Department of Oral and Maxillofacial Surgery, Center for Dental Education and Research, All India Institute of Medical Sciences, New Delhi 110029, India.
Med Hypotheses. 2013 Oct;81(4):561-3. doi: 10.1016/j.mehy.2013.06.031. Epub 2013 Aug 1.
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.
颞下颌关节（TMJ）强直是亚洲国家的一个重大问题，最常见的病因是下颌骨髁突创伤。其他较少见的病因包括感染、产钳分娩创伤和类风湿关节炎。有许多假说被提出来解释其发病机制。所有提出的假说都围绕着关节创伤及其随后的愈合导致强直。然而，这仅适用于少数患者，大多数其他患者在 TMJ 创伤后即使不寻求治疗也不会进展为强直。在本文中，我们试图回答一个问题，即为什么只有一小部分髁突损伤进展为强直，而其他的则没有？这一假说源于 4 例双侧 TMJ 强直合并肝外门静脉阻塞（EHPVO）继发于蛋白 C 缺乏的报告。据推测，这些 TMJ 强直伴 EHPVO 以及非 EHPVO 患者的高凝状态/纤维蛋白溶解活性降低可能使他们易发生关节强直。解释了可能的机制，并与 TMJ 强直的其他原因以及蛋白 C 缺乏/活化蛋白 C 抵抗的已知事实相关联。
