Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy
Abstract Aims Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association...
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| Veröffentlicht in: | European heart journal 2019-11, Vol.40 (42), p.3459-3470 |
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| creator | Czesnikiewicz-Guzik, Marta Osmenda, Grzegorz Siedlinski, Mateusz Nosalski, Richard Pelka, Piotr Nowakowski, Daniel Wilk, Grzegorz Mikolajczyk, Tomasz P Schramm-Luc, Agata Furtak, Aneta Matusik, Pawel Koziol, Joanna Drozdz, Miroslaw Munoz-Aguilera, Eva Tomaszewski, Maciej Evangelou, Evangelos Caulfield, Mark Grodzicki, Tomasz D'Aiuto, Francesco Guzik, Tomasz J |
| description | Abstract
Aims
Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.
Methods and results
We performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of −11.1 mmHg; 95% CI 6.5–15.8; P |
| doi_str_mv | 10.1093/eurheartj/ehz646 |
| format | Article |
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Aims
Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.
Methods and results
We performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of −11.1 mmHg; 95% CI 6.5–15.8; P < 0.001). Systolic BP reduction was correlated to periodontal status improvement. Diastolic BP and endothelial function (flow-mediated dilatation) were also improved by IPT. These cardiovascular changes were accompanied by reductions in circulating IFN-γ and IL-6 as well as activated (CD38+) and immunosenescent (CD57+CD28null) CD8+T cells, previously implicated in hypertension.
Conclusion
A causal relationship between periodontitis and BP was observed providing proof of concept for development of clinical trial in a large cohort of hypertensive patients. ClinicalTrials.gov: NCT02131922.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehz646</identifier><identifier>PMID: 31504461</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Editor's Choice ; Fast Track Clinical Research ; Female ; Humans ; Hypertension - complications ; Hypertension - epidemiology ; Hypertension - genetics ; Inflammation ; Male ; Mendelian Randomization Analysis ; Middle Aged ; Periodontitis - complications ; Periodontitis - epidemiology ; Periodontitis - genetics ; Vasodilation - physiology</subject><ispartof>European heart journal, 2019-11, Vol.40 (42), p.3459-3470</ispartof><rights>The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology. 2019</rights><rights>The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-138be75431a5ddd51c8e17c55e79d2c2b9808f554a7bab0d6ab152fcf2cb63823</citedby><cites>FETCH-LOGICAL-c498t-138be75431a5ddd51c8e17c55e79d2c2b9808f554a7bab0d6ab152fcf2cb63823</cites><orcidid>0000-0001-8215-6567 ; 0000-0002-9759-011X ; 0000-0002-5039-7849 ; 0000-0002-7444-1373 ; 0000-0001-5788-575X ; 0000-0003-0159-4915 ; 0000-0002-7990-2896 ; 0000-0002-6594-9386 ; 0000-0001-8654-935X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31504461$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Czesnikiewicz-Guzik, Marta</creatorcontrib><creatorcontrib>Osmenda, Grzegorz</creatorcontrib><creatorcontrib>Siedlinski, Mateusz</creatorcontrib><creatorcontrib>Nosalski, Richard</creatorcontrib><creatorcontrib>Pelka, Piotr</creatorcontrib><creatorcontrib>Nowakowski, Daniel</creatorcontrib><creatorcontrib>Wilk, Grzegorz</creatorcontrib><creatorcontrib>Mikolajczyk, Tomasz P</creatorcontrib><creatorcontrib>Schramm-Luc, Agata</creatorcontrib><creatorcontrib>Furtak, Aneta</creatorcontrib><creatorcontrib>Matusik, Pawel</creatorcontrib><creatorcontrib>Koziol, Joanna</creatorcontrib><creatorcontrib>Drozdz, Miroslaw</creatorcontrib><creatorcontrib>Munoz-Aguilera, Eva</creatorcontrib><creatorcontrib>Tomaszewski, Maciej</creatorcontrib><creatorcontrib>Evangelou, Evangelos</creatorcontrib><creatorcontrib>Caulfield, Mark</creatorcontrib><creatorcontrib>Grodzicki, Tomasz</creatorcontrib><creatorcontrib>D'Aiuto, Francesco</creatorcontrib><creatorcontrib>Guzik, Tomasz J</creatorcontrib><title>Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Abstract
Aims
Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.
Methods and results
We performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of −11.1 mmHg; 95% CI 6.5–15.8; P < 0.001). Systolic BP reduction was correlated to periodontal status improvement. Diastolic BP and endothelial function (flow-mediated dilatation) were also improved by IPT. These cardiovascular changes were accompanied by reductions in circulating IFN-γ and IL-6 as well as activated (CD38+) and immunosenescent (CD57+CD28null) CD8+T cells, previously implicated in hypertension.
