The use of rodent models to investigate host-bacteria interactions related to periodontal diseases

被引:293
作者
Graves, Dana T. [1 ]
Fine, Daniel [2 ]
Teng, Yen-Tung A. [3 ]
Van Dyke, Thomas E. [1 ]
Hajishengallis, George [4 ,5 ]
机构
[1] Boston Univ, Sch Dent Med, Dept Periodontol & Oral Biol, Boston, MA 02118 USA
[2] Univ Med & Dent New Jersey, Dept Oral Biol, Div Peridontol, Eastman Dept Dent, Newark, NJ 07103 USA
[3] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Ctr Oral Biol, Rochester, NY 14642 USA
[4] Univ Louisville, Hlth Sci Ctr, Ctr Oral Hlth & Systemat Dis, Louisville, KY 40292 USA
[5] Univ Louisville, Hlth Sci Ctr, Dept Periodont, Louisville, KY 40292 USA
关键词
animal model; bacteria; bone; cytokine; infection; inflammation; mouse; murine; osteoclast; periodontitis; rat;
D O I
10.1111/j.1600-051X.2007.01172.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Even though animal models have limitations, they are often superior to in vitro or clinical studies in addressing mechanistic questions and serve as an essential link between hypotheses and human patients. Periodontal disease can be viewed as a process that involves four major stages: bacterial colonization, invasion, induction of a destructive host response in connective tissue and a repair process that reduces the extent of tissue breakdown. Animal studies should be evaluated in terms of their capacity to test specific hypotheses rather than their fidelity to all aspects of periodontal disease initiation and progression. Thus, each of the models described below can be adapted to test discrete components of these four major steps, but not all of them. This review describes five different animal models that are appropriate for examining components of host-bacteria interactions that can lead to breakdown of hard and soft connective tissue or conditions that limit its repair as follows: the mouse calvarial model, murine oral gavage models with or without adoptive transfer of human lymphocytes, rat ligature model and rat Aggregatibacter actinomycetemcomitans feeding model.
引用
收藏
页码:89 / 105
页数:17
相关论文
共 142 条
[1]  
ADELMAN N, 1978, J IMMUNOL, V121, P209
[2]   Diabetes enhances mRNA levels of proapoptotic genes and caspase activity, which contribute to impaired healing [J].
Al-Mashat, HA ;
Kandru, S ;
Liu, RK ;
Behl, Y ;
Desta, T ;
Graves, DT .
DIABETES, 2006, 55 (02) :487-495
[3]   Deficiency of iNOS contributes to Porphyromonas gingivalis-induced tissue damage [J].
Alayan, J. ;
Ivanovski, S. ;
Gemmell, E. ;
Ford, P. ;
Hamlet, S. ;
Farah, C. S. .
ORAL MICROBIOLOGY AND IMMUNOLOGY, 2006, 21 (06) :360-365
[4]   Lipopolysaccharides indirectly stimulate apoptosis and global induction of apoptotic genes in fibroblasts [J].
Alikhani, MI ;
Alikhani, ZB ;
He, HB ;
Liu, RK ;
Popek, BI ;
Graves, DT .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (52) :52901-52908
[5]   Dendritic cells at the osteo-immune interface: Implications for inflammation-induced bone loss [J].
Alnaeeli, Mawadda ;
Park, Jaekweon ;
Mahamed, Deeqa ;
Penninger, Joseph M. ;
Teng, Yen-Tung A. .
JOURNAL OF BONE AND MINERAL RESEARCH, 2007, 22 (06) :775-780
[6]   Immune interactions with CD4+ T cells promote the development of functional osteoclasts from murine CD11c+ dendritic cells [J].
Alnaeeli, Mawadda ;
Penninger, Josef M. ;
Teng, Yen-Tung Andy .
JOURNAL OF IMMUNOLOGY, 2006, 177 (05) :3314-3326
[7]   Solubility properties of human tooth mineral and pathogenesis of dental caries [J].
Aoba, T .
ORAL DISEASES, 2004, 10 (05) :249-257
[8]  
Assuma R, 1998, J IMMUNOL, V160, P403
[9]   Genetic control of susceptibility to Porphyromonas gingivalis-induced alveolar bone loss in mice [J].
Baker, PJ ;
Dixon, M ;
Roopenian, DC .
INFECTION AND IMMUNITY, 2000, 68 (10) :5864-5868
[10]   Genetic control of the immune response in pathogenesis [J].
Baker, PJ .
JOURNAL OF PERIODONTOLOGY, 2005, 76 (11) :2042-2046