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World J Orthop. Mar 18, 2026; 17(3): 115770
Published online Mar 18, 2026. doi: 10.5312/wjo.v17.i3.115770
Published online Mar 18, 2026. doi: 10.5312/wjo.v17.i3.115770
Machine learning identifies complement factor I as a shared mediator of periodontitis and ossification of posterior longitudinal ligament
Yu-Nan Man, Lu-Yang Zhong, Yue-Liang Wen, Mao-Lin He, Division of Spinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Co-first authors: Yu-Nan Man and Lu-Yang Zhong.
Author contributions: Man YN and Zhong LY contributed equally to this work; Man YN, Zhong LY, and Wen YL designed the research study; Man YN, Zhong LY, and Wen YL performed the research and analyzed the data; He ML contributed to funding acquisition and supervision; Man YN wrote the manuscript; all authors have read and approved the final manuscript.
Supported by National Natural Science Foundation of China, No. 82160536.
Conflict-of-interest statement: All authors declare no competing interests.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Corresponding author: Mao-Lin He, PhD, Division of Spinal Surgery, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. hemaolin@stu.gxmu.edu.cn
Received: October 27, 2025
Revised: November 29, 2025
Accepted: December 25, 2025
Published online: March 18, 2026
Processing time: 142 Days and 20.9 Hours
Revised: November 29, 2025
Accepted: December 25, 2025
Published online: March 18, 2026
Processing time: 142 Days and 20.9 Hours
Core Tip
Core Tip: By integrating transcriptomics with machine learning across two distinct conditions, we identified complement factor I (CFI) as a candidate molecular mediator linking periodontitis and ossification of the posterior longitudinal ligament. This study provides the first computational evidence implicating a potential immune-endothelial axis, mediated by CFI, in the shared pathophysiology of these conditions.