Conclusion
A causal relationship between periodontitis and BP was observed providing proof of concept for development of clinical trial in a large cohort of hypertensive patients. ClinicalTrials.gov: NCT02131922.</description><subject>Editor's Choice</subject><subject>Fast Track Clinical Research</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - complications</subject><subject>Hypertension - epidemiology</subject><subject>Hypertension - genetics</subject><subject>Inflammation</subject><subject>Male</subject><subject>Mendelian Randomization Analysis</subject><subject>Middle Aged</subject><subject>Periodontitis - complications</subject><subject>Periodontitis - epidemiology</subject><subject>Periodontitis - genetics</subject><subject>Vasodilation - physiology</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNqFkc1u1TAQhS1ERS-FPSvkJRIKtZPYcVggVVf8SUVsQGJnOfakcZXYwXaKbh-oz4mvUqJ2xcrj8ZnvjHwQekXJO0ra6hyWMIAK6fochlte8ydoR1lZFi2v2VO0I7RlBefi1yl6HuM1IURwyp-h04oyUtec7tDdXi1RjVjF6LVVyXqHO0h_AByeIVhvvEs22YiVM3g45F4CF7PsPYYba8BpwH3wE_4GzsBolcMhS_1kb1facU5tPTBYZ2Lw45jLFGz29j123hVxCVdW5_vmm-s0QFDz4QU66dUY4eX9eYZ-fvr4Y_-luPz--ev-4rLQdStSQSvRQcPqiipmjGFUC6CNZgya1pS67FpBRM9YrZpOdcRw1eX_6nVf6o5XoqzO0IeVOy_dBEZDXlWNcg52UuEgvbLy8Yuzg7zyN5KLqqGcZsCbe0DwvxeISU42ahhH5cAvUZalEE1JquroRVapDj7GAP1mQ4k8xiu3eOUabx55_XC9beBfnlnwdhX4Zf4_7i-Bibs9</recordid><startdate>20191101</startdate><enddate>20191101</enddate><creator>Czesnikiewicz-Guzik, Marta</creator><creator>Osmenda, Grzegorz</creator><creator>Siedlinski, Mateusz</creator><creator>Nosalski, Richard</creator><creator>Pelka, Piotr</creator><creator>Nowakowski, Daniel</creator><creator>Wilk, Grzegorz</creator><creator>Mikolajczyk, Tomasz P</creator><creator>Schramm-Luc, Agata</creator><creator>Furtak, Aneta</creator><creator>Matusik, Pawel</creator><creator>Koziol, Joanna</creator><creator>Drozdz, Miroslaw</creator><creator>Munoz-Aguilera, Eva</creator><creator>Tomaszewski, Maciej</creator><creator>Evangelou, Evangelos</creator><creator>Caulfield, Mark</creator><creator>Grodzicki, Tomasz</creator><creator>D'Aiuto, Francesco</creator><creator>Guzik, Tomasz J</creator><general>Oxford University Press</general><scope>TOX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8215-6567</orcidid><orcidid>https://orcid.org/0000-0002-9759-011X</orcidid><orcidid>https://orcid.org/0000-0002-5039-7849</orcidid><orcidid>https://orcid.org/0000-0002-7444-1373</orcidid><orcidid>https://orcid.org/0000-0001-5788-575X</orcidid><orcidid>https://orcid.org/0000-0003-0159-4915</orcidid><orcidid>https://orcid.org/0000-0002-7990-2896</orcidid><orcidid>https://orcid.org/0000-0002-6594-9386</orcidid><orcidid>https://orcid.org/0000-0001-8654-935X</orcidid></search><sort><creationdate>20191101</creationdate><title>Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy</title><author>Czesnikiewicz-Guzik, Marta ; Osmenda, Grzegorz ; Siedlinski, Mateusz ; Nosalski, Richard ; Pelka, Piotr ; Nowakowski, Daniel ; Wilk, Grzegorz ; Mikolajczyk, Tomasz P ; Schramm-Luc, Agata ; Furtak, Aneta ; Matusik, Pawel ; Koziol, Joanna ; Drozdz, Miroslaw ; Munoz-Aguilera, Eva ; Tomaszewski, Maciej ; Evangelou, Evangelos ; Caulfield, Mark ; Grodzicki, Tomasz ; D'Aiuto, Francesco ; Guzik, Tomasz J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-138be75431a5ddd51c8e17c55e79d2c2b9808f554a7bab0d6ab152fcf2cb63823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Editor's Choice</topic><topic>Fast Track Clinical Research</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - complications</topic><topic>Hypertension - epidemiology</topic><topic>Hypertension - genetics</topic><topic>Inflammation</topic><topic>Male</topic><topic>Mendelian Randomization Analysis</topic><topic>Middle Aged</topic><topic>Periodontitis - complications</topic><topic>Periodontitis - epidemiology</topic><topic>Periodontitis - genetics</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Czesnikiewicz-Guzik, Marta</creatorcontrib><creatorcontrib>Osmenda, Grzegorz</creatorcontrib><creatorcontrib>Siedlinski, Mateusz</creatorcontrib><creatorcontrib>Nosalski, Richard</creatorcontrib><creatorcontrib>Pelka, Piotr</creatorcontrib><creatorcontrib>Nowakowski, Daniel</creatorcontrib><creatorcontrib>Wilk, Grzegorz</creatorcontrib><creatorcontrib>Mikolajczyk, Tomasz P</creatorcontrib><creatorcontrib>Schramm-Luc, Agata</creatorcontrib><creatorcontrib>Furtak, Aneta</creatorcontrib><creatorcontrib>Matusik, Pawel</creatorcontrib><creatorcontrib>Koziol, Joanna</creatorcontrib><creatorcontrib>Drozdz, Miroslaw</creatorcontrib><creatorcontrib>Munoz-Aguilera, Eva</creatorcontrib><creatorcontrib>Tomaszewski, Maciej</creatorcontrib><creatorcontrib>Evangelou, Evangelos</creatorcontrib><creatorcontrib>Caulfield, Mark</creatorcontrib><creatorcontrib>Grodzicki, Tomasz</creatorcontrib><creatorcontrib>D'Aiuto, Francesco</creatorcontrib><creatorcontrib>Guzik, Tomasz J</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Czesnikiewicz-Guzik, Marta</au><au>Osmenda, Grzegorz</au><au>Siedlinski, Mateusz</au><au>Nosalski, Richard</au><au>Pelka, Piotr</au><au>Nowakowski, Daniel</au><au>Wilk, Grzegorz</au><au>Mikolajczyk, Tomasz P</au><au>Schramm-Luc, Agata</au><au>Furtak, Aneta</au><au>Matusik, Pawel</au><au>Koziol, Joanna</au><au>Drozdz, Miroslaw</au><au>Munoz-Aguilera, Eva</au><au>Tomaszewski, Maciej</au><au>Evangelou, Evangelos</au><au>Caulfield, Mark</au><au>Grodzicki, Tomasz</au><au>D'Aiuto, Francesco</au><au>Guzik, Tomasz J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2019-11-01</date><risdate>2019</risdate><volume>40</volume><issue>42</issue><spage>3459</spage><epage>3470</epage><pages>3459-3470</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Abstract
Aims
Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.
Methods and results
We performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of −11.1 mmHg; 95% CI 6.5–15.8; P < 0.001). Systolic BP reduction was correlated to periodontal status improvement. Diastolic BP and endothelial function (flow-mediated dilatation) were also improved by IPT. These cardiovascular changes were accompanied by reductions in circulating IFN-γ and IL-6 as well as activated (CD38+) and immunosenescent (CD57+CD28null) CD8+T cells, previously implicated in hypertension.
Conclusion
A causal relationship between periodontitis and BP was observed providing proof of concept for development of clinical trial in a large cohort of hypertensive patients. ClinicalTrials.gov: NCT02131922.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>31504461</pmid><doi>10.1093/eurheartj/ehz646</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8215-6567</orcidid><orcidid>https://orcid.org/0000-0002-9759-011X</orcidid><orcidid>https://orcid.org/0000-0002-5039-7849</orcidid><orcidid>https://orcid.org/0000-0002-7444-1373</orcidid><orcidid>https://orcid.org/0000-0001-5788-575X</orcidid><orcidid>https://orcid.org/0000-0003-0159-4915</orcidid><orcidid>https://orcid.org/0000-0002-7990-2896</orcidid><orcidid>https://orcid.org/0000-0002-6594-9386</orcidid><orcidid>https://orcid.org/0000-0001-8654-935X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | European heart journal, 2019-11, Vol.40 (42), p.3459-3470 |
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| language | eng |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Editor's Choice Fast Track Clinical Research Female Humans Hypertension - complications Hypertension - epidemiology Hypertension - genetics Inflammation Male Mendelian Randomization Analysis Middle Aged Periodontitis - complications Periodontitis - epidemiology Periodontitis - genetics Vasodilation - physiology |
| title | Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy |
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