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Tumor Necrosis Factor Modulates Fibroblast Apoptosis, PMN Recruitment, and Osteoclast Formation in Response to P. gingivalis Infection

Department of Peri odontology and Oral Biology, dgraves{at}bu.edu

M. Oskoui

Department of Endodontics, Boston University School of Dental Medicine, Division of Oral Biology, 700 Albany Street, Rm. W-202, Boston, MA 02118

S. Voleinikova

Department of Peri odontology and Oral Biology

G. Naguib

Department of Peri odontology and Oral Biology

S. Cai

Department of Peri odontology and Oral Biology

T. Desta

Department of Peri odontology and Oral Biology

A. Kakouras

Department of Peri odontology and Oral Biology

Y. Jiang

Department of Endodontics, Boston University School of Dental Medicine, Division of Oral Biology, 700 Albany Street, Rm. W-202, Boston, MA 02118

P. gingivalis is an important oral pathogen, which has been closely linked to periodontal disease as well as lesions of endodontic origin. Both infections are associated with a decrease in fibroblast numbers, formation of an inflammatory infiltrate, and bone resorption. The goal of this study was to investigate the role that the host response plays in the capacity of P. gingivalis to stimulate fibroblast apoptosis, PMN recruitment, and osteoclastogenesis. This was accomplished by the use of an in vivo calvarial model in mice with targeted deletion of TNF receptors p55 and p75 and matched wild-type mice. The results indicate that P. gingivalis induces fibroblast apoptosis in vivo and establish for the first time that this involves the stimulation of a host response. Moreover, bacteria-stimulated PMN recruitment and osteoclastogenesis were also dependent upon the host response. The results suggest that much of the damage caused by P. gingivalis infection, including fibroblast apoptosis, at least under some circumstances, results from stimulation of the host response rather than the direct effect of bacterial products. Furthermore, this may represent a more general mechanism by which bacterial challenge induces apoptosis of matrix-producing cells through the induction of TNF.

Key Words: cytokine • bacteria • inflammation • cell death.

Journal of Dental Research, Vol. 80, No. 10, 1875-1879 (2001)
DOI: 10.1177/00220345010800100301


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