THE PATHOPHYSIOLOGY OF ALVEOLAR OSTEONECROSIS OF THE JAW - ANTICARDIOLIPIN ANTIBODIES, THROMBOPHILIA, AND HYPOFIBRINOLYSIS

We studied 55 patients (50 women, 5 men) with severe facial pain and b iopsy-proven neuralgia-inducing cavilational osteonecrosis (NICO) of t he alveolar bone of the jaws. Our aim was to assess the pathophysiolog ic contributions to NICO of anticardiolipin antibodies (aCLA), thrombo philia (increased tendency to intravascular thrombi), and hypofibrinol ysis (reduced ability to lyse thrombi). Of the 55 patients, 43 (78%) h ad one or more tests positive for thrombophilia or hypofibrinolysis (o r both), and only 12 (22%) were normal. Eighteen of 55 (33%) patients had high aCLA (>2 SD above mean value for control subjects); immunoglo bulin G (IgG) (p = 0.01) and immunoglobulin A (IgA)(p = 0.001) levels were higher in patients than in controls. The distribution of elevated aCLA immunoglobulin classes among patients was as follows: lgG alone, 5 (9%); IgA alone, 7 (13%); and IgM alone, 3 (5%). Three patients (5% ) had high levels of both IgG and IgA aCLA. Other defects of the throm botic or fibrinolytic systems in the 55 patients included high lipopro tein(a) in 36% (vs 20% in control subjects (p = 0.03)), low stimulated tissue plasminogen activator activity (IPA-Fx) in 22% (vs 7% in contr ol subjects (p = 0.08)), high plasminogen activator inhibitor activity (PAI-Fx) in 18% (vs 8% in control subjects (p = 0.03)), resistance to activated protein C in 16% (vs 0% in control subjects (p = 0.007)), l ow antigenic protein C in 4% (vs 0% in control subjects (p > 0.2)), an d low antigenic protein S in 4% (vs 0% in control subjects (p > 0.2)). Anticardiolipin antibodies and other defects of the thrombotic and fi brinolytic systems appear to be common, potentially reversible pathoge netic risk factors associated with osteonecrosis of the jaw.