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.

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