Objective: To investigate the size and morphology of the temporomandibular joint (TMJ) articular disc and condyle in young asymptomatic adults by using magnetic resonance imaging (MRI) and to provide a reference for clinical diagnosis and scientific study of temporomandibular disorders (TMD). Methods: Overall, 93 undergraduate volunteers without TMD were enrolled from the freshmen pool at the Qingdao University. All participants underwent MRI of the oblique sagittal and oblique coronal TMJ planes. The articular disc and condyle were subsequently measured, and their morphology was evaluated. The obtained data were then grouped and analyzed statistically. Finally, intragroup correlation coefficient (ICC) was used to evaluate the interobserver measurement reliability. Results: We totally received 186 TMJ imaging samples. Based on our analysis, disc’s anterior band in young asymptomatic adult females were thicker than males of the same age (p = 0.024). Moreover, the media-lateral dimensions of the condylar head of adult females were shorter than males of equal age (P<0.001). The bilateral articular disc morphology was the same in 72.4% of subjects while the condylar morphology was the same in 63.4% of participants. Finally, using measurement reliability assessment, we demonstrated that our conclusions are reliable (ICC ≥0.7). Conclusion: The thickness of the anterior band of the disc and the media-lateral dimensions of the condylar head were gender-related. Additionally, the morphology of the bilateral articular disc and condyle was different among the subset of young asymptomatic adults.
Intervertebral disc degeneration (IDD) is a common chronic inflammatory degenerative disease that causes lower back pain. However, the underlying mechanisms of IDD remain unclear. Ferroptosis suppressor protein 1 (FSP1) is a newly identified suppressor for ferroptosis. This study aims to investigate the role of FSP1 in IDD. Nucleus pulposus (NP) tissues in humans were collected and NP cells from rats were isolated to detect FSP1 expression pattern. The relationship between FSP1-mediated ferroptosis and apoptosis was identified using FSP1 inhibitor iFSP1. RNA sequencing was utilized to seek downstream molecules and related signaling pathways. Moreover, both exogenous recombinant FSP1 protein and endogenous small interfering RNA were implemented in this study to clarify the role of FSP1 in tumor necrosis factor-alpha (TNFα)-mediated NP cell apoptosis. Ultimately, the underlying mechanisms of FSP1-related signaling pathway in IDD were uncovered both in vitro and in vivo. As a result, FSP1 was up-regulated in human degenerative NP tissues and after TNFα stimulation. FSP1 inhibition by iFSP1 fails to trigger ferroptosis in NP cells while inhibiting TNFα-mediated apoptosis. Further experiments demonstrated that FSP1 was closely related to TNFα-reliant caspase 3 activation and mitochondrial damage. However, the exogenous addition of recombinant protein FSP1 does not induce cell death or intensify the efficacy of TNFα. Mechanically, FSP1 is involved in TNFα-mediated NF-κB signaling activation to accelerate the development of IDD. This study demonstrated that FSP1 promotes IDD through TNFα-reliant NF-κB signaling activation and caspase 3-dependent apoptosis. These findings suggested a novel therapeutic target for the treatment of IDD.