Background: We evaluated the comparative effectiveness of all intra-articular injection corticosteroids for treating internal temporomandibular joint (TMJ) disorders. Methods: We searched MEDLINE, CENTRAL, EMBASE, SCOPUS, and LILACS through December 2023. We included randomized clinical trials (RCTs) enrolling patients with symptomatic internal disorders of the TMJ comparing any type of intra-articular corticosteroid therapy against another or to another minimally invasive therapy. The outcomes of interest were pain, range of mandibular motion (RoM), quality of life (QoL) and adverse effects at 1, 3, 6, and 12 months. We assessed the risk of bias using the Cochrane Collaboration’s tool. We conducted a frequentist network meta-analysis and assessed the certainty of the evidence (CoE) using GRADE. Results: We included 20 RCTs enrolling 810 participants, which assessed five corticosteroids alone or combined with arthrocentesis or hyaluronic acid. Based on moderate CoE, betamethasone is among the most effective corticosteroids for reducing pain at one (mean difference compared to arthrocentesis [MD], −3.80; 95% confidence interval [CI], −4.55 to −3.05) and three months (MD, −2.74; 95%CI, −3.42 to −2.06), and arthrocentesis plus dexamethasone at six months (MD, −0.80; 95%CI, −1.57 to −0.03). There was no convincing evidence that any intervention was better than arthrocentesis for improving the RoM and QoL at any follow-up time. Methylprednisolone may be more harmful than arthrocentesis for adverse effects. Discussion: Betamethasone and arthrocentesis plus dexamethasone are the most effective in managing pain in the short and medium term compared to arthrocentesis (moderate CoE). Decisions about their use should consider other factors, such as costs, feasibility, and acceptability. Future research should consider QoL as an outcome and assess participants at longer follow-up periods.

The aim of this study was to perform a literature review regarding the role of hyaluronic acid (HA) in the homeostasis and therapeutics of temporomandibular joint (TMJ) osteoarthritis (OA). The TMJ has characteristics that give it special adaptation and recovery abilities, where HA plays a fundamental role in helping to maintain joint homeostasis, which is affected in pathological processes like OA. OA is a chronic degenerative multi-factor disease that can affect all the components of the synovial joints, causing degradation of the articular cartilage, extracellular matrix and breakage in the HA molecules. HA is a non-branched linear polysaccharide with viscosupplementation, anti-inflammatory, lubrication and pain relief effects; it also activates the intrinsic repair processes of the cartilage and normalizes the endogenous production of HA by the synoviocytes. In recent years, the therapeutic use of HA has shown evidence that supports its application in TMJ OA, improving viscosupplementation capacity, acting at the cellular and molecular levels, reducing various inflammatory mediators and improving the reparative characteristics. Its use has been studied in animal models and in humans. However, no consensus has been reached in terms of concentrations, dose, application frequency or molecular weight to be used.

Osteoarthritis (OA) of the temporomandibular joint (TMJ) is a progressive disease characterized by the progressive destruction of the internal surfaces of the joint. Certain epigenetic biomarkers have been detected in TMJ-OA. We summarized the available evidence on the epigenetic biomarkers in TMJ-OA. There is an increase in the expression of non-coding RNAs related to the degradation of the extracellular matrix, chondrocyte apoptosis, and proinflammatory cytokines, while there is a decrease in the expression of those related to COL2A1, as well as the osteogenic and chondrogenic differentiation of mesenchymal stem cells. Certain methylated genes and histone modifications in TMJ-OA were also identified. In the early stage, DNA methylation was significantly decreased; that is, the expression of inflammation-related genes such as TNF and genes associated with extracellular matrix degradation, such as Adamts, were increased. While in the late stage, there was an increase in the expression of genes associated with the TGF-β and MAPK signaling pathway and angiogenesis-related genes. Although research on the role of epigenetic markers in TMJ-OA is still ongoing, the results here contribute to improving the basis for the identification of accurate diagnostic and prognostic markers and the development of new therapeutic molecules for the prevention and management of TMJ-OA. It also represents a significant advancement in elucidating its pathogenesis.

La percepción del dolor resulta de múltiples y dinámicos mecanismos en el sistema nervioso central (SNC) y periférico que inhiben o facilitan el estímulo y respuesta nociceptiva. Sin embargo, la principal capacidad de modulación esta a cargo del SNC. Los estímulos nociceptivos son detectados por terminaciones nerviosas libres de neuronas periféricas que sinaptan con neuronas aferentes secundarias de la médula espinal. Luego estas fibras decusan para formar las vías nociceptivas ascendentes. Una vez alcanzadas las estructuras subcorticales, se activan las neuronas del tálamo, quienes envían el estímulo hacia la corteza somatosensorial, desencadenando la percepción consciente del dolor y activando el sistema inhibitorio descendente. Para que la modulación nociceptiva se realice, es necesaria la participación de diversas sustancias o neurotransmisores que conectan áreas del SNC especializadas. Por lo tanto, el objetivo de este estudio fue realizar una revisión de la literatura respecto de los mecanismos que participan en los procesos de modulación central del dolor.