Single-Cell Atlas Maps Human Periodontal Ligament Remodeling During Tooth Movement

Edited by Orthotown staff

Researchers have produced what they describe as the first single-cell transcriptomic atlas of the human periodontal ligament during orthodontic tooth movement, identifying a pressure-side fibroblast population that appears to contribute to early bone remodeling, according to a study published online Oct. 26 in the Journal of Dental Research.

The team profiled control tissue along with pressure-side and tension-side tissue collected three and seven days after force application. Analysis of 65,032 cells identified 15 cell populations and showed pronounced remodeling across stromal, immune, vascular, and neural compartments that varied with force direction and stage.

Within the fibroblasts, a subset marked by CTHRC1 was enriched on the pressure side at day 3 and showed heightened mechanotransduction, inflammatory signaling, and chemokine activity. The mechanosensitive channel TRPA1 was preferentially expressed in this subset.

Ligand-receptor and functional analyses implicated complement component C3 as a downstream mediator linking regions rich in these fibroblasts to monocyte recruitment and osteoclastogenic activity.

In a mouse model of tooth movement, blocking TRPA1, either systemically with the inhibitor HC-030031 or through local gene knockdown, reduced tooth movement, and the inhibitor also reduced osteoclast surface. Local C3a supplementation partially restored tooth movement during TRPA1 inhibition.

W. Zhao, S. Wu, Y. Lin, B. Yan, and colleagues in the Department of Orthodontics at the Affiliated Stomatological Hospital of Nanjing Medical University in China conducted the study.

The authors said the findings provide a human single-cell framework for understanding periodontal remodeling during orthodontic tooth movement. The intervention experiments were conducted in mice, not patients.

Sources:
Journal of Dental Research, “Single-Cell Atlas of Human Orthodontic Tooth Movement,” published online Oct. 26, 2026: journals.sagepub.com/doi/10.1177/00220345261491310
National Library of Medicine, PubMed, PMID 42934893: pubmed.ncbi.nlm.nih.gov/42934893