Temporomandibular Joint Osteoarthritis Research Articles

An artificial intelligence model for the radiographic diagnosis of osteoarthritis of the temporomandibular joint

The interpretation of the signs of Temporomandibular joint (TMJ) osteoarthritis on cone-beam computed tomography (CBCT) is highly subjective that hinders the diagnostic process. The objectives of this study were to develop and test the performance of an artificial intelligence (AI) model for the diagnosis of TMJ osteoarthritis from CBCT. A total of 2737 CBCT images from 943 patients were used for the training and validation of the AI model. The model was based on a single convolutional network while object detection was achieved using a single regression model. Two experienced evaluators performed a Diagnostic Criteria for Temporomandibular Disorders (DC/TMD)-based assessment to generate a separate model-testing set of 350 images in which the concluded diagnosis was considered the golden reference. The diagnostic performance of the model was then compared to an experienced oral radiologist. The AI diagnosis showed statistically higher agreement with the golden reference compared to the radiologist. Cohen’s kappa showed statistically significant differences in the agreement between the AI and the radiologist with the golden reference for the diagnosis of all signs collectively (P = 0.0079) and for subcortical cysts (P = 0.0214). AI is expected to eliminate the subjectivity associated with the human interpretation and expedite the diagnostic process of TMJ osteoarthritis.

Bergapten exerts a chondroprotective effect in temporomandibular joint osteoarthritis by combining intestinal flora alteration and reactive oxygen species reduction

Bergapten, a furanocoumarin naturally occurring in bergamot essential oil, has been demonstrated to have the potential to alleviate osteoarthritis-related symptoms via its anti-inflammatory activity. Although its systemic bioavailability is limited, its precise mechanisms of action and effects on temporomandibular joint osteoarthritis (TMJOA) and its relationship with the intestinal flora remain unclear. Here, we explored the anti-TMJOA effect of BGT combined with the interleukin-1β-induced inflammatory response of chondrocytes in a monosodium iodoacetate (MIA)-induced TMJOA rat model. It was confirmed that BGT effectively reduced proinflammatory mediators and increased type II collagen, bone volume, and trabecular number of condyles in TMJOA rats. Importantly, the oral administration of BGT altered the intestinal flora of rats by increasing the relative abundances of nine prebiotic species and decreasing the relative abundance of one potential species. In addition, BGT considerably reduced reactive oxygen species (ROS) levels by suppressing glutathione, oxidized glutathione, and superoxide dismutase in the serum and malondialdehyde in urine. These results suggest that BGT exerts a chondroprotective effect, most likely by improving the intestinal flora and reducing ROS production associated with TMJOA in rats. This finding indicates a novel beneficial effect of BGT on the prevention and treatment of TMJOA.

Bone marrow aspirate concentrate – A novel approach to alter the course of temporomandibular joint osteoarthritis (a clinical study)

IntroductionTMJ OA is characterized by severe osteocartilaginous degradation of the joint structure resulting in severe deterioration of both joint function as well as joint structure. bone marrow aspirate concentrate (BMAC) gained wide acceptance as an auspicious addition for regenerative medicine as it is confirmed to be a rich source of pluripotent mesenchymal stem cells and growth factors that produce promising relief of clinical symptoms with significant repair of the joint structure. Thus, the study aims at assessing the efficacy of bone marrow aspirate concentrate (BMAC) as a treatment modality for TMJ osteoarthritis and compare its efficacy with that of hyaluronic acid (HA). Methods24 patients were included in the present study and divided into 12 patients in each group. Joint arthrocentesis was performed to all patients followed by intra-articular BMAC injection in Group I. While Group II received HA acid injection ResultsA trend towards long term joint repair at 12 and 18 months follow up period was observed in the bone marrow aspirate concentrate (BMAC) group as a therapeutic modality for TMJ OA by providing necessary growth factors and anti-inflammatories that impedes the progression of the osteoarthritic degeneration. On the contrary to the viscosupplementary action of hyaluronic acid (HA) that showed relapse of patients conditions. ConclusionBone marrow aspirate concentrate (BMAC) is able to reverse the degenerative effects of TMJ OA however,further studies are mandatory with larger population and longer follow-up time.

