Journal of Bone Metabolism

"Cytokines"

Review Articles

Mechanisms of Osteoclastogenesis in Orthodontic Tooth Movement and Orthodontically Induced Tooth Root Resorption: Yuta Nakai, Natnicha Praneetpong, Wanida Ono, Noriaki Ono; J Bone Metab 2023;30(4):297-310.
Published online November 30, 2023; DOI: https://doi.org/10.11005/jbm.2023.30.4.297

Orthodontic tooth movement (OTM) is achieved by the simultaneous activation of bone resorption by osteoclasts and bone formation by osteoblasts. When orthodontic forces are applied, osteoclast-mediated bone resorption occurs in the alveolar bone on the compression side, creating space for tooth movement. Therefore, controlling osteoclastogenesis is the fundamental tenet of orthodontic treatment. Orthodontic forces are sensed by osteoblast lineage cells such as periodontal ligament (PDL) cells and osteocytes. Of several cytokines produced by these cells, the most important cytokine promoting osteoclastogenesis is the receptor activator of nuclear factor-κB ligand (RANKL), which is mainly supplied by osteoblasts. Additionally, osteocytes embedded within the bone matrix, T lymphocytes in inflammatory conditions, and PDL cells produce RANKL. Besides RANKL, inflammatory cytokines, such as interleukin-1, tumor necrosis factor-α, and prostaglandin E2 promote osteoclastogenesis under OTM. On the downside, excessive osteoclastogenesis activation triggers orthodontically-induced external root resorption (ERR) through pro-osteoclastic inflammatory cytokines. Therefore, understanding the mechanisms of osteoclastogenesis during OTM is essential in reducing the adverse effects of orthodontic treatment. Here, we review the current concepts of the mechanisms underlying osteoclastogenesis in OTM and orthodontically induced ERR.

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Differential Role of Transforming Growth Factor-beta in an Osteoarthritic or a Healthy Joint: Peter M. van der Kraan; J Bone Metab 2018;25(2):65-72.
Published online May 31, 2018; DOI: https://doi.org/10.11005/jbm.2018.25.2.65

Transforming growth factor-β (TGF-β) is a cytokine that plays an important role in both normal joints and joints affected by osteoarthritis (OA), the most common joint disease. However, the role of this pleiotropic cytokine in a normal healthy joint is very different from its role in an OA joint. In a normal synovial joint, active TGF-β is only present after joint loading and only for a short period. In contrast, permanent and high levels of active TGF-β are detected in OA joints. Due to this difference in levels and exposure period of joint cells to active TGF-β, the function of TGF-β is strikingly different in normal and OA joints. The consequences of this difference in TGF-β levels on joint homeostasis and pathological changes in OA joints are discussed in this review.

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