IMMUNOCYTOCHEMICAL STUDY OF THE EFFECT OF SUPEROXIDE DISMUTASE ON THE PERIODONTAL LIGAMENT CELLS

Superoxide Dismutase가 치주인대 세포에 미치는 면역세포학적 연구

The cells associated with normal defense mechanism in inflammation release free oxygen radicals, hydroxy radicals, and various protease, all of which can damage the surrounding cells(fibroblasts) and matrix molecules(collagen). The objective of this study was to evaluate the effects of "scavenger" enzyme, superoxide dismutase(SOD). to periodontal ligament (PDL) cells. Human PDL cells were cultured from the teeth extracted for non-periodontal reason. Cultured PDL cells in vitro were treated with SOD and LPS according to dosage and culture times. Cellular activity was exaimed by Microtitration(MTT) assay. The quantitative expression of cellular proliferation by proliferating cell nuclear antigen(PCNA), collagen type I and fibronectin by indirect immunocytochemically stain in PDL cells were done. The results were as follows: 1. As only SOD treated group at 2 and 3 days, PDL cell activity was significantly increased at more than 150U(P<0.05). 2. When LPS(0.5, $5{\mu}g/m{\ell}$) and SOD(more than 150U) were added together, it was significantly increased than LPS only treated and control groups at 2 days(P<0.05). 3. When LPS($5{\mu}g/m{\ell}$) and SOD(150, 300U) were added together, PCNA index was significantly increased than LPS only treated and control groups at 2 and 3 days(P<0.05). 4. When LPS($5{\mu}g/m{\ell}$) and SOD(150U) were added together, collagen type I was significantly increased than LPS only treated and control groups at 3 days(P<0.05). 5.When LPS($5{\mu}g/m{\ell}$) and SOD(300U) were added together, fibronectin was significantly increased than LPS only treated and control groups at 3 days(P<0.05). On the above the results, the SOD in association with collagen type I, fibonectin, and PCNA may afford biological protection to oxy-radicals that were typically liberated during normal inflammatory response. Thus, the exogenous application of SOD may be effective in sthe treatment of the localized breakdown associated with chronic periodontal disease.