Objectives To describe the radiographic evolution after 13 years of follow-up in a monographic consultation of patients with Axial Spondyloarthritis (EspAax) included in REGISPONSER at the Reina Sofía University Hospital in Córdoba. Methods Seventy eight SpA patients from the REGISPONSER registry were analysed in an observational study, which were evaluated for the first time in the year 2004–2005. The last x-rays analysis of the cervical and lumbar spine, pelvis and hips were recorded. Two independent observers evaluated the radiographs and calculated the BASRI index. The interobserver concordance was studied using Cohen’s Kappa statistic. Finally, radiographic progression was assessed using the McNemar test. Results Sixty one SpA patients were radiographicaly evaluated at baseline and after 11 (1.7) years of follow-up. A complete radiographic study was recorded in 38 of them. The baseline characteristics, including BASRI values, as well as the treatment received are listed in table 1. The strength of the interobserver concordance in the radiographic analysis was considerable in hips (k=0.77, p<0.001) and almost perfect at the levels of the cervical spine (k=0.88, p<0.001), lumbar spine (k=0.87, p<0.001) and sacroiliac joints (k=0.84, p<0.001). The BASRIs and BASRIt scores were 7.5 (2.9) and 8.8 (4.1) respectively. Moreover, during the follow-up, the BASRIt was increased in 1.23 (p=0.014). Individual analysis of the different components of BASRI, showed that 42.1% of SpA patients got worse regarding the score corresponding to the cervical spine (p<0.001), 28.9% to the lumbar spine (p=0.057), 15.8% to the hip (p=0.754) and no worsening was found in sacroiliac (p=0.500). Conclusions This study provides information related to the structural progression of patients followed in a monographic consultation of SpA after 13 years of follow-up. Radiographic evolution was significantly noticed in relation to the total score of the BASRI. However, analysing the individual scores it seems that the cervical spine was the segment where there was greater radiographic progression. We did not find worsening of BASRI in sacroiliac due to the fact that the most of patients already had an advanced degree of sacroileitis in the first visit of the registry. Disclosure of Interest None declared

OBJECTIVES Dactylitis is a typical feature of psoriatic arthritis. However, dactylitis was included as a spondyloarthritis (SpA) feature for both (axial and peripheral) of the ASAS classification criteria, but data about its prevalence are scarce, especially in patients with a recent onset of the disease. Our objective was to determine the prevalence and characteristics associated with dactylitis in patients with early SpA. METHODS A baseline dataset from the ESPeranza cohort was used. This programme included patients who were suspected of having SpA (age <45 years, symptoms duration of 3-24 months and with inflammatory back pain, or asymmetrical arthritis, or spinal/joint pain plus ≥1 of the SpA features). For this study, 609 patients who were diagnosed with SpA by their physician were included. Descriptive, univariable and multivariable logistic regression analyses were employed to investigate the association between the presence of dactylitis and the characteristics associated with SpA. RESULTS Fifty-eight (9.5%) patients currently or previously had dactylitis. In the multivariable analysis, dactylitis was independently associated with peripheral arthritis (OR= 4.83; p<0.001), enthesitis (OR= 2.49; p=0.01), psoriasis (OR= 3.62; p<0.01) and the physician's visual analogue scale (OR= 0.82; p=0.01). However, 67% of the patients who had dactylitis did not have peripheral arthritis or psoriasis and 15% had predominantly axial disease. CONCLUSIONS Dactylitis is a frequent manifestation in patients with SpA, even during the early stages of the disease. Its presence is mainly associated with peripheral manifestations and psoriasis. Nevertheless, dactylitis is not exclusive of patients with PsA or peripheral manifestations.