BNTA attenuates temporomandibular joint osteoarthritis progression by directly targeting ALDH3A1: An in vivo and in vitro study

BNTA is known to have a therapeutic effect on knee osteoarthritis and inflammatory osteoclastogenesis. However, the protective effect of BNTA regarding temporomandibular mandibular joint osteoarthritis (TMJOA) and its underlying mechanism and physiological target remains unclear. In the present study, BNTA ameliorated cartilage degradation and inflammation responses in monosodium iodoacetate (MIA)-induced TMJOA in vivo. In IL-1β-induced condylar chondrocytes, BNTA prevents oxidative stress, inflammatory responses and increasing synthesis of cartilage extracellular matrix through activating nuclear factor-E2-related factor 2 (NRF2) signaling. Suppression of NRF2 signaling abolishes the protective effect of BNTA in TMJOA. Notably, BNTA may bind directly to ALDH3A1 and act as a stabilizer, as evidenced by drug affinity responsive target stability assay (DARTS), cellular thermal shift assay (CETSA) and molecular docking results. Further investigation of the underlying molecular and cellular mechanism infers a positive correlation of ALDH3A1 regulating NRF2 signaling. In conclusion, BNTA may attenuate TMJOA progression via the ALDH3A1/NRF2 axis, inferring that BNTA is a therapeutic target for treating temporomandibular mandibular joint osteoarthritis.

MiR-335-5p inhibits endochondral ossification by directly targeting SP1 in TMJ OA.

During the development of temporomandibular joint osteoarthritis, endochondral ossification is compromised which leads to condylar degeneration; miR-335-5p in endochondral ossification in osteoarthritic condylar cartilage tissue remains unclear. Up-regulated microRNA and its target gene were searched for endochondral ossification in osteoarthritis articular cartilage. The effect of increased or decreased miR-335-5p on endochondral ossification was evaluated by transfecting miR-335-5p mimics or miR-335-5p inhibitor in vitro in chondrocytes C28/I2. Finally, we injected the temporomandibular joint of rats intra-articularly with agomiR-335 in a unilateral anterior crossbite rat model to determine the in vivo regulation of miR-335. After the onset of temporomandibular joint osteoarthritis, miR-335-5p levels were gradually up-regulated, whereas endochondral ossification-related genes were down-regulated in condylar cartilage specimens. Our results showed that miR-335 inhibited endochondral ossification after administration of a miR-335 antagonist into the temporomandibular joint articular cavity of a unilateral anterior crossbite rat model. AgomiR-335, a miR-335 agonist, inhibited matrix mineralization in fibrocartilage stem cells in vitro and then miR-335-5p negatively regulated chondrocyte activity by directly targeting SP1 via promoting transforming growth factor-β/Smad signalling. miR-335-5p can significantly inhibit endochondral ossification; therefore, its inhibition may be beneficial for the treatment of temporomandibular joint osteoarthritis.

Comparing apparent diffusion coefficient values of the masticatory muscles on diffusion‐weighted magnetic resonance imaging in patients with temporomandibular joint osteoarthrosis

