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IL‐8 and MCP‐1 induced by excessive orthodontic force mediates odontoclastogenesis in periodontal tissues
Author(s) -
Asano M,
Yamaguchi M,
Nakajima R,
Fujita S,
Utsunomiya T,
Yamamoto H,
Kasai K
Publication year - 2011
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2010.01780.x
Subject(s) - periodontal fiber , bone resorption , chemokine , osteoclast , resorption , root resorption , chemotaxis , rankl , interleukin 8 , ccl2 , medicine , monocyte , immunohistochemistry , molar , chemistry , dentistry , endocrinology , cytokine , inflammation , receptor , activator (genetics)
Oral Diseases (2011) 17 , 489–498 Objective: The aim of this study was to investigate how interleukin (IL)‐8 (cytokine‐induced neutrophil chemoattractant; CINC‐1) and monocyte chemotactic protein (MCP)‐1/CCL2 contribute to root resorption during orthodontic tooth movement. Materials and methods: Forty 6‐week‐old male Wistar rats were subjected to orthodontic force of 10 or 50 g to induce a mesially tipping movement of the upper first molars for 7 days. We determined the expressions of CINC‐1, CXCR2, and MCP‐1 proteins in root resorption area using immunohistochemistry. Furthermore, we investigated the effects of compression forces (CF) on IL‐8 and MCP‐1 production by human periodontal ligament (hPDL) cells. We observed an effect of chemokine treatment on rat odonto/osteoclasts in dentin slices that recapitulated root resorption. Results: The immunoreactivity for CINC‐1/CXCR2 and MCP‐1 was detected in odontoclasts and PDL fibroblasts by the orthodontic force of 50 g on day 7. CF increased the secretion and the expression of mRNA of IL‐8 and MCP‐1 from PDL cells in a magnitude‐dependent manner. Moreover, CINC‐1 and MCP‐1 stimulated osteoclastogenesis from rat osteoclast precursor cells. Conclusion: IL‐8 (CINC‐1) and MCP‐1 may therefore facilitate the process of root resorption because of excessive orthodontic force.