Early collagen degeneration in the temporomandibular intradiscal junction portends the onset of discal pathogenesis

IF 9.4 1区 医学 Q1 ENGINEERING, BIOMEDICAL
Jiahao Zhou , Liang Xie , Jie Zhang, Xinyi Deng, Haozhe Chen, Songsong Zhu, Nan Jiang
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Abstract

The temporomandibular intradiscal junction is a structural transition region connecting anteroposterior and circumferential aligned collagens fibers in the temporomandibular joint disc. Despite inherent stiffness, this region is incredibly susceptible to perforation under pathological conditions. This study aimed to determine whether the intradiscal junction was the initiation destructive site for discal degeneration. Utilizing high-resolution microscopy and nanoindentation, we characterized the structural and mechanical properties of the intradiscal junction. In rabbit models of anterior disc displacement-mediated temporomandibular osteoarthritis, we observed a significant reduction in collagen fibril diameter and an increase in denatured procollagen within the intradiscal junction as early as one week post-surgery, further spreading across the whole disc. Mass spectrometry proteomics showed that the alteration of the intradiscal junction was the consequence of mechanical stimuli mediated by tenascin-C and metalloproteinase-3. Notably, these degenerative changes were blocked by early reduction of the discal position. In vitro monotonic loading confirmed the dominant contribution of the intradiscal junction to the overall mechanical function of the disc. The present findings underscore the pivotal role of the intradiscal junction in the pathogenesis of discal degeneration, providing early detection indicators and therapeutics.

Statement of significance

Temporomandibular joint osteoarthritis (TMJOA) is a prevalent disorder affecting the structure and mechanics of the TMJ disc, with no effective early detection or treatment strategies. This study identifies the temporomandibular intradiscal junction (IJ) as the site where discal pathogenesis begins. Degeneration at the IJ involves reduced collagen fibril diameter and denatured procollagens, compromising the mechanical properties of the entire disc. Rescuing the IJ's position through TMJ anchorage surgery may restore mechanosensitive homeostasis and prevent further discal degeneration. These findings highlight the importance of the IJ in the discal progression, payving the way for early detection methods and treatment strategies that target aberrant remodeling in this critical region to slow or reverse disease.

Abstract Image

颞下颌盘内连接处的早期胶原变性预示着椎间盘发病的开始。
颞下颌盘内连接处是连接颞下颌关节盘前后和周向排列的胶原纤维的结构过渡区。尽管具有固有的刚度,但在病理条件下,该区域非常容易穿孔。本研究旨在确定椎间盘内连接处是否是椎间盘退变的起始破坏部位。利用高分辨率显微镜和纳米压痕,我们表征了椎间盘内连接处的结构和力学性能。在兔椎间盘前移位介导的颞下颌骨关节炎模型中,我们观察到早在手术后一周,椎间盘内连接处的胶原纤维直径显著减少,变性前胶原增加,并进一步扩散到整个椎间盘。质谱分析显示,椎间盘内连接处的改变是腱蛋白c和金属蛋白酶-3介导的机械刺激的结果。值得注意的是,这些退行性改变被椎间盘位置的早期复位所阻断。体外单调负荷证实了椎间盘内连接处对椎间盘整体力学功能的主要贡献。目前的研究结果强调了椎间盘内连接处在椎间盘退变发病机制中的关键作用,提供了早期检测指标和治疗方法。意义声明:颞下颌关节骨关节炎(TMJOA)是一种影响TMJ椎间盘结构和力学的常见疾病,没有有效的早期发现或治疗策略。本研究确定了颞下颌盘内交界处(IJ)是椎间盘发病开始的部位。IJ的退变包括胶原纤维直径减小和前胶原变性,损害整个椎间盘的力学性能。通过TMJ锚固手术挽救IJ位置可以恢复机械敏感的内稳态并防止进一步的椎间盘退变。这些发现强调了IJ在椎间盘进展中的重要性,为早期发现方法和治疗策略铺平了道路,这些方法和治疗策略针对这一关键区域的异常重塑,以减缓或逆转疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Acta Biomaterialia
Acta Biomaterialia 工程技术-材料科学:生物材料
CiteScore
16.80
自引率
3.10%
发文量
776
审稿时长
30 days
期刊介绍: Acta Biomaterialia is a monthly peer-reviewed scientific journal published by Elsevier. The journal was established in January 2005. The editor-in-chief is W.R. Wagner (University of Pittsburgh). The journal covers research in biomaterials science, including the interrelationship of biomaterial structure and function from macroscale to nanoscale. Topical coverage includes biomedical and biocompatible materials.
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