Inflammatory and degenerative effects of induced osteoarthritis/rheumatoid arthritis models on temporomandibular joint of rats

Temporomandibular joint (TMJ) disorders can affect jaw and masticatory muscles. Factors that include age, sex, hormonal factors, trauma, and psychological stress can lead to physiological adaptation or disorganization of TMJs (Figueroba et al., 2014).

Rheumatoid arthritis (RA) is a chronic autoimmune, systemic, degenerative inflammation that can affect several tissues and organs, causing damage to the joints (Cairns, 2010). RA can cause pain, swelling, and bone and cartilage changes in the affected joints, in addition to stiffness and limitation of daily joint activities (Napimoga et al., 2020). The percentage of patients with RA and TMJ involvement varies from 67% to 92% (Lin et al., 2014).

In addition to RA, osteoarthritis (OA) is another form of arthritis. OA is a degenerative disease that begins due to the loss of cartilage and bone remodeling. OA features synovial inflammation (Napimoga et al., 2020), joint degradation, abrasion, and subchondral bone remodeling (Tolba et al., 2020). The symptoms of OA in TMJ are not evident in the initial stage, but ultimately present as decreased joint space and pain (Kang et al., 2007).

In both inflammatory pathologies, an imbalance in the repair/remodeling process controlled by chondrocytes can cause progressive damage to the articular cartilage, involving inflammatory cells and cytokine synthesis (Lemos et al., 2018). Elevated concentrations of the pro-inflammatory cytokines interleukin 1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) are present in the synovial fluid in diseases involving intra-articular degenerative processes. IL-6 and IL-11 are associated with the joint adaptive process, and IL-10 has anti-inflammatory activity (Kristensen et al., 2014).

Collagen-induced arthritis in rodents is one of the most commonly used models for evaluating drugs aimed at controlling inflammation caused by RA and degeneration caused by OA. Complete Freund's adjuvant (CFA) is a suspension of inactivated and dried Mycobacterium tuberculosis in mineral oil. When introduced along with type II bovine collagen (CII), CFA allows the development of inflammation and arthritis in rodents with characteristics very similar to those observed in humans (Flake et al., 2005, Liu et al., 2015).

Arthritis induction can be performed systemically by intradermal injection of CFA and CII at the base of the tail (Morin et al., 2015), or directly into the TMJ (Wang et al., 2012, Wang et al., 2017). No studies have compared the effects of established models on the TMJ. The objective of this study was to compare three models of RA/OA induction in rats.

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