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Telomere Length in Leukocytes and Cultured Gingival Fibroblasts from Patients with Aggressive Periodontitis
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Background: The association of genetic risk factors with the pathogenesis of aggressive periodontitis (AgP) has been a focus of attention. Telomeres, which are nucleoprotein complexes at the ends of chromosomes, could be a genetic marker for Down's syndrome and Hutchinson‐Gilford progeria, in which patients' premature aging is involved in the pathogenesis. It has been reported that these patients tend to experience severe periodontitis. Therefore, we investigated the telomere length of peripheral blood leukocytes (PBL) obtained from patients with AgP and that in the patients' gingival fibroblasts undergoing cellular aging in vitro.Methods: Twenty‐one patients with AgP and 50 age‐matched, periodontally healthy subjects (HS) participated in this study. Genomic DNA from PBL and from human gingival fibroblasts (HGF) was analyzed by Southern blotting for telomere length. The percentage of HGF positive for β‐galactosidase (β‐gal), a marker for cellular senescence, was also investigated.Results: There was no significant difference in the telomere length (P = 0.20, Student's t test) between the two groups, and wide interindividual variation was found (5.93 to 11.4 kbp, average 8.35 ± 1.19 kbp). The telomere length from PBL negatively correlated with donor age, but no significant difference in telomere loss between the two groups was observed. With HGF undergoing aging in culture, the mean telomere length of these cells from six patients with AgP and seven HS decreased an average of –67.5 bp and –81.0 bp, respectively. No association was found in the telomere length between PBL and HGF from the same donors (r = 0.56, P = 0.20). A significant association was found between the telomere length and the percentages of β‐ gal–positive HGF during cell passages (r = 0.70, P <0.001).Conclusions: These results indicate that patients with AgP do not have excessive telomere loss and thus do not support the notion of the occurrence of a generalized premature cellular aging in patients with AgP. Further studies are required to investigate the association between telomere length and β‐gal in HGF. J Periodontol 2004;75:84‐90.
Title: Telomere Length in Leukocytes and Cultured Gingival Fibroblasts from Patients with Aggressive Periodontitis
Description:
Background: The association of genetic risk factors with the pathogenesis of aggressive periodontitis (AgP) has been a focus of attention.
Telomeres, which are nucleoprotein complexes at the ends of chromosomes, could be a genetic marker for Down's syndrome and Hutchinson‐Gilford progeria, in which patients' premature aging is involved in the pathogenesis.
It has been reported that these patients tend to experience severe periodontitis.
Therefore, we investigated the telomere length of peripheral blood leukocytes (PBL) obtained from patients with AgP and that in the patients' gingival fibroblasts undergoing cellular aging in vitro.
Methods: Twenty‐one patients with AgP and 50 age‐matched, periodontally healthy subjects (HS) participated in this study.
Genomic DNA from PBL and from human gingival fibroblasts (HGF) was analyzed by Southern blotting for telomere length.
The percentage of HGF positive for β‐galactosidase (β‐gal), a marker for cellular senescence, was also investigated.
Results: There was no significant difference in the telomere length (P = 0.
20, Student's t test) between the two groups, and wide interindividual variation was found (5.
93 to 11.
4 kbp, average 8.
35 ± 1.
19 kbp).
The telomere length from PBL negatively correlated with donor age, but no significant difference in telomere loss between the two groups was observed.
With HGF undergoing aging in culture, the mean telomere length of these cells from six patients with AgP and seven HS decreased an average of –67.
5 bp and –81.
0 bp, respectively.
No association was found in the telomere length between PBL and HGF from the same donors (r = 0.
56, P = 0.
20).
A significant association was found between the telomere length and the percentages of β‐ gal–positive HGF during cell passages (r = 0.
70, P <0.
001).
Conclusions: These results indicate that patients with AgP do not have excessive telomere loss and thus do not support the notion of the occurrence of a generalized premature cellular aging in patients with AgP.
Further studies are required to investigate the association between telomere length and β‐gal in HGF.
J Periodontol 2004;75:84‐90.
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