Abstract

Interleukin-1 beta (IL-1 beta) has been proven to be a multi-effect mediator of inflammation including in the promotion of inflammatory cells to move from blood to inflamed tissues, the regulation of the synthesis and decomposition of extra-cellular matrix, and indirectly in causing bone resorption and inhibition of bone growth. In this study, the amounts of IL-1 beta in the biopsied specimens of normal oral mucosa, oral submucous fibrosis (OSF), oral squamous cell carcinoma (OSCC), and verrucous hyperplasia (VerH) were quantified by ELISA. The results showed that the amounts of IL-1 beta (pg per mg tissue, mean +/- SD) in normal oral mucosa, OSF, OSCC, and VerH were 1.07 +/- 0.53, 0.76 +/- 0.56, 4.37 +/- 0.87 and 3.97 +/- 1.93 respectively. There were no significant differences (p > 0.05, Mann-Whitney U Test) between the amounts of IL-1 beta in normal oral mucosa and OSF, and between VerH and OSCC. However, a significant difference in IL-1 beta level was found (p < 0.001) between normal oral mucosa and OSCC or VerH. Immunohistochemistry staining technique using antibody against IL-1 beta showed positive staining in hyperplastic epithelium (VerH) and tumor cells of OSCC. These results might suggest a correlation between the amounts of IL-1 beta in oral precancerous and cancerous lesions and cell transformation. On the other hand, the amount of IL-1 beta did not change significantly as OSF progressed. Thus, IL-1 beta levels may not be useful to gauge the seriousness of fibrosis, but the gradual increase in IL-1 beta level from normal oral mucosa through VerH to OSCC suggests that IL-1 beta may play an important role in oral carcinogenesis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.