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Conference Paper: Periodontal treatment increases circulating EPC counts in patients with T2DM

TitlePeriodontal treatment increases circulating EPC counts in patients with T2DM
Authors
Issue Date2018
PublisherInternational Association for Dental Research. The Journal's web site is located at http://www.iadr.org/
Citation
The 96th General Session and Exhibition of the International Association for Dental Research (IADR) and IADR Pan European Regional (PER) Congress, London, UK, 25-28 July 2018. In Journal of Dental Research, 2018, v. 97 n. Spec Iss B, abstract no. 1114 How to Cite?
AbstractObjectives: It is evident that a decreased level of circulating endothelial progenitor cells (EPCs) reflects a poor glycemic control and increased risk of cardiovascular disease (CVD). Our recent study shows that chronic periodontitis is significantly associated with the reduction of EPCs in patients with type 2 diabetes (T2DM). This study extended to investigate the effects of periodontal treatment on EPC counts in subjects with T2DM. Methods: A single-blind randomized controlled trial was conducted in 44 Chinese adults with both T2DM and moderate to severe chronic periodontitis. They were randomly assigned into the Treatment group (n=22) with immediate periodontal treatment including oral hygiene instruction, scaling and root debridement, and the Control group (n=22) with a postponement of the same treatment after 6-month follow-up. Four subsets of circulating EPCs, namely CD34+, CD133+, CD34+/KDR+ and CD133+/KDR+ cells in peripheral blood were quantified by flow cytometry analysis at baseline and 6-month recall. Results: The overall periodontal condition in the Treatment group was greatly improved following the treatment. Meanwhile, there was a notable increase in the levels of CD133+ and CD133+/KDR+ cells (log transformed: 2.00±1.18 vs. 3.16±1.50, p< 0.01; 0.78±0.76 vs. 1.69±1.10, p<0.05), whereas, no significant change was found in the Control group. Furthermore, the increase in CD133+/KDR+ cell counts was reversely correlated with the reduction in sites% with probing depth ≥ 4mm (R2=0.105, p=0.04). No significant therapeutic effect was observed in the levels of CD34+ and CD34+/KDR+ cells. Conclusions: This study provides the first evidence that periodontal treatment may account for the increase of circulating CD133+ and CD133+/KDR+ cell counts in subjects with T2DM, implying that effective control of periodontal infection/inflammation could be beneficial for diabetes care and reduction of CVD risks.
DescriptionPoster Presentation - no. 1114
Persistent Identifierhttp://hdl.handle.net/10722/259657

 

DC FieldValueLanguage
dc.contributor.authorWang, Y-
dc.contributor.authorLiu, HN-
dc.contributor.authorZhen, Z-
dc.contributor.authorYiu, KH-
dc.contributor.authorTse, HF-
dc.contributor.authorZhang, C-
dc.contributor.authorPelekos, G-
dc.contributor.authorJin, L-
dc.date.accessioned2018-09-03T04:11:38Z-
dc.date.available2018-09-03T04:11:38Z-
dc.date.issued2018-
dc.identifier.citationThe 96th General Session and Exhibition of the International Association for Dental Research (IADR) and IADR Pan European Regional (PER) Congress, London, UK, 25-28 July 2018. In Journal of Dental Research, 2018, v. 97 n. Spec Iss B, abstract no. 1114-
dc.identifier.urihttp://hdl.handle.net/10722/259657-
dc.descriptionPoster Presentation - no. 1114-
dc.description.abstractObjectives: It is evident that a decreased level of circulating endothelial progenitor cells (EPCs) reflects a poor glycemic control and increased risk of cardiovascular disease (CVD). Our recent study shows that chronic periodontitis is significantly associated with the reduction of EPCs in patients with type 2 diabetes (T2DM). This study extended to investigate the effects of periodontal treatment on EPC counts in subjects with T2DM. Methods: A single-blind randomized controlled trial was conducted in 44 Chinese adults with both T2DM and moderate to severe chronic periodontitis. They were randomly assigned into the Treatment group (n=22) with immediate periodontal treatment including oral hygiene instruction, scaling and root debridement, and the Control group (n=22) with a postponement of the same treatment after 6-month follow-up. Four subsets of circulating EPCs, namely CD34+, CD133+, CD34+/KDR+ and CD133+/KDR+ cells in peripheral blood were quantified by flow cytometry analysis at baseline and 6-month recall. Results: The overall periodontal condition in the Treatment group was greatly improved following the treatment. Meanwhile, there was a notable increase in the levels of CD133+ and CD133+/KDR+ cells (log transformed: 2.00±1.18 vs. 3.16±1.50, p< 0.01; 0.78±0.76 vs. 1.69±1.10, p<0.05), whereas, no significant change was found in the Control group. Furthermore, the increase in CD133+/KDR+ cell counts was reversely correlated with the reduction in sites% with probing depth ≥ 4mm (R2=0.105, p=0.04). No significant therapeutic effect was observed in the levels of CD34+ and CD34+/KDR+ cells. Conclusions: This study provides the first evidence that periodontal treatment may account for the increase of circulating CD133+ and CD133+/KDR+ cell counts in subjects with T2DM, implying that effective control of periodontal infection/inflammation could be beneficial for diabetes care and reduction of CVD risks.-
dc.languageeng-
dc.publisherInternational Association for Dental Research. The Journal's web site is located at http://www.iadr.org/-
dc.relation.ispartofJournal of Dental Research (Spec Issue)-
dc.relation.ispartofIADR/PER 96th General Session & Exhibition-
dc.titlePeriodontal treatment increases circulating EPC counts in patients with T2DM-
dc.typeConference_Paper-
dc.identifier.emailLiu, HN: drdhnl@hku.hk-
dc.identifier.emailZhen, Z: zhenzhe@hku.hk-
dc.identifier.emailYiu, KH: khkyiu@hku.hk-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.emailZhang, C: zhangcf@hku.hk-
dc.identifier.emailPelekos, G: george74@hku.hk-
dc.identifier.emailJin, L: ljjin@hkucc.hku.hk-
dc.identifier.authorityYiu, KH=rp01490-
dc.identifier.authorityTse, HF=rp00428-
dc.identifier.authorityZhang, C=rp01408-
dc.identifier.authorityPelekos, G=rp01894-
dc.identifier.authorityJin, L=rp00028-
dc.identifier.hkuros288112-
dc.identifier.volume97-
dc.identifier.issueSpec Iss B-
dc.identifier.spageno. 1114-
dc.identifier.epageno. 1114-
dc.publisher.placeUnited States-

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