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ID PMID Title PublicationDate abstract
21188451 Disseminated cutaneous and visceral Kaposi's sarcoma in a patient with rheumatoid arthriti 2011 Jun Kaposi's sarcoma (KS) is a vascular lesion of low-grade malignant potential caused by the complex interactions between geographic, genetic, environmental, and immunological factors. We recently experienced a rare case of KS associated with rheumatoid arthritis in a patient receiving corticosteroids and tacrolimus; the KS demonstrated unusually aggressive clinical behavior. We herein report the details of the clinical course and discuss the possible contribution of corticosteroids and tacrolimus to the development of aggressive KS in the present case.
20849003 How to reduce morbidity and mortality from chest infections in rheumatoid arthritis. 2010 Aug Morbidity and mortality from pneumonia is increased in patients with rheumatoid arthritis. Factors contributing to this have been recently identified and a number of recommendations have been implemented in an attempt to reverse this trend. The present paper shows that these measures have combined to produce a fourfold reduction in both admissions and case fatality rates. In the study population, immunisation rates against influenza and pneumococcus have improved to 86% and 65%, oral steroid consumption has halved and disease modifying drugs were usually appropriately suspended during acute infection. These measures may now merit more widespread adoption.
19604464 Denosumab for joints and bones. 2009 Jul Denosumab is an investigational, fully human monoclonal antibody with a high affinity and specificity for receptor activator of nuclear factor kappaB ligand (RANKL), a cytokine member of the tumor necrosis factor family. RANKL, an essential mediator of osteoclast formation, function, and survival, plays a major role in the pathogenesis of postmenopausal osteoporosis, structural damage in rheumatoid arthritis, and bone loss associated with other skeletal disorders. Denosumab suppresses bone turnover by inhibiting the action of RANKL on osteoclasts. Denosumab reduces bone turnover and increases bone mineral density in postmenopausal women with low bone mineral density, reduces fracture risk in women with postmenopausal osteoporosis, and inhibits structural damage in patients with rheumatoid arthritis when added to ongoing methotrexate treatment. It is generally well tolerated, with a good safety profile. Adverse and serious adverse events, including infections and malignancy, are similar in patients treated with denosumab or placebo.
20143116 Etanercept-induced anti-Jo-1-antibody-positive polymyositis in a patient with rheumatoid a 2010 May Antitumor necrosis factor (TNF) therapy has been associated with adverse immunologic events including systemic lupus erythematosus. However, the development of polymyositis (PM)/dermatomyositis (DM) associated with anti-TNF therapy is extremely rare. We experienced a case of a 48-year-old female with rheumatoid arthritis (RA) who had anti-Jo-1 antibodies and interstitial lung disease but no previous history of PM/DM and who developed PM soon after the initiation of etanercept (ETN) therapy for RA. The patient recovered upon withdrawal from ETN and corticosteroid (CS) therapies. Only four reports of PM/DM associated with anti-TNF therapy for RA could be found in the literature. The patients described in three of the four reports were positive for anti-Jo-1 antibodies before the initiation of anti-TNF therapy, and in all the cases, recovery occurred after the cessation of anti-TNF-agent administration and CS therapy. These results suggest a relationship between the onset of PM/DM with anti-Jo-1 antibody and anti-TNF therapy for RA.
19929953 Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoi 2009 Dec AIM: To identify periodontal bacterial DNA (PBDNA) by PCR in subgingival dental plaque (SDP), serum and synovial fluid (SF) of rheumatoid arthritis (RA) with periodontal disease (PD) patients and to explore the possible PBDNA transport pathways from mouth to joints. METHODS: This cross-sectional prolective study involved 19 subjects with RA and PD. Informed consent, health and dental questionnaires were obtained. SDP, SF and serum samples were obtained, and leucocytes were isolated from blood. DNA was extracted and PCR assays to detect main PD species were carried out. Cultures on agar plates and broth, from each sample, were performed. RESULTS: Hundred percentage of patients showed PBDNA in SDP and SF and 83.5% in serum. Prevotella intermedia (89.4% and 73.6%) and Porphyromonas gingivalis (57.8% and 42.1%) were the species most frequently detected in SDP and SF, respectively. In SDP, 4.05 different bacterial species were found followed by 1.19 in serum and 2.26 in SF. Culture onto agar plates and broth did not show any bacterial growth, leucocytes were not positive to PBDNA by PCR. CONCLUSION: This study suggests that PBDNA could have a role on the RA aetiology. The possible pathway of transport of PBDNA from mouth to joints could be via the free form of DNA.
