Adhesion Molecule Expression and Cellular Infiltrate Within Gingival Tissue

Moughal, Naureen Arshad (1992) Adhesion Molecule Expression and Cellular Infiltrate Within Gingival Tissue. PhD thesis, University of Glasgow.

Abstract

The development of gingival inflammation is not well understood, despite many years of investigation. Accordingly, the main aims of this thesis were, to study the immune and inflammatory cellular infiltrate during the development of gingival inflammation and to examine the effect of proinflammatory cytokines on adhesion molecule expression using gingival organ culture. Two studies were performed which utilised the experimental gingivitis model. In the model, experimental gingival inflammation was induced in two groups of healthy volunteers by withdrawing oral hygiene procedures and allowing plaque to accumulate undisturbed for 21-days and 10-days. Tissue for analysis was obtained from the experimental gingivitis studies and from patients undergoing routine periodontal treatment. Immunohistology and computerised image planimetry were employed for assessing changes within periodontal cellular infiltrate and adhesion molecules; and a bioassay was used to assess changes in the levels of interleukin-1. Initial studies showed that a single staining avidin-biotin-complex method utilising peroxidase as the substrate, gave the optimal immunohistological staining procedure. Clinical parameters during the experimental gingivitis studies changed as expected, with the 10-day study demonstrating minimal changes and the 21-day study showing large increases as expected. The 10-day study was aimed at analysing changes during very early 'histological' inflammation and the 21-day study during 'clinically detectable' inflammation. The cytokine, interleukin-1 was demonstrated in crevicular fluid during the 21-day study in healthy human volunteers. A sensitive and specific bioassay allowed detection of biologically active interleukin-1 in inflamed gingiva. Interleukin-1 levels increased rapidly with plaque accumulation and in advance of the subsequent gingival inflammation, peaking within 7 days of the start of gingivitis. Monoclonal antibodies to CD1a (specific for Langerhans cells and thymocytes) and HLA-DR (class II major histocompatibility antigens - (MHC)) were used to identify Langerhans cells within gingival biopsies taken every 7 days of the 21-day study and every 3 days of the 10-day study. HLA-DR antibody stained dendritic cells within the oral epithelium which were morphologically identical to the CDla+ Langerhans cells. During the 10-day study the number of CDla+ Langerhans cells and HLA-DR+ Langerhans cells did not change with time. However, within the 21-day study. Class II MHC Langerhans cell numbers rose and plateaued between day 7 and 14, then decreased to baseline by day 21. As plaque accumulated and inflammation developed there was an initial increase, followed by a decrease in CDla+ Langerhans cells. It was hypothesised that this may reflect the antigen presenting and migrating role of Langerhans cells to lymph nodes. The cellular infiltrate of gingival tissue was also analysed and it was found that all of the cell types studied (neutrophils; T-cells and T-cell subsets i.e. helper, suppressor, naive and memory) were present in varying quantities. Periodontal cellular infiltrate was seen within healthy tissue and within experimentally inflamed gingival tissue; and demonstrated preferential accumulation in the connective tissue subjacent to the junctional epithelium. Higher numbers of memory-T cells than naive-T cells were found within healthy gingival tissue; with subsequent inflammation development their was no change in memory-T cells numbers, with a simultaneous decrease in the number of naive-T cells. This suggests that the naive-T cells were maturing into memory-T cells, and in turn are maintaining the numbers of memory-T cells within the gingival tissue. Vascular endothelium expressed ELAM-1 (endothelial cell leukocyte adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1) both in clinically 'healthy' tissue (day 0) and in experimentally inflamed tissue (day 3 to 10 and day 7 to 21). Positive vessels were found mainly in the connective tissue subjacent to the junctional epithelium where the highest numbers of T cells (CD11a+) and neutrophils were also seen.

• Item Type: Thesis (PhD)
• Qualification Level: Doctoral
• Additional Information: Adviser: D F Kinane
• Keywords: Dentistry
• Date of Award: 1992
• Depositing User: Enlighten Team
• Unique ID: glathesis:1992-75453
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 19 Nov 2019 20:04
• Last Modified: 19 Nov 2019 20:04
• URI: https://theses.gla.ac.uk/id/eprint/75453