AbstractAimThis study aimed to compare the apparent diffusion coefficient (ADC) values of the masticatory muscles between patients with and without temporomandibular joint osteoarthritis (TMJ‐OA) on diffusion‐weighted magnetic resonance imaging.MethodsThis prospective study included 120 patients with temporomandibular disorders (TMD), including 60 patients with TMJ‐OA and 60 without TMJ‐OA, and 60 without TMD patients. All patients underwent magnetic resonance imaging of the TMJs at our hospital between November 2011 and January 2017. The regions of interest included the right and left lateral pterygoid muscles, medial pterygoid muscles, and masseter muscles on axial slices. Magnetic resonance images from the TMJ‐OA and control groups were independently evaluated by two oral and maxillofacial radiologists. ADC values were compared between the two groups using Mann–Whitney U tests.ResultsThe respective mean ADC values of the lateral pterygoid muscles in patients with TMJ‐OA and controls were 1.18 × 10−3 and 1.33 × 10−3 mm2/s, respectively. Those for the medial pterygoid muscles were 1.14 × 10−3 and 1.25 × 10−3 mm2/s, while those for the masseter muscles were 1.20 × 10−3 and 1.28 × 10−3 mm2/s, respectively. The mean ADC values of the normal lateral pterygoid, normal medial pterygoid, and normal masseter muscles were 1.29 × 10−3, 1.09 × 10−3, and 1.08 × 10−3 mm2/s, respectively.ConclusionAmong patients with TMDs, the ADC values of the masticatory muscles were significantly higher in patients without TMJ‐OA than in those with TMJ‐OA.

Comparison of Four Treatment Protocols with Intra-Articular Medium Molecular Weight Hyaluronic Acid in Induced Temporomandibular Osteoarthritis: An Experimental Study.

The aim was to compare the effect between a single intra-articular infiltration (1i) and two infiltrations (2i) of medium molecular weight hyaluronic acid (MMW-HA) of high viscosity (HV) and low viscosity (LV) on the histopathological characteristics of temporomandibular joint (TMJ) osteoarthritis (OA) induced in rabbits. An experimental study was conducted on Oryctolagus cuniculus rabbits, including 42 TMJs, distributed between (1) TMJ-C, control group; (2) TMJ-OA, group with OA; (3) TMJ-OA-wt, group with untreated OA; (4) group treated with HA-HV-1i; (5) group treated with HA-HV-2i; (6) group treated with HA-LV-1i; and (7) group treated with HA-LV-2i. The results were evaluated using the Osteoarthritis Research Society International (OARSI) scale and descriptive histology considering the mandibular condyle (MC), the articular disc (AD), and the mandibular fossa (MF). The Kruskal-Wallis test was used for the statistical analysis, considering p < 0.05 significant. All treated groups significantly decreased the severity of OA compared to the TMJ-OA-wt group. The HA-HV-2i group showed significant differences in the degree of OA from the TMJ-OA group. The degree of OA in the HA-HV-2i group was significantly lower than in the HA-LV-1i, HA-LV-2i, and HA-HV-1i groups. The protocol that showed better results in repairing the joint was HA-HV-2i. There are histological differences depending on the protocol of the preparation used: two infiltrations seem to be better than one, and when applying two doses, high viscosity shows better results.

Loss of miR-204 and miR-211 shifts osteochondral balance and causes temporomandibular joint osteoarthritis.

Temporomandibular joint (TMJ) osteoarthritis (OA) is a common type of TMJ disorders causing pain and dysfunction in the jaw and surrounding tissues. The causes for TMJ OA are unknown and the underlying mechanism remains to be identified. In this study, we generated genetically-modified mice deficient of two homologous microRNAs, miR-204 and miR-211, both of which were confirmed by in situ hybridization to be expressed in multiple TMJ tissues, including condylar cartilage, articular eminence, and TMJ disc. Importantly, the loss-of-function of miR-204 and miR-211 caused an age-dependent progressive OA-like phenotype, including cartilage degradation and abnormal subchondral bone remodeling. Mechanistically, the TMJ joint deficient of the two microRNAs demonstrated a significant accumulation of RUNX2, a protein directly targeted by miR-204/-211, and upregulations of β-catenin, suggesting a disrupted balance between osteogenesis and chondrogenesis in the TMJ, which may underlie TMJ OA. Moreover, the TMJ with miR-204/-211 loss-of-function displayed an aberrant alteration in both collagen component and cartilage-degrading enzymes and exhibited exacerbated orofacial allodynia, corroborating the degenerative and painful nature of TMJ OA. Together, our results establish a key role of miR-204/-211 in maintaining the osteochondral homeostasis of the TMJ and counteracting OA pathogenesis through repressing the pro-osteogenic factors including RUNX2 and β-catenin.

