Periodontitis induced by bacterial infection exacerbates features of Alzheimer\u27s disease in transgenic mice.

Periodontitis is a localized infectious disease caused by periodontopathic bacteria,such as Porphyromonas gingivalis. Recently, it has been suggested that bacterial infections may contribute to the onset and the progression of Alzheimer’s disease (AD). However, we do not have any evidence about a causative relationship between periodontitis and AD. In this study, we investigated by using a transgenic mouse model of AD whether periodontitis evoked by P. gingivalis modulates the pathological features of AD. Cognitive function was significantly impaired in periodontitis-induced APP-Tg mice, compared to that in control APP-Tg mice. Levels of Amiloid β (Aβ) deposition, Aβ40, and Aβ42 in both the hippocampus and cortex were higher in inoculated APP-Tg mice than in control APP-Tg mice. Furthermore, levels of IL-1β and TNF-α in the brain were higher in inoculated mice than in control mice. The levels of LPS were increased in the serum and brain of P. gingivalis-inoculated mice. P. gingivalis LPS-induced production of Aβ40 and Aβ42 in neural cell cultures and strongly enhanced TNF-α and IL-1β production in a culture of microglial cells primed with Aβ. Periodontitis evoked by P. gingivalismay exacerbate brain Aβ deposition, leading to enhanced cognitive impairments, by a mechanism that involves triggering brain inflammation

AB0800 HEMATOLOGICAL MARKERS OF SYSTEMIC INFLAMMATION IN PATIENTS RHEUMATOID ARTHRITIS (RA) AND SPONDYLOARTHRITIS (SPA)

Background:An appropriate assessment of disease activity is essential in the management of patients with chronic inflammatory joint diseases, rheumatoid arthritis (RA) and spondyloarthritis (SpA). Hematological parameters [Neutrophil-To-Lymphocyte (NLR), Platelet-To-Lymphocyte (PLR) and Monocyte-To- Lymphocyte (MLR) ratios] have been demonstrated to be good, promising indicators of systemic inflammation status in different diseases, additionally to conventional inflammatory markers [erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)]. However results remain conflicting in rheumatic patients.Objectives:The goal of the study was to determine the role of NLR, PLR, MLR in assessing inflammatory disease activity and to compare the biomarkers in RA and SpA patients.Methods:An observational study was conducted in patients with RA and SpA (ankylosing spondylitis and psoriatic arthritis) treated in the Department of Rheumatology and Connective Tissue Diseases, Medical University of Lublin, Poland. Demographic and clinical information was obtained through structured interview, review of medical records and laboratory tests. The following disease activity and functional scores were registered: CRP and ESR levels, swollen and tender joints counts (SJC, TJC), DAS28 (ESR), HAQ, BASDAI, BASFI, patient global assessment (PtGA) and physician global assessment (PGA) rated on a visual analogue scale (VAS).The study group consisted of 95 patients (58 women, 37 men), with the mean (SD) age 45.4 (9.9), disease duration 10.0 (8.4) years. There were 58 (61.1%) patients with RA (44 women, 14 men) and 37 (38.9%) patients with SpA. The mean age and disease duration were statistically not different in both patients’ groups. The mean (SD) DAS28 was 4.21 (1.8) in RA patients; in SpA patients BASDAI 4.9 (2.6) and BASFI 5.0 (2.8).Results:In the whole group (95 patients) and in the SpA group, we found positive correlations between the PLR value and the following parameters CRP, ESR; between NLR and CRP, ESR; between MLR and CRP. In the RA group positive correlations were observed between PLR and CRP, ESR; NLR and CRP; MLR did not correlate with CRP and ESR.In RA patients, there were statistically significant correlations between values of PLR and DAS28 (r=0.356, p=0.006), TJC (r=0.308, p=0.02), SJC (r=0.318, p=0.016), PtGA (r=0.372, p=0.008). No significant correlation was found between NLR, MLR and other disease activity scores.In SpA patients, we found a significant correlation between NLR and PtGA (r=0.488, p=0.04). No significant correlations were found between NLR, PLR, MLR and BASDAI, BASFI.The group of RA patients as compared with SpA, was characterized by significantly higher value of PLR [respectively 207.8 (94.0) vs 169.9 (77.7), p=0.04]. In turn, SpA patients compared with RA, were characterized by unfavorable metabolic parameters: higher atherogenic index [respectively 4.03 (0.8) vs 3.57 (1.1), p=0.03], lower HDL-cholesterol [47.4 (10.7) vs 56.1 (16.4) mg/dl (p=0.006); higher serum uric acid [5.6 (1.2) vs 4.5 (1.4) mg/dl (p=0.0001)], higher waist measurement [96.1 (14.2) vs 85.9 (11.5) cm (p=0.0003).Conclusion:In our study we found, that in patients with RA, PLR was associated with both clinical and inflammatory markers of disease activity; in SpA patients NLR, PLR and MLR were associated with conventional inflammatory markers (CRP, ESR). Hematological inflammatory biomarkers may reflect disease activity and could represent potential parameters to evaluate disease activity not only in RA, but also in SpA.Disclosure of Interests:Bozena Targonska-Stepniak Speakers bureau: Berlin-Chemie/Menarini, KRKA, Medac, Santen, Krzysztof Grzechnik: None declared, Maria Majdan Speakers bureau: Roche, Medac</jats:sec

