NDLI: Inflammation, C-reactive protein, and atherothrombosis.

Please wait, while we are loading the content...

Year: 2017 Volume: 88

Year: 2016 Volume: 87

Year: 2015 Volume: 86

Year: 2014 Volume: 85

Year: 2013 Volume: 84

Year: 2012 Volume: 83

Year: 2011 Volume: 82

Year: 2010 Volume: 81

Year: 2009 Volume: 80

Year: 2008 Volume: 79

Year: 2008 Volume: 79 Issue: 12

Year: 2008 Volume: 79 Issue: 11

Year: 2008 Volume: 79 Issue: 10

Year: 2008 Volume: 79 Issue: 9

Year: 2008 Volume: 79 Issue: 8

Year: 2008 Volume: 79 Issue: 8 Supplementary

Inflammation and periodontal diseases: a reappraisal.

Inflammation and factors that may regulate inflammatory response.

Gene-environment interactions and susceptibility to metabolic syndrome and other chronic diseases.

Epigenetic regulation of gene expression in the inflammatory response and relevance to common diseases.

Controlling the resolution of acute inflammation: a new genus of dual anti-inflammatory and proresolving mediators.

The role of inflammatory cytokines in diabetes and its complications.

The inflammatory response in Alzheimer's disease.

Inflammation, C-reactive protein, and atherothrombosis.

Understanding and managing periodontal diseases: a notable past, a promising future.

Mapping the pathogenesis of periodontitis: a new look.

Inflammation and bone loss in periodontal disease.

Rethinking periodontal inflammation.

Cytokines that promote periodontal tissue destruction.

Host-response therapeutics for periodontal diseases.

The management of inflammation in periodontal disease.

Clinical innovations in managing inflammation and periodontal diseases: the workshop on inflammation and periodontal diseases.

Year: 2008 Volume: 79 Issue: 7

Year: 2008 Volume: 79 Issue: 6

Year: 2008 Volume: 79 Issue: 5

Year: 2008 Volume: 79 Issue: 4

Year: 2008 Volume: 79 Issue: 3

Year: 2008 Volume: 79 Issue: 2

Year: 2008 Volume: 79 Issue: 1

Year: 2007 Volume: 78

Year: 2005 Volume: 76

Year: 2004 Volume: 75

Year: 2003 Volume: 74

Year: 2002 Volume: 73

Year: 2001 Volume: 72

Year: 2000 Volume: 71

Year: 1998 Volume: 69

Inflammation, C-reactive protein, and atherothrombosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ridker, Paul M. Silvertown, Josh D.
Description	Country affiliation: United States Author Affiliation: Ridker PM ( Department of Medicine, Harvard Medical School, 900 Commonwealth Avenue East, Boston, MA 02215, USA.)
Abstract	Atherothrombosis of the coronary and cerebral vessels is understood to be a disorder of inflammation and innate immunity, as well as a disorder of lipid accumulation. From a vascular biology perspective, the processes of cellular adhesion, monocyte and macrophage attachment, and transmigration of immune cells across the endothelium are crucial steps in early atherogenesis and in the later stages of mature plaque rupture, particularly the transition of unstable plaque at the time of acute thrombosis. There is abundant clinical evidence demonstrating that many biomarkers of inflammation are elevated years in advance of first ever myocardial infarction (MI) or thrombotic stroke and that these same biomarkers are highly predictive of recurrent MI, recurrent stroke, diabetes, and cardiovascular death. In daily practice, the inflammatory biomarker in widest use is high-sensitivity C-reactive protein (hsCRP); when interpreted within the context of usual risk factors, levels of hsCRP <1, 1 to 3, and >3 mg/l denote lower, average, and higher relative risk for future vascular events. Risk-prediction models that incorporate hsCRP, such as the Reynolds Risk Score, have been developed that improve risk classification and the accuracy for global risk prediction, particularly for those deemed at 'intermediate risk' by usual algorithms, such as the Framingham Risk Score. With regard to cerebral vessels, increased biomarkers of inflammation, including hsCRP, have been associated with increased stroke risk as well as an increased rate of atherosclerosis progression in the carotid vessels. Although the proportion of variation in hsCRP explained by genetic factors may be as large as 20% to 40%, diet, exercise, and smoking cessation remain critical tools for risk reduction and CRP reduction. Statin therapy reduces hsCRP in a largely low-density lipoprotein (LDL)-independent manner, and the 'anti-inflammatory' properties of these agents have been suggested as a potential mechanism beyond LDL reduction for the efficacy of these agents. The ongoing multinational Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial of 17,802 initially healthy men and women with low levels of LDL cholesterol but increased levels of hsCRP will help to define whether vascular protection can be achieved with statin therapy, even in the absence of hyperlipidemia. Targeted anti-inflammatory therapies are being developed that may provide a direct method of translating the biology of inflammation into new clinical treatments across multiple vascular beds. This article summarizes data supporting a role for inflammation in cardiovascular disease and offers the possibility that other disorders characterized by inflammation, such as periodontal disease, may have an indirect role by influencing the risk, manifestation, and progression of vascular events.
File Format	HTM / HTML
ISSN	00223492
Issue Number	8 Suppl
Volume Number	79
e-ISSN	19433670
Journal	Journal of Periodontology
Language	English
Publisher	American Academy of Periodontology
Publisher Date	2008-08-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Dentistry Atherosclerosis Immunology C-reactive Protein Anti-inflammatory Agents Therapeutic Use Biological Markers Analysis Coronary Artery Disease Humans Hydroxymethylglutaryl-coa Reductase Inhibitors Immunity, Innate Inflammation Inflammation Mediators Intracranial Arteriosclerosis Protective Agents Risk Assessment Journal Article Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Review
Content Type	Text
Resource Type	Article
Subject	Periodontics

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in