RESEARCH - Non-traumatic necrosis of bone (osteonecrosis) is associated with endothelial cell activation but not thrombophilia

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Rheumatology Advance Access published online on June 4, 2008

Rheumatology, doi:10.1093/rheumatology/ken206

Non-traumatic necrosis of bone (osteonecrosis) is associated with

endothelial cell activation but not thrombophilia

C. Séguin1,2, J. Kassis3, L. Busque3, A. Bestawros4, J.

Theodoropoulos5, M.-L. Alonso3 and E. J. Harvey5

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.

Abstract

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.

http://rheumatology.oxfordjournals.org/cgi/content/abstract/ken206v1?papetoc

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