Osteoarthritis, a degenerative joint disease, causes pain and limits mobility; it currently affects 303 million people worldwide (Gourdine, 2019). The temporomandibular joint (TMJ) is the only bilateral synovial joint in the human body with complex movement patterns and is closely associated with important functions such as chewing and facial expression (Roberts and Goodacre, 2020, Wang et al., 2015). Osteoarthritis of the TMJ (TMJ-OA) is characterised by condylar bone changes, including cortical erosion, subcortical cystic changes, and osteophyte formation (Liu, Xu, et al., 2023). TMJ-OA occurs in 9.8 % of adults and can cause TMJ dysfunction and facial deformities, substantially affecting patients’ health (Chantaracherd et al., 2015, Valesan et al., 2021).

Inflammation is a key pathological feature of TMJ-OA (Wang et al., 2015). Mechanical trauma and stress induce synovial cell production of inflammatory mediators, which accumulate in the joint causing pain and symptoms of osteoarthritis (Sanchez-Lopez et al., 2022, Wood et al., 2022). The inflammatory-induced pain associated with TMJ can result in alterations in dietary patterns (Nogueira et al., 2025) and depression (Sójka et al., 2019), potentially leading to fluctuations in body weight. Inflammatory cytokines induce catabolism and inhibit metabolism, resulting in sustained cartilage and osteochondral injury (Wang et al., 2014). Current TMJ-OA treatment strategies include non-steroidal anti-inflammatory drug administration, physical therapy, and other measures for controlling synovial inflammation and alleviating pain (Al-Moraissi et al., 2020).

Conducting pathological research on human TMJ-OA is challenging; therefore, animal models are typically used. Rats are considered a suitable TMJ-OA model animal owing to their anatomical and biomechanical similarities with humans (Orset et al., 2014). Surgical procedures, mechanical stress induction, occlusal changes, and drug administration are used to establish TMJ-OA models (Liu et al., 2021, Togni et al., 2018, Zhao et al., 2022). Surgical methods may cause considerable trauma, irreversible joint damage, and disruption of normal joint stress in animals (Lampropoulou-Adamidou et al., 2014). The unilateral anterior crossbite method, which causes cartilage damage through occlusal changes, is not standardised. However, chemical reagent induction methods involving injection of papain, hyaluronidase, collagenase, and monoiodoacetic acid (MIA) offer suitable alternatives (Nicot et al., 2021).

Intra-articular MIA injection is a well-established method for inducing osteoarthritis in animal models (Udo et al., 2016). This technique is simple, highly reproducible, and effectively simulates key pathological features of human osteoarthritis. MIA injection induces inflammation within the joint cavity, elevating levels of inflammatory cytokines similar to those observed in patients with osteoarthritis (Kawarai et al., 2018). This leads to a cascade of pathological changes, including articular cartilage degeneration, subchondral bone sclerosis, synovitis, and osteophyte formation. Furthermore, the MIA-induced model exhibits behavioural signs of joint pain, such as tenderness, which aligns with the clinical manifestations of patients with osteoarthritis (Wang et al., 2012). This model also results in long-term facial pain symptoms (Jiang et al., 2022), further emphasising its relevance to human TMJ-OA. However, comprehensive studies on pathological changes in the TMJ condyle and the molecular mechanisms underlying MIA-induced TMJ-OA are lacking. Therefore, in this study, we aimed to establish a simple, minimally invasive MIA-induced TMJ-OA rat model and evaluate the effects on weight, pain, and pathological changes in the condyle of rats. Additionally, we sought to explore the possible mechanism underlying MIA-induced TMJ-OA through transcriptome sequencing and reverse transcription-polymerase chain reaction (RT-PCR) of condylar surface cartilage in rats.