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A Clinician's Guide to Systemic Effects of Periodontal DiseasesPeriodontal Infections and Rheumatoid Arthritis

A Clinician's Guide to Systemic Effects of Periodontal Diseases: Periodontal Infections and... [Rheumatoid arthritis (RA) is a chronic, destructive, autoimmune disorder characterized by autoantibody production and predilection for the joints that can lead to accelerated morbidity, mortality, and disability [1]. Current understanding of RA pathogenesis posits that a combination of host predisposition and risk factors is most likely required for the initiation and sustainability of the inflammatory process. However, the exact combination of factors and the precise timing for clinical manifestations are still insufficiently understood [2]. Mounting evidence suggests that environmental risk factors such as commensal and infectious microbiota may contribute to RA in patients with genetic susceptibility [3]. New findings suggest that germ-free mice, lacking all microbiota, are resistant to development of spontaneous autoimmune arthritis [4]. Intriguingly, recent evidence suggests that, in the right genetic background [5], the presence of certain predisposing factors (i.e., periodontitis (PD) and smoking) [6–9] along with serological markers (i.e., autoantibodies and proinflammatory cytokines) may predict the emergence of RA [10].] http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png

A Clinician's Guide to Systemic Effects of Periodontal DiseasesPeriodontal Infections and Rheumatoid Arthritis

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Publisher
Springer Berlin Heidelberg
Copyright
© Springer-Verlag Berlin Heidelberg 2016
ISBN
978-3-662-49697-8
Pages
107 –115
DOI
10.1007/978-3-662-49699-2_9
Publisher site
See Chapter on Publisher Site

Abstract

[Rheumatoid arthritis (RA) is a chronic, destructive, autoimmune disorder characterized by autoantibody production and predilection for the joints that can lead to accelerated morbidity, mortality, and disability [1]. Current understanding of RA pathogenesis posits that a combination of host predisposition and risk factors is most likely required for the initiation and sustainability of the inflammatory process. However, the exact combination of factors and the precise timing for clinical manifestations are still insufficiently understood [2]. Mounting evidence suggests that environmental risk factors such as commensal and infectious microbiota may contribute to RA in patients with genetic susceptibility [3]. New findings suggest that germ-free mice, lacking all microbiota, are resistant to development of spontaneous autoimmune arthritis [4]. Intriguingly, recent evidence suggests that, in the right genetic background [5], the presence of certain predisposing factors (i.e., periodontitis (PD) and smoking) [6–9] along with serological markers (i.e., autoantibodies and proinflammatory cytokines) may predict the emergence of RA [10].]

Published: May 18, 2016

Keywords: Rheumatoid Arthritis; Rheumatoid Arthritis Patient; Root Plane; Rheumatoid Arthritis Pathogenesis; Early Rheumatoid Arthritis Patient

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