Temporomandibular joint osteoarthritis (TMJOA) is a prevalent source of temporomandibular joint disorder (TMD). Women are more commonly diagnosed with TMD and are more likely to seek care at tertiary orofacial pain clinics. Limited knowledge regarding mechanisms underlying temporomandibular joint (TMJ) pain impairs development of improved pain management strategies. In a rat model of unilateral TMJOA, monosodium iodoacetate (MIA) produces joint pathology in a concentration-dependent manner. Unilateral MIA produces alterations in meal patterns in males and females without altering overnight time spent eating or weight across 2 weeks. Monosodium iodoacetate (80 mg/mL)-treated males develop ongoing pain within 2 weeks after MIA injection. Females develop ongoing pain at a 5-fold lower MIA concentration (16.6 mg/m). Monosodium iodoacetate (80 mg/mL)-treated males show spread of tactile hypersensitivity across the face during the first week after injection and then to the fore paws and hind paws during the second week after injection, indicating development of central sensitization. At the lower dose, female rats demonstrate a similar spread of tactile hypersensitivity, whereas male rats do not develop ongoing pain or spread of tactile hypersensitivity outside the area of the ipsilateral temporomandibular joint. These observations indicate that females have a higher susceptibility to development of ongoing pain and central sensitization compared with male rats that is not due to differences in MIA-induced joint pathology. This model of TMJOA pain can be used to explore sex differences in pain processes implicated in development of neuropathic pain, ongoing pain, and central sensitization, allowing for development of individualized strategies for prevention and treatment of TMD joint pain.
Females show increased susceptibility to development of temporomandibular joint pain and central sensitization compared with males in a rat model of unilateral temporomandibular joint pain.
aDepartment of Biomedical Sciences, College of Osteopathic Medicine, Biddeford, ME, United States
bCenter for Excellence in the Neurosciences, University of New England, Biddeford, ME, United States
cCenter for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, ME, United States
dDepartment of Anatomy and Cell Biology, Temple University, Lewis Katz School of Medicine, Philadelphia, PA, United States
Corresponding author. Address: Department of Biomedical Sciences, Center for Excellence in the Neurosciences, College of Osteopathic Medicine, 11 Hills Beach Rd, Biddeford, ME 04005, United States. Tel.: (207) 602-2981; fax: (207) 602-5931. E-mail address: email@example.com (T. King).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received December 11, 2018
Received in revised form April 12, 2019
Accepted April 19, 2019
Online date: April 23, 2019