Mast Cells in Human Periodontal Disease - Periodontal (Gum) Disorders

Mast Cells in Human Periodontal Disease
2004
E. Gemmell*, C.L. Carter, and G.J. Seymour
Journal of Dental Research

© 2004 International and American Associations for Dental Research

Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane 4072, Australia;

* corresponding author, e.gemmell@uq.edu.au

ABSTRACT

Recently, mast cells have been shown to produce cytokines which can direct the development of T-cell subsets. The aim of the present study was to determine the relationship between mast cells and the Th1/Th2 response in human periodontal disease. Tryptase+ mast cell numbers were decreased in chronic periodontitis tissues compared with healthy/gingivitis lesions. Lower numbers of c-kit+ cells, which remained constant regardless of clinical status, indicate that there may be no increased migration of mast cells into periodontal disease lesions. While there were no differences in IgG2+ or IgG4+ cell numbers in healthy/gingivitis samples, there was an increase in IgG4+ cells compared with IgG2+ cells in periodontitis lesions, numbers increasing with disease severity. This suggests a predominance of Th2 cells in periodontitis, although mast cells may not be the source of Th2-inducing cytokines.

KEY WORDS: mast cells Ô periodontal disease Ô immunohistology

INTRODUCTION

Mast cells are a heterogeneous population which can be divided into two phenotypes on the basis of neutral serine proteases (Irani et al., 1986). Connective tissue mast cells (CTMC)s are found throughout the connective tissues of the skin and peritoneal cavity, whereas mucosal mast cells (MMC)s are present in the intestinal lamina propria and lung (Irani and Schwartz, 1989; Wasserman, 1994).

While the primary role for mast cells was thought to be in the innate defense against intestinal and cutaneous parasitic and bacterial infections, they are now believed also to play a role in the induction of acquired immune responses (M»cheri and David, 1997). Mast cells have been reported to reside close to T-cells (Mekori and Metcalf, 1999), can phagocytose and process bacterial antigens prior to presentation of antigens to T-cells (Malaviya et al., 1996), and are a source of Th1- and Th2-inducing cytokines (Plaut et al., 1989; Smith et al., 1994; Marietta et al., 1996).

The aim of the present study was to determine the relationship between mast cells and the Th1/Th2 response in human periodontal disease. Tryptase+ and c-kit+ mast cells were first demonstrated in biopsies from healthy/gingivitis and chronic periodontitis patients. Stem cell factor is a differentiation and proliferation factor for mast cells and is a ligand for the receptor that is encoded by the c-kit proto-oncogene (Galli et al., 1995). Second, mast cells produce IL-4, IL-10, and IL-13 (Plaut et al., 1989; Marietta et al., 1996), which direct Th2 responses, and IL-12 (Smith et al., 1994), which induces IFN-gamma production (Chan et al., 1991), contributing to the development of a Th1 response. Since interferon gamma and IL-4 induce T-cell-dependent isotype switching in B-cells to IgG2 and IgG4, respectively (Agresti and Vercelli, 2002; Tanaka et al., 2003), IgG2+ and IgG4+ B-cells/plasma cell numbers were also examined.

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