Salubrinal alleviates cartilage degradation in a rabbit temporomandibular joint osteoarthritis model.

To investigate and explain the beneficial effects of local intra-articular injection of Salubrinal on temporomandibular joint osteoarthritis (TMJOA) using a rabbit model of anterior disc displacement (ADD). Rabbits were divided and subjected to surgical ADD. Salubrinal was administered by intra-articular injection in the TMJ every other day for 2 and 4 weeks after operation. Histological examination and TUNEL staining were then performed. Immunohistochemistry, quantitative real-time PCR, and Western blot analysis were employed to evaluate the expression of endoplasmic reticulum (ER) stress-related markers, catabolic factors, extracellular matrix proteins, inflammatory factors, and nuclear factor-kappa B (NF-κB) activation. In the ADD groups, we found that Salubrinal partly reversed condylar cartilage deterioration according to the histological analysis. Salubrinal reduced chondrocytes apoptosis while increased matrix components including Collagen II and Aggrecan. Meanwhile, Salubrinal downregulated the catabolic expression of MMP13, ADAMTS5, VEGF, TNF-α, and IL-1β. We also observed that Salubrinal inhibited ER stress activation by reducing the expression of GRP78, CHOP, ATF4, and Caspase-12. Additionally, Salubrinal suppressed the phosphorylation of NF-κB. These results indicate that Salubrinal alleviates cartilage degradation following ADD, suggesting that intra-articular injection of Salubrinal is a potential therapeutic approach for preventing TMJOA.

Upregulated Mitochondrial Dynamics Is Responsible for the Procatabolic Changes of Chondrocyte Induced by α2-Adrenergic Signal Activation.

Activation of sympathetic tone is important for cartilage degradation in osteoarthritis (OA). Recent studies reported that sympathetic signals can affect the mitochondrial function of target cells. It is unknown whether this effect exits in chondrocytes and affects chondrocyte catabolism. The contribution of mitochondrial dynamics in the activation of α2-adrenergic signal-mediated chondrocyte catabolism was investigated in this study. Primary chondrocytes were stimulated with norepinephrine (NE) alone, or pretreated with an α2-adrenergic receptor (Adra2) antagonist (yohimbine) and followed by stimulation with NE. Changes in chondrocyte metabolism and their mitochondrial dynamics were investigated. We demonstrated that NE stimulation induced increased gene and protein expressions of matrix metalloproteinase-3 and decreased level of aggrecan by chondrocytes. This was accompanied by upregulated mitochondriogenesis and the number of mitochondria, when compared with the vehicle-treated controls. Mitochondrial fusion and fission, and mitophagy also increased significantly in response to NE stimulation. Inhibition of Adra2 attenuated chondrocyte catabolism and mitochondrial dynamics induced by NE. The present findings indicate that upregulation of mitochondrial dynamics through mitochondriogenesis, fusion, fission, and mitophagy is responsible for activation of α2-adrenergic signal-mediated chondrocyte catabolism. The hypothesis that "α2-adrenergic signal activation promotes cartilage degeneration in temporomandibular joint osteoarthritis (TMJ-OA) by upregulating mitochondrial dynamics in chondrocytes" is validated. This represents a new regulatory mechanism in the chondrocytes of TMJ-OA that inhibits abnormal activation of mitochondrial fusion and fission is a potential regulator for improving mitochondrial function and inhibiting chondrocyte injury and contrives a potentially innovative therapeutic direction for the prevention of TMJ-OA.

Alleviation of temporomandibular joint osteoarthritis by targeting RIPK1-mediated inflammatory signalling.