20448280 Current evidence for a strategic approach to the management of rheumatoid arthritis with d 2010 Jun OBJECTIVES: To perform a systematic literature review of effective strategies for the treatment of rheumatoid arthritis (RA). METHODS: As part of a European League Against Rheumatism (EULAR) Task Force investigation, a literature search was carried out from January 1962 until February 2009 in PubMed/Ovid Embase/Cochrane and EULAR/American College of Rheumatism (ACR)) abstracts (2007/2008) for studies with a treatment strategy adjusted to target a predefined outcome. Articles were systematically reviewed and clinical outcome, physical function and structural damage were compared between intensive and less intensive strategies. The results were evaluated by an expert panel to consolidate evidence on treatment strategies in RA. RESULTS: The search identified two different kinds of treatment strategies: strategies in which the reason for treatment adjustment differed between the study arms ('steering strategies', n=13) and strategies in which all trial arms used the same clinical outcome to adjust treatment with different pharmacological treatments ('medication strategies', n=7). Both intensive steering strategies and intensive medication strategies resulted in better outcome than less intensive strategies in patients with early active RA. CONCLUSION: Intensive steering strategies and intensive medication strategies produce a better clinical outcome, improved physical function and less structural damage than conventional steering or treatment. Proof in favour of any steering method is lacking and the best medication sequence is still not known.
19184362 Combination therapies that inhibit cyclooxygenase-2 and leukotriene synthesis prevent dise 2009 Feb OBJECTIVE AND DESIGN: To determine the effect of combinations of cyclooxygenase (COX) inhibitors and inhibitors of leukotriene (LT) syntheses on collagen induced arthritis (CIA) in mice. METHODS: The CIA model was evaluated for the presence of eicosanoids in the paw tissue. Several selective cyclooxygenase 2 (COX-2) inhibitors or non-selective non-steroidal anti inflammatory drugs (NSAIDs) were evaluated alone or in combination with leukotriene (LT) synthesis inhibitors in the CIA model. RESULTS: Arthritic paw tissue showed increased levels of prostaglandins and leukotrienes in comparison to normal paws. Analysis of mRNA levels indicated the inducible form of the COX-2 enzyme to be the source of prostaglandins. NSAIDs, COX-2 or leukotriene synthesis inhibitors administered alone in CIA decreased severity but had little effect on disease incidence. However, the combination of selective COX-2 inhibitors with leukotriene synthesis inhibitors produced significant decreases in both incidence and severity, suggesting an additive or synergistic effect. This effect was reversible with removal of drug. Little decrease in incidence was observed with the NSAID/5-LO inhibitor combinations. CONCLUSIONS: These results suggest that the induction of the disease in CIA is mediated by products of the COX-2 enzyme and LTB4 production, and that blockade of both pathways is required to prevent CIA.
19620209 Medico-economic evaluation of infliximab in rheumatoid arthritis--prospective French study 2009 Oct OBJECTIVES: To perform, in real conditions of prescription, the medico-economic evaluation of infliximab in severe RA. METHODS: A cost-effectiveness analysis of the annual costs was done with a comparison between the previous and the following year under infliximab. The effectiveness, determined from the HAQ, was expressed in clinically significant units and in quality-adjusted life years (QALYs). The incremental net benefit (INB), defined as willingness to pay (lambda), was used to express the results. RESULTS: A cohort of 635 patients was formed. Before the use of infliximab, after 1 and 2 years, the mean annual cost per patient for the care of RA was 9832, 27,723 and 46,704 euro, respectively. Among the direct costs, infliximab accounts for 21,182 euro for the first year. The distribution of the different costs was similar after 2 years. By using the INB, the difference before and after 1 year under infliximab is significant, on average by 1.86 (S.E.M. = 0.76) when the effectiveness is expressed in clinically significant units. For severe HAQ, lambda is 9841 euro (18,593 for all HAQ). When it is expressed in QALYs, also for severe HAQ, lambda > 100,000 euro. This can be explained by a short follow-up although severe complication of RA appears later. CONCLUSION: An evaluation of the more long-term costs is required in order to determine whether there are any full economic benefits with this treatment.
