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ID PMID Title PublicationDate abstract
19013374 Deforming arthropathy in systemic lupus erythematosus. 2008 Nov Systemic lupus erythematosus is an autoimmune and inflammatory disease characterized by a variety of symptoms, including arthropathy. The clinical presentation of joint involvement varies, ranging from arthralgia without erosions or deformity to an erosive arthropathy and severe functional disability. This paper reviews the main forms of deforming arthropathy observed in lupus patients. It includes a) non-erosive arthropathy (it is the most frequent form and characterized as Jaccoud's), b) erosive symmetrical polyarthritis with deformities similar to rheumatoid arthritis, named as rhupus, and c) mild deforming arthropathy. Even though enough such cases of patients have been reported in the international bibliography, no definite criteria for their diagnosis have been published yet. The use of contemporary radiological and immunological methods will facilitate their prevention and treatment.
17317618 Interleukin-18 in chronic joint diseases. 2007 Mar Interleukin-18 is a cytokine member of the IL-1 super family that seems to exert powerful Th1-promoting activities in synergy with IL-12. Here we describe the participation of IL-18 in inflammatory joint diseases, in particular rheumatoid arthritis, adult onset Still's disease and juvenile idiopathic arthritis. The emphasis of this study was to summarize in vivo and in vitro studies that focused the action of this pro-inflammatory cytokine on the arthritic process as well as its role in the complex network of chemical mediators involved.
18227193 Incidence and characteristics of arthritis in Norwegian children: a population-based study 2008 Feb OBJECTIVE: The purpose of this work was to assess the annual incidence of arthritis in children and describe early disease and patient characteristics, microbiologic features, and immunogenetic factors in children with different subgroups of childhood arthritis. PATIENTS AND METHODS: A population-based multicenter study was performed in southeastern Norway between June 1, 2004, and May 31, 2005. The total population of children under 16 years of age was 255,303. Physicians were asked to refer their patients with suspected arthritis to the local department of pediatrics or rheumatology. The children were assessed on the basis of clinical, radiologic, and laboratory examinations at inclusion and followed up at 6 weeks, 6 months, and thereafter as long as clinically indicated. A chart review was performed to identify patients with arthritis who had not been included prospectively. RESULTS: The total annual incidence of arthritis was 71 per 100,000 children. Transient arthritis, juvenile idiopathic arthritis, postinfectious arthritis, and infectious arthritis were found in 43, 14, 9, and 5 of 100,000 children, respectively. The incidence was higher in children under the age of 8 years than in older children (107 vs 34 per 100,000). Arthritis occurred more frequently in boys than in girls before the age of 8 years but not thereafter. The median age of onset was lower in children with infectious arthritis than in those with other types of arthritis. Monarthritis was less frequent in patients with juvenile idiopathic arthritis than in the other subgroups (64% vs 83%-100%). Ten percent of the patients had poststreptococcal reactive arthritis, and only 1 had enteropathic arthritis. Autoantibodies and the presence of HLA-B27 were associated with juvenile idiopathic arthritis. CONCLUSIONS: The annual incidence of childhood arthritis was 71 per 100,000 children. We found several factors that may help in differentiating between subgroups of arthritis.
17828345 Laboratory findings in psoriatic arthritis. 2007 Psoriatic arthritis (PsA) has been classically defined as an inflammatory arthritis associated with psoriasis. However, in comparison with other relevant inflammatory arthropathies, in which a definite diagnosis is frequently possible only by means of laboratory investigations, in PsA true laboratory diagnostic markers are lacking. Some markers are utilised more to differentiate other diseases than to characterise PsA. For example in polyarticular PsA, which may be in some cases indistinguishable from RA, the rheumatoid factor (RF) or the more specific and recently introduced antibodies to cyclic citrullinated peptides (anti-CCP), may be useful to better identify RA. However, RF was found in 5% to 13% of patients with PsA, and anti-CCP may be observed in almost similar percentage. The determination of ESR and/or CRP is frequently disappointing in PsA, since they are both elevated in only half of the patients with PsA. However, ESR and/or CRP are included in the most utilised response criteria for RA, such as ACR and DAS, and, in addition are also considered reliable in the assessment of PsA. Furthermore, elevated levels of ESR have been proposed as one of the best predictors of damage progression and, in addition, a low ESR seems protective, while an ESR >15 mm/h is one of the factors associated with an increased mortality in PsA. The synovial fluid (SF) effusion is much higher in PsA, in comparison with other arthropathies. When available, SF analysis may offer additive information useful for the diagnosis, such as the increased number of leukocytes, which underlines the inflammatory nature of the effusion even in a patient with normal serum levels of acute phase response. We found that elevated IL-1 levels in SF of patients with early disease (<6 months), may be predictive of an evolution in polyarticular form at follow-up. This observation is in keeping with the crucial role that inflammatory cytokines play in PsA, probably related to a genetic predisposition. The recent introduction in PsA of anti-TNF-alpha agents and the demonstration of their efficacy in the management of many clinical disease expressions including peripheral arthropathy, axial involvement, enthesopathy and skin manifestations, have stimulated the research also in the field of the possible laboratory markers.
