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The association between rheumatoid arthritis and periodontal disease

DOI: 10.1186/ar3106

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Abstract:

Periodontitis (PD), the most common oral disease, is a destructive inflammatory disease of the supporting tissues of the teeth and is caused by specific microorganisms [1]. As a rule, PD develops through gingivitis, an inflammation of the marginal periodontium. However, not every gingivitis develops further into PD. Both the amount and virulence of the microorganisms and the resistance factors of the host (risk factors and immune status) are crucial for the progression of the periodontal destruction (Figure 1). PD has been proposed as having an etiologic or modulating role in cardiovascular and cerebrovascular disease, diabetes, and respiratory disease and adverse pregnancy outcome, and several mechanisms have been proposed to explain or support such theories. Moreover, oral lesions are indicators of disease progression, and the oral cavity can be a window to overall health and body systems. In recent years, remarkable epidemiological and pathological relationships between periodontal diseases and rheumatic diseases, especially rheumatoid arthritis (RA), have been presented.Chronic, plaque-associated inflammation of the periodontium is among the most common oral diseases and has a prevalence of 80% to 90% [1], resulting in soft and hard periodontal tissue destruction and ultimately in tooth loss [2]. Both the amount and virulence of the microorganisms and the resistance factors of the host (risk factors and immune status) are crucial for the initiation and progression of the periodontal destruction [3]. Besides detailed concepts about microbiological, molecular, and cellular mechanisms, which determine the strength and balance of the cellular and humoral host response in tissues, it became apparent that a complex and primarily endogenous periodontal microflora is responsible for disease initiation and progression.PD is to be understood as an opportunistic infection [4]. It results directly in tissue injury or provokes excessive, autodestructive inflammatory response

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