In the skeleton, prostaglandins, mainly PGE(2) produced by osteoblasts under COX-2 stimulation, play either a stimulatory or an inhibitory role in bone metabolism, depending on the physiological or pathological conditions. The anabolic effect occurs largely in response to mechanical forces and in bone fracture healing, whereas PGE(2)-mediated resorption contributes significantly to bone loss in inflammatory diseases and in response to prolonged immobilization. Many reports have shown that conventional nonsteroidal anti-inflammatory drugs (NSAIDs) may delay fracture healing and negatively interfere with spinal fusion in both humans and other animals, whereas the alleged inhibitory effects of COX-2-selective NSAIDs still lacks experimental and clinical evidence. Pertaining to clinical dentistry, recent studies have suggested a potential adjuvant role for NSAIDs in periodontal therapy. There are few experimental reports addressing the deleterious effects of conventional NSAIDs on alveolar bone healing; clinical reports, relating mostly to short-term administration of NSAIDs for management of post-extraction edema and pain, are just as rare and have noted no clinically perceptible delay in bone healing. Additional studies are necessary in order to elucidate whether patients who require reparational bone formation can safely receive prolonged treatment with NSAIDs, and which drug types are less harmful.