Background Ankylosing spondylitis (AS) is a chronic inflammatory disease, of unknown etiology, that mainly affects the axial skeleton and the sacroiliac joints in the pelvis. Neutrophils are critical actors in innate immunity and their activation has been involved in the progression of AS symptoms. Recently, NETosis has been suggested to play a central role in several pathologic states, including rheumatology diseases. Nevertheless, this process has not been described yet in AS patients Objectives 1) To evaluate and characterise the presence of NETosis in AS patients. 2) To explore the relationship among NETosis markers and clinical characteristics of this disease Methods Thirty patients with AS and 32 healthy donors (HD) were included in the study. Disease activity was determined by BASDAI index and, CRP and ESR levels; in parallel, inflammatory markers were determined in plasma by ELISA kits. Spinal mobility of AS patients was measured by the BASMI index, and structural damage was calculated by the mSASSS index. Ex vivo, spontaneous NETosis generation in purified neutrophils from AS patients and HDs were measured by fluorescence (n=6) and scanning electron (n=3) microscopy after 6 hour of incubation. PMA, known to promote NETosis, was used as positive control. DNA extrusion was analysed by fluorescence microscopy and fluorimetry after SYTOX staining, whereas elastase percentage (NE) was analysed by fluorescence microscopy after staining of neutrophils with NE antibody. In vivo, mieloperoxidase (MPO) and NE protein expression were measured by flow cytometry (FACSCalibur), whereas extracellular DNA was examined in plasma using fluorimetry after SYTOX staining Results Compared to HDs, AS neutrophils showed spontaneous extracellular release of a meshwork of DNA nuclear and granule proteins (NETs), as demonstrated by fluorescence microscopy, fluorimetry, and scanning electron microscopy. Indeed, analysis of DNA fibres staining by SYTOX revealed that NETosis rate was above baseline levels after 6 hour of ex vivo AS neutrophil incubation as compared to those from HDs (p<0.05). Furthermore, higher cell free-DNA levels were observed between AS patients and HDs at 6 hour (p<0.05). Increased spontaneous NETs production in this pathology was additionally corroborated by the observation of an enhanced percentage of NE-staining cells after 6 hour of incubation (p<0.05). In vivo, higher intracellular NE levels (p=0.036), and plasma DNA concentrations (p=0.021) were also found in AS patients as compared to HDs. Correlation studies showed that plasma DNA levels positively correlated with inflammatory markers (i.e. CRP, ESR and TNFα), and with the spinal mobility index BASMI. In addition, a positive correlation was found between intracellular NE levels and plasma IL-1β concentration Conclusions 1) NETosis is increased in AS patients. 2) Raised NETosis in AS is associated with several markers of inflammation and mobility. Thus, NETosis might act as a key mediator in the etiopathogenesis of AS. Funded by JA PI-0314–2012, SER, ISCIII (RIER RD16/0012/0015) Disclosure of Interest None declared

Background Dose optimization, such as dose reduction or dose spacing, is nowadays presented as a therapeutic strategy to be followed in patients with rheumatoid arthritis (RA) who have managed to reach and maintain clinical remission for a while. This strategy reduces the frequency of adverse effects and promotes cost savings Methods Patients with RA (Criteria ACR 1987) of the CREATE registry (patients who was treated in real life conditions) who had clinical remission (DAS28 <2.6) of at least 6 months of duration on November 1, 2013, constituted the cohort of patients who were optimized for the dose received. According to the consensus of the Spanish Societies of Rheumatology and Hospital Pharmacy, the optimization of doses meant the reduction of between 20 and 50% of the same. A multidisciplinary team of rheumatologists and clinical pharmacists in a third-level hospital was involved in decision-making on treatment and dose reduction, which involved the application of protocols and the follow-up of patients at least every two months. Results A prospective follow-up of 70 patients with RA who had received optimized doses of biological therapy for 3 years, with a mean age of 56.9 (13.7) years, of which 78.6% were women, 68.8% were positive rheumatoid factor and 66.7% ACPA +. The relapse occurred in 41.8% (at first year), 56.7% (at second year) and 62.7% (at third year). There were no statistical differences between these last 2 percentages. The median survival time of the optimization regimen was 15.24 (4.65) months (95% CI: 4.66–25.83). No statistically significant differences were found when comparing patients according to the optimized drug (antiTNF versus non-anti-TNF) (test log.rank: 0.239, p: 0.625). When relapse occurs, the patient returns to normal doses prior to optimization of the drug. Our data show that 62.7% of the patients in