18035319 Infections, B cell receptor activation and autoimmunity: different check-point impairments 2007 Dec B cells as autoantibody producing cells are major players in several autoimmune chronic inflammatory diseases (ACIDs). In some particular settings (i.e. Sjogren's syndrome, rheumatoid arthritis), the activated B cells could undergo malignant clonal expansion. Chronic infections by lymphotropic viruses (hepatitis C virus, Epstein Barr Virus, Herpes 6 and 8 viruses) could amplify the activation process by inducing antiapoptotic signals that lead to a longer survival of B cell subsets. This might then lead, through multiple oncogenic events, to benign first and malignant thereafter clonal B cell expansion. Understanding how the B cell are activated, how the B cell receptor activation can be maintained under control, which check-points could be deregulated and lead to a persistent activation is of crucial importance in benign and malignant diseases. The evidence suggests that the B cells faulty check-points are different in chronic lymphocytic leukaemia, in cryoglobulinemia, rheumatoid arthritis, systemic lupus erythematosus and systemic sclerosis.
16788537 [Ultrasound features of entesopathy in patients with psoriatic dactylitis]. 2006 Jun PURPOSE: To describe the sonographic features of entesopathy in patients with psoriatic dactylitis. Materials and methods. Clinical, radiographic and sonographic evaluation of 120 hand joints with clinical abnormality including 20 fingers in 17 patients with rheumatoid arthritis (RA) and 20 fingers in 17 patients with psoriatic arthritis (PA). RESULTS: Forty cases of dactylitis. In patients with RA: 29 cases of synovitis, 15 cases of tenosynovitis, and 2 cases of tendinitis; in patients with PA: 21 cases of synovitis and 3 cases of tenosynovitis. Bone erosions were present in RA patients whereas erosions with bone production were present in PA patients. A total of 60% of RA and PA patients showed erosions on conventional radiographs. Features suggesting entesopathy were present in PA patients only: specific changes of P3, capsular hyperostosis and periarticular periostitis. CONCLUSION: Based on evaluation of PA patients, it seems that sonographic features suggesting entesopathy in patients with dactylitis may be present.
18759291 Extracellular high mobility group box chromosomal protein 1 is a coupling factor for hypox 2008 Sep OBJECTIVE: Tissue hypoxia is closely associated with arthritis pathogenesis, and extracellular high mobility group box chromosomal protein 1 (HMGB-1) released from injured cells also has a role in arthritis development. This study was thus undertaken to investigate the hypothesis that extracellular HMGB-1 may be a coupling factor between hypoxia and inflammation in arthritis. METHODS: Concentrations of tumor necrosis factor alpha, interleukin-6, vascular endothelial growth factor, lactic acid, lactate dehydrogenase, and HMGB-1 were measured in synovial fluid (SF) samples from patients with inflammatory arthropathy (rheumatoid arthritis and pseudogout) and patients with noninflammatory arthropathy (osteoarthritis). The localization of tissue hypoxia and HMGB-1 was also examined in animal models of collagen-induced arthritis (CIA). In cell-based experiments, the effects of hypoxia on HMGB-1 release and its associated cellular events (i.e., protein distribution and cell viability) were studied. RESULTS: In SF samples from patients with HMGB-1-associated inflammatory arthropathy (i.e., samples with HMGB-1 levels >2 SD above the mean level in samples from patients with noninflammatory arthropathy), concentrations of HMGB-1 were significantly correlated with those of lactic acid, a marker of tissue hypoxia. In CIA models in which the pathologic phenotype could be attenuated by HMGB-1 neutralization, colocalization of HMGB-1 with tissue hypoxia in arthritis lesions was also observed. In cell-based experiments, hypoxia induced significantly increased levels of extracellular HMGB-1 by the cellular processes of secretion and/or apoptosis-associated release, which was much more prominent than the protein release in necrotic cell injury potentiated by oxidative stress. CONCLUSION: These findings indicate that tissue hypoxia and its resultant extracellular HMGB-1 might play an important role in the development of arthritis.
