore, further research with an emphasis in human clinical studies comparing the effect of the COX selectivity of NSAIDs on osseointegration is required.