whom the relapse occurs at 3 years, maintains DAS28 <2,6 (P<0.05) when dose was returned to the manufacturer recommended dose. The 37.3% (95% CI: 26.72%, 49.28%) patients maintained the optimization pattern throughout the follow-up without relapse, with an average DAS28 of 1.99 (1.07) at 3 years. Comparing these patients with those who relapse, they achieved significantly lower DAS28 values at both (p: 0.028) and at three years (p: 0.025) Conclusions The strategy of dose reduction of biological therapies in patients with established RA that achieve sustained remission is possible in 37.3% of cases in real clinical practice (CREATE Registry) and it was maintained for 3 years. The probability of occurrence of relapse decreases after 2 years of treatment with an optimized regimen in those patients who have not relapsed before. This strategy is possible in patients with persistently controlled disease and in view of our results, it is independent of the drug administered (antiTNF versus non-antiTNF). After 3 years of follow-up, all patients maintained clinical remission (DAS 28 <2.6) despite relapses, and after resumption of the usual dose, all of them reached the therapeutic goal again. Patients who maintain clinical remission for 3 years achieve DAS28 values statistically lower than those who did not after 2 years. Disclosure of Interest None declared

Background Ankylosing spondylitis (AS) is a chronic inflammatory disease, of unknown aetiology, associated to the development of several comorbidities such as atherosclerosis. Splicing is a post-transcriptional process involved in the RNA maturation. Recent studies have revealed that a pathological dysregulation of the splicing machinery or spliceosome is associated to several human diseases. Yet, the spliceosome alterations have not been described in AS. Objectives 1) To analyze whether dysregulation of the spliceosome is present in AS. 2) To evaluate the association between the alteration of this process and the clinical, inflammatory, oxidative, and atherogenic profiles present in this pathology. Methods Fourteen AS patients and 14 healthy donors (HDs) were included in the study. Disease function and activity status were analyzed using the BASFI and BASDAI. The expression of selected components of the major-(n=12) and minor-spliceosome (n=4), and splicing factors (n=28) was evaluated in purified monocytes, lymphocytes and neutrophils from patients and HDs (n=14 each) by Fluidigm methodology. Oxidative stress, inflammation and atherogenesis were evaluated by flow cytometry and RT-PCR. Endothelial function was determined by the post occlusive hyperaemia test using Laser-Doppler. Results Compared to HDs, a significant dysregulation in the expression of relevant splicing factors and spliceosome components was found in all the leukocyte subtypes from AS patients, being neutrophils which displayed higher number of altered molecules. Interestingly, a specific altered profile of major- and minor-spliceosome members, and splicing factors was observed when compared lymphocytes (U4, U6, NOVA1, RMB17), monocytes (PRP8, SF3B TV2, CELF4, ESRP2, RBM3, SAM68 TV1, SRSF10, TIA1) and neutrophils (U11, U2, U2AF2, U11, CA 150, ESRP1, PSF, PTB, SRM160). Correlation studies revealed that disease activity (CRP, ESR, BASDAI) was associated to the alteration of a vast number of spliceosome components in the three subtypes of analyzed leukocytes. In addition, the BASFI index correlated with the expression of splicing factors ESRP1, SRSF1 and TRA2B in neutrophils. The inflammatory, atherogenic and oxidative profile of AS leukocytes was related to the expression of a number of spliceosome molecules in the three leukocyte subsets, although neutrophils exhibited the highest number of deregulated spliceosome components related to inflammation (STAT3, TNF-α, IL-1α, IL-1β, IL-5) and cell adhesion (ICAM-1, SELL, THBS4, CDH5). Finally, endothelial dysfunction correlated with the expression of several components of the major-spliceosome and splicing factors in monocytes and neutrophils. Conclusions 1) AS patients display a dysregulation of the splicing machinery components associated to disease function and activity. 2) The expression of spliceosome members in the different leukocyte subsets is related to the inflammatory, oxidative and proatherogenic profile of AS patients. Alteration of the spliceosome may provide new biomarkers for diagnosis and clinical monitoring of AS Acknowledgements Funding by: JA PI-0314–2012, SER, ISCIII (RIER RD16/0012/0015) Disclosure of Interest None declared

