A Novel Ex vivo Culture Model for Inflammatory Bone Destruction

被引:17
作者
Sloan, A. J. [1 ,2 ]
Taylor, S. Y. [1 ]
Smith, E. L. [1 ,4 ]
Roberts, J. L. [1 ,2 ]
Chen, L. [3 ]
Wei, X. Q. [1 ]
Waddington, R. J. [1 ,2 ]
机构
[1] Cardiff Univ, Sch Dent, Mineralised Tissue Grp, Cardiff CF10 3AX, S Glam, Wales
[2] Cardiff Univ, Sch Dent, Cardiff Inst Tissue Engn & Repair, Cardiff CF10 3AX, S Glam, Wales
[3] Capital Med Univ, Sch Stomatol, Beijing, Peoples R China
[4] Univ Southampton, Inst Dev Sci, Bone & Joint Res Grp, Southampton SO9 5NH, Hants, England
基金
中国国家自然科学基金; 英国国家替代、减少和改良动物研究中心;
关键词
periodontal disease; osteoclast; LPS; RANKL; MCSF; inflammation; bone; GINGIVAL CREVICULAR FLUID; PERIODONTAL-DISEASE; OSTEOCLAST DIFFERENTIATION; RECEPTOR ACTIVATOR; RESORPTION; INTERLEUKIN-6; INDUCTION; LIPOPOLYSACCHARIDE; OSTEOBLASTS; MEDIATORS;
D O I
10.1177/0022034513495240
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Pathological alterations in the balance of bone metabolism are central to the progression of inflammatory bone diseases such as periodontal disease. We have developed and characterized a novel ex vivo murine mandible model of inflammatory bone destruction. Slices of mandible were cultured for 14 days in the presence or absence of P. gingivalis lipopolysaccharide (LPS) or pro-inflammatory cytokines. Following culture, cell viability and tissue histomorphometry were assessed with quantification of matrix proteins, resident osteoclasts, ligament cells, monocytes, macrophages, and neutrophils. In the absence of inflammatory factors, culture viability, osteoclasts, and matrix components were maintained. LPS or TNF stimulation demonstrated an increase in cellular proliferation, monocyte cells, osteoclast differentiation, and matrix degradation. Pathophysiological bone metabolism can be induced via exposure to LPS and direct influence of TNF within the model despite the absence of systemic circulation, providing a model for inflammatory bone destruction and investigation of the effects of novel therapeutics.
引用
收藏
页码:728 / 734
页数:7
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