18073234 Polysomnography and self-reported sleep, pain, fatigue, and anxiety in children with activ 2008 Apr OBJECTIVE: To compare polysomnography (PSG) and self-reported sleep, symptoms (pain and fatigue), and anxiety between children with active and inactive juvenile rheumatoid arthritis (JRA) and examine relations among sleep, symptoms, and anxiety. METHODS: Two consecutive nights of PSG, self-reported sleep, and symptoms were obtained in 70 children 6-11 years of age with active (n = 35) or inactive (n = 35) JRA. RESULTS: On the second (study) night, PSG and self-reported sleep variables were not different, but pain and fatigue were significantly higher (both p <.02) in children with active compared to inactive disease. In a stepwise regression, age, medications, disease status, anxiety, evening pain, total sleep time, and arousals explained 36% of the variance in fatigue and age, disease status, and evening pain were significant (all p <.04) predictors of fatigue. All children showed longer sleep latency and reduced sleep efficiency on the first night in the laboratory. CONCLUSIONS: Sleep was not altered in children with active JRA, however, the "first night effect" suggests that valid laboratory sleep assessments require an adaptation night.
17442092 Livedoid vasculopathy and hypercoagulability in a patient with primary Sjögren's syndrome 2007 Apr BACKGROUND: A 31-year-old woman presented with a 5-year history of painful ulcerations, palpable purpura, porcelain-white atrophic scars of the malleolar region and dorsal aspect of the feet, livedo reticularis on the limbs, arthralgia, xerophthalmia, and xerostomia. METHODS: Skin biopsy revealed vessel wall hyalinization and thrombosis of the microvasculature with a very scarce dermal inflammatory infiltrate. Biopsy of the oral mucosa showed mononuclear infiltration of an intralobular duct of a salivary gland. RESULTS: Laboratory studies, including autoantibodies and inflammation markers, were normal, except for a positive rheumatoid factor. Coagulation screening revealed C677T methylenetetrahydrofolate reductase (MTHFR) mutation, with a normal serum homocysteine. The patient was treated with oral methylprednisolone (32 mg/day with progressive reduction) and enoxaparin (20 mg/day subcutaneously), with complete ulcer healing within 4 months. CONCLUSION: Livedoid vasculitis or vasculopathy has not been referred to previously in association with Sjögren's syndrome, but may be associated with other autoimmune disorders and anomalies of coagulation, namely factor V Leiden mutation, protein C deficiency, and MTHFR mutation, associated or not with hyperhomocysteinemia, a condition that seems to confer an increased risk of recurrent arterial and venous thrombosis. We stress the importance of anticoagulant therapy for ulcer healing and for the prevention of other thrombotic events.
18577440 Therapeutic effect of tripterine on adjuvant arthritis in rats. 2008 Aug 13 AIMS OF THE STUDY: Tripterygium wilfordii Hoog f., a perennial vine, is used in traditional Chinese medicine for treatment of rheumatoid arthritis. This study was to determine whether tripterine, isolated from Tripterygium wilfordii Hoog f., had therapeutic effects on adjuvant arthritis. MATERIALS AND METHODS: Adjuvant arthritis (AA) was induced in rats on day 0. Tripterine 5, 10 and 20 mg kg(-1)day(-1), or prednisone 10 mg kg(-1)day(-1) was given to rats intragastrically from day 19 to day 24. RESULTS: Tripterine significantly inhibited paw swelling and bone destruction in AA rats. Serum level of IgG anti-Mycobacterium tuberculosis antibodies and delayed-type hypersensitivity (DTH) induced by Mycobacterium tuberculosis were also decreased by tripterine. The effects of tripterine were associated with decreased interleukin-1beta (IL-1beta) mRNA expression in ankle joint synovial membrane and tumor necrosis factor-alpha (TNF-alpha) mRNA expression in homogenized paws from adjuvant-induced arthritic rats. CONCLUSIONS: These findings suggested that tripterine had a therapeutic effect on adjuvant arthritis.
