Haemostasis in oral surgery--the possible pathogenetic implications of oral fibrinolysis on bleeding. Experimental and clinical studies of the haemostatic balance in the oral cavity, with particular reference to patients with acquired and congenital defects of the coagulation system.
Activation and inhibition of the haemostatic system was reviewed including the interaction between the four biological systems involved in haemostasis: the vessel wall, the platelets, the coagulation system and the fibrinolytic system. The haemostatic mechanism is initiated at the site of injury through local activation of surfaces and release of tissue thromboplastin, resulting in formation and deposition of fibrin. The coagulation process is regulated by physiological anticoagulants. Activation of fibrinolysis is triggered by the presence of fibrin, and the role of tissue-type plasminogen activators (t-PA) at the site of fibrin formation in particular is emphasized. The process is regulated by physiological inhibitors, of which alpha 2-antiplasmin, histidine-rich glycoprotein and plasminogen activator inhibitor are reported to be of major physiological significance. The role of fibrinolysis in the regulation of the dynamic haemostatic balance is discussed, elucidated through examples of congenital deficiencies of the coagulation and the fibrinoytic system. Pharmacological inhibitors of fibrinolysis (i.e. epsilon-aminocaproic acid and tranexamic acid) and their possible effect on the haemostatic system are described. The systemic effects on the fibrinolytic system of surgery and oral surgery is reviewed, and it is concluded, that oral surgery has insignificant effects on blood fibrinolysis. In contrast, oral surgery induces changes of fibrinolysis in the oral environment; initially the fibrinolytic activity of saliva is reduced, due to the presence of inhibitors of fibrinolysis originating from the blood and the wound exudate. When bleeding and exudation cease, the fibrinolytic activity of the saliva will increase. Plasminogen and plasminogen activator, identified as t-PA are present in the oral environment under physiological conditions. Plasminogen is secreted in the saliva and the sources of t-PA include oral epithelial cells and gingival crevicular fluid. The presence of plasminogen and t-PA in the oral environment implies that when fibrin is present (i.e. after surgery), fibrinolysis is triggered. Haemorrhagic complications to oral surgery in patients without known defects of the coagulation system is reviewed. It is concluded that the investigations conducted to the present day do not permit final conclusions with respect to the pathophysiological role of defects in the coagulation and the fibrinolytic systems for the development of bleeding after oral surgery. Further investigations are necessary in order to clarify these aspects, and should include extensive laboratory analyses to reveal rare congenital defects such as factor XIII- and alpha 2-antiplasmin deficiencies.(ABSTRACT TRUNCATED AT 400 WORDS)
Sindet-Pedersen
S
S
Department of Clinical Chemistry, Ribe County Hospital, Esbjerg.
D000925:Anticoagulants / Q000009:adverse effects; D001777:Blood Coagulation / Q000502:physiology; D001792:Blood Platelets / Q000502:physiology; D003894:Deamino Arginine Vasopressin / Q000627:therapeutic use; D005337:Fibrin / Q000502:physiology; D005342:Fibrinolysis / Q000502:physiology*; D005881:Gingiva / Q000502:physiology; D006467:Hemophilia A; D006470:Hemorrhage / Q000503:physiopathology / Q000517:prevention & control; D006487:Hemostasis / Q000502:physiology*; D006488:Hemostasis, Surgical / Q000379:methods*; D006801:Humans; D009061:Mouth Mucosa / Q000502:physiology; D012463:Saliva / Q000502:physiology; D013515:Surgery, Oral; D010959:Tissue Plasminogen Activator / Q000502:physiology; D014842:von Willebrand Diseases
D000925:Anticoagulants; D005337:Fibrin; D010959:Tissue Plasminogen Activator; D003894:Deamino Arginine Vasopressin