Osteocyte Mechanotransduction in Orthodontic Tooth Movement

Abstract

Purpose of review: Orthodontic tooth movement is characterized by periodontal tissue responses to mechanical loading, leading to clinically relevant functional adaptation of jaw bone. Since osteocytes are significant in mechanotransduction and orchestrate osteoclast and osteoblast activity, they likely play a central role in orthodontic tooth movement. In this review, we attempt to shed light on the impact and role of osteocyte mechanotransduction during orthodontic tooth movement.

Recent findings: Mechanically loaded osteocytes produce signaling molecules, e.g., bone morphogenetic proteins, Wnts, prostaglandins, osteopontin, nitric oxide, sclerostin, and RANKL, which modulate the recruitment, differentiation, and activity of osteoblasts and osteoclasts. The major signaling pathways activated by mechanical loading in osteocytes are the wingless-related integration site (Wnt)/β-catenin and RANKL pathways, which are key regulators of bone metabolism. Moreover, osteocytes are capable of orchestrating bone adaptation during orthodontic tooth movement. A better understanding of the role of osteocyte mechanotransduction is crucial to advance orthodontic treatment. The optimal force level on the periodontal tissues for orthodontic tooth movement producing an adequate biological response, is debated. This review emphasizes that both mechanoresponses and inflammation are essential for achieving tooth movement clinically. To fully comprehend the role of osteocyte mechanotransduction in orthodontic tooth movement, more knowledge is needed of the biological pathways involved. This will contribute to optimization of orthodontic treatment and enhance patient outcomes.

Keywords: Bone remodeling; Jaw bone; Mechanical loading; Mechanotransduction; Orthodontic tooth movement; Osteocyte.

Fig. 1

Schematic diagram of bone remodeling at the “compression side” and “tension side” during orthodontic tooth movement. Mechanical force is applied to the teeth. Bone remodeling starts at the “compression side” by means of osteoclastic bone resorption regulated by several (bio)chemical factors, e.g. NO, PGE₂, sclerostin, TNF-α, IL-1β/6, RANK/RANKL, M-CSF, VEGF, cathepsin K, and MMPs. At the “tension side” osteoblastic bone formation is also regulated by (bio)chemical factors, e.g. NO, PGE₂, IL-10, RANK/RANKL, BMP, VEGF, OPG, IGF, TGF-β, TIMP, and MMPs. NO, nitric oxide; PGE₂, prostaglandin E₂; TNF-α, tumor necrosis factor-α; IL-1β/6, interleukin-1β/6; RANK, receptor activator of nuclear-κB; RANKL, receptor activator of nuclear factor- κB ligand; M-CSF, macrophage-colony stimulating factor; VEGF, vascular endothelial growth factor; OPG, osteoprotegerin; IGF, insulin-like growth factor; TGF-β, transforming growth factor-β; TIMP, tissue inhibitor of metalloproteinases; MMPs, matrix metalloproteinases