17849730 A conversation with Arthur Kavanaugh. 2007 Jul Biologic therapies play a greater role in the treatment of human autoimmune diseases than they did in the past. Arthur Kavanaugh, MD, Professor of Clinical Medicine, University of California, San Diego, School of Medicine, talked with Managed Care Interface about the use of these agents, ongoing research in this area, and genetic factors that can come into play when treating rheumatoid arthritis.
17309127 High prevalence of serum metabolic alterations in primary Sjögren's syndrome: influence o 2007 Apr OBJECTIVE: To analyze the prevalence and clinical significance of associated metabolic alterations [dyslipidemia, diabetes mellitus (DM), and hyperuricemia] in a large series of unselected patients with primary Sjögren's syndrome (SS). METHODS: We analyzed 254 consecutive patients with primary SS who had a complete analytical followup study for at least 5 consecutive years. The control group consisted of 254 age and sex-matched patients without systemic autoimmune diseases consecutively followed during the same period in a primary care center. RESULTS: In comparison with controls, patients with primary SS showed a higher frequency of dyslipidemia (47% vs 33%; p = 0.002), DM (28% vs 18%; p = 0.006), and hyperuricemia (9% vs 4%; p = 0.007). The mean age at SS diagnosis was 10 years greater in patients with DM (p < 0.001) and hyperuricemia (p = 0.009). Hypercholesterolemia was associated with a lower frequency of immunological markers such as anti-Ro/SSA antibodies (p = 0.001), anti-La/SSB antibodies (p = 0.005), low C3 (p = 0.047), and low C4 levels (p = 0.030), while hypertriglyceridemia and DM were associated with a higher prevalence of extraglandular features, especially renal, liver, and vasculitic involvement. A higher prevalence of DM was found in patients treated with corticosteroids (40% vs 19%; p = 0.001). CONCLUSION: Patients with primary SS showed a higher prevalence of associated dyslipidemia, DM, and hyperuricemia in comparison with an age and sex-matched control group. Metabolic alterations were associated with a differentiated pattern of clinical and immunological SS expression, but not with SS-related therapies (except for the higher frequency of DM observed in patients treated with corticosteroids).
18466539 Identifying single-nucleotide polymorphisms responsible for the linkage signal of rheumato 2007 This study evaluated the utility of unrelated controls and flanking markers when performing joint modeling of linkage and association by the LAMP software (version 0.0.6) [Am J Hum Genet 2005, 76:934-949; Am J Hum Genet 2006, 78:778-792]. Analyses were conducted on the simulated rheumatoid arthritis (RA) data in Genetic Analysis Workshop 15 (GAW15), using single-nucleotide polymorphisms (SNPs) on chromosome 6 over the 100 simulated replicates. We found that the LOD score for testing association in the presence of linkage dramatically increased when unrelated controls were added to affected sib pairs (ASPs), and that choosing a sufficient number of flanking markers is critical in order to distinguish between perfect linkage disequilibrium (which leads to the conclusion of a measured SNP explaining a linkage signal) and incomplete linkage disequilibrium (which leads to the conclusion of other undetected causal variants in a linkage region).
22096344 Synergistic induction of CX3CL1 by TNF alpha and IFN gamma in osteoblasts from rheumatoid 2008 To explore the regulation of CX3CL1 in inflammatory bone diseases, CX3CL1 expression by osteoblasts (OB) was examined. Human OB isolated from rheumatoid arthritis (RA) patients, osteoarthritis patients, and normal individuals were incubated in the presence of cytokines. Soluble CX3CL1 levels were determined with an enzyme-linked immunosorbent assay. Expression of CX3CL1 mRNA was examined using quantitative real-time polymerase chain reaction. Although tumor necrosis factor (TNF)-α or interferon (IFN)-γ alone RA OB induced negligible CX3CL1 secretion, the combination of TNF-α and IFN-γ induced dramatic increases in both soluble CX3CL1 protein and mRNA transcripts. This synergistic effect was more pronounced in OB from RA than in OB from either osteoarthritis or normal individuals. The expression of CX3CL1 was markedly reduced by specific inhibitors of the nuclear factor-κB (NF-κB) or STAT-1 transcription factor. These findings suggest that osteoblasts are an important cellular source of CX3CL1 and may play roles in inflammatory bone/joint diseases.