Background Monocytes play a key role in the pathogenesis of the cardiovascular disease (CVD). Three monocyte subsets have been described based on their CD14 and CD16 profile, with different actions in the vascular pathology. The distribution of these monocytes subsets and their epigenetic profile associated with CVD in rheumatoid arthritis (RA) remain unravelled Objectives To functionally characterize the monocytes subsets in RA patients and analyze their role in the endothelial dysfunction, altered oxidative status and proinflammatory/prothrombotic profile associated to RA. Methods Fifty RA patients and 30 healthy donors were included. Endothelial function was measured through post occlusive hyperaemia using Laser-Doppler. Carotid intima media thickness (CIMT) was used as atherosclerosis marker. The monocyte subsets were characterized by flow cytometry and isolated by immuno-magnetic selection. Proinflammatory cytokines, peroxides levels and cellular activation markers were analyzed. NanoString nCounter miRNA Expression Array was used to profile 800 microRNAs in isolated CD14+ and CD16+ monocytes. PCR array gene expression was used to analyze the expression of 84 genes related to atherosclerosis. Target genes of the differentially expressed miRNAs were identified by using the Ingenuity Pathway Analysis Software (IPA). The predicted microRNA-mRNA interactions were characterized by the microRNA Target Filter tool of IPA. The resulting identified interactions were revalidated by RT-PCR on the whole cohort of RA patients Results CD16+ monocytes were significantly extended in RA patients. These subsets had increased protein and gene expression of proinflammatory cytokines, markers of atherosclerosis and peroxide levels. miRNA expression profiling showed that 38 miRNAs were significantly altered (≥2 fold) in CD14+ RA monocytes compared to CD16+ RA monocytes. Functional classification of those miRNAs showed a preponderance of targets mRNAs involved in the pathological process of RA such as inflammatory state, immune response and CVD. RA patients had impaired endothelial function, with a reduced perfusion value after ischemia. Increased CD16+ monocytes and reduced CD14+ cells percentage were associated with a pathologic CIMT. Clinical parameters strongly correlated with endothelial dysfunction, decreased percentage of CD14+ monocytes and increased number of CD16+ subsets. Conclusions 1) RA patients exhibit an increased number of CD16+ monocytes, which display a specific atherogenic and inflammatory pattern directly associated to the autoimmune profile, the progression of the disease and the altered microvascular function. This atherogenic profile might be associated with an altered epigenetic pattern. That data suggest that CD16+ subpopulation might play a key role in the CVD pathogenesis associated with RA. Acknowledgement Funded by CTS7940, PI15/01333, PI2013–0191, CP15/00158 Disclosure of Interest None declared

Background Neutrophil extracellular traps (NETs) have recently been implicated in vascular damage and atherothrombosis. Extruded DNA fibers containing multiple proinflammatory and thrombotic molecules induce the activation and recruitment of monocytes and dendritic cells to the vessel wall. Enhanced NETosis occurs in rheumatoid arthritis (RA), which has been shown related to the pathogenesis of this disorder. However, the relevance of this abnormality in the development of atherosclerosis has not been elucidated yet. Objectives To evaluate the association of netosis-derived products with the development of atherosclerosis in RA. Methods One hundred RA patients and 30 healthy donors were included. Carotid intima media thickness (CIMT) was used as atherosclerosis marker. Inflammatory and prothrombotic molecules, nitric oxide (NO), total antioxidant capacity (TAC) and protein nitration (NTyr) were analyzed in plasma. Neutrophils were isolated from RA patients and controls. Spontaneous and induced NETs formation from RA and control neutrophils was assessed in vitro through fluorescence microscopy. Oxidative stress status (JC1 and DCFH) and myeloperoxidase (MPO), neutrophil elastase (NE) protein expression were measured in neutrophils through flow cytometry. Cell-free DNA plasma levels were analyzed using Sytox staining. mRNA expression of peptidyl arginine deiminase 4 (PAD4) was analyzed in neutrophils by RT-PCR. Receiver operator characteristic (ROC) curves were calculated. Results Induced NETosis was increased in RA patients alongside MPO and NE protein expression in neutrophils. Cell-free DNA plasma levels were found significantly increased in RA patients. ROC curve analysis showed an area under the curve (AUC): 84, with a high sensitivity (69%) and specificity (86%). Those DNA levels strongly correlated with clinical parameters such as evolution time, DAS28, CRP and ESR and autoimmunity state (RF and anti-CCPs levels). In addition, high levels of cell-free DNA were associated with elevated levels of IL-6, MCP-1, spSelectin and tPA in plasma. Moreover, high levels of cell-free DNA correlated with increased NTyr and TAC and decreased NO. At cellular level, cell-free DNA plasma levels correlated with increased oxidative status in RA neutrophils (JC1 and DCFH) and mRNA expression of PADI4. Those patients having pathologic CIMT showed increased cell-free DNA plasma levels (ROC curve analysis: AUC 77, sensitivity 60%, specifity 72%). Conclusions 1) Elements associated with the extrusion of NETs are significantly enhanced in RA compared with healthy controls. 2) NETosis-derived products, such as cell-free DNA strongly correlated with clinical parameters, inflammatory and oxidative status in RA patients. Thus, NETosis-derived products demonstrated diagnostic potential for atherosclerosis, which might be a complementary tool to discriminate between normal and pathologic CIMT in RA patients. Acknowledgement Funded by CTS7940, PI2013–0191, PI15/01333, CP15/00158. Disclosure of Interest None declared