AB0782 Serum pentraxin 3 as a biomarker in patients with spondyloarthritis.

BackgroundA proper evaluation and management of patients with spondyloarthritis (SpA) requires the use of biomarkers, facilitating early diagnosis, reflecting disease activity and clinical response to therapies. The chronic, systemic inflammatory process is responsible for increased CV risk in SpA patients. Pentraxin 3 (PTX3) is an inflammatory marker, a member of long pentraxin superfamily, argued to be involved in pathogenesis of both inflammation and atherosclerosis. PTX3 is produced locally in the inflamed tissue, by different cell types including macrophages, endothelial cells, synoviocytes, but not hepatocytes. PTX3 is produced in walls of blood vessels, in atherosclerotic plaques, as a response to pro-inflammatory cytokines.ObjectivesThe aim of the study was to assess the role of PTX3 as a biomarker in patients with SpA and to evaluate the relationship between PTX3 and CV risk markers (carotid intima-media thickness (cIMT), lipid profile).MethodsThe study group consisted of 40 consecutive patients with SpA: 29 patients with psoriatic arthritis (PsA) and 11 patients with ankylosing spondylitis (AS). The group consisted of 16 (40%) women and 24 (60%) men, with the mean (SD) age 43.9 (12.0) (range 25–68) and disease duration 7,8 (7,6) years (range 1–32). An assessment of the disease activity included: laboratory inflammatory parameters (erythrocyte sedimentation rate (ESR), C-reactive protein, CRP) and clinical assessment (in patients with peripheral SpA (pSpA) joints counts and disease activity score in 28 joints (DAS28); in patients with axial SpA (axSpA) Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI) and pain of the spine according to the patient in visual analogue scale (VAS). A measurement of carotid intima-media thickness (cIMT) was performed using high-resolution B-mode ultrasonography to estimate features of atherosclerosis (cIMT&gt; 0.9 mm and/or presence of atherosclerotic plaques).ResultsThe median (IQR) PTX3 concentration in SpA patients was 3.39 (2.22-3.88) ng/ml. The mean (SD) value of ESR was 27.7 (28.3) mm/h and CRP concentration 13.6 (19.9) mg/l.The mean values of clinical indices were as follows: DAS28 3.8 (1.1), BASDAI 4.02 (2.1), BASFI 4.22 (2.2), VAS spine pain 41.4 (24.0).The mean (SD) cIMT value was 0.77 (0.23) mm (range 0.48-1.33). The features of atherosclerosis were detected in 7 (17.5%) patients.No significant correlations were found between PTX3 and other inflammatory markers (ESR, CRP). There were no correlations between PTX3 concentration the clinical indices of the disease activity (DAS28, BASDAI, BASFI, VAS spine pain). No differences of PTX3 concentrations were detected between pSpA and axSpA patients.The PTX3 concentrations were significantly higher in patients with definite atherosclerosis (cIMT &gt; 0.9 mm) than in patients with subclinical or no atherosclerosis (cIMT=&lt; 0.9) (5.79 (3.84-8.59) vs 3.06 (2.0-3.52) ng/ml, p=0.01), as well as in patients with atherosclerotic plaques in comparison with no plaques (6.79 (4.86-8.59) vs 3.26 (2.0-3.71) ng/ml, p=0.02) (Figure 1).ConclusionThe results of our study suggest that in patients with SpA, PTX3 could be regarded as a biomarker indicating intensity of atherosclerosis. However PTX3 was not associated with parameters of disease activity in patients with SpA.References[1]Maksymowych WP. Biomarkers in axial spondyloarthritis. Curr Opin Rheumatol. 2015 Jul;27(4):343-8. doi: 10.1097/BOR.0000000000000180.[2]Nisihara R, Skare TL, Zeni JO, Rasera H, Lidani K, Messias-Reason I. Plasma levels of pentraxin 3 in patients with spondyloarthritis. Biomarkers. 2018 Feb;23(1):14-17. doi: 10.1080/1354750X.2016.1278265.Disclosure of InterestsNone declared</jats:sec

