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PubMed2001

From reactive arthritis to rheumatoid arthritis.

Reactive arthritis was initially described as a sterile synovitis, without microbial components present in the joint tissue. It has, however, become evident that bacterial degradation products, and even bacterial DNA, are present in the synovium of patients with this disease. Since intestinal pathogens are important causes of reactive arthritis, and since cellular homing allows transport of bacterial products from the gut to synovium, we have approached the etiology of rheumatoid arthritis from this point of view. A series of observations has led to a hypothesis that patients with rheumatoid arthritis might favour, for genetic reasons, intestinal bacteria which are capable of inducing arthritis. In the long-run, with continuous seeding of bacterial products from the gut, the synovial inflammation is followed by erosion, exposition of cartilage antigens, and autoimmunity.

Animals↗

PubMed2002

Immunization of rats with homologous type XI collagen leads to chronic and relapsing arthritis with different genetics and joint pathology than arthritis induced with homologous type II collagen.

The most commonly used animal model for rheumatoid arthritis (RA) is collagen-induced arthritis (CIA), induced by immunization with type II collagen (CII), a cartilage restricted protein. In this work we show that type XI collagen (CXI), which is a minor component in cartilage, induces a different form of erosive and chronic relapsing polyarthritis in rats. Using a series of inbred rat strains involving various genetic backgrounds (DA, LEW, E3), and congenic MHC regions (a, u, f, n, c, d), we found that CXI induced arthritis (C(XI)IA) is associated with the RT1f haplotype in contrast to CII induced arthritis (C(II)IA), which is associated with the RT1a and RT1u haplotypes. The C(XI)IA follows a chronic disease course affecting peripheral joints with both progression and relapses, which appear not to cease (occurring >800 days). Susceptible strains showed a sustained antibody response to CXI with time indicating that the autoimmune response was self-perpetuated. Microscopic analysis of the joints at different stages demonstrated the severe destruction of bone and cartilage by pannus tissue consisting of activated macrophages and T cells. The main difference to joints from rats with C(II)IA was larger numbers of infiltrating lymphocytes and these tended to form follicle-like aggregates. Surprisingly, males were more susceptible to C(XI)IA than females whereas the opposite has been observed in other rat arthritis models, including C(II)IA. Taken together, C(XI)IA is a chronic relapsing and erosive polyarthritis that is MHC associated, which in fact fulfills the criteria for diagnosis of RA. Thus the C(XI)IA model will be useful as a novel and relevant animal model for RA.

Animals↗

PubMed1997

Septic arthritis due to bacteroides fragilis after pilonidal sinus resection in a patient with rheumatoid arthritis.

Bacteroides fragilis is a rare cause of septic arthritis. Most patients with B. fragilis septic arthritis have a chronic joint disease, particularly rheumatoid arthritis, and sources of infection are lesions of the gastrointestinal tract and the skin. We report a 69-year-old male, who developed B. fragilis septic arthritis after pilonidal sinus resection. High level of suspicion of development B. fragilis septic arthritis must be present in patients with chronic joint disease in whom gastrointestinal or skin surgery was previously performed.

Aged↗

PubMed1996

Expression of TNF alpha in arthritis caused by caprine arthritis encephalitis virus.

Goats infected with caprine arthritis encephalitis virus (CAEV) develop chronic arthritis sharing many features with