Abstract
Orthodontic tooth movement (OTM) requires the orthodontic forces (compressive and tensile strain) to subject to the periodontal ligament and mechanosensory cells in the periodontium and to achieve mechanotransduction by mechanoreceptors. In the context of OTM, a diverse array of signaling pathways are activated in mechanosensory cells that modulate bone resorption and formation in in vitro and in vivo models. The underlying molecular signal transduction, such as MAPK and β-Catenin signaling, that is involved in OTM, has been partially identified. It includes, but is not limited to genes and proteins which are related to osteogenesis, osteoclastogenesis, cementogenesis and inflammation. However, the interactive relation of β-Catenin and MAPK signaling remains ambiguous and diverse cross-talks are acting with each other. In this comprehensive text, we review the biology of OTM and reported experimental results on the activation/inhibition of these two signaling pathways during OTM. Here, we also focus on the implications and interplays between the MAPK and β-Catenin signaling in mechanosensory cells in response to orthodontic forces. Finally, the potential of further investigation strategies aimed at supporting orthodontic interventions are discussed. This review provides a conceptual framework for more comprehensive knowledge about signaling interaction during OTM.
Highlights
The conventional mitogen-activated protein kinase (MAPK) signaling is known as one of the fundamental pathways in cellular response during orthodontic tooth movement (OTM), and its activation regulates periodontal cell homeostasis [1] and innate immune responses [2]
To adapt to the particular circumstances that are induced by orthodontic forces, the MAPK pathway and β-Catenin pathway must be integrated into the overall signaling activities of the mechanosensory cells
The precise molecular basis about how these two signaling pathways interact with each other and their impacts on OTM and orthodontically induced inflammatory root resorption (OIIRR) remains largely unresolved. It is unclear, how the various isoforms (i.e., ERK1/2, P38, c-Jun N-terminal kinase (JNK)) of MAPK signaling differentially regulate the glycogen synthase kinase-3β (GSK-3β) and β-Catenin and how this distinctly alters OIIRR. It has not been revealed yet, if the MAPK pathway is involved in the interaction with β-Catenin in other mechanosensory cells such as bone mesenchymal stem cells (BMSCs) during OTM
Summary
The conventional mitogen-activated protein kinase (MAPK) signaling is known as one of the fundamental pathways in cellular response during orthodontic tooth movement (OTM), and its activation regulates periodontal cell homeostasis [1] and innate immune responses [2]. This pathway is of vital importance in bone/cementum mineralization, and for modulation of the periodontal ligament in response to orthodontic force [3]. It will cover the interaction roles how these two pathways relate to each other and their functions in the formation and maintenance of bone/cementum
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