Temporomandibular joint osteoarthritis (TMJOA), prevalent in adolescents and the elderly, has serious physical and psychological consequences. TMJOA is a degenerative disease of the cartilage and bone, mostly driven by inflammation, and synoviocytes are the first and most important inflammatory factor releasers. Receptor-interacting serine/threonine-protein kinase (RIPK1) promotes inflammatory response and cell death during an array of illnesses. This research aimed to explore the impacts of RIPK1 inhibitor therapy in TMJOA and the mechanism of RIPK1 in inducing inflammation during TMJOA. Herein, inhibition of RIPK1 suppressed the elevated levels of inflammatory factors, nuclear factor kappa B (NF-κB), along with markers of apoptosis and necroptosis after tumour necrosis factor (TNF)-α/cycloheximide (CHX) treatment in synoviocytes. Moreover, inflammation models were constructed in vivo through complete Freund's adjuvant (CFA) induction and disc perforation, and the findings supported that RIPK1 inhibition protected TMJ articular cartilage against progressive degradation. RIPK1 regulates NF-κB activation via cellular inhibitor of apoptosis proteins (cIAP), apoptosis via caspase-8, and necroptosis via RIPK3/mixed lineage kinase domain-like (MLKL) in synoviocytes, which in turn facilitates TMJOA inflammation progression.

Divergent chondro/osteogenic transduction laws of fibrocartilage stem cell drive temporomandibular joint osteoarthritis in growing mice

The anterior disc displacement (ADD) leads to temporomandibular joint osteoarthritis (TMJOA) and mandibular growth retardation in adolescents. To investigate the potential functional role of fibrocartilage stem cells (FCSCs) during the process, a surgical ADD-TMJOA mouse model was established. From 1 week after model generation, ADD mice exhibited aggravated mandibular growth retardation with osteoarthritis (OA)-like joint cartilage degeneration, manifesting with impaired chondrogenic differentiation and loss of subchondral bone homeostasis. Lineage tracing using Gli1-CreER+;Tmfl/-mice and Sox9-CreER+;Tmfl/-mice showed that ADD interfered with the chondrogenic capacity of Gli1+ FCSCs as well as osteogenic differentiation of Sox9+ lineage, mainly in the middle zone of TMJ cartilage. Then, a surgically induced disc reposition (DR) mouse model was generated. The inhibited FCSCs capacity was significantly alleviated by DR treatment in ADD mice. And both the ADD mice and adolescent ADD patients had significantly relieved OA phenotype and improved condylar growth after DR treatment. In conclusion, ADD-TMJOA leads to impaired chondrogenic progenitor capacity and osteogenesis differentiation of FCSCs lineage, resulting in cartilage degeneration and loss of subchondral bone homeostasis, finally causing TMJ growth retardation. DR at an early stage could significantly alleviate cartilage degeneration and restore TMJ cartilage growth potential.

Pyroptosis of chondrocytes activated by synovial inflammation accelerates TMJ osteoarthritis cartilage degeneration via ROS/NLRP3 signaling

ObjectivesSynovial inflammation and chondrocyte death have been widely acknowledged as key contributors to the pathological progression of temporomandibular joint osteoarthritis (TMJ-OA), a degenerative joint disease currently lacking definitive treatments. This study aims to understand the regulatory role of chondrocyte pyroptosis in condylar cartilage degradation during TMJ-OA. MethodsThe levels of cytokines, cartilage degeneration markers, and pyroptotic biomarkers in the synovium and synovial fluid of temporomandibular disorders (TMD) patients were examined. The synovitis, cartilage degradation, and chondrocyte pyroptosis in wild-type and alpha-kinase 1 (ALPK1)-deficient TMJ-OA mice were then compared following monosodium iodoacetate (MIA) induction. Subsequently, we investigated the downstream mechanisms of cytokines- or macrophage supernatants-induced metabolic disorders and pyroptosis in chondrocytes using primary TMJ chondrocytes and ATDC5 chondrocyte cultures. ResultsWe found a positive correlation between pyroptotic biomarkers and cartilage degradation mediators and cytokines in the synovial fluid of TMD patients. MIA-induced TMJ-OA mice demonstrated significant synovitis, cartilage degradation, and chondrocyte pyroptosis, which were mitigated in ALPK1-deficient TMJ-OA mice, inflammation-restrained mice. Ex-vivo study revealed the contribution of reactive oxygen species (ROS) to inflammation-irritated macrophage supernatants-induced pyroptosis and metabolic disorders in chondrocytes. Targeting NOD-like receptor protein 3 (NLRP3) alleviated cytokines- or ROS-induced pyroptosis and metabolic disorders in chondrocytes by inhibiting caspase-1 activation and interleukin-1β (IL-1β) secretion. ConclusionOur findings offer novel insight into the role of synovial inflammation-induced chondrocyte pyroptosis in promoting cartilage degradation during TMJ-OA via the ROS and NLRP3 signaling pathway.