18992831 Luteolin inhibits proliferation and affects the function of stimulated rat synovial fibrob 2009 Feb Hyperproliferation of synovial fibroblasts is considered to be a pivotal event in the pathogenesis of rheumatoid arthritis (RA). Luteolin, a flavonoid, inhibits the proliferation of synovial fibroblasts in collagen-induced arthritic rats. Treatment with luteolin also decreases the secretion of matrix metalloprotease-1 and -3 and the expression of IL-6, IL-8, IL-15, and TGF-beta. Luteolin treatment caused a delay of cells in the G(2)/M phase. Interestingly, combination treatment with luteolin and TNF-alpha exhibited a synergistic inhibitory effect in all experiments. Western blotting demonstrated that treatment with luteolin alone or combined with TNF-alpha inhibited the MAPK/ERKs and PI3K-Akt pathways. These results indicate that luteolin inhibits the proliferation and partially blocks the pathogenic function of synovial fibroblasts in rheumatoid arthritis.
20165551 Update on Targets of Biologic Therapies for Rheumatoid Arthritis. 2008 Nov 1 With the advent of biological therapies, considerable progress has been made in the treatment of rheumatoid arthritis (RA). These revolutionary therapies owe their origin to the role that cytokines play in the pathophysiology of the disease and are best exemplified by the wide use of tumor necrosis factor (TNF) blockade. The identification of additional pro-inflammatory factors and an understanding of their effector function now offer major possibilities for the generation of additional novel biological therapeutics to address unmet clinical needs. Such interventions will ideally fulfill several of the following criteria: control of inflammation, modulation of underlying immune dysfunction by promoting the reestablishment of immune tolerance, protection of targeted tissues such as bone and cartilage, and preservation of host immune capability to avoid profound immune suppression and amelioration of co-morbidity associated with underlying RA. The identification and characterization of the intracellular signaling pathways, in particular, the mitogen-activated protein kinase pathway, the nuclear factor-κB pathway and the cross-talk between these pathways offer several potential therapeutic opportunities. This review will provide an update on cytokine activities and signal transduction pathways that represent, in our opinion, optimal utility as future therapeutic targets.
16785825 Cyclooxygenase-2 and nitric oxide. 2006 Nitric oxide (NO) is a simple but pluripotent molecule that is mainly released from vascular endothelial cells where it is formed intracellularly by nitric oxide synthase from L-arginine in response to several stimuli, including shear stress or muscarinic receptor stimulation. NO stimulates guanylyl cyclase to form cyclic guanosine monophosphate, which results in relaxation and vasodilatation of vascular smooth muscle cells (VSMCs). In addition, NO prevents adhesion and aggregation of platelets, and it possesses anti-inflammatory, antiproliferative, and antimigratory effects on leukocytes, endothelial cells, and VSMCs, thus offering protection from atherosclerosis. Dysfunction of the vascular endothelium has been documented in most conditions that promote or are associated with atherosclerosis and is characterized by a reduced bioavailability of NO. The healthy endothelium prevents adhesion and migration of leukocytes, proliferation of VSMCs, and platelet adhesion and aggregation. Maintaining the balance of blood flow and thrombus formation is also a major task of the vascular endothelium. It has been shown that both NO and prostacyclin, a cyclooxygenase-derived relaxing factor, inhibit activation of platelets and regulate vasomotion. Reduced NO and prostacyclin levels can result in endothelial dysfunction, which is recognized as the first step in the atherogenic process. It is of note that chronic inflammation conditions, such as rheumatoid arthritis, are associated with endothelial dysfunction. The reduced NO bioavailability may therefore explain the increased risk for cardiovascular events in patients with chronic low-grade inflammation, such as rheumatoid arthritis and osteoarthritis. Thus, this article provides an overview of the impact of inflammation and anti-inflammatory treatment with cyclooxygenase inhibitors on endothelial function.