Background Inhibition of the interleukin IL6 receptor pathway by tocilizumab (TCZ) is an effective treatment for rheumatoid arthritis (RA). TCZ reduces atherosclerosis markers and improves endothelial function. In peripheral blood, TCZ increases the percentage of natural killer and regulatory T cells and decreases the number of inflammatory Th1/Th17 lymphocytes. Monocytes activation and neutrophil extracellular traps (NETs) are key players in the development of cardiovascular disease; however, the specific effect of TCZ on these cells has not been described yet. Objectives To analyze the molecular changes (focused on monocyte and neutrophil abnormalities) underlying the beneficial effect of TCZ on atherosclerosis and endothelial dysfunction in rheumatoid arthritis. Methods Fifteen RA patients received 162 mg/week subcutaneous TCZ as combined therapy. Endothelial function was measured through post occlusive hyperemia using Laser-Doppler. To analyze the specificity of TCZ, blood samples from 5 RA patients with high disease activity no taking TCZ was used to perform in vitro studies. Isolated monocytes and neutrophils were treated in vitro with IL6 and blocking FCRII plus TCZ for 18 and 6 hours, respectively. Oxidative stress markers in leukocytes were analyzed by flow cytometry. NETosis was measured through Sytox staining of DNA fibers. Myeloperoxidase (MPO) and neutrophil elastase (NE) were analyzed in neutrophils by flow cytometry. mRNA expression of peptidyl arginine deiminase (PAD4) was measured by RT-PCR. Percentage of low density granulocytes (LDGs) was analyzed through flow cytometry. mRNA expression of genes involved in monocyte activation, prothrombotic state, lipid uptake and insulin resistance was analyzed in monocytes through RT-PCR. Activation of intracellular pathways was analyzed in monocytes using pathscan intracellular signaling array. Expression of miRNAs was evaluated in plasma. Results After 6 months of treatment, TCZ reduced clinical parameters of inflammation, autoimmunity and joint damage. Endothelial function was significantly restored. TCZ decreased peroxide and peroxinitrite levels in RA leukocytes, most significantly in monocytes and neutrophils. Percentage of LDGs was also reduced after treatment. TCZ in vivo treatment reduced the expression of MPO, NE and PAD4 in RA neutrophils. The generation of in vitro induced NETs was also inhibited by TCZ. The expression of inflammatory and prothrombotic molecules, genes involved in lipid uptake and cellular activation and insulin signaling and the activation of various intracellular pathways were modulated in monocytes after in vivo TCZ treatment. All these results were recapitulated after in vitro TCZ treatment of RA monocytes and neutrophils. Plasma levels of miRNA-223, miRNA-146 and miRNA-23, previously reported to be modified by anti-TNFalpha drugs, were also upregulated after TCZ treatment. Conclusions TCZ improves endothelial dysfunction and atherothrombosis through the restoration of the oxidative status, inhibition of the monocyte prothrombotic and inflammatory profile and the generation of NETosis Acknowledgement Funded by CTS7940, PI2013–0191, CP15/00158, PI15/01333 Disclosure of Interest None declared

Background MicroRNAs (miRNA) have recently emerged as a new class of modulators of gene expression. Several studies have shown a deregulation of miRNAs in peripheral blood mononuclear cells or T lymphocytes, in synovial tissue and fibroblasts that might contribute to inflammation, degradation of extracellular matrix and invasive behavior of the resident cells in rheumatoid arthritis (RA). Neutrophils are key cells participating in the joint destruction. Objectives To investigate the miRNA expression profile in synovial and blood neutrophils in RA and its role in the pathogenesis of this disorder. Methods Neutrophils were isolated from peripheral blood of 20 healthy donors and 20 RA patients. Synovial neutrophils were isolated from paired synovial fluid of 10 RA patients. nCounter microRNA Assay was used to detect simultaneously 800 human microRNAs in each sample.100 ng of RNA from peripheral blood and synovial neutrophils were prepared by ligating a specific DNA tag (miR-tag) onto the 30 end of each mature microRNA according to the manufacturer9s instructions. Altered miRNAs were analyzed for potential mRNA targets using Ingenuity pathways analysis (IPA) software. miRNA