Even though it was observed that halitosis has a predominantly oral origin, a multidisciplinary approach remains necessary to identify ear, nose and throat or extra-oral pathologies and/or pseudo-halitosis/halitophobia.
We concluded that the measurement of the VSC levels can be used as an adjunct to the organoleptic assessment. Thresholds should be revisited in order to improve their clinical utility. These devices can prove the absence of malodour in case of pseudo-halitosis.
IntroductionRheumatoid arthritis–associated autoantibodies (RA-AAB) can be present in serum years before clinical onset of rheumatoid arthritis (RA). It has been hypothesized that initiation of RA-AAB generation occurs at inflamed mucosal surfaces, such as in the oral cavity or lungs. The aim of this study was to assess systemic presence of RA-AAB in patients without RA who had oral or lung mucosal inflammation.MethodsThe presence of RA-AAB (immunoglobulin A [IgA] and IgG anti-cyclic citrullinated peptide 2 antibodies (anti-CCP2), IgM and IgA rheumatoid factor (RF), IgG anti-carbamylated protein antibodies and IgG and IgA anti-citrullinated peptide antibodies against fibrinogen, vimentin and enolase) were determined in sera of non-RA patients with periodontitis (PD, n = 114), bronchiectasis (BR, n = 80) or cystic fibrosis (CF, n = 41). Serum RA-AAB levels were compared with those of periodontally healthy controls (n = 36). Patients with established RA (n = 86) served as a reference group. Association of the diseases with RA-AAB seropositivity was assessed with a logistic regression model, adjusted for age, sex and smoking.ResultsLogistic regression analysis revealed that IgG anti-CCP seropositivity was associated with BR and RA, whereas the association with PD was borderline significant. IgA anti-CCP seropositivity was associated with CF and RA. IgM RF seropositivity was associated with RA, whereas the association with BR was borderline significant. IgA RF seropositivity was associated with CF and RA. Apart from an influence of smoking on IgA RF in patients with RA, there was no influence of age, sex or smoking on the association of RA-AAB seropositivity with the diseases. Anti-CarP levels were increased only in patients with RA. The same held for IgG reactivity against all investigated citrullinated peptides.ConclusionAlthough overall levels were low, RA-AAB seropositivity was associated with lung mucosal inflammation (BR and CF) and may be associated with oral mucosal inflammation (PD). To further determine whether mucosal inflammation functions as a site for induction of RA-AAB and precedes RA, longitudinal studies are necessary in which RA-AAB of specifically the IgA isotype should be assessed in inflamed mucosal tissues and/or in their inflammatory exudates.
a b s t r a c tRheumatoid Arthritis (RA) and chronic and aggressive periodontitis are chronic inflammatory disorders characterized by deregulation of the host inflammatory response. Increased secretion of pro-inflammatory mediators results in soft and hard tissue destruction of the synovium and periodontium respectively. Both diseases share risk factors and have pathological pathways in common, resulting in loss of function and disability as a final clinical outcome. This article discusses possible interactions, particularly related to the periodontal pathogen Porphyromonas gingivalis, which could explain the observed association between these two prevalent diseases.
From an epidemiologic point of view, patients with RA have a higher incidence of periodontal disease than individuals without RA. In addition, there is a dose-response pattern in the association between the severity of periodontitis and RA disease activity. There are indications that periodontitis precedes RA, but there is no evidence yet available to show that Pg plays a direct role in this temporal relationship. The role of the unique characteristic of citrullination by Pg remains unexplained. However, in animal models, citrullination by Pg plays a distinct role in the development and aggravation of experimental arthritis. Although the role of Pg in RA remains speculative, a causative role for periodontitis as a chronic inflammatory disease caused by infectious agents in RA seems biologically plausible.
PD patients are exposed to citrullinated histone H3 in inflamed periodontal tissue. Citrullinated histone H3 is targeted by autoantibodies present in RA sera. This supports a role for periodontitis in generation of antigens targeted by autoantibodies directed against citrullinated proteins.
In this study the similarities in immune response and tissue degradation between RA and periodontitis are reviewed. It is shown that the two diseases share the same environmental and genetic risk factors, apart from the fact that there is a link between both diseases via citrullination of proteins by human PAD and P. gingivalis PAD.
Objective
Rheumatoid arthritis (RA) and periodontitis share several pathological features including bone and soft tissue destruction and high levels of circulating inflammatory proteins. Studies related to cytokines in the periodontal inflammatory exudate (gingivocrevicular fluid, GCF) of RA patients might provide insight into the association between periodontitis and RA. The aim of our study was to review the literature on cytokines in GCF of RA patients including the effect of anti‐rheumatic treatment with biological disease‐modifying anti‐rheumatic drugs (DMARDs) and periodontal treatment on these cytokines.
Materials and methods
MedLine/PubMed searches with different combinations of keywords “rheumatoid arthritis or RA” and “crevicular fluid or GCF” until June 2019 revealed 64 articles. Ten cross‐sectional observational studies and nine treatment studies fulfilled the inclusion criteria.
Results
Rheumatoid arthritis patients have increased circulating and GCF levels of pro‐inflammatory cytokines and proteins, despite anti‐rheumatic treatment with biological DMARDs. Presence of periodontitis was accompanied by higher cytokine and protein levels. Treatment of periodontitis resulted in a decrease of these levels.
Conclusion
Analysis of GCF of RA patients reveals that the relationship between periodontitis and RA is bidirectional, probably caused by a non‐specific inflammatory burden. Data for a specific relationship are barely present in GCF.
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