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Objective: To investigate the effects of congenital unilateral first permanent molar occlusal loss (CUMOL) on the morphology and position of temporomandibular joint (TMJ). Materials and Methods: Cone‐beam computed tomography (CBCT) images of 37 patients with CUMOL (18 males and 19 females, mean age: 13.60 ± 4.38 years) were divided into two subgroups according to the status of second molar (G1: the second molar not erupted, n = 18, G2: second molar erupted, n = 19). The control group consisted of 33 normal occlusion patients (9 males and 24 females, mean age: 16.15 ± 5.44 years) and was divided into 2 subgroups accordingly (G3: the second molar had not erupted, n = 18, G4: the second molar had erupted and made contact with the opposing tooth, n = 15). Linear and angular measurements were used to determine the characteristics of TMJ. Results: In G1, the condyle on the side of the CUMOL shifts posteriorly, with significant side differences observed in Anterior space (AS, P <.05) and Posterior space (PS, P <.05). However, with the eruption of the second permanent molars, in G2, the condyle on the CUMOL side moves posteriorly and inferiorly. This results in significant lateral differences in the AS (P <.05), PS (P <.05), and Superior space (SS, P <.05). Additionally, there is an increase in the thickness of the roof of the glenoid fossa (TRF) on the CUMOL side (P <.05), and a decrease in the inclination of the bilateral articular eminences (P <.05). Conclusions: CUMOL can affect the position and the morphology of the condyle and was associated with the eruption of the second permanent molars. Before the eruption of the second permanent molars, CUMOL primarily affects the position of the condyle. After the emergence of the second permanent molars, CUMOL leads to changes in both the condyle's position and the morphology of the glenoid fossa. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Macrophage‐mediated regulation of chondrocytes plays an important role in promoting temporomandibular joint (TMJ) inflammation. We investigated whether extracellular vesicles (EVs) derived from M1 macrophages (M1‐EVs) have a proinflammatory effect on TMJ inflammation and what the associated mechanisms are. In vitro, purified THP‐1 cell–derived M1‐EVs were applied to human TMJ condylar chondrocytes, and in vivo M1‐EVs derived from bone marrow–derived macrophages (BMDMs) were injected into rat TMJs. The levels of IL‐6, IL‐8, IL‐1β, and matrix metalloproteinase were then evaluated and found to be upregulated in the chondrocytes and rat TMJs. MicroRNA sequencing analysis was performed to identify differential expression of miRNAs, including miR‐1246. High expression of miR‐1246 in M1‐EVs from synovial fluid of patients with TMJ osteoarthritis and synovitis was verified by RT‐PCR. We then identified miR‐1246 targets GSK3β and Axin2 and found that miR‐1246 inhibits GSK3β and Axin2 expression, causing activation of the Wnt/β‐catenin pathway and inflammation in condylar chondrocytes. Our study found that M1‐EVs promote inflammation by transfer of miR‐1246 to condylar chondrocytes, thus providing new insight into one mechanism that can promote TMJ inflammation. [ABSTRACT FROM AUTHOR]

Botulinum toxin A (BoNT-A) has emerged as a treatment option for temporomandibular disorder (TMD). By injecting BoNT-A into the masseter muscle, it is possible to reduce mechanical loading on the temporomandibular joint (TMJ). However, numerous prior studies have indicated excessive reduction in mechanical loading can have detrimental effects on TMJ cartilage. This study proposes that autophagy, a process influenced by mechanical loading, could play a role in BoNT-A-induced mandibular condyle cartilage degeneration. To explore this hypothesis, we employed both BoNT-A injection and an excessive biting model to induce variations in mechanical loading on the condyle cartilage of C57BL/6 mice, thereby simulating an increase and decrease in mechanical loading, respectively. Results showed a significant reduction in cartilage thickness and downregulation of Runt-related transcription factor 2 (Runx2) expression in chondrocytes following BoNT-A injection. In vitro experiments demonstrated that the reduction of Runx2 expression in chondrocytes is associated with autophagy, possibly dependent on decreased YAP expression induced by low mechanical loading. This study reveals the potential involvement of the YAP/LC3/Runx2 signaling pathway in BoNT-A mediated mandibular condylar cartilage degeneration. [Display omitted] • BoNT-A injection reduced mechanical loading in the mandibular condyle, decreased expression of YAP in chondrocytes. • YAP modulates Runx2 in response to the mechanical loading change on chondrocytes. • Autophagy is potentially involved in the regulation of YAP on Runx2. [ABSTRACT FROM AUTHOR]