Release from optimal compressive force suppresses osteoclast differentiation

Ikeda,Masaaki; Yoshimura,Yoshitaka; Kikuiri,Takashi; Matsuno,Mino; Hasegawa,Tomokazu; Fukushima,Kumu; Hayakawa,Takako; Minamikawa,Hajime; Suzuki,Kuniaki; Iida,Junichiro

doi:10.3892/mmr.2016.5801

Release from optimal compressive force suppresses osteoclast differentiation

Authors:
- Masaaki Ikeda
- Yoshitaka Yoshimura
- Takashi Kikuiri
- Mino Matsuno
- Tomokazu Hasegawa
- Kumu Fukushima
- Takako Hayakawa
- Hajime Minamikawa
- Kuniaki Suzuki
- Junichiro Iida
View Affiliations

Affiliations: Department of Orthodontics, Hokkaido University Graduate School of Dental Medicine, Sapporo, Hokkaido 060‑8586, Japan, Department of Molecular Cell Pharmacology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Hokkaido 060‑8586, Japan, Department of Pediatric Dentistry, Hokkaido University Graduate School of Dental Medicine, Sapporo, Hokkaido 060‑8586, Japan, Department of Pediatric Dentistry, Faculty of Dentistry, Tokushima University, Tokushima 770‑8504, Japan
Published online on: October 5, 2016 https://doi.org/10.3892/mmr.2016.5801
Pages: 4699-4705

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

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.

