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National Journal of Maxillofacial Surgery
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Table of Contents
Year : 2020  |  Volume : 11  |  Issue : 1  |  Page : 154-155  

Pathogenesis of temporomandibular joint ankylosis: A perspective

Department of Oral and Maxillofacial Surgery, All India Institute of Medical Sciences, New Delhi, India

Date of Submission27-Dec-2018
Date of Acceptance28-May-2019
Date of Web Publication18-Jun-2020

Correspondence Address:
Krushna V Bhatt
Department of Oral and Maxillofacial Surgery, All India Institute of Medical Sciences, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njms.NJMS_91_18

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How to cite this article:
Bhatt KV, Roychoudhury A, Bhutia O. Pathogenesis of temporomandibular joint ankylosis: A perspective. Natl J Maxillofac Surg 2020;11:154-5

How to cite this URL:
Bhatt KV, Roychoudhury A, Bhutia O. Pathogenesis of temporomandibular joint ankylosis: A perspective. Natl J Maxillofac Surg [serial online] 2020 [cited 2023 Feb 5];11:154-5. Available from: https://www.njms.in/text.asp?2020/11/1/154/287131


The following write-up is to string the known facts in one thread to explain all the etiologies of temporomandibular joint (TMJ) ankylosis.

While being the most common etiology, a very minor percentage of condylar trauma patients progress to ankylosis; others regain normal function despite conservative/no treatment. Besides, computed tomography scans of TMJ ankylosis show hyperdense bone beyond the anatomical boundaries of the joint, in the mandibular ramus, and at the cranial base. Likely, there are differences in response to injury between ankylosis cases and others.

A significant percentage (21.9%) of ankylosis patients have procoagulant states of blood, pointing to hitherto unknown links between processes, leading to TMJ ankylosis.[1] The prevalence of hypercoagulability in ankylosis patients goes quite above the figures for general population. Following trauma, the extent of hypoxia at the fracture site plays an important role in determining the amount of callus formation and course of healing. Hypoxia induces HIF-1 α and its downstream gene VEGF. Posttrauma expression of TGF-β superfamily genes, importantly many BMPs, initiate angiogenesis; osteoblast precursor cells accompany these newly forming endosteal blood vessels and penetrate hematoma from the adjacent medullary cavity.[2] In a procoagulant/hypofibrinolytic state, conceivably, clotting process may involve more of medullary capillaries and the hypoxia would be enhanced. The scaffold of hematoma stays longer in situ, allowing the newly forming blood vessels to spread. Just enough immobilization at this vascularization phase can then lead to callus formation [Figure 1]. In addition, protein C has anti-inflammatory properties; hence, in deficiency states, children might have more and prolonged duration of swelling and pain posttrauma, thereby reducing their use of joints and causing indirect immobilization.
Figure 1: Proposed pathway of ankylosis in procoagulant state

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Hypoxia induces multiple effects on different cell types [Figure 2]. It causes a reversible state of quiescence in osteoblasts and promotes osteoclastic activity. However, osteoblasts survive and start osteogenesis once hypoxia reverse.[3] Hypoxia also facilitates recruitment and osteogenic differentiation of multipotent mesenchymal stromal cells using HIF-1 α and RUNX-2 genes.[4] However, some reports suggest that on the contrary, hypoxia rather promotes chondrogenesis.[5] This incongruity among experiments may be due to laboratory conditions such as different levels and duration of hypoxia to treat different cell types. In a real scenario, if prolonged hypoxia causes suppression of osteogenesis and promotion of chondrogenesis, it can explain the radiolucent zone in ankylosis and its longer course to ossification. It is plausible that the internal milieu and external mechanical factors together govern the pathogenesis.
Figure 2: Effects of hypoxia on mesenchymal stem cells, osteoblasts, and osteoclasts

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During varicella infection and childhood sepsis (other known causes behind ankylosis), protein S levels are reduced. In many cases, there is physiologic protein C deficiency in the perinatal period; increasing risk of ankylosis even with minor trauma by forceps delivery. In vitro studies have suggested protective effects of activated protein C in rheumatoid arthritis. In deficiency states, there could be excessive destruction during an active inflammatory period followed by surge in bone deposition. Activated protein C in a hypoxic wound can also play its tweaking role on type of differentiation the mesenchymal stem cells undergo. Hence, research on effects of different levels of hypoxia and activated protein C (APC) on stem cells is the way forward.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Bhatt KV, Roychoudhury A, Bhutia O, Saxena R, Subbiah V, Chattopadhyay P, et al. Study of risk factors for developing post-traumatic temporomandibular joint ankylosis. Eu J Oral Maxillofac Surg 2019;3:12-6.  Back to cited text no. 1
Ferretti C, Bryant R, Becker P, Lawrence C. Temporomandibular joint morphology following post-traumatic ankylosis in 26 patients. Int J Oral Maxillofac Surg 2005;34:376-81.  Back to cited text no. 2
Utting JC, Robins SP, Brandao-Burch A, Orriss IR, Behar J, Arnett TR. Hypoxia inhibits the growth, differentiation and bone-forming capacity of rat osteoblasts. Exp Cell Res 2006;312:1693-702.  Back to cited text no. 3
Wagegg M, Gaber T, Lohanatha FL, Hahne M, Strehl C, Fangradt M, et al. Hypoxia promotes osteogenesis but suppresses adipogenesis of human mesenchymal stromal cells in a hypoxia-inducible factor-1 dependent manner. PLoS One 2012;7:e46483.  Back to cited text no. 4
Huang J, Deng F, Wang L, Xiang XR, Zhou WW, Hu N, et al. Hypoxia induces osteogenesis-related activities and expression of Core binding factor α 1 in mesenchymal stem cells. Tohoku J Exp Med 2011;224:7-12.  Back to cited text no. 5


  [Figure 1], [Figure 2]

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