Transcriptomic response to compressive force simulating orthodontic tooth movement in cultured porcine epithelial cell rests of Malassez.

Mechanical stress on the periodontal ligaments, such as orthodontic force, causes the failure of homeostasis-inducing inflammation leading to inflammatory root resorption and replacement resorption. Despite these developments during orthodontic treatment, little is known about its relationship to the epithelial cell rests of Malassez (ERM) located in the periodontal ligament. To address this gap, RNA sequencing was performed on non-compression and compression forced porcine ERM groups subjected to 4.0 g/cm2 for 12 h. The results showed 529 upregulated and 273 downregulated genes with more than a twofold change. Pathway analyses indicated that the differentially expressed genes were significantly enriched in 13 pathways, including the TNF signaling pathway, viral protein interaction with cytokine and cytokine receptor IL-17 signaling pathway, and NF-kappa B signaling pathway. The differentially expressed genes such as BMP2, NFKBIA, CXCL8, CCL4, SOCS3, and FOS were commonly significantly upregulated within these pathways. The levels of BMP2 protein increased, while the NF-kB protein did not translocate intranuclearly, with no change in CXCL8 protein levels. Through ERM-induced mechanical compression, BPM2 can regulate root resorption and bone addition to maintain periodontal ligament homeostasis. CCL4, SOCS3, and c-fos may suppress root resorption by angiogenesis, preventing excessive osteoclast formation and inhibiting hyalinization.