Abstract
Chronic periodontitis (CP) and rheumatoid arthritis (RA) are chronic inflammatory conditions, and share many pathologic features. Plasma amino acid profiles have been shown to be associated with RA, but their relevance to CP remains unclear. The aim of the present study is to evaluate amino acid profiles in relation to CP and RA. The study participants consisted of 62 patients with RA (RA group), 30 patients with CP (CP group) and 29 healthy controls (H group) in age-, gender-, smoking status-balanced condition. Clinical periodontal and rheumatologic parameter values and plasma levels of 21 amino acids, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were determined. Multiple comparison analyses revealed that the RA group exhibited similar periodontal conditions but significantly higher levels of CRP, IL-6, and TNF-α than the CP group (P P P P P = 0.006) in the RA group. These results suggest a possibility that profiles of four amino acids may play a role in the pathogenesis of CP and RA.
Highlights
Similarities in the clinical and pathological features have been suggested between periodontitis and rheumatoid arthritis (RA) [1,2]
Multiple comparison analyses revealed that the RA group exhibited similar periodontal conditions but significantly higher levels of C-reactive protein (CRP), IL-6, and TNF-α than the Chronic periodontitis (CP) group (P < 0.01)
The CP group showed significantly higher alpha-aminobutyric acid level than the RA and H groups (P < 0.01). Of these four amino acids, a significantly positive correlation was found between ornithine level and % of sites with bleeding on probing (P = 0.006) in the RA group. These results suggest a possibility that profiles of four amino acids may play a role in the pathogenesis of CP and RA
Summary
Similarities in the clinical and pathological features have been suggested between periodontitis and rheumatoid arthritis (RA) [1,2]. Patients with RA were more likely to exhibit periodontits [3,4], while individuals with moderate-to-severe periodontitis had a higher prevalence of RA than those without periodontitis [5,6] These observations imply that certain features of the inflammatory response are common to both diseases, which might be underpinned by biological pathways [2]. There is evidence to suggest the similarities in the plasma cytokine and gene expression profiles between patients with RA and those with periodontitis [7,8]. The pathogenesis of both diseases is characterized by increased levels of circulating matrix metalloproteinases, reactive oxygen species, lipid mediators, and neutrophil-
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