Systemic and Local Humoral Immune Response in Periodontal Diseases

Mooney, John (1994) Systemic and Local Humoral Immune Response in Periodontal Diseases. Master in Management Studies thesis, University of Glasgow.

Abstract

The precise role of the humoral immune response in periodontal diseases is not known. Previous workers have investigated the relationship between systemic antibody levels and disease status in great detail. However, areas such as local antibody levels, antibody avidity, differentiation of specific disease states, treatment effects and oral implants have been investigated to a much lesser extent. Therefore, in this study, these and other aspects were investigated in order to further elucidate the effects of the humoral immune response on the initiation and progression of periodontal disease. An early study investigated systemic antibody levels to Gram-positive organisms during the course of experimental gingivitis. No significant changes in antibody levels were detected. However, at this stage, the ELISA technology employed was not sensitive enough to permit estimation of gingival crevicular fluid (GCF) antibody levels. Levels of alpha2-macroglobulin (alpha2-M) and transferrin were assayed to monitor the progression of inflammation. Because many studies of the humoral immune response in periodontal disease have concentrated on antibody titre and very little has been published on antibody avidity, or binding strength, three studies were conducted into the relationship between antibody avidity and disease progression, disease state and response to treatment respectively. The first study assayed antibody avidities to Porphyromonas gingivalis and Actinohacillus actinomycetemcomitans in adult periodontitis (AP) patients on a longitudinal basis. IgM antibodies to P. gingivalis were found to be higher in patients who did not go on to experience further attachment loss than in those who did. IgG avidities to P. gingivalis were significantly higher in AP patients than in control subjects, confirming a previous finding. The second of these studies investigated the relationship between antibody avidity and periodontal disease classification, i.e. AP or rapidly progressive periodontitis (RPP). It had previously been shown that antibody avidities were lower in RPP patients than in controls, in complete contrast to the earlier finding for AP patients. However, this study demonstrated that IgG and IgM avidities to P. gingivalis were lower in RPP patients than in AP, when directly compared. The third of these studies investigated the effect of periodontal treatment on antibody avidity. The scope of previous studies in this area was increased to include IgG, IgM and IgA avidities to both P. gingivalis and A. actinomycetemcomitans. The avidity of IgG antibodies to P. gingivalis and IgG, IgM and IgA titres to A. actinomycetemcomitans increased after therapy. Overall, the data suggest that therapy induces the production of higher avidity antibodies. Modification of the ELISA technology by utilising biotin-avidin amplification increased sensitivity allowing antibody levels in GCF to be quantified. Four studies were conducted. Two of these were cross-sectional studies investigating healthy, gingivitis and periodontitis sites in periodontitis patients. Two compared cross-sectionally matched oral implant and natural tooth sites in oral implant patients. The first of these studies demonstrated a strong correlation between IgG antibody levels to P. gingivalis in serum and GCF, confirming earlier findings. IgG levels to P. gingivalis were found to be significantly different in sites with different disease status, i.e. sites with deeper pockets and more inflammation had lower antibody levels than sites with shallower pockets and less inf Icimmat ion. The second of these studies focused on a comparison of IgG levels to P. gingivalis around oral implants and natural teeth. This is a field in which no previous work has been conducted on the humoral immune response, and very little on the infIcimmatory response. Therefore, assays of the acute-phase proteins, alpha2-M and alpha1-antitrypsin (al-AT), and the iron-binding proteins, TF and lactoferrin (LF), were also performed. This study indicated great similarity between oral implants and natural teeth. However, there was also a suggestion that implants and natural teeth may differ in their local plasma cell infiltrate. Because of the provocative conclusion of the first study, that antibody levels were paradoxically lower in deeper pockets and more inflamed sites, it was decided to conduct another cross-sectional study in periodontitis patients. This differed in that three sites were sampled in each patient - one healthy, one gingivitis and one periodontitis. Paired comparisons were performed by multivariate repeated measures analysis of variance (MANOVA). In addition, levels of the tissue metalloproteinase, stromelysin, and tissue inhibitor of metalloproteinases (TIMP) were assayed to provide an indication of local tissue degradation. IgG levels against P. gingivalis alone showed a significant difference between health and gingivitis. Additionally, there was a definite trend towards specific IgG levels being lower in periodontitis sites than in gingivitis sites; bearing out the findings of the previous study and suggesting that specific antibody levels may provide a more sensitive indicator of local disease progression than other parameters, e.g. metalloproteinases or TIMP.

• Item Type: Thesis (Master in Management Studies)
• Qualification Level: Masters
• Additional Information: Adviser: D F Kinane
• Keywords: Dentistry, Immunology
• Date of Award: 1994
• Depositing User: Enlighten Team
• Unique ID: glathesis:1994-75645
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 19 Nov 2019 19:01
• Last Modified: 19 Nov 2019 19:01
• URI: https://theses.gla.ac.uk/id/eprint/75645