Compressive mechanical stress promotes osteoclast formation through RANKL expression on synovial cells

Ichimiya, Hisashi; Takahashi, Tsuneo; Ariyoshi, Wataru; Takano, Hiroshi; Matayoshi, Takaaki; Nishihara, Tatsuji

doi:10.1016/j.tripleo.2006.05.026

Cited by 35 publications

(18 citation statements)

References 35 publications

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“…Mechanical stimuli elicit biochemical and morphological responses in a variety of cell types [20,21]. It has been reported that excessive mechanical loading causes articular dysfunctions such as temporomandibular joint disorders (TMD) and osteoarthritis through the production of inflammatory cytokines [3,22,23].…”

Section: Discussionmentioning

confidence: 99%

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

et al. 2011

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“…Mechanical stimuli include tensile force (8,9,(11)(12)(13)(14), compressive force (7,10,(15)(16)(17), hydrostatic pressure (18), sheer stress (19,20), rotative stress (21) and others (22,23). Stimulation with tensile force using a Flexercell tension system suppresses osteoclast differentiation and fusion.…”

Section: Introductionmentioning

confidence: 99%

Release from optimal compressive force suppresses osteoclast differentiation

Ikeda

Yoshimura

Kikuiri

et al. 2016

Molecular Medicine Reports

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Abstract. Bone remodeling is an important factor in orthodontic tooth movement. During orthodontic treatment, osteoclasts are subjected to various mechanical stimuli, and this promotes or inhibits osteoclast differentiation and fusion. It has been previously reported that the release from tensile force induces osteoclast differentiation. However, little is known about how release from compressive force affects osteoclasts. The present study investigated the effects of release from compressive force on osteoclasts. The number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts derived from RAW264.7 cells was counted, and gene expression associated with osteoclast differentiation and fusion in response to release from compressive force was evaluated by reverse transcription-quantitative polymerase chain reaction. Osteoclast number was increased by optimal compressive force application. On release from this force, osteoclast differentiation and fusion were suppressed. mRNA expression of NFATc1 was inhibited for 6 h subsequent to release from compressive force. mRNA expression of the other osteoclast-specific genes, TRAP, RANK, matrix metalloproteinase-9, cathepsin-K, chloride channel 7, ATPase H + transporting vacuolar proton pump member I, dendritic cell-specific transmembrane protein and osteoclast stimulatory transmembrane protein (OC-STAMP) was significantly inhibited at 3 h following release from compressive force compared with control cells. These findings suggest that release from optimal compressive force suppresses osteoclast differentiation and fusion, which may be important for developing orthodontic treatments.

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“…A number of studies in vitro and in vivo have described the effects of mechanical stress on the bone cells. To investigate the influence of mechanical stress on the cells, several in vitro models have been established with varying methods, including sheer stress (fluid flow) (13,14) compressive (15,16) and tensile force (17), hydrostatic pressure (18), microgravity (19), and so on (20,21). Furthermore, in addition to an in vivo experimental system including transgenic mice, many studies have indicated the effect of mechanical stress on the bone's adaptive remodeling behavior in osteocytes (22), osteoblasts (23) and in a co-culture between osteoblasts and osteoclasts (24).…”

Section: Introductionmentioning

confidence: 99%

Effect of the release from mechanical stress on osteoclastogenesis in RAW264.7 cells

Yoshimura¹

2011

Int J Mol Med

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Abstract. The effects of mechanical stress release on osteoclastogenesis may be as important as those of mechanical stress application. However, the direct effects of mechanical stress on the behavior of osteoclasts has not been thoroughly investigated and there is limited information on the results of the release from mechanical stress. In this study, the effects of mechanical stress application and its release on osteoclast differentiation were examined. The number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts derived from RAW264.7 cells were measured and the expression of osteoclast differentiation genes, which was altered in response to the release from mechanical stress according to the Flexercell tension system was evaluated by real-time PcR. Osteoclast differentiation and fusion were suppressed by mechanical stress application and were rapidly induced after mechanical stress release. The mRNA expression of the osteoclast specific genes, TRAP, matrix metalloproteinase-9 (MMP-9), cathepsin-K (cath-k), calcitonin receptor (cTR), ATPase H + transporting vacuolar proton pump member I (ATP6i), chloride channel-7 (clc7) and dendritic cell-specific transmembrane protein (dc-STAMP) was decreased with mechanical stress application, and increased up to 48 h after the release from it. These alterations in gene mRNA expression were associated with the number of osteoclasts and large osteoclasts. Inducible nitric oxide synthetase (iNOS) mRNA was increased with mechanical stress and decreased after its release. Nitric oxide (NO) production was increased with mechanical stress. Nuclear factor of activated T cells cytoplasmic (NFATc) family mRNAs were not altered with mechanical stress, but were up-regulated up to 48 h after the release from it. These findings indicate that the suppression of osteoclast differentiation and fusion induced by mechanical stress is the result of NO increase via iNOS, and that the promotion of osteoclast differentiation and fusion after the release from mechanical stress is related to the NFATc family genes, whose expression remained constant during mechanical stress but was up-regulated after the release from mechanical stress.

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Compressive mechanical stress promotes osteoclast formation through RANKL expression on synovial cells

Cited by 35 publications

References 35 publications

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

Release from optimal compressive force suppresses osteoclast differentiation

Effect of the release from mechanical stress on osteoclastogenesis in RAW264.7 cells

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