Experimental Model of Zymosan‐Induced Arthritis in the Rat Temporomandibular Joint: Role of Nitric Oxide and Neutrophils

Abstract

Aims. To establish a new model of zymosan-induced temporomandibular joint (TMJ) arthritis in the rat and to investigate the role of nitric oxide. Methods. Inflammation was induced by an intra-articular injection of zymosan into the left TMJ. Mechanical hypernociception, cell influx, vascular permeability, myeloperoxidase activity, nitrite levels, and histological changes were measured in TMJ lavages or tissues at selected time points. These parameters were also evaluated after treatment with the nitric oxide synthase (NOS) inhibitors L-NAME or 1400 W. Results. Zymosan-induced TMJ arthritis caused a time-dependent leucocyte migration, plasma extravasation, mechanical hypernociception, and neutrophil accumulation between 4 and 24 h. TMJ immunohistochemical analyses showed increased inducible NOS expression. Treatment with L-NAME or 1400 W inhibited these parameters. Conclusion. Zymosan-induced TMJ arthritis is a reproducible model that may be used to assess both the mechanisms underlying TMJ inflammation and the potential tools for therapies. Nitric oxide may participate in the inflammatory temporomandibular dysfunction mechanisms.

Prevention of 1-palmitoyl lysophosphatidylcholine-induced inflammation by polyunsaturated acyl lysophosphatidylcholine

“…Additionally, LPC16:0 could also activate endothelial cells to release AA from the cell membrane [6], available for the formation of pro-inflammatory lipid chemokines such as PGE 2 and 12-HETE, which in turn further amplifies the extravasation of leukocytes into the peritoneum compartment. Subsequently, leukocytes presented at inflamed areas continuously produce a variety of pro-inflammatory mediators that express chemo-taxis for other leukocyte migrations [36]. Presumably consistent with this hypothesis, the time period for the Fig.…”

Nitric Oxide Interferes With Hypoxia Signaling During Colonic Inflammation

“…In this state, O 2 utilization by the mitochondrial chain is reduced and free O 2 can induce the PHD-mediated de gradation of HIF-1a (25) , resulting in inadequate cellular signaling during hypoxia. L-NAME administration to rats with TNBS-induced colitis with reactivation at a dose previously described to block NO synthesis in vivo (4,5) , improved HIF-1a expression and increased apelin and VEGF protein expression. These results suggest that iNOS inhibition restored HIF-1a signaling during intestinal inflammation and that this restoration was not dependent on an anti-inflammatory response induced by L-NAME.…”

Lectin from Abelmoschus esculentus reduces zymosan-induced temporomandibular joint inflammatory hypernociception in rats via heme oxygenase-1 pathway integrity and tnf-α and il-1β suppression

“…As previously shown by our group [2], during the time course of zymosan TMJ inflammatory hypernociception development, it is maximal at 4 h of arthritis whereas cell influx peaks at 6 h. Based on these results we used these time points to assess both nociceptive (head withdrawal threshold) and inflammatory parameters (total cell counting and myeloperoxidase assay)…”

“…Experimental models that allow the study of the mechanisms underlying these conditions are of great clinical relevance. In this regard, we developed a rat model of TMJ inflammation using intra-articular injection of the pro-inflammatory agent zymosan [2].…”