A rabbit model for temporomandibular joint intracapsular adhesion

2009 ◽  
Vol 38 (5) ◽  
pp. 591
Author(s):  
S.Y. Zhang ◽  
C. Yang ◽  
K.J. Wei ◽  
Y.J. Xu ◽  
Y.T. Qiu ◽  
...  
Author(s):  
Sarah E. Henderson ◽  
Alejandro J. Almarza ◽  
Scott Tashman ◽  
Amy L. McCarty

Degeneration of the articulating surfaces and pain associated with temporomandibular joint (TMJ) dysfunction are the primary symptoms of TMJ disorders (TMDs), where normal life activities such as eating, talking, and even sleeping may be drastically impaired [1–3]. To accelerate the discovery of effective therapeutic interventions for the treatment of TMD pain, we have been establishing a novel non-invasive approach for objectively assessing the presence of joint hypersensitivity. Our approach to identify chronic joint pain is based on evidence that all of the etiological factors associated with TMD pain implicate remodeling and degeneration of the joint in response to alterations in motion and loading. The injury model used for this study was a reversible, mechanical model through splint placement on the molars. It is hypothesized that arthrokinematic analysis will identify a specific pattern of functional changes that constitute a signature for the presence of irreversible damage.


Author(s):  
Steven B. Nicoll ◽  
Christopher K. Hee ◽  
Martin B. Davis ◽  
Beth A. Winkelstein

Orofacial pain associated with osteoarthritis (OA) in the temporomandibular joint (TMJ) is a significant clinical problem [1]. The pathophysiologic and cellular mediators that underlie the development of such chronic orofacial pain are not well understood, nor has a relationship to mechanical loading been defined. Several experimental models have been developed to examine causative factors in TMJ OA progression and joint pathology. Such models often involve intra-articular injections or surgical manipulation of tissue structures in order to alter joint kinematics and stability [2–6]. For example, severing of the discal attachments followed by anterior displacement of the disc has been employed in a rabbit model, while disc perforation and scraping of the condylar surface have been used in sheep models to induce OA symptoms [2,3]. A limitation of the above approaches is that they introduce artificial damage to the joint structures and do not approximate the clinical disorder of mechanically-induced TMJ OA. Therefore, the goal of this pilot study was to develop a novel model of TMJ OA via non-invasive and mechanically relevant methods that could produce behavioral hypersensitivity (mechanical allodynia) suggestive of pain symptoms and histological changes in the TMJ consistent with osteoarthritic pathology.


Author(s):  
Joao L.G.C. Monteiro ◽  
Toru Takusagawa ◽  
Belmiro C.E. Vasconcelos ◽  
Sara I. Pai ◽  
Joseph P. McCain ◽  
...  

2016 ◽  
Vol 54 (5) ◽  
pp. e33-e37 ◽  
Author(s):  
Felipe Ernesto Artuzi ◽  
Renan Langie ◽  
Maíra Cavallet de Abreu ◽  
Alexandre Silva Quevedo ◽  
Adriana Corsetti ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hyunjeong Kim ◽  
Gwanghyun Yang ◽  
Jumi Park ◽  
Jene Choi ◽  
Eunju Kang ◽  
...  

Abstract Osteoarthritis (OA) is a degenerative condition of the temporomandibular joint (TMJ) characterised by chronic inflammation and damage to joint structures. Because of the complexity of TMJ-OA, only symptomatic treatments are currently available. Recent reports have shown that many of stem cells can exert anti-inflammatory and tissue-regenerating effects. In this study, we investigated the potential cartilage-regenerating and anti-inflammatory effects of human umbilical cord matrix-mesenchymal stem cells (hUCM-MSCs) for the treatment of TMJ-OA. hUCM-MSC lines, isolated from different donors, which showed different activities in vitro. Using a selected cell line, we used different concentrations of hUCM-MSCs to assess therapeutic effects in a rabbit model of monosodium iodoacetate-induced TMJ-OA. Compared with the untreated control group, the potential regenerative result and anti-inflammatory effects of hUCM-MSCs were evident at all the tested concentrations in rabbits with induced TMJ-OA. The median dose of hUCM-MSCs showed the prominent cartilage protective effect and further cartilage regeneration potential. This effect occurred via upregulated expression of growth factors, extracellular matrix markers, and anti-inflammatory cytokines, and reduced expression of pro-inflammatory cytokines. The anti-inflammatory effect of hUCM-MSCs was comparable to that of dexamethasone (DEX). However, only hUCM-MSCs showed potential chondrogenesis effects in this study. In conclusion, our results indicate that hUCM-MSCs may be an effective treatment option for the treatment of TMJ-OA.


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