A Comprehensive Review of Artificial Intelligence Based Algorithms Regarding Temporomandibular Joint Related Diseases.

Today, with rapid advances in technology, computer-based studies and Artificial Intelligence (AI) approaches are finding their place in every field, especially in the medical sector, where they attract great attention. The Temporomandibular Joint (TMJ) stands as the most intricate joint within the human body, and diseases related to this joint are quite common. In this paper, we reviewed studies that utilize AI-based algorithms and computer-aided programs for investigating TMJ and TMJ-related diseases. We conducted a literature search on Google Scholar, Web of Science, and PubMed without any time constraints and exclusively selected English articles. Moreover, we examined the references to papers directly related to the topic matter. As a consequence of the survey, a total of 66 articles within the defined scope were assessed. These selected papers were distributed across various areas, with 11 focusing on segmentation, 3 on Juvenile Idiopathic Arthritis (JIA), 10 on TMJ Osteoarthritis (OA), 21 on Temporomandibular Joint Disorders (TMD), 6 on decision support systems, 10 reviews, and 5 on sound studies. The observed trend indicates a growing interest in artificial intelligence algorithms, suggesting that the number of studies in this field will likely continue to expand in the future.

Effective technical protocol for producing a mono-iodoacetate-induced temporomandibular joint osteoarthritis in a rat model.

An animal model of osteoarthritis (OA) induced by monosodium iodoacetate (MIA) can be effectively adjusted based on the concentration of MIA to control the onset, progression, and severity of OA as required. The rat temporomandibular joint osteoarthritis (TMJOA) model using MIA is a useful tool for studying the effectiveness of disease-modifying OA drugs in TMJOA research. However, the intricate and complex anatomy of the rat TMJ often poses challenges in achieving consistent TMJOA induction during experiments. In the previous paper, a reference point was established by drawing parallel lines based on the line connecting the external ear and the zygomatic arch. However, this is not suitable for the anatomical characteristics of the rat. We used the zygomatic arch as a reference, which is a technical protocol that considers it. In our protocol, we designated a point approximately 1 mm away from the point where the zygomatic arch bends towards the ear as the injection site. To ensure precise injection of MIA and increase the likelihood of inducing OA, it is recommended to insert the needle at a 45° angle so that the needle tip contacts the joint projection. To confirm TMJOA induction, we identified changes in the condyle using in vivo micro-computed tomography (CT) in a rat model of MIA-induced OA and measured the degree of pain-related inflammation using head withdrawal threshold (HWT) measurements. Micro-CT scanning revealed typical OA-like lesions, including degenerative changes and subchondral bone remodeling induced by MIA in the TMJ. Pain, a major clinical feature of OA, showed an appropriate response corresponding to the structural changes shown in micro-CT scanning. In addition, the MIA concentration suitable for long-term observation of lesions was determined through ex vivo micro-CT imaging and HWT measurements. The 8 mg concentration exhibited a significant difference compared to others, confirming the sustained presence of lesions, particularly through changes in subchondral bone over an extended period. Consequently, we have successfully established a reliable rat TMJOA induction model and identified the MIA concentration suitable for long-term observation of subchondral bone research, which will greatly contribute to the study of TMJOA-an incurable disease lacking specific treatment options.

