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Advisory Committee Chair

Ping Zhang

Advisory Committee Members

Suzanne M Michalek

Jannet Katz

Amjad Javed

Document Type

Thesis

Date of Award

2011

Degree Name by School

Master of Science in Dentistry (MScD) School of Dentistry

Abstract

Porphyromonas gingivalis is one of the etiologic factors of periodontal disease, a chronic inflammatory disorder characterized by the destruction of periodontal connective tissue and the subsequent loss of alveolar bone. Epidemiological and genetic studies have indicated an association between periodontal disease and the vitamin D system. However, little is known regarding how vitamin D signaling regulates the inflammatory immune process of this disease. The purpose of the study was to understand the role of the vitamin D receptor (VDR) in regulating the host response to P. gingivalis infection by using a dual chamber mouse model. These chambers served both as infection and sample collection sites. Chamber exudates of wild type (WT) and VDR knock out (VDR-/-) mice were sampled for neutrophil and monocyte levels, bacterial clearance and levels of TNF-α, IL-6, IL-12p40, and IL-10 cytokines. In addition, serum cytokines, P. gingivalis specific CD4+ T cell cytokine responses and serum antibody responses were assessed. Our results showed similar levels of neutrophil and monocyte infiltration in WT and VDR-/- mice following P. ginigvalis infection. However, VDR-/- mice exhibited a significantly higher level of bacteria than WT mice. Furthermore, significant higher levels of IL-6, IL-10, IL-12p40 and TNF-α were observed in the chamber exudates of VDR-/- mice. Although a similar level of serum IL-6 was seen in WT and VDR-/- mice 4 hr after P. gingivalis infection, 24 hr post infection, the levels were increased in VDR-/- mice. Assessment of P. gingivalis-specific CD4+ T cell cytokine responses suggested that in the presence of the VDR a Th1 response was favored following P. gingivalis infection. Furthermore, VDR-/- mice exhibited lower levels of serum IgG anti-P. gingivalis antibodies than that observed in WT mice. Taken together, these results suggest that VDR deficient mice have an increased susceptibility to P. gingivalis infection, implicating the VDR in the control of bacterial growth and in modulating inflammatory responses that could be detrimental to the host during infection by P. ginigvalis. These findings provide valuable insight on the role of the VDR in P. gingivalis infection

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Dentistry Commons

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