Temporomandibular joint (TMJ) disc displacement is one of the most significant subtypes of temporomandibular joint disorders, but its etiology and mechanism are poorly understood. In this study, we elucidated the mechanisms by which destruction of inflamed collagen fibrils induces alterations in the mechanical properties and positioning of the TMJ disc. By constructing a rat model of TMJ arthritis, we observed anteriorly dislocated TMJ discs with aggravated deformity in vivo from five weeks to six months after a local injection of Freund's complete adjuvant. By mimicking inflammatory conditions with interleukin-1 beta in vitro, we observed enhanced expression of collagen-synthesis markers in primary TMJ disc cells cultured in a conventional two-dimensional environment. In contrast, three-dimensional (3D)-cultivated disc cell sheets demonstrated the disordered assembly of inflamed collagen fibrils, inappropriate arrangement, and decreased Young's modulus. Mechanistically, inflammation-related activation of the nuclear factor kappa-B (NF-κB) pathway occurs during the progression of TMJ arthritis. NF-κB inhibition reduced the collagen fibril destruction in the inflamed disc cell sheets in vitro, and early NF-κB blockade alleviated collagen degeneration and dislocation of the TMJ discs in vivo. Therefore, the NF-κB pathway participates in the collagen remodeling in inflamed TMJ discs, offering a potential therapeutic target for disc displacement.
Animals ; NF-kappa B/metabolism* ; Temporomandibular Joint Disorders/pathology* ; Temporomandibular Joint Disc/metabolism* ; Rats ; Rats, Sprague-Dawley ; Disease Models, Animal ; Male ; Collagen/metabolism* ; Cells, Cultured ; Joint Dislocations/pathology* ; Interleukin-1beta ; Arthritis, Experimental

Collagen is the building component of temporomandibular joint (TMJ) discs and is often affected by inflammation in temporomandibular disorders.The macromechanical properties of collagen are deteriorated by chronic inflammation.However,the mechanism by which inflammation influences disc function remains unknown.The relationship between the ultrastructure and nanomechanical properties of collagen in inflamed discs should be clarified.Seven-week-old female Sprague-Dawley rats were randomly divided into two groups.Chronic TMJ inflammation was induced by intra-articular injection of complete Freund's adjuvant,and samples were harvested after 5 weeks.Picrosirius staining revealed multiple colours under polarized light,which represented alternative collagen bundles in inflamed discs.Using atomic force microscopy scanning,the magnitude of Young's modulus was reduced significantly accompanied with disordered collagen fibril arrangement with porous architecture of inflamed discs.Transmission electron microscopy scanning revealed a non-uniform distribution of collagen fibres,and oversized collagen fibrils were observed in inflamed discs.Fourier transform infrared microspectroscopy revealed a decrease in 1 338 cm-1/amide Ⅱ area ratio of collagen in different regions.The peak positions of amide Ⅰ and amide Ⅱ bands were altered in inflamed discs,indicating collagen unfolding.Our results suggest that sustained inflammation deteriorates collagen structures,resulting in thedeterioration of the ultrastructure and nanomechanical properties of rat TMJ discs.

Objective To study the etiological effect between the spatial variation of lumbar facet orientation and the degenerative lumbar spondylolisthesis(DLS)in axial,sagittal and coronal plane.Methods 85 patients with DLS at L4 and 110 controlsreceived X-ray and CT scanning.The facet angle at L4-L5 was measured in axial,sagittal and coronal plane.Results Compared with the control group, the DLS-angles were lesser and the difference between the left and right was greater in axial,coronal plane(P <0.05).But were greater in sagittal plane(P <0.05).Conclusion The DLS-angles are more sagittal in axial plane,more level in sagittal plane and more erect in coronal plane.The change of spatial orientation in the facet joint is one of etiological factors of degenerative lumbar spondylolisthesis.