This represents the first ultrasonographic study focusing on the analysis of interobserver reliability between sonographers with different levels of experience in demonstrating inflammatory and structural abnormalities in knee OA. Globally, even considering some variable results that were mainly obtained by the evaluation of single components of bone involvement, US offered a reliable assessment of a wide set of abnormalities in knee OA.

BackgroundSpondyloarthropathies (SpA) comprise an inflammatory spectrum that can involve peripheral and axial joints, enthesial sites and extra-articular tissues. We hypothesized that oxidation of fibrocartilage matrix proteins collagen type II (CII) at enthesial sites might generate oxidative posttranslational modification (oxPTM)-associated neoepitopes that provoke humoral autoimmunity.Our objectives were to test for the presence and clinical significance of antibodies to oxPTM-CII in patients with SpA. MethodsLevels of antibodies specific to native CII and oxPTM-CII were assessed by enzyme-linked immunosorbent assays (ELISA). Reactivity in serum samples obtained from patients with axial SpA (axSpA, n=242) was compared to reactivity in samples from patients with predominantly peripheral arthritis such as psoriatic arthritis (PsA, n=69), undifferentiated arthritis (UA, n=48) and early rheumatoid arthritis (RA, n=60). Controls included psoriasis without musculoskeletal symptoms (Ps, n=35), fibromyalgia (FM, n=19) and healthy subjects (HC, n=178). 97 th percentile of the healthy individuals cut-off point absorbance units obtained for healthy control samples was used to construct a contingency table of positive binders to oxPTM-CII and tested it by Fishers Exact Test. ResultsIgG binding to oxPTM-CII was observed in serum samples from axSpA (52%) compared to RA (83%), PsA (28%), UA (35%), and FM (15%). Importantly, while strong IgA anti-oxPTM-CII was detected in axSpA and PsA patients, with 47% and 84% respective binders, no IgA anti-oxPTM-CII was detected in RA patients. IgA anti-oxPTM-CII reactivity in axSpA patients treated with biologics was higher and more frequent with 85% binders compared to 9% binders in patients treated with synthetic DMARDs. Sensitivity values for both IgG and IgA anti-oxPTM-CII for RA samples were 3 91% and 32%, respectively. IgG and IgA anti-oxPTM-CII for axSpA were 64% and 80%, respectively. Similartly, sensitivity for IgA anti-oxPTM-CII in PsA was doubled to 87%. Conclusions:Our data implies that axSpA is associated with the presence of antibodies specific for oxPTM-CII, suggesting that there may be a humoral component to disease-associated inflammation that may stratify patients with SpA from RA.

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In a previous report of two married cohabiting couples affected by polymyalgia rheumatica (PMR), we noticed that the wife of one couple and both members of the other couple suffered from symptomatic diverticular disease (DD), whose diagnosis was made before the onset of PMR. We investigated whether DD might be a risk factor for the development of PMR. We conducted a case-control study informed on a database containing the prospectively collected medical records of consecutive PMR patients. Among comorbidities, attention was focused on symptomatic DD, provided that the diagnosis had been made by colonoscopy and/or computed tomography scan. As controls, we identified one control per case at random among those matched by age and sex attending the ophthalmic and orthopedic outpatient clinics, as long as a PMR diagnosis had been excluded. A logistic regression model was used, following a multiplicative model, and results were presented as odds ratio (OR) and 95% confidence intervals (95% CI). The most frequent comorbidities in the two groups of patients (121 cases and 121 controls) were chronic coronary artery disease, atrial fibrillation, diabetes mellitus, hypertension, DD, hypercholesterolemia, osteoporosis, chronic obstructive pulmonary disease, gastroesophageal reflux disease, and cholelithiasis. The association between PMR and DD (OR = 4.06; 95% CI: 1.76-9.35) was by far stronger than that found comparing PMR with the other comorbidities. The chronic bowel inflammation induced by dysbiosis in patients with symptomatic DD could be a critical immunopathological mechanism supporting the development or exacerbation of PMR in susceptible individuals.