Relationships between clinical parameters, Interleukin 1B and histopathologic findings of gingival tissue in periodontitis patients
Journal
Cytokine
Journal Volume
8
Journal Issue
2
Date Issued
1996-02
Author(s)
Abstract
IL-1 beta is one of the cytokines which can induce bone resorption and connective tissue destruction. Previous studies demonstrated that the amount of IL-1 beta in gingival crevicular fluid (GCF) was closely related to the severity of gingival index (GI) and probing depth (PD). To further investigate whether the amount of IL-1 beta in GCF and the tissues adjacent to the periodontal pockets can reflect the degree of inflammation and destruction of these tissues, the GCF and inflamed gingival specimens were harvested from 14 periodontal patients and IL-1 beta in these samples was measured by ELISA. Clinical parameters of the sampled teeth were also recorded. Possible relations among periodontal parameters, GCF or tissue IL-1 beta and the degrees of inflammation in tissue sections were analysed statistically. The results showed that with increasing GI and PD, there was an elevation of GCF and tissue IL-1 beta activity. GCF flow also showed a tendency to increase with a higher percentage of inflammatory infiltrate. The GCF and tissue IL-1 beta activity were significantly correlated with clinical parameters (GI, PD and GCF flow), as well as with the percentage of inflammatory infiltrate and tissue alterations. With the exception of a significantly negative correlation with the extent of inflammation, no obvious relation between the GCF or tissue concentration of IL-1 beta and the state of tissue pathology could be detected. In conclusion, measurements of IL-1 beta activity in GCF or diseased tissues based on the classification of clinical parameters can reflect the degree of inflammation within periodontal disease tissue. These observations indicate that clinical parameters can provide reliable means of evaluation of the severity of periodontal disease, and that IL-1 beta plays a pivotal role in the pathogenic mechanism of periodontal tissue destruction.
Subjects
ELISA | Histomorphometry | Interleukin-1β | Periodontal disease activity | Periodontitis
SDGs
Type
journal article