Journal of clinical periodontology · 2002
Sister chromatid exchange (SCE) analysis in periodontitis.
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Emingil Gülnur, Sapmaz Gül, Biçakçi Nurgün, Ozkinay Ferda
Аннотация
BACKGROUND: Emerging data indicate that genetic factors may be associated with the etiopathogenesis of aggressive periodontitis. Sister chromatid exchange (SCE) is a sensitive method that might reflect an instability of DNA or a deficiency of DNA repair. The aim of the present study was to investigate SCE frequency of patients with different forms of periodontal disease and to determine whether this cytogenetic marker in patients with aggressive periodontitis can be differential compared to patients with chronic periodontitis and control subjects.
METHODS: SCE was analysed in peripheral blood lymphocyte chromosomes of 13 patients with generalised aggressive periodontitis (G-AP), 10 patients with chronic periodontitis (CP) and 10 control subjects. The periodontal parameters of probing depth, clinical attachment level, the presence of bleeding on probing and plaque were recorded. Peripheral blood lymphocytes obtained from both patient groups and control subjects were cultured in the presence of 5-Bromo-2-deoxyuridine in complete darkness for 72 h. For scoring SCE frequency, 20 metaphases were studied from each donor.
RESULTS: The frequency of SCE was found to be 6.7 +/- 0.9 per cell in patients with G-AP, 6.5 +/- 1.5 per cell in CP patients and 6.9 +/- 1.1 in control subjects. No statistically significant differences were found between groups (p > 0.05).
CONCLUSIONS: The data indicate that there the cyotogenetic damage in the aggressive type of periodontal disease is not greater than in chronic periodontitis and control subjects. Although no aberrant cytogenetic damage was observed in different forms of periodontitis compared to control, this does not discount the importance of other genetic factors in the pathogenesis of periodontal disease.
METHODS: SCE was analysed in peripheral blood lymphocyte chromosomes of 13 patients with generalised aggressive periodontitis (G-AP), 10 patients with chronic periodontitis (CP) and 10 control subjects. The periodontal parameters of probing depth, clinical attachment level, the presence of bleeding on probing and plaque were recorded. Peripheral blood lymphocytes obtained from both patient groups and control subjects were cultured in the presence of 5-Bromo-2-deoxyuridine in complete darkness for 72 h. For scoring SCE frequency, 20 metaphases were studied from each donor.
RESULTS: The frequency of SCE was found to be 6.7 +/- 0.9 per cell in patients with G-AP, 6.5 +/- 1.5 per cell in CP patients and 6.9 +/- 1.1 in control subjects. No statistically significant differences were found between groups (p > 0.05).
CONCLUSIONS: The data indicate that there the cyotogenetic damage in the aggressive type of periodontal disease is not greater than in chronic periodontitis and control subjects. Although no aberrant cytogenetic damage was observed in different forms of periodontitis compared to control, this does not discount the importance of other genetic factors in the pathogenesis of periodontal disease.