Rheumatology Advance Access originally published online on June 4, 2008
Rheumatology 2008 47(8):1151-1155; doi:10.1093/rheumatology/ken206
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Non-traumatic necrosis of bone (osteonecrosis) is associated with endothelial cell activation but not thrombophilia
1Department of Medicine, Division of Haematology, 2Department of Oncology, McGill University Health Centre, 3Department of Medicine, Division of Haematology, Maisonneuve-Rosemont Hospital, 4Department of Medicine, Division of Internal Medicine and 5Department of Orthopaedic Surgery, McGill University Health Centre, Montreal, Quebec, Canada.
Correspondence to: C. Séguin, Montreal General Hospital, McGill University Health Center, 1650 Cedar Avenue, room A7-117, Montreal, Quebec, Canada. E-mail: chantal.seguin{at}muhc.mcgill.ca
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Abstract |
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Objective. The pathophysiology of non-traumatic osteonecrosis (ON) or avascular necrosis (AVN) of the femoral head remains poorly understood. Some studies have suggested the contribution of underlying thrombophilia as a mechanism; however, no specific thrombophilic factor has been consistently found in association with the disease. We are presenting data suggesting a role for endothelial cell activation rather than thrombophilia in ON.
Methods. A prospective consecutive cohort of 49 patients with a diagnosis of ON. The disease was considered idiopathic in five and secondary in 44 patients. The investigation included a coagulation and thrombophilia profile, endothelial cell activation and non-specific inflammatory markers as well as a biochemical profile. Statistical analysis using Fisher's exact test was obtained to assess correlation between endothelial cell markers and variables of inflammation.
Results. Patients with non-traumatic ON were not found to have a specific underlying thrombophilic factor compared with the general population. Out of 49 patients,19 had elevation of at least one endothelial cell markers. We found that activation of endothelial cell markers was independently correlated to ON but not correlated to the presence of inflammation (P = 1.0000).
Conclusion. These results suggest that non-traumatic ON is not associated with a specific thrombophilic abnormality in those affected. This study demonstrates a potential association between regional endothelial dysfunction and ON. More studies are needed at a molecular level to further investigate the specific role of endothelium in the physiopathology of ON. A better understanding of the underlying mechanism could lead to potential preventive and therapeutic strategies of this devastating disease.
KEY WORDS: Avascular necrosis, Osteonecrosis, Thrombophilia, Endothelial cell activation, Inflammation
Submitted 9 February 2008; Accepted 17 April 2008