19224981 Are individuals with an autoimmune disease at higher risk of a second autoimmune disorder? 2009 Mar 15 Limited evidence suggests that autoimmune diseases tend to co-occur, although data are needed to determine whether individuals with an existing autoimmune disorder are at increased risk of a second disorder. The authors conducted a series of population-based cohort studies, utilizing the United Kingdom General Practice Research Database, to assess intraindividual risks of coexistence of rheumatoid arthritis (RA), autoimmune thyroiditis (AIT), multiple sclerosis (MS), and insulin-dependent diabetes mellitus (IDDM) during 1990-1999. Sex-specific age- and calendar-period standardized incidence ratios (SIRs) were calculated for development of a second autoimmune disease among index populations including 22,888 RA, 26,198 AIT, 4,332 MS, and 6,170 IDDM patients compared with the general population. Among those with IDDM, adjusted AIT rates were higher than expected for both males (SIR = 646.0, 95% confidence interval (CI): 466, 873) and females (SIR = 409.6, 95% CI: 343, 485), as were RA rates for females (SIR = 181.6, 95% CI: 136, 238). Coexistence of AIT and RA was also shown for either disease sequence (sex-specific SIRs = 130.4-162.0). However, point estimates suggested an inverse relation between RA and MS, irrespective of diagnostic sequence. This study demonstrates coexistence of RA, AIT, and IDDM at higher than expected rates but reduced comorbidity between RA and MS.
20731114 [Severe disseminated constrictive polyserositis in a patient with rheumatoid arthritis]. 2010 Constrictive polyserositis (pleuritis, pericarditis) is a syndrome within the underlying disease (tuberculosis, periodic disease, rheumatoid arthritis, systemic lupus erythematosus, asbestos, silicosis, uremia, some genetic diseases), a complication due to chest surgery or radiation or drug therapy, is occasionally idiopathic (fibrosing mediastinitis). There are frequently great difficulties in making its nosological diagnosis. The paper describes a patient in whom the onset of disease was exudative pleurisy with the signs of constriction, arthralgias; pleural punctures provided serous exudates with 80% lymphocytes. A year later there was ascitis and shin and foot edemas, which concurrent with hepatomegaly and cholestasis was regarded as cryptogenic liver cirrhosis. The signs of constrictive pericarditis were further revealed. The disease was complicated by the development of pulmonary artery thromboembolism (PATE) (which required the use of warfarin) and hemorrhagic vasculitis. Therapy with metipred in combination with isoniazid yielded a slight effect. The diagnoses of tuberculosis, liver cirrhosis, and autoimmune hepatitis, systemic vasculitis were consecutively rejected; the diagnosis of rheumatoid polyarthritis with systemic manifestations was made, by taking into account persistent arthalgias with the minimum signs of arthritis, noticeably increased C-reactive protein, rheumatoid factor, and cyclic citrullinated peptide antibodies (CCPA); plasmapheresis, therapy with metipred and methotrexate, and subtotal pericardectomy were performed. Constrictive polyserositis concurrent with PATE, hemorrhagic vasculitis (probably, drug-induced one), and hepatic lesion has been first described in a CCPA-positive patient with rheumatoid arthritis in the presence of moderate true arthritis (during steroid therapy).
20388060 Nuclear imaging of autoimmunity: focus on IBD and RA. 2010 Nov There is a need for methods to improve the diagnosis, patient staging and evaluation of therapeutic response in patients with autoimmune conditions to improve patient care. Inflammatory bowel disease (IBD) and rheumatoid arthritis (RA) are two inflammatory diseases characterized by involvement of innate and adaptive immune components that change the metabolic state of their respective target tissues, thus providing an opportunity for molecular imaging probes to detect such changes. Optimally, such probes and the imaging methods employed would be non-invasive, robust and reproducible, give a quantitative result, report on the status of the affected tissue(s) and respond to the effects of a therapeutic molecule. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) are nuclear imaging approaches that have the potential to satisfy such requirements. In this review, the work to date and the potential of PET and SPECT imaging probes in these two inflammatory conditions, IBD and RA, are discussed.
