Although all the theories reported of the etiopathol- ogy of dry socket still need to be established, some evidence has suggested that an interaction exists be- tween excessive local trauma and bacterial invasion. This association results in the formation of plasmin and, consequently, fibrinolysis inside the socket.1,27 In 1989, Catellani28 stated that the pyrogens secreted by the bacteria are indirect activators of fibrinolysis in vivo. Catellani28 studied the effectiveness of those pyrogens on the treatment of thromboembolic dis- ease, injecting the products intravenously. An inter- esting fact is that dry socket does not occur until after the first postoperative day. The explanation is that the