View Figures

View References

1	Karsenty G and Wagner EF: Reaching a genetic and molecular understanding of skeletal development. Dev Cell. 2:389–406. 2002. View Article : Google Scholar : PubMed/NCBI
2	Teitelbaum SL and Ross FP: Genetic regulation of osteoclast development and function. Nat Rev Genet. 4:638–649. 2003. View Article : Google Scholar : PubMed/NCBI
3	Roberts-Harry D and Sandy J: Orthodontics. Part 11: Orthodontic tooth movement. Br Dent J. 196:391–394. 2004. View Article : Google Scholar : PubMed/NCBI
4	Bourauel C, Vollmer D and Jäger A: Application of bone remodeling theories in the simulation of orthodontic tooth movements. J Orofac Orthop. 61:266–279. 2000.(In English, German). View Article : Google Scholar : PubMed/NCBI
5	Boyle WJ, Simonet WS and Lacey DL: Osteoclast differentiation and activation. Nature. 423:337–342. 2003. View Article : Google Scholar : PubMed/NCBI
6	Takayanagi H: The role of NFAT in osteoclast formation. Ann N Y Acad Sci. 1116:227–237. 2007. View Article : Google Scholar : PubMed/NCBI
7	Zhang F, Wang CL, Koyama Y, Mitsui N, Shionome C, Sanuki R, Suzuki N, Mayahara K, Shimizu N and Maeno M: Compressive force stimulates the gene expression of IL-17s and their receptor in MC3T3-E1 cells. Connect Tissue Res. 51:359–369. 2010. View Article : Google Scholar : PubMed/NCBI
8	Shibata K, Yoshimura Y, Kikuiri T, Hasegawa T, Taniguchi Y, Deyama Y, Suzuki K and Iida J: Effect of the release from mechanical stress on osteoclastogenesis in RAW264.7 cells. Int J Mol Med. 28:73–79. 2011.PubMed/NCBI
9	Kameyama S, Yoshimura Y, Kameyama T, Kikuiri T, Matsuno M, Deyama Y, Suzuki K and Iida J: Short-term mechanical stress inhibits osteoclastogenesis via suppression of DC-STAMP in RAW264.7 cells. Int J Mol Med. 31:292–298. 2013.PubMed/NCBI
10	Hayakawa T, Yoshimura Y, Kikuiri T, Matsuno M, Fukushima K, Shibata K, Deyama Y, Suzuki K and Iida J: Optimal compressive force accelerates osteoclastogenesis in RAW264.7 cells. Mol Med Rep. 12:5879–5885. 2015.PubMed/NCBI
11	Suzuki N, Yoshimura Y, Deyama Y, Suzuki K and Kitagawa Y: Mechanical stress directly suppresses osteoclast differentiation in RAW264.7 cells. Int J Mol Med. 21:291–296. 2008.PubMed/NCBI
12	Rubin J, Murphy TC, Fan X, Goldschmidt M and Talor WR: Activation of extracellular signal-regulated kinase is involved in mechanical strain inhibition of RANKL expression in bone stromal cells. J Bone Miner Res. 17:1452–1460. 2002. View Article : Google Scholar : PubMed/NCBI
13	Koike M, Shimokawa H, Kanno Z, Ohya K and Soma K: Effects of mechanical strain on proliferation and differentiation of bone marrow stromal cell line ST2. J Bone Miner Metab. 23:219–225. 2005. View Article : Google Scholar : PubMed/NCBI
14	Kanzaki H, Chiba M, Sato A, Miyagawa A, Arai K, Nukatsuka S and Mitani H: Cyclical tensile force on periodontal ligament cells inhibits osteoclastogenesis through OPG induction. J Dent Res. 85:457–462. 2006. View Article : Google Scholar : PubMed/NCBI
15	Nishijima Y, Yamaguchi M, Kojima T, Aihara N, Nakajima R and Kasai K: Levels of RANKL and OPG in gingival crevicular fluid during orthodontic tooth movement and effect of compression force on release from periodontal ligament cells in vitro. Orthod Cranifac Res. 9:63–70. 2006. View Article : Google Scholar
16	Ichimiya H, Takahashi T, Ariyoshi W, Takano H, Matayoshi T and Nishihara T: Compressive mechanical stress promotes osteoclast formation through RANKL expression on synovial cells. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 103:334–341. 2007. View Article : Google Scholar : PubMed/NCBI
17	Liu J, Zhao Z, Zou L, Li J, Wang F, Li X, Zhang J, Liu Y, Chen S, Zhi M and Wang J: Pressure-loaded MSCs during early osteodifferentiation promote osteoclastogenesis by increase of RANKL/OPG ratio. Ann Biomed Eng. 37:794–802. 2009. View Article : Google Scholar : PubMed/NCBI
18	Rubin J, Biskobing D, Fan X, Rubin C, McLeod K and Taylor WR: Pressure regulates osteoclast formation and MCSF expression in marrow culture. J Cell Physiol. 170:81–87. 1997. View Article : Google Scholar : PubMed/NCBI
19	Mehrotra M, Saegusa M, Wadhwa S, Voznesensky O, Peterson D and Pilbeam C: Fluid flow induceds RANKL expression in primary murine calvarial osteoblasts. J Cell Biochem. 98:1271–1283. 2006. View Article : Google Scholar : PubMed/NCBI