LincRNA-EPS Alleviates Inflammation in TMJ Osteoarthritis by Binding to SRSF3

Temporomandibular joint osteoarthritis (TMJOA) is a common inflammatory disease that can cause pain, cartilage degradation, and subchondral bone loss. However, the key regulatory factors and new targets for the treatment of TMJOA have yet to be determined. Long noncoding RNAs (lncRNAs) have shown remarkable potential in regulating tissue homeostasis and disease development. The long intergenic RNA–erythroid prosurvival (lincRNA-EPS) is reported to be an effective inhibitor of inflammation, but its role in TMJOA is unexplored. Here, we found that lincRNA-EPS is downregulated and negatively correlated with inflammatory factors in the condyles of TMJOA mice. LincRNA-EPS knockout aggravated inflammation and tissue destruction after TMJOA modeling. The in vitro studies confirmed that loss of lincRNA-EPS facilitated inflammatory factor expression in condylar chondrocytes, while recovered expression of lincRNA-EPS showed anti-inflammatory effects. Mechanistically, RNA sequencing revealed that the inflammatory response pathway nuclear factor–kappa B (NF-κB) was mostly affected by lincRNA-EPS deficiency. Moreover, lincRNA-EPS was proved to effectively bind to serine/arginine-rich splicing factor 3 (SRSF3) and inhibit its function in pyruvate kinase isoform M2 (PKM2) formation, thus restraining the PKM2/NF-κB pathway and the expression of inflammatory factors. In addition, local injection of the lincRNA-EPS overexpression lentivirus significantly alleviated inflammation, cartilage degradation, and subchondral bone loss in TMJOA mice. Overall, lincRNA-EPS regulated the inflammatory process of condylar chondrocytes by binding to SRSF3 and showed translational application potential in the treatment of TMJOA.

Artificial intelligence for detecting temporomandibular joint osteoarthritis using radiographic image data: A systematic review and meta-analysis of diagnostic test accuracy.

In this review, we assessed the diagnostic efficiency of artificial intelligence (AI) models in detecting temporomandibular joint osteoarthritis (TMJOA) using radiographic imaging data. Based upon the PRISMA guidelines, a systematic review of studies published between January 2010 and January 2023 was conducted using PubMed, Web of Science, Scopus, and Embase. Articles on the accuracy of AI to detect TMJOA or degenerative changes by radiographic imaging were selected. The characteristics and diagnostic information of each article were extracted. The quality of studies was assessed by the QUADAS-2 tool. Pooled data for sensitivity, specificity, and summary receiver operating characteristic curve (SROC) were calculated. Of 513 records identified through a database search, six met the inclusion criteria and were collected. The pooled sensitivity, specificity, and area under the curve (AUC) were 80%, 90%, and 92%, respectively. Substantial heterogeneity between AI models mainly arose from imaging modality, ethnicity, sex, techniques of AI, and sample size. This article confirmed AI models have enormous potential for diagnosing TMJOA automatically through radiographic imaging. Therefore, AI models appear to have enormous potential to diagnose TMJOA automatically using radiographic images. However, further studies are needed to evaluate AI more thoroughly.

Imaging signs of temporomandibular joint osteoarthritis in an urban population of 65-year-olds: a cone beam computed tomography study.

