The changes in vascular adhesion molecule expression and numbers of infiltrating leukocytes during a 21-day experimental gingivitis episode were investigated immunohistochemically. Monoclonal antibodies to ELAM-1 (1.2B6), ICAM-1 (6.5B5), CD3 (OKT3-pan-T cell) and neutrophils (PMN-elastase) were used to identify positive vessels and leukocytes within gingival biopsies taken on d 0, 7, 14 and 21. Vascular endothelium expressed ELAM-1 and ICAM-1 both in clinically 'healthy' tissue (d 0) and in experimentally inflamed tissue (d 7 to 21). Positive vessels were found mainly in the connective tissue subjacent to the junctional epithelium where the highest numbers of T cells and neutrophils were also seen. Although T cells were found in all tissue areas studied, neutrophils were largely concentrated in the junctional epithelium and the subjacent connective tissue but were absent from the oral epithelial region. As the experimental gingivitis developed, the number of T cells or neutrophils in the different tissue regions did not change significantly although the most intense vascular ICAM-1 and ELAM-1 staining redistributed to the CT adjacent to the junctional epithelium. A prominent feature was the intense ICAM-1 positive staining of the junctional epithelium and its absence in the closely adjacent oral epithelium, in both clinically 'healthy' and inflamed tissue. The gradient of ICAM-1 in junctional epithelium, with the strongest staining on the crevicular aspect plus the vascular expression of ELAM-1 and ICAM-1 in both clinically 'healthy' and inflamed tissue may be crucial processes which direct leukocyte migration towards the gingival crevice.

The ability of stromelysin (SL), fibroblast-type collagenase (FIB-CL) and tissue inhibitor of metalloproteinases (TIMP), to differentiate between healthy, gingivitis and periodontitis sites was investigated. SL and FIB-CL are members of a family of enzymes which are capable of degrading most of the extracellular matrix macromolecules. Extracellular control of these enzymes is performed by TIMP. 40 patients each provided 3 GCF samples from healthy, gingivitis and periodontitis sites. GCF samples were collected by means of sterile paper strips. GCF samples were eluted into 500 microliters of assay buffer and assays for SL, FIB-CL and TIMP were performed by a sandwich ELISA. The mean amounts of SL and TIMP in diseased sites (gingivitis and periodontitis) were significantly higher than the mean amount of these GCF components in healthy sites (MANOVA p values were: 0.006 for SL and 0.001 for TIMP). GCF SL and TIMP differentiated healthy from diseased sites. Both SL and TIMP showed moderate correlation with clinical indices. FIB-CL was detectable in only 20.8% of all sites and did not correlate with disease status.

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This study examined lactoferrin (LF) levels in gingival crevicular fluid (GCF) and set out to test the hypothesis that LF could act as a marker of crevicular polymorphonuclear leucocytes (PMN). Therefore, 2 experiments were conducted: (a) to quantify total LF (ng/30 s sample) in GCF; (b) to correlate LF levels (ng/microliters) and PMN numbers (PMNs/microliters) in gingival crevicular washings (GCW). GCF was collected from 71 sites in a total of 22 patients. These sites were classified on the basis of clinical indices of gingivitis (GI) and pocket depth (PD) into three clinical groups: 'healthy', 'gingivitis' and 'periodontitis'. GCWs were obtained from an additional 63 sites in 21 patients. LF in GCF and GCWs was assayed by a sandwich ELISA. Total leucocyte and differential counts were performed on the GCWs. GCF LF (ng/30 s) correlated positively with GI (r = 0.418, p < 0.001), PD (r = 0.415, p < 0.001) and GCF volume (r = 0.624, p < 0.001). Gingivitis (n = 21) and periodontitis sites (n = 24) demonstrated significantly higher (p < 0.05) total GCF LF than healthy (n = 26) sites. In GCWs LF (ng/microliters) showed stronger correlations with clinical indices (GI: r = 0.452, PD: r = 0.513, p < 0.001) than did PMN numbers (PMNs/microliters) (GI: r = 0.279, PD: r = 0.388, p < 0.05). LF correlated strongly with PMNs in GCWs (r = 0.531, p < 0.001) and provides a simple and effective marker of crevicular PMN numbers.

This study assessed the effect of periodontal therapy on specific serum antibody concentration, expressed as titer, and antibody binding strength, expressed as relative avidity. The immune responses to Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans were investigated. Antibody titer was assayed by enzymelinked immunosorbent assay (ELISA) and relative avidity was measured by thiocyanate elution in 17 adult periodontitis patients before and after therapy. Immunoglobulin G (IgG) avidities (expressed as thiocyanate molarity) to P. gingivalis increased from 1.01 to 1.38 M (P ‫؍‬ 0.05) and IgA titers (expressed as ELISA units [EU]) increased from 89 to 237 EU (P ‫؍‬ 0.012). There were no significant changes in avidity to A. actinomycetemcomitans, but the titer of all three immunoglobulin classes increased significantly (P < 0.03). More specifically, when patients were divided into subgroups which had originally been either IgG seropositive (i.e., having an IgG titer to this organism >2 times the control median) or seronegative for P. gingivalis, only patients who were initially seropositive showed a significant increase in antibody avidity (P ‫؍‬ 0.026; mean difference, 0.69 M). Patients who were originally seropositive in terms of IgG and IgA titer to P. gingivalis had demonstrably better treatment outcomes in terms of a reduced number of deep pockets and sites which bled on probing (P < 0.05). These findings suggest that periodontal therapy affects the magnitude and quality of the humoral immune response to suspected periodontopathogens, that this effect is dependent on initial serostatus, and that initial serostatus may have a bearing on treatment outcome.