Temporomandibular joint ankylosis: Is hypercoagulable state of blood a predisposing factor?

Abstract

Temporomandibular joint (TMJ) ankylosis is a significant problem in Asian countries and the most common etiology is trauma to the mandibular condyle. Other less common etiologies are infection, forceps delivery trauma and rheumatoid arthritis. Many hypotheses are given to explain the pathogenesis. All the proposed hypotheses revolve around trauma to the joint and subsequent healing causing ankylosis. This is however true for only few patients, most of the others do not progress to ankylosis after trauma to TMJ irrespective of seeking treatment or not. In this paper, we try to answer the question that why only a minor subset of condylar injuries progress to ankylosis and why others do not? The hypothesis follows a report of 4 cases that had bilateral TMJ ankylosis with extrahepatic portal venous obstruction (EHPVO) secondary to protein C deficiency. It is postulated that hypercoagulability/reduced fibrinolytic activity in these as well as non-EHPVO patients with TMJ ankylosis cases may have predisposed them to the development of joint ankylosis. The possible mechanism is explained and correlated with other causes of TMJ ankylosis and known facts of protein C deficiency/activated protein C resistance.