expression levels were validated through RT-PCR. Several mRNA targets of these miRNAs were analyzed by RT-PCR. Healthy neutrophils were treated in vitro with anti-CCPs isolated from RA patients. mRNA expression of DICER, Ago1, Ago2, exportin was evaluated through RT-PCR. DICER protein expression was analyzed by western blot. Results Among 800 miRNAs analyzed, 121 were detected in neutrophils from peripheral blood or synovial fluid. Using a 2 fold change cut off, 97 miRNAs were altered in peripheral blood neutrophils from RA patients compared to healthy donors. Most of them were downregulated (94 downregulated and 3 upregulated). Accordingly, RA neutrophils showed a downregulation of the proteins participating in miRNA biogenesis, including DICER, Ago1, Ago2, exportin 5. In addition, treatment of healthy neutrophils with IgGs anti-CCPs isolated from RA patients decreased the expression of these proteins, thus pointing at these autoantibodies as main modulators of microRNA neutrophil expression. Functional IPA analysis showed that altered miRNAs regulated cellular functions such as development, growth, proliferation and movement and were mainly involved in immunological disease. Among the miRNAs found deregulated blood, 34 miRNAs were found even more significantly reduced in synovial neutrophils compared to paired blood neutrophils from RA patients. These miRNAs were mainly involved in inflammatory response, suggesting the abnormal activation of this cell subtype in the joint. Conclusions 1) RA neutrophils exhibit a defect in the miRNAs processing, showed by a decrease in most of the detected miRNAs and the concomitant downregulation of proteins involved in their biogenesis. This defect seems to be modulated, at least partially, by anti-CCPs antibodies. 2) miRNA downregulation is even more pronounced in synovial resident neutrophils, which may contribute to the high inflammatory profile of these cells in the joint. Acknowledgement Funded by CTS7940, PI2013–0191, CP15/00158, PI15/01333 Disclosure of Interest None declared

Background RELATIONSHIP BETWEEN CHRONIC LOW BACK PAIN AND MRI OF SACROILIAC JOINTS Objectives To determine the relationship between chronic low back pain and presence of edema on MRI of sacroiliac joints and to establish the value of MRI as a method of early diagnosis of SpA without considering others characteristics Methods An Observational cross-sectional study, which included 95 patients with chronic low back pain suggestive of spondyloarthritis from primary care, was carried out. The criteria for inflammatory back pain were aplicated to these patients and the relationship between chronic inflammatory back pain according to (PCM) prymary care physicians (gold standar) and the presence or absence of signs of inflammatory activity in MRI, was assessed. Results Results: 51.6% of the patients were male, with a mean age of 32.6 (8.86) years, 84’2% of patients fulfilled the criteria for inflammatory back pain according to PCM. Their mean evolution time was 8.43 (16.5) months. 42.1% showed HLA-B27 and only 22.1% had a family history of spondyloarthritis. Of the group of patients who fulfilled PCM criteria for inflammatory back pain, 42 (44.2%) showed RM SI joint (+). No differences in age, gender or form onset of symptoms in another group (with edema or without edema), wasn’t fond. However, a prevalence of HLA B27 (57’8% vs. 24’5%) p=0.001, night waking in 2nd half of the night (64’4% vs 18.4% p=0.0001), morning stiffness>1 hour (73.3% vs. 40’8%, P=0.001) and pain in alternating buttocks (42’2% vs. 14’3%, P=0.002), were recorded. The number was higher if the criteria was classified according to the experts. The MRI showed edema in 52’5% patients classificated of inflammatory by PCM criteria, increasing it to 67% if applied to experts’ criteria. This means that nearly half of the patients classified by the PMC had negative MRI Conclusions Although MRI appears to be a safe and useful tool to detect inflammatory lesions in patients with early axial SpA and thus is widely used in clinical practice (having been included it in the new classification criteria) data was from our study indicates that in cases of chronic low back pain, if not properly classified as inflammatory, MRI is not sensitive. Therefore, in clinical practice (outside of clinical trials) the RM has no value, and it implies the need to incluid other more sensitive markers and/or other clinical or laboratory caracteristics to establish the diagnosis in the early stages of the disease. References Rudwaleit, M. et al. Ann. Rheum. Dis. 68, 770–776(2009) Rudwaleit M, van der Heijde D, Landewé R, et al. Ann Rheum Dis2009; 68: 777–83. M. Rudwaleit, A. G. Jurik, K-G A Hermann. Ann Rheum Dis. January, 2009; 68; 1520–1527. M. Rudwaleit, A. G. Jurik, K-G A Hermann. Ann Rheum Dis. January, 2009; 68; 1520–1527. N Bennett, A Rehman,E M A Hensor, H Marzo-Ortega, P Emery, D McGonagle. Ann Rheum Dis 2010;69:891–8942 Disclosure of Interest None Declared