FRI0080 CLINICAL CHARACTERISTICS OF PATIENTS WITH ELDERLY-ONSET RHEUMATOID ARTHRITIS (EORA)

Background:The onset of rheumatoid arthritis (RA) occurs usually between 35-50 years of age. Since the general population is ageing, beginning of RA in older age is more common. The termelderly onset of rheumatoid arthritis(EORA) describes the disease with onset at age over 60. The termyounger-onset rheumatoid arthritis(YORA) refers to the disease with typical, earlier onset. Observational studies indicate, that substantial differences do occur between the two RA subtypes (EORA and YORA).Objectives:The goal of the study was to analyze the course of disease and treatment in EORA in comparison to YORA patients.Methods:The study was conducted in consecutive RA patients, treated in the Department of Rheumatology and Connective Tissue Diseases, Medical University of Lublin, Poland. The study group consisted of 113 patients (93 women, 20 men), with the mean (SD) age 59.4 (19.0), disease duration 12.9 (10.3) years.The cut off between EORA and YORA was set at 60 years of age. There were 63 (55.8%) EORA and 50 (44.2%) YORA patients. Demographic and clinical information was obtained through structured interview, review of medical records and laboratory tests. Disease activity was assessed based on joint counts and Disease Activity Score of 28 joints (DAS28).Results:In patients with EORA vs YORA, the mean (SD) age was 73.64 (6,6) vs 41.5 (13.7) (p&lt;0.001), the age of RA diagnosis 65.0 (4.2) vs 23.3 (4.8) (p&lt;0.001), RA duration 8.6 (5.4) vs 18.3 (12.3) years (p&lt;0.001).The group of patients with EORA compared with YORA, was characterized by: significantly higher number of men [respectively 16 (25.4%) vs 4 (8.0%)], unfavorable metabolic parameters [higher body mass index (BMI): 26.0 (5.8) vs 23.4 (4.1) kg/m2(p=0.04); serum uric acid: 5.7 (1.5) vs 4.4 (1.6) mg/dl (p=0.001)], as well as unfavorable parameters of RA activity [higher DAS28: 4.4 (1.5) vs 3.2 (1.6) (p&lt;0.001); higher tender joints count (TJC): 6.1 (6.2) vs 3.2 (3.7) (p=0.01); higher erythrocyte sedimentation rate (ESR) 45.9 (30.3) vs 24.1 (25.6) (p&lt;0.001) and white blood cell count (WBC): 8.3 (2.7) vs 7.0 (2.4)x103/ml (p=0.01)]. At the time of assessment, remission or low disease activity was achieved in significantly fewer EORA vs YORA patients [15 (23.8%) vs 25 (50%) (p=0.007)].In EORA patients methotrexate was used as the first disease modifying drug (DMARD) more often [54 (85.7%) vs 26 (52%) (p&lt;0.001)], the use of biological DMARDs was less common [5 (7.9%) vs 23 (46.0%) (p&lt;0.001)], as well as glucocorticoids (GC) [49 (77.8%) vs 47 (94.0%) (p=0.04)]. Significantly more patients with EORA than YORA, were affected by concomitant diseases [62 (98.4%) vs 41 (82%) (p=0.007)].The prevalence of joint erosions, extra-articular manifestations and antibodies typical for RA (rheumatoid factor, RF-IgM and/or anti-citrullinated peptide, ACPA) did not differ significantly between the groups.Conclusion:In our study group, EORA patients were characterized by higher proportion of men, higher inflammatory parameters and higher disease activity, in comparison with YORA. In patients with EORA we also found unfavorable metabolic parameters and higher incidence of concomitant diseases, which could affect the method of treatment (less common use of GC and biological DMARDs).Disclosure of Interests:Bozena Targonska-Stepniak Consultant of: Berlin-Chemie Mennarini, Sandoz, Speakers bureau: KRKA, Sandoz, Krzysztof Grzechnik: None declared, Katarzyna Kolarz: None declared, Danuta Gagol: None declared, Maria Majdan Consultant of: Roche, Amgen, Speakers bureau: Roche, Amgen</jats:sec

Smoking cessation advice by rheumatologists: results of an international survey

The aim of this study was to understand practices regarding smoking cessation among rheumatologists for patients with inflammatory rheumatic diseases