The systemic immune response is more prominent than the mucosal immune response in the pathogenesis of periodontal disease.
OBJECTIVE
The diseased periodontium appears to express features of a systemic and a mucosal immune response. Our aims were to determine differences in immunoglobulin expression between gingivitis and periodontitis lesions and to ascertain whether immune and inflammatory cells were recruited into the diseased periodontium by the mucosal addressin adhesion molecule (MAdCAM-1).


METHODS
In situ hybridization and immunohistochemistry were used to detect the expression of chemokines, adhesion molecules and immunoglobulins in tissue sections of gingival and granulation tissues excised from periodontitis-affected sites and of healthy tissue and gingivitis-affected tissue excised during crown-lengthening procedures.


RESULTS
Greater numbers of plasma cells were observed in periodontitis gingival/granulation tissue lesions compared with gingivitis lesions. While IgA1 were predominant in all lesions, IgA2 and J-chain expressing plasma cells were present in increased proportions in gingival tissues compared with granulation tissue. Intracellular adhesion molecule-1 (ICAM-1) was higher in periodontitis than in gingivitis and interleukin-8 mRNA was higher in lesions with a pronounced neutrophil infiltrate. Vascular cell adhesion molecule-1 (VCAM-1) localized to the deep connective tissue and indicated the presence of a systemic type of immune response in this region. Periodontal tissues (n=71 biopsies) did not appear to express MAdCAM-1, in positive control sections of small intestine where it was detected.


CONCLUSIONS
Overall, the systemic-type immune response is predominant, and although the mucosal immune response is minor and limited to the superficial tissues it may have an important role in the host defense to periodontal pathogens.
Lappin
D F
DF
Periodontology and Oral Immunology, Glasgow University Dental School, Glasgow, Scotland, UK. d.lappin@dental.gla.ac.uk
McGregor
A M P
AM
Kinane
D F
DF
D000328:Adult; D015815:Cell Adhesion Molecules; D003238:Connective Tissue / Q000276:immunology; D005881:Gingiva / Q000276:immunology; D005891:Gingivitis / Q000276:immunology*; D006097:Granulation Tissue / Q000276:immunology; D006801:Humans; D018928:Immunity, Mucosal / Q000276:immunology; D007070:Immunoglobulin A / Q000032:analysis; D007144:Immunoglobulin J-Chains / Q000032:analysis; D007136:Immunoglobulins / Q000032:analysis; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008875:Middle Aged; D009088:Mucoproteins / Q000032:analysis; D009504:Neutrophils / Q000276:immunology; D010518:Periodontitis / Q000276:immunology*; D010519:Periodontium / Q000276:immunology; D010950:Plasma Cells / Q000276:immunology; D016201:Receptors, Lymphocyte Homing / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
D015815:Cell Adhesion Molecules; D007070:Immunoglobulin A; D007144:Immunoglobulin J-Chains; D007136:Immunoglobulins; D016209:Interleukin-8; C504265:MADCAM1 protein, human; D009088:Mucoproteins; D016201:Receptors, Lymphocyte Homing; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1