17569223 Curcumin and autoimmune disease. 2007 The immune system has evolved to protect the host from microbial infection; nevertheless, a breakdown in the immune system often results in infection, cancer, and autoimmune diseases. Multiple sclerosis, rheumatoid arthritis, type 1 diabetes, inflammatory bowel disease, myocarditis, thyroiditis, uveitis, systemic lupus erythromatosis, and myasthenia gravis are organ-specific autoimmune diseases that afflict more than 5% of the population worldwide. Although the etiology is not known and a cure is still wanting, the use of herbal and dietary supplements is on the rise in patients with autoimmune diseases, mainly because they are effective, inexpensive, and relatively safe. Curcumin is a polyphenolic compound isolated from the rhizome of the plant Curcuma longa that has traditionally been used for pain and wound-healing. Recent studies have shown that curcumin ameliorates multiple sclerosis, rheumatoid arthritis, psoriasis, and inflammatory bowel disease in human or animal models. Curcumin inhibits these autoimmune diseases by regulating inflammatory cytokines such as IL-1beta, IL-6, IL-12, TNF-alpha and IFN-gamma and associated JAK-STAT, AP-1, and NF-kappaB signaling pathways in immune cells. Although the beneficial effects of nutraceuticals are traditionally achieved through dietary consumption at low levels for long periods of time, the use of purified active compounds such as curcumin at higher doses for therapeutic purposes needs extreme caution. A precise understanding of effective dose, safe regiment, and mechanism of action is required for the use of curcumin in the treatment of human autoimmune diseases.
20706557 Targeting Angiogenesis in Rheumatoid Arthritis. 2008 Nov 1 Angiogenesis, the development of new capillaries, is a crucial process in health and disease. The perpetuation of neovascularization in rheumatoid arthritis is highly involved in leukocyte extravasation into the synovium and pannus formation. Numerous soluble and cell surface-bound angiogenic mediators, including growth factors, cytokines, proteases, matrix macromolecules, cell adhesion receptors, chemokines and chemokine receptors, have been implicated in the process of neovascularization. Endogenous angiostatic factors, primarily angiostatin, endostatin, IL-4, IL-13, some angiostatic chemokines may be used to downregulate neovascularization. In addition, angiogenesis might be targeted by several specific approaches against VEGF, angiopoietin, α(v)β(3) integrin or by exogenously administered compounds including DMARDs, anti-TNF agents, fumagillin analogues or thalidomide. Potentially all anti-angiogenic could be tried in order to control synovitis.
17401566 Outcome of patients with arthritis and parvovirus B19 DNA in synovial membranes. 2007 Jun To investigate the follow-up of the 17 patients during the period of 1995-2001 of the outpatient Clinic for Rheumatology at the University Hospital of Zurich with arthritis and the presence of parvovirus B19 DNA demonstrated by PCR in synovial biopsies. Seventeen patients of 163 with arthritis, which were routinely examined by needle arthroscopy during 1995-2001 with a positive parvovirus B19 DNA by PCR of synovial biopsy were reevaluated. Investigations included medical history, clinical examination and blood tests. Joint fluid was taken on patients with joint effusion. The observation period of the 17 patients (F:M = 11:6) was 2-8 years (Ø = 6.5 years). In 8 of 17 patients the arthritis could not be classified neither at entry nor during the follow up of the study. The arthritis could be diagnosed in six patients early in the onset of the disease and included three cases of lyme arthritis of the knee joint, two cases with arthritis following a gastrointestinal infection (one with Salmonella typhimurium--positive faecal test--and the other one with a culture negative agent), one patient probably had an infection-associated arthritis after a gastrointestinal infection with Entamöeba histolytica (Schirmer et al. in Rheumatol Int 18:37-38, 1998; Kasliwal in Am J Proctol Gastroenterol Colon Rectal Surg 32:12, 16, 28, 1981; Haslock and Wright in J R Coll Phys Lond 8:1554-162, 1974; Than-Saw et al. in Trop Geogr Med 44:355-358, 1992) with remission after antibiotic therapy. After a disease course of 9 months one patient could be classified as rheumatoid arthritis in the presence of anti-cyclic citrullinated antibodies but lack of rheumatoid factor. One patient with polyarthritis developed psoriasis of the skin 22 months later. From the nine patients with unclassified arthritis 4 (45%) got into complete remission with no symptoms or signs of joint inflammation after a disease course of 9-45 months, whereas 5 (55%) still demonstrate active non erosive arthritis (disease duration between 3 and 10 years). The presence of parvovirus B19 DNA in synovial tissue of patients with joint inflammation does not allow the diagnosis of parvovirus induced arthritis. If the arthritis remains unclassified and without erosions over time a virus associated aetiology may be assumed. However, no definitive diagnosis is possible even in the presence of parvovirus B19 DNA in synovial tissue.