Malocclusion model of temporomandibular joint osteoarthritis in mice with and without receptor for advanced glycation end products

Matias, Emilyn Martins; Mecham, David; Black, C.S.; Graf, Justin; Steel, Sharon; Wilhelm, Spencer K.; Andersen, Karl; Mitchell, J. A.; Macdonald, J. R.; Hollis, Weston R.; Eggett, Dennis L.; Reynolds, Paul; Kooyman, David L.

doi:10.1016/j.archoralbio.2016.05.007

Cited by 18 publications

(20 citation statements)

References 65 publications

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“…17 This hypothesis was supported by evidence that RAGE −/− had anti-inflammatory effects in a meniscal destabilization model and in a model of temporomandibular joint OA. 18,19 In addition, RAGE −/− has been shown to decrease osteoclast activity and to improve bone mineral density and bone strength in diabetic mice, results that are consistent with our findings that −/− mitigates bone loss in the IAF model 20,21 …”

Section: Discussionsupporting

confidence: 91%

Effects of knockout of the receptor for advanced glycation end‐products on bone mineral density and synovitis in mice with intra‐articular fractures

Seol

Tochigi

Bogner

et al. 2018

Journal Orthopaedic Research

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Our group employed the mouse closed intra-articular fracture (IAF) model to test the hypothesis that the innate immune system plays a role in initiating synovitis and post-traumatic osteoarthritis (PTOA) in fractured joints. A transgenic strategy featuring knockout of the receptor for advanced glycation end-products (RAGE ) was pursued. The 42 and 84 mJ impacts used to create fractures were in the range previously reported to cause PTOA at 60 days post-fracture. MicroCT (μCT) was used to assess fracture patterns and epiphyseal and metaphyseal bone loss at 30 and 60 days post-fracture. Cartilage degeneration, synovitis, and matrix metalloproteinase (MMP-3, -13) expression were evaluated by histologic analyses. In wild-type mice, μCT imaging showed that 84 mJ impacts led to significant bone loss at 30 days (p< 0.05), but recovered to normal at 60 days. Bone losses did not occur in RAGE mice. Synovitis was significantly elevated in 84 mJ impact wild-type mice at both endpoints (30 day, p = 0.001; 60 day, p = 0.05), whereas in RAGE mice synovitis was elevated only at 30 days (p = 0.02). Mankin scores were slightly elevated in both mouse strains at 30 days, but not at 60 days. Immunohistochemistry revealed significant fracture-related increases in MMP-3 and -13 expression at 30 days (p < 0.05), with no significant difference between genotypes. These findings indicated that while RAGE accelerated recovery from fracture and diminished synovitis, arthritic changes were temporary and too modest to detect an effect on the pathogenesis of PTOA. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2439-2449, 2018.

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Section: Discussionsupporting

confidence: 91%

Effects of knockout of the receptor for advanced glycation end‐products on bone mineral density and synovitis in mice with intra‐articular fractures

Seol

Tochigi

Bogner

et al. 2018

Journal Orthopaedic Research

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“…In the present study, malocclusion was not significantly associated with either the total score or any domain score of the OHIP‐C14. Based on previous literature, involving both human research and animal research, TMJ‐OA tended to be associated with malocclusion and the association was bidirectional. However, there was no literature focusing on the relationship between malocclusion and OHRQoL in patients with TMJ‐OA.…”

Section: Discussionmentioning

confidence: 99%

“…No evidence has proved that malocclusion affected patients’ taste and pronunciation. Also, it was reported that malocclusion may be associated with the development and exacerbation of TMJ‐OA mainly based on morphological changes of TMJ condylar cartilage in human or animal models but no evidence in humans indicates that malocclusion is associated with pain in the mouth or orofacial regions. Besides, on one hand, if the malocclusion was present before TMJ‐OA occurred, it means that the malocclusion was more likely to have been present for a long time and patients may already be used to the malocclusion in daily life and are not likely to report feel discomfort in eating in the preceding 1 month.…”

Section: Discussionmentioning

confidence: 99%

Association of malocclusion, self-reported bruxism and chewing-side preference with oral health-related quality of life in patients with temporomandibular joint osteoarthritis

Liu

Yang

et al. 2018

International Dental Journal

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“…For instance, there are nearly half a million joint replacements performed annually in the United States alone [193]. Many studies, including mouse knee destabilization and TMJ misalignment models, have demonstrated a pattern of biomarker expression associated with the progression of OA [194,195,196,197]. The disease appears to be associated with an initial rise in Tgf-β1 expression, followed by the upregulation of HtrA1, Ddr2 and Mmp13 expression, resulting in OA as assessed by standardized joint scoring methods such as the Mankin and the Osteoarthritis Research Society International (OARSI) scoring systems [198,199,200,201].…”

Section: Health Outcomes and Comorbiditiesmentioning

confidence: 99%

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Lewis

Hirschi

Arroyo

et al. 2017

IJMS

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Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First-and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.

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Malocclusion model of temporomandibular joint osteoarthritis in mice with and without receptor for advanced glycation end products

Cited by 18 publications

References 65 publications

Effects of knockout of the receptor for advanced glycation end‐products on bone mineral density and synovitis in mice with intra‐articular fractures

Effects of knockout of the receptor for advanced glycation end‐products on bone mineral density and synovitis in mice with intra‐articular fractures

Association of malocclusion, self-reported bruxism and chewing-side preference with oral health-related quality of life in patients with temporomandibular joint osteoarthritis

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

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