Intracellular localization of Porphyromonas gingivalis thiol proteinase in periodontal tissues of chronic periodontitis patients
Article first published online: 17 AUG 2004
Volume 10, Issue 5, pages 298–305, September 2004
How to Cite
Rautemaa, R., Järvensivu, A., Kari, K., Wahlgren, J., DeCarlo, A., Richardson, M. and Sorsa, T. (2004), Intracellular localization of Porphyromonas gingivalis thiol proteinase in periodontal tissues of chronic periodontitis patients. Oral Diseases, 10: 298–305. doi: 10.1111/j.1601-0825.2004.01021.x
- Issue published online: 17 AUG 2004
- Article first published online: 17 AUG 2004
- Received 28 August 2003; revised 6 February 2004; accepted 12 March 2004
- Porphyromonas gingivalis;
- cellular invasion;
- immune evasion;
- chronic periodontitis;
- thiol proteinase
Objectives: Porphyromonas gingivalis is a significant periodontal pathogen that has been shown in vitro to be able to invade gingival epithelial cells and grow intracellularly. The aim of the present study was to detect P. gingivalis in gingival tissues from chronic periodontitis (CP) patients.
Materials and methods: Monoclonal antibodies specific to a cell membrane-bound thiol proteinase of P. gingivalis were used to detect the microbe in gingival tissues of CP patients (n = 13) by immunohistochemistry. The presence of P. gingivalis was also analysed by polymerase chain reaction (PCR).
Results: Immunohistochemical analysis of the periodontal tissues revealed positive staining for P. gingivalis thiol proteinase in 11 of the 13 patients. Positive staining was mainly located intracellularly in the perinuclear region of the cytoplasm in the periodontal epithelial cells and it could be detected throughout the whole depth of both pocket and oral epithelium. The sensitivity of immunohistochemistry was found to be comparable with that of PCR.
Conclusions: Our results provide in vivo evidence of the ability of P. gingivalis to enter human gingival epithelial cells. Intracellular localization of P. gingivalis contributes to its evasion of the host immune surveillance and eventually increases its resistance to conventional treatments of periodontal diseases.