Symptoms of osteoarthritis (OA) in the temporomandibular joint (TMJ) may vary and possible causes should be further explored, such as prevalence and characteristics of imaging features. Investigate prevalence, gender differences and characteristics of imaging signs of TMJ-OA by cone beam computed tomography (CBCT) in a population-based sample of 65-year-old Oslo citizens. 159 (86 women, 73 men) individuals randomly recruited from a cohort of 460 Oslo citizens were examined with CBCT. The TMJs were categorized as with imaging signs of OA, no OA or indeterminate for OA. CBCT signs of TMJ-OA were found in 35 % of the 159 participants: 47% of the women and 22% of the men. CBCT signs of TMJ-OA were unilateral in two-thirds of the TMJs and characterized by articular surface flattening and condylar osteophytes. In almost all joints with bone erosive findings, bone productive findings were also found. Participants with and without CBCT signs of TMJ-OA showed no significant difference in TMD pain screener. Fourteen of the 159 participants (9%) had pain-related TMD and 12 (8%) had been in contact with health care services due to TMD. CBCT signs of TMJ-OA was common in this study group of 65-year-old Oslo citizens, found in every second woman and every fifth man. Articular surface flattening and bone productive changes, in particular condylar osteophytes, were the most frequent imaging features. Despite the high frequency of CBCT signs of TMJ-OA, few of the participants had pain-related TMD.

Intra-articular injection of kartogenin promotes fibrocartilage stem cell chondrogenesis and attenuates temporomandibular joint osteoarthritis progression.

Introduction: Kartogenin (KGN) is a small-molecule compound that has been reported to improve the chondrogenic differentiation of mesenchymal stem cells in vitro and to alleviate knee joint osteoarthritis in animal models. However, whether KGN has any effect on temporomandibular joint osteoarthritis (TMJOA) remains unclear. Methods: We first performed partial temporomandibular joint (TMJ) discectomy to induce TMJOA in rats. Histological analysis, tartrate-resistant acid phosphatase staining, and immunohistochemistry were used to assess the therapeutic effect of KGN on TMJOA in vivo. CCK8 and pellet cultures were used to determine whether KGN treatment could promote the proliferation and differentiation of FCSCs in vitro. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression of aggrecan, Col2a1, and Sox9 in FCSCs. Furthermore, we performed western blot to analysis the effect of KGN treatment on the expression of Sox9 and Runx2 in FCSCs. Results and discussion: Histological analysis, tartrate-resistant acid phosphatase staining, and immunohistochemistry showed that intra-articular injection of KGN attenuated cartilage degeneration and subchondral bone resorption in vivo. Further analyses of the underlying mechanisms revealed that KGN enhanced chondrocyte proliferation, increased the number of cells in both superficial and proliferative zones of TMJ condylar cartilage in vivo, enhanced the proliferation and chondrogenic differentiation of fibrocartilage stem cells (FCSCs), and upregulated the expression of chondrogenesis-related factors in vitro. Collectively, in our study, KGN was shown to promote FCSC chondrogenesis and restore TMJ cartilage, suggesting that KGN injections might be a potential treatment for TMJOA.

Understanding of Tempormandibular joint osteoarthritis: pathophysiology, epidemiology and diagnosis

Temporomandibular joint Osteoarthritis (TMJ OA) is a subtype of temporomandibular disorders (TMDs) andrefers to a debilitating degenerative disorder involving inflammatory conditions accompanying bone changes of the TMJ. Once the physical load exceeds physiologic resistance of TMJ, gradual damage to the cartilage layer occurs and leads to bone destruction with various signs and symptoms related to the defect of adjacent tissues.TMJ OA is a relatively common phenomenon, not only in patients complaining of TMJ symptoms, but also found incidentally through radiographs taken for any other dental treatments. TMJ OA is known to be more common in women and related to age closely, but the results of the studies are inconsistent.Deformity of the TMJ condyle due to OA can be easily confirmed with radiography and diagnosis is becom-ing more effective with the development of imaging modalities such as computed tomography. Also, as osseous changes of TMJ OA cause dysfunction of TMJ due to pain and/or restriction of motion and eventually can lead to irreversible changes in occlusion and facial morphology, accurate and in-depth understanding based on sci-entific evidence is essential for dentists. Therefore, this review on the basis of the documents published so far will describe the pathophysiologic mechanisms, epidemiology and diagnosis of TMJ OA.