20	Tan SD, Vries TJ, Kujipers-Jagtman AM, Semeins CM, Everts V and Klein-Nulend J: Osteocytes subjected to fluid flow inhibits osteoclast formation and formation and bone resorption. Bone. 41:745–751. 2007. View Article : Google Scholar : PubMed/NCBI
21	Hong Z Qing, Tao L Meng, Yi Z, Wei L, Ju Xiang S and Li L: The effect of rotative stress on CAII, FAS, FASL, OSCAR, and TRAP gene expression in osteoclasts. J Cell Biochem. 114:388–397. 2013. View Article : Google Scholar : PubMed/NCBI
22	Makihira S, Kawahara Y, Yuge L, Mine Y and Nikawa H: Impact of the microgravity environment in a 3-dimentional clinostat on osteoblast- and osteoclast-like cells. Cell Biol Int. 32:1176–1181. 2008. View Article : Google Scholar : PubMed/NCBI
23	Kadow-Romacker A, Haffman JE, Duga G, Wildemann B and Schmidmaier G: Effect of mechanical stimulation on osteoblast- and osteoclast-like cells in vitro. Cell Tissues Organs. 190:61–68. 2009. View Article : Google Scholar
24	Takeyama S, Yoshimura Y, Deyama Y, Sugawara Y, Fukuda H and Matsumoto A: Phosphate decreases osteoclastogenesis in coculture of osteoblast and bone marrow. Biochem Biophys Res Commum. 282:798–802. 2001. View Article : Google Scholar
25	Nakamura K, Deyama Y, Yoshimura Y, Suzuki K and Morita M: Toll-like receptor 3 ligand-induced antiviral response in mouse osteoblastic cells. Int J Mol Med. 19:771–775. 2007.PubMed/NCBI
26	Livak KJ and Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(−Delta Delta C(T)) Method. Methods. 25:402–408. 2001. View Article : Google Scholar : PubMed/NCBI
27	Reitan K: Tissue behavior during orthodontic tooth movement. Am J Orthod. 46:881–900. 1960. View Article : Google Scholar
28	Zhao Q, Wang X, Liu Y, He A and Jia R: NFATc1: Functions in osteoclasts. Int J Biochem Cell Biol. 42:576–579. 2010. View Article : Google Scholar : PubMed/NCBI
29	Nakagawa N, Kinosaki M, Yamaguchi K, Shima N, Yasuda H, Yano K, Morinaga T and Higashio K: RANK is essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Biochem Biophys Res Commun. 253:395–400. 1998. View Article : Google Scholar : PubMed/NCBI
30	Blavier L and Delaissé JM: Matrix metalloproteinases are obligatory for the migration of preosteoclasts to the developing marrow cavity of primitive long bones. J Cell Sci. 108:3649–3659. 1995.PubMed/NCBI
31	Sato T, Foged NT and Delaissé JM: The migration of purified osteoclasts through collagen is inhibited by matrix metalloproteinase inhibitors. J Bone Miner Res. 13:59–66. 1998. View Article : Google Scholar : PubMed/NCBI
32	Hill PA, Murphy G, Docherty AJ, Hembry RM, Millican TA, Reynolds JJ and Meikle MC: The effects of selective inhibitors of matrix metalloproteinase (MMPs) on bone resorption and the identification of MMPs and TIMP-1 in isolated osteoclasts. J Cell Sci. 107:3055–3064. 1994.PubMed/NCBI
33	Spessotto P, Rossi FM, Degan M, Di Francia R, Perris R, Colombatti A and Gattei V: Hyaluronan-CD44 interaction hampers migration of osteoclast-like cells by down-regulation MMP-9. J Cell Biol. 158:1133–1144. 2002. View Article : Google Scholar : PubMed/NCBI
34	Saftig P, Hunziker E, Wehmeyer O, Jones S, Boyde A, Rommerskirch W, Moritz JD, Schu P and von Figura V: Impaired osteoclastic bone resorption leads to osteopeterosis in cathepsin-K-deficient mice. Proc Natl Acad Sci USA. 95:13453–13458. 1998. View Article : Google Scholar : PubMed/NCBI
35	Kornak U, Kasper D, Bösl MR, Kaiser E, Schweizer M, Schulz A, Friedrich W, Delling G and Jentsch TJ: Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man. Cell. 104:205–215. 2001. View Article : Google Scholar : PubMed/NCBI
36	Li YP, Chen W, Liang Y, Li E and Stashenko P: Atp6i-deficient mice exhibit severe osteopetrosis due to loss of osteoclast-mediated extracellular acidfiction. Nat Genet. 23:447–451. 1999. View Article : Google Scholar : PubMed/NCBI
37	Miyamoto H, Suzuki T, Miyauchi Y, Iwasaki R, Kobayashi T, Sato Y, Miyamoto K, Hoshi H, Hashimoto K, Yoshida S, et al: Osteiclasts stimulatory transmembrane protein and dendritic cell-specific transmembrane protein cooperatively modulate cell-cell fusion to form osteoclasts and foreign body giant cells. J Bone Miner Res. 27:1289–1297. 2012. View Article : Google Scholar : PubMed/NCBI