20118145 Golimumab: a tumor necrosis factor alpha inhibitor for the treatment of rheumatoid arthrit 2010 Jan OBJECTIVE: To review the pharmacologic, pharmacokinetic, efficacy, and safety data of golimumab, an anti-tumor necrosis factor alpha (TNF-alpha) monoclonal antibody. DATA SOURCES: A search of MEDLINE (1950-September 2009) was performed to identify any published clinical trials or review articles pertaining to golimumab. Key search terms included golimumab, rheumatoid arthritis, CNTO 148, and anti-TNF-alpha inhibitors. Bibliographies of selected articles were reviewed to identify other relevant citations. Abstracts from national and international meetings and information from the manufacturer were also reviewed. STUDY SELECTION AND DATA EXTRACTION: All available published articles and abstracts describing golimumab's pharmacologic or pharmacokinetic profile, efficacy, and safety were included. DATA SYNTHESIS: Golimumab is a fully humanized TNF-alpha monoclonal antibody that is specific for human TNF-alpha. Trials have investigated the use of golimumab in patients who have rheumatoid arthritis (RA) and are on methotrexate, are methotrexate-naïve, and have previously tried TNF-alpha inhibition therapy. When used in combination with methotrexate or another disease-modifying antirheumatic drug, golimumab therapy results in improvements of clinical outcomes including the American College of Rheumatology parameters in all of the aforementioned populations. Although multiple doses and dosing regimens have been studied, the Food and Drug Administration-approved dose is 50 mg subcutaneously every 4 weeks. The most common adverse effects include injection site erythema, headaches, and nausea. There were a limited number of incidences of serious infection or malignancy. CONCLUSIONS: With 4 TNF-alpha monoclonal antibodies currently on the market, it is unclear what golimumab's place in therapy for RA will be. Some benefits include monthly injections, proven efficacy after previous TNF-alpha inhibitor therapy, and limited antibody development during therapy. However, with a lack of longer-term trials assessing efficacy and safety compared with other TNF-alpha inhibitors, golimumab should be reserved for use after other therapies fail.
21073898 The role of Natural Killer cells in the pathogenesis of rheumatoid arthritis: major contri 2011 May Natural Killer (NK) cells are lymphocytes of the innate immune system, originally described by their capacity to control tumour cells and eliminate virus-infected cells. However accumulating evidence suggests that NK cells can interact with various components of the immune system and play a critical role in autoimmune diseases by limiting or exacerbating immune responses. Rheumatoid arthritis is a chronic inflammatory disease characterised by joint inflammation and cartilage and bone destruction. NK cells are enriched within the joints of patients with rheumatoid arthritis but how they contribute to disease pathology is currently not fully elucidated. This review will outline the current understanding of NK cell biology and how these cells may modulate disease pathogenesis in rheumatoid arthritis through interactions with other immune cells.
20510237 B cell therapies for rheumatoid arthritis: beyond B cell depletion. 2010 May Initially suggested by the presence of rheumatoid factor autoantibodies, multiple pathogenic roles for B cells (both antibody-mediated and antibody-independent) in rheumatoid arthritis (RA) now are supported by a growing body of experimental observations and human studies. The pathogenic significance of B cells in this disease also has been established conclusively by the proven benefit of Rituximab-induced B cell depletion in RA patients refractory to tumor necrosis factor (TNF) blockade. This article reviews the rationale for the use of B cell-targeting therapies in RA and discusses the caveats and limitations of indiscriminate B cell depletion as currently applied, ncluding incomplete depletion of pathogenic B cells and elimination of protective B cells. Finally, it presents alternative therapeutic strategies that exploit current knowledge of B cell activation, survival, and differentiation to provide more selective B cell and plasma cell targeting.
19758178 Immmunopathogenesis of rheumatoid arthritis; induction of arthritogenic autoimmune respons 2009 Sep Rheumatoid arthritis (RA) is a severe autoimmune disorder of unknown etiology. Major autoantigens include immunoglobulin G (which is targeted by rheumatoid factor), citrullinated proteins, and the heterogeneous nuclear ribonucleoprotein (hnRNP) A2. To obtain more insight into the pathogenic role of arthritogenic autoantigens, we studied autoimmune responses in two animal models of RA, which are independent of immunization with exogenous antigens, namely human tumor necrosis factor-alpha (TNF-alpha)-transgenic (hTNFtg) mice and rats with pristane-induced arthritis (PIA). Serologic and cellular studies revealed autoantibodies to hnRNP-A2 in these animals and pronounced T-cell reactivity to hnRNP-A2 and the presence of rheumatoid factor in PIA, while citrullinated antigens were not targeted. Furthermore, hnRNP-A2 was found to be highly overexpressed in the joints of mice and rats affected by arthritis. Thus, unspecific proinflammatory stimuli, such as TNF-alpha or pristane, may induce pathogenic autoimmune reactions that may drive an inflammatory process, leading to the development of erosive arthritis.
20546209 The effect of desmopressin on blood loss in patients with rheumatoid arthritis undergoing 2010 Aug BACKGROUND: Blood loss is an important issue for patients with rheumatoid arthritis undergoing hip surgery. We hypothesised that intraoperative desmopressin treatment would result in a reduction in blood loss in rheumatoid patients undergoing total hip arthroplasty. METHODS: Seventy-five patients scheduled for elective total hip arthroplasty were randomised to three groups to receive 0.4 microg/kg desmopressin (D 0.4), 0.2 microg/kg desmopressin (D 0.2) or placebo intraoperatively in a double-blind fashion. Blood transfusions were based on calculated safe allowable blood loss and haemoglobin measurements (trigger 90 g/l, 5.59 mmol/l). The primary endpoint was the total blood loss measured till the end of the fourth post-operative day. Secondary endpoints included red cell transfusion requirements and haemoglobin. RESULTS: Total blood loss during the study period was not significantly different between the groups (D 0.4 1829 +/- 1068; D 0.2 2240 +/- 843 and placebo 2254 +/- 1040 ml; P= 0.50). The total amount of red cell transfusions was fewer in group D 0.4 (3.6 +/- 1.6 U) when compared with D 0.2 (4.4 +/- 1.7 U; P=0.009) and placebo (4.5 +/- 2.0 U; P= 0.011) groups. Haemoglobin concentration was lower in the placebo group in the first (5.42 +/- 1.16 vs. 5.98 +/- 0.47 mmol/l; P=0.033) and the second (6.28 +/- 0.66 vs. 6.69 +/- 0.47 mmol/l; P=0.033) post-operative mornings compared with group D 0.4. CONCLUSION: Despite a lack of difference in the primary outcome, total blood loss, intraoperative administration of 0.4 microg/kg desmopressin resulted in fewer total red cell transfusion requirements in rheumatoid patients undergoing total hip arthroplasty when compared with 0.2 microg/kg treatment and placebo.
20440528 Serological investigation of IgG levels and subclasses in rheumatoid arthritis patients fo 2011 Feb The purpose of this study was to investigate whether clinical improvement in patient with rheumatoid arthritis (RA) taking oral Bovine type II collagen (bCII) is associated with changes in levels of anti-bCII total IgG antibody and its subclasses. Four groups were given either 5, 0.5 or 0.05 mg of bCII or a placebo in a double-blind randomised control trial. The sera IgG anti-collagen type II and antibodies of the IgG subclasses, IgG1-4, were measured at the start and end of the trial by ELISA. Total IgG anti-collagen II antibodies in the pooled active treatment groups were statistically significantly reduced compared with the placebo group (p = 0.021). Decreasing total IgG titres were observed in the 0.5-mg group (p = 0.008), 0.05-mg group (p = 0.004) and 5-mg group (p = 0.078) before and after treatment. For IgG1, IgG2, IgG3 and IgG4 subclasses, in the 0.5-mg group in which the best clinical response was observed, there was statistically significant decreases observed in the IgG2 and IgG3 subclasses (p = 0.047, p = 0.046). Treatment with bCII in patients with RA led to a reduction in anti-collagen II antibody titre indicating an active biological effect as observed previously in animal model of RA. The largest decrease in total and subclasses of anti-collagen antibody titres occurred in the groups of patients with the best therapeutic response to bCII, supporting the conclusion of the clinical trial and suggests that immune regulation explains the therapeutic effect.
20349066 Patterns of preventive health services in rheumatoid arthritis patients compared to a prim 2011 Sep To determine the proportion of rheumatoid arthritis (RA) patients receiving preventive health care according to US Preventive Services Task Force recommendations compared with a community-based population sample, with emphasis on dyslipidemia testing, given the increased risk of cardiovascular disease (CVD) in RA patients. Patients with RA (ICD-9 code 714.0 at ≥2 office visits with a rheumatologist) and a primary care physician (PCP) at the Geisinger Health System (GHS) were identified through electronic health records. The records were searched back from 3/31/08 for the length of time required to satisfy each outcome measure. Percentages were compared with population testing rates using the Pearson Chi-square test. Eight hundred and thirty-one RA patients were compared to 169,476 subjects with a PCP at GHS, stratified by gender and age. Patients with RA were more likely to have had dyslipidemia and osteoporosis testing compared with the general population (86 vs. 75 and 75 vs. 55%, respectively, P < 0.0001 for both). The proportion of RA patients receiving breast and cervical cancer testing was similar to the general population. The majority (79%) of lipid testing was ordered by PCPs. Those RA patients with recommended lipid testing had more traditional CVD factors (hypertension, diabetes, coronary artery disease). RA patients are screened more than the general population for two RA-related co-morbidities, i.e. dyslipidemia and osteoporosis. The RA patients with traditional cardiovascular risk factors are more likely to be tested for dyslipidemia. Further work is warranted to improve testing for modifiable CVD risk factors in this group with multiple co-morbidities.
20346239 Visfatin is not associated with inflammation or metabolic syndrome in patients with severe 2010 Jan BACKGROUND AND OBJECTIVE: Visfatin is an insulin-mimetic adipokine. In non-rheumatoid arthritis (RA) patients circulating levels of visfatin are correlated with the amount of visceral fat. Recent studies have disclosed an implication of visfatin in inflammation. Chronic systemic inflammation is of major importance in the development of atherosclerosis in RA. In the present study we investigated whether inflammation, obesity or metabolic syndrome are potential determinants of circulating visfatin concentrations in a group of RA patients on periodical treatment with the TNF-alpha blocker infliximab due to severe disease. We also assessed whether the infusion of infliximab may alter circulating visfatin concentrations in patients with severe RA. METHODS: We investigated 33 non-diabetic patients with RA on periodical treatment with infliximab. Serum visfatin levels were determined immediately prior to and after infliximab infusion. RESULTS: There was no correlation between body mass index of RA patients and baseline serum level of visfatin. Also, no significant correlations between baseline visfatin levels and the age at the time of the study or at the onset of the disease, disease duration, ESR and CRP levels, DAS28, lipids, insulin sensitivity, resistin or the cumulative prednisone dose at the time of the study were found. Visfatin levels did not change upon infliximab infusion. CONCLUSIONS: In RA patients on TNF-alpha blocker treatment, circulating visfatin levels are unrelated to disease activity, adiposity or metabolic syndrome. The beneficial effect of anti-TNF-alpha therapy on cardiovascular mortality in RA does not seem to be mediated by changes in serum levels of visfatin.
19492413 CCL20/CCR6 chemokine/receptor expression in bone tissue from osteoarthritis and rheumatoid 2009 Oct Subchondral bone remodeling in osteoarthritis (OA) and rheumatoid arthritis (RA) is mainly characterized by the formation of osteophytes/fibrosis and by the presence of infiltrating cells associated to bone resorption. In this study we analyzed CC (cysteine cysteine motif) chemokine ligand (CCL)20 and CC chemokine receptor (CCR)6 function in subchondral bone tissue and osteoblasts isolated from OA and RA patients. CCL20/CCR6 expression was evaluated by immunohistochemical techniques in bone tissue from OA and RA patients. CCL20-functional tests were performed on osteoblasts isolated from OA and RA patients to evaluate enzymatic response and cell proliferation. Moreover, we assessed Akt phosphorylation as the major signaling pathway for CCL20. In bone tissue biopsies we found that osteoblasts from both OA and RA patients expressed CCR6 while CCL20 was expressed only by RA osteoblasts. Both CCR6 and CCL20 were highly expressed in osteocytes and mononuclear cells from only RA patients. CCL20-stimulated OA osteoblasts showed a significant increase in beta-N-acetylhexosaminidase release compared to RA. Conversely, a significant increase in cellular proliferation was found only in CCL20-stimulated RA osteoblasts associated to Akt phosphorylation. These data were confirmed in bone tissue biopsies. This study demonstrates a different expression of CCL20-positive osteoblasts in OA versus RA disease that seem to be associated with the presence of infiltrating mononuclear cells. Moreover, CCL20 stimulation resulted in a greater proliferative response in RA osteoblasts compared to OA osteoblasts, mediated by Akt signaling, while OA osteoblasts showed increased enzymatic activity, thus suggesting a differential role of this chemokine in OA and RA.