A Yamasaki1, H Ito, J Yusa, Y Sakurai, N Okuyama, R Ozawa. 1. Division of Oral Pathology, Department of Oral Medical Sciences, Ohu University School of Dentistry, Koriyama, Fukushima, Japan. a-yamasaki@den.ohu-u.ac.jp
Abstract
BACKGROUND AND OBJECTIVE: The therapeutic rationale of low-energy pulsed CO(2) laser coagulation mode has not been clarified yet. We conducted this study to characterize the effect of low-energy pulsed CO(2) laser coagulation mode irradiation of the rat gingiva in terms of the expression of heat shock proteins. MATERIAL AND METHODS: Laser irradiation was achieved with the parameters of 5 W, 600 mus pulse duration, and fluence of 326 J/cm(2). The gingiva dissected at different times after irradiation was processed for immunohistochemical examination of the expression of the heat shock proteins, Hsp70 and Hsp25. RESULTS: One hour after irradiation, the epithelial keratinocytes facing the laser wound exhibited an overexpression of Hsp70 in their nucleus. The connective tissue cells facing the laser wound, which included fibroblasts and capillary endothelial cells, showed de novo expression of Hsp70 at 3 h post-irradiation, the level of which peaked at 1 d and thereafter decreased. An enhanced and/or de novo expression of Hsp25 in the connective tissue cells facing the laser wound became evident at 3 h after irradiation, and after 1 d the Hsp25-expressing cells increased in number and spread over the wound as wound repair progressed. There was a temporospatial difference in the expression pattern between Hsp70 and Hsp25, with only a few cells appearing to co-express both heat shock proteins. CONCLUSION: The CO(2) laser treatment in coagulation mode produced the expression of heat shock proteins, and the findings suggest that while Hsp70 mainly conferred cell protection, Hsp25 was involved in the progress of wound repair as well as cell protection.
BACKGROUND AND OBJECTIVE: The therapeutic rationale of low-energy pulsed CO(2) laser coagulation mode has not been clarified yet. We conducted this study to characterize the effect of low-energy pulsed CO(2) laser coagulation mode irradiation of the rat gingiva in terms of the expression of heat shock proteins. MATERIAL AND METHODS: Laser irradiation was achieved with the parameters of 5 W, 600 mus pulse duration, and fluence of 326 J/cm(2). The gingiva dissected at different times after irradiation was processed for immunohistochemical examination of the expression of the heat shock proteins, Hsp70 and Hsp25. RESULTS: One hour after irradiation, the epithelial keratinocytes facing the laser wound exhibited an overexpression of Hsp70 in their nucleus. The connective tissue cells facing the laser wound, which included fibroblasts and capillary endothelial cells, showed de novo expression of Hsp70 at 3 h post-irradiation, the level of which peaked at 1 d and thereafter decreased. An enhanced and/or de novo expression of Hsp25 in the connective tissue cells facing the laser wound became evident at 3 h after irradiation, and after 1 d the Hsp25-expressing cells increased in number and spread over the wound as wound repair progressed. There was a temporospatial difference in the expression pattern between Hsp70 and Hsp25, with only a few cells appearing to co-express both heat shock proteins. CONCLUSION: The CO(2) laser treatment in coagulation mode produced the expression of heat shock proteins, and the findings suggest that while Hsp70 mainly conferred cell protection, Hsp25 was involved in the progress of wound repair as well as cell protection.