SLPI in periodontal Ligament is not sleepy during biophysical force‐induced tooth movement

• Published in: Journal of clinical periodontology Vol. 48; no. 4; pp. 528 - 540
• Main Authors: Lee, Su‐Young, Moon, Jung‐Sun, Yang, Dong‐Wook, Yoo, Hong‐Il, Jung, Ji‐Yeon, Kim, Ok‐Su, Kim, Min‐Seok, Koh, Jeong‐Tae, Chung, Hyun‐Ju, Kim, Sun‐Hun
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01-04-2021
• Subjects: Alveolar bone; Animals; biophysical force; Bone remodeling; Cbfa-1 protein; Cells, Cultured; Compression; Differential display; Homeostasis; Immunofluorescence; Ligaments; Localization; Macrophages; Mineralization; PDL; Peptidase; Periodontal Ligament; RANK Ligand; Rats; Secretory Leukocyte Peptidase Inhibitor; SLPI; Therapeutic applications; tooth movement; Tooth Movement Techniques; TRANCE protein; Western blotting; alveolar bone; biophysical force; PDL; tooth movement; SLPI
• ISSN: 0303-6979; 1600-051X
• DOI: 10.1111/jcpe.13416

Aim
We aimed to identify a key molecule that maintains periodontal tissue homeostasis during biophysical force‐induced tooth movement (BTM) by orchestrating alveolar bone (AB) remodelling.
Materials and Methods
Differential display‐PCR was performed to identify key molecules for BTM in rats. To investigate the localization and expression of the identified molecules, immunofluorescence, real‐time RT‐PCR and Western blotting were performed in rats and human periodontal ligament (PDL) cells. Functional test and micro‐CT analysis were performed to examine the in vivo effects of the identified molecules on BTM.
Results
Secretory leucocyte peptidase inhibitor (SLPI) in the PDL was revealed as a key molecule for BTM‐induced AB remodelling. SLPI was enhanced in the PDL under both compression and tension, and downregulated by an adenyl cyclases inhibitor. SLPI induced osteoblastogenic genes including runt‐related transcription factor 2 (Runx2) and synergistically augmented tension‐induced Runx2 expression. SLPI augmented mineralization in PDL cells. SLPI induced osteoclastogenic genes including receptor activator of nuclear factor kappa‐Β ligand (RANKL) and synergistically augmented the compression‐induced RANKL and macrophage colony‐stimulating factor (MCSF) expression. Finally, the in vivo SLPI application into the AB significantly augmented BTM.
Conclusions
SLPI or its inhibitors might serve as a biological target molecule for therapeutic interventions to modulate BTM.