Wang Yanfang, Xu Yili, Lu Yutong, Su Xinying, Lei Yonghua
Department of Orthodontics, Center of Stomatology, Xiangya Hospital, Central South University, Changsha, China.
Department of Orthodontics, Center of Stomatology, Xiangya Hospital, Central South University, Changsha, China; Department of Stomatology, Liuzhou People's Hospital, Liuzhou, China.
Int Dent J. 2025 May 1;75(4):100810. doi: 10.1016/j.identj.2025.03.019.
Gingival recession is a common complication of orthodontic treatment that affects both aesthetics and periodontal health. While traditionally associated with bone resorption, recent research suggests that Cathepsin K (CTSK) play a significant role in collagen fibre degradation within periodontal connective tissues. This study combines animal experiments and clinical research to investigate whether CTSK plays a role in the process of gingival recession during orthodontic tooth movement (OTM).
An OTM model was created using the maxillary first molar in mice. Differences in gingival tissue thickness and height between experimental and control groups were statistically analysed. Additionally, in the clinical study, CTSK expression in gingival crevicular fluid (GCF) was assessed. CTSK mRNA expression in gingival crevicular fluid was evaluated in orthodontic patients, comparing healthy and gingival recession groups.
High-force OTM significantly decreased the thickness and height of mesial gingival tissues (P < .005). In the gingival recession group, the number of cells within the region of interest (ROI) decreased, while the number of CTSK+ cells increased significantly (P < .0005). RT-qPCR analysis showed that CTSK mRNA expression in GCF of gingival recession patients was significantly higher than in the control group (P < .05).
High-force orthodontic tooth movement induced gingival recession in mice. The results of the animal experiment suggested that CTSK contributes to collagen fibre degradation in gingival connective tissue, leading to recession. Studies of human GCF have further supported the role of CTSK as a marker of collagen degradation in gingival recession.
These findings may offer new insights for the clinical management of complications such as "black triangles" following orthodontic treatment.
牙龈退缩是正畸治疗中常见的并发症，会影响美观和牙周健康。虽然传统上认为与骨吸收有关，但最近的研究表明，组织蛋白酶K（CTSK）在牙周结缔组织中的胶原纤维降解过程中起重要作用。本研究结合动物实验和临床研究，探讨CTSK在正畸牙齿移动（OTM）过程中牙龈退缩的发生过程中是否起作用。
利用小鼠上颌第一磨牙建立OTM模型。对实验组和对照组之间牙龈组织厚度和高度的差异进行统计学分析。此外，在临床研究中，评估龈沟液（GCF）中CTSK的表达。对正畸患者龈沟液中CTSK mRNA表达进行评估，比较健康组和牙龈退缩组。
高力OTM显著降低了近中牙龈组织的厚度和高度（P < .005）。在牙龈退缩组，感兴趣区域（ROI）内的细胞数量减少，而CTSK+细胞数量显著增加（P < .0005）。RT-qPCR分析显示，牙龈退缩患者GCF中CTSK mRNA表达显著高于对照组（P < .05）。
高力正畸牙齿移动诱导小鼠牙龈退缩。动物实验结果表明，CTSK导致牙龈结缔组织中的胶原纤维降解，进而导致牙龈退缩。对人龈沟液的研究进一步支持了CTSK作为牙龈退缩中胶原降解标志物的作用。
这些发现可能为正畸治疗后诸如“黑三角”等并发症的临床处理提供新的见解。
