Periodontal tissue remodeling is the foundation for Orthodontic Tooth Movement (OTM) during orthodontic treatment. Periodontal tissue's dynamic balance between bone formation and resorption is disrupted by mechanical force. The tension side of alveolar bone experiences bone formation, while the compression zone experiences bone resorption. The speed of OTM is significantly influenced by the rate of remodeling in periodontal tissue. Osteoclast-mediated bone resorption and osteoblast-mediated bone formation are two tightly coupled processes that are regulated by a variety of cytokines, chemokines and their receptors, as well as other inflammatory mediators. The process involves communication and regulation between varieties of cells. As a membrane-associated cytokine, receptor activator of NF-kappa (NK-B) ligand (RANKL) is essential for osteoclastogenesis. Bone resorption factors stimulate the expression of RANKL by osteoocytes, osteoblasts, and stromal cells. RANK, a receptor for RANKL, is expressed by osteoclast precursor cells. Osteoclastic differentiation is triggered when RANKL binds to RANK, which sets off a number of signal transduction pathways in the next step. Osteoprotegerin (OPG), a RANKL decoy receptor, is also produced by osteoblasts and stromal cells. Osteoclast differentiation and bone resorption can be inhibited by OPG by inhibiting the interaction between RANKL and RANK. Local RANKL gene transfection has the potential to significantly increase bone resorption, speed up bone remodeling, and promote OTM. Similarly, local OPG gene transfection can prevent OTM and bone resorption. On the other hand, severe RANKL genetic defects may result in a particular form of autosomal recessive osteopetrosis (ARO) that is characterized by the failure of osteoclasts to resorb bone, resulting in increased bone mineral density. Due to the inability of osteoblasts to induce the formation of osteoclasts, OPG-deficient mice have been shown to have severe osteopetrosis, difficulty erupting teeth, and a complete absence of osteoclasts. The periodontal ligament is a connective tissue that is soft and fibrous and is buried between the cementum and the inner wall of the alveolar bone. Periodontal ligament tissue can be used to isolate periodontal ligament stem cells (PDLSCs).They are capable of self-renewal and differentiation across multiple lineages. PDLSCs are essential for maintaining periodontal homeostasis.  PDLSCs can differentiate into a variety of cell lineages, including osteoblast-like cells, cementoblast-like cells, adipocytes, and fibroblast-like cells, under the right conditions for induction. PDLSCs have been shown to promote the formation of new alveolar bone tissue, periodontal ligament, and cementum from damaged periodontal tissue in vivo. PDLSCs have been identified as the most promising source of differentiation for alveolar bone regeneration. In conclusion, it is believed that PDLSCs have numerous potential applications in periodontal tissue regeneration engineering. During orthodontic tooth movement, PDLSCs also play a crucial role in remodeling the periodontal ligament and alveolar bone. Zhang created an OTM rat model and monitored the response of PDLSCs in vivo. The study found that PDLSCs could be reactivated during orthodontic treatment on both the compression and tension sides. After orthodontic treatment, PDLSCs also participate in the process of relapse. PDLSCs' osteogenic differentiation and proliferation could be aided by mechanical stress, according to in vitro studies. PDLSCs typically play a significant role in OTM, which may involve a wide range of mechanoreceptors and pathways, including the cytoskeleton, MAPK signal, TGF-/Smad, Wnt/-Catenin pathway, and RANKL/OPG axis.

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Regards,
Catherine
Journal Co-Ordinator
Journal of Clinical Immunology and Allergy