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

Abstract

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.

Sclerostin in periodontal ligament: Homeostatic regulator in biophysical force‐induced tooth movement

“…A balanced cross-talk between these cells is mandatory for maintaining periodontal homeostasis (Liu et al, 2017;Aveic et al, 2021). Accordingly, PDL-derived biological molecules in BFTM have been widely investigated (Krishnan & Davidovitc, 2009;Lee et al, 2015Lee et al, , 2021Yang et al, 2015). Nevertheless, the homeostatic regulation of compression-induced AB resorption and tension-induced formation during BFTM, which occur concurrently and synchronized, has yet to be elucidated.…”

“…The factor that directly triggers BF‐induced TM (BFTM) is the transfiguration experienced by PDL cells and the extracellular matrix. This morphological modification causes the alteration of gene expression, subsequently inducing the release of cytokines from PDL cells (Meeran, 2013; Lee et al, 2021). Notably, the time‐dependent increase of BFTM while using orthodontic appliances is attenuated.…”

Extracellular Matrix-Oriented Proteomic Analysis of Periodontal Ligament Under Mechanical Stress

“…The process and pathway enrichment analysis showed that ossification (GO:0001503) and negative regulation of proteolysis (GO:0045861) were enriched at mesial and distal sides of the PDL. It has been well accepted that the cells in PDL maintain the adjacent alveolar bone by resorption and apposition of the bone matrix ( Jiang et al, 2016 ; Moon et al, 2019 ; Lee et al, 2021 ). The enrichment of the “negative regulation of proteolysis” indicated that antagonizing mechanisms against ECM degradation were enhanced in response to the mechanical loading.…”

C‑X‑C receptor 7 agonist acts as a C‑X‑C motif chemokine ligand 12 inhibitor to ameliorate osteoclastogenesis and bone resorption

“…LPS induces RANKL expression from osteoblasts and production of proinflammatory cytokines, such as TNF-α and IL-1, from macrophages and other cells ( 37 ). It has been reported that periodontal ligament cells also express numerous types of proinflammatory cytokines to regulate osteoclastogenesis by LPS ( 38 ). RANKL and TNF-α contribute to LPS-induced osteoclastogenesis and bone resorption ( 39 ).…”