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Increased Bacterial Invasion and Differential Expression of Tight-Junction Proteins, Growth Factors, and Growth Factor Receptors in Periodontal Lesions

Cited 29 time in Web of Science Cited 30 time in Scopus
Authors

Choi, Yun S.; Kim, Yong C.; Ji, Suk; Choi, Youngnim

Issue Date
2014-08
Publisher
American Academy of Periodontology
Citation
Journal of Periodontology, Vol.85 No.8, pp.E313-E322
Abstract
Background: Many pathogens are known to modulate epithelial physical barriers, particularly tight-junction (TJ) proteins, to enter host cells and/or tissues. Growth factors have been implicated in the regulation of TJ proteins. The aim of this study is to determine differences in the levels of TJ proteins, growth factors, and their receptors in relation to bacterial invasion in diseased gingival tissues obtained from patients with periodontitis. Methods: The presence of bacteria and expression of junctional adhesion molecule (JAM)-A, occludin, epidermal growth factor (EGF), keratinocyte growth factor (KGF), insulin-like growth factor-I (IGF-I), EGF receptor, KGF receptor, and IGF-1 receptor (IGF-1R) were evaluated in gingival tissues from healthy (n = 10) and diseased (n = 10) sites in patients with periodontitis by in situ hybridization and immunohistochemistry. Results: The bacterial invasion of gingival tissue was increased in periodontal lesions compared with healthy sites. Although the levels of JAM-A and occludin were not significantly different between the healthy and diseased sites, aberrant cytoplasmic expression of JAM-A and occluding was often observed in the lesions. In addition, more leukocytes expressing JAM-A or occludin were observed within the disease-associated epithelia. Compared with the healthy sites, the differential expression of KGF, IGF-I, and IGF-1R was observed in the periodontal lesions. The levels of TJ proteins showed positive correlations with those of growth factors. Conclusion: The aberrant expression of growth factors and TJ proteins may contribute to increased bacterial invasion and disease progression in periodontal lesions.
ISSN
0022-3492
URI
https://hdl.handle.net/10371/190699
DOI
https://doi.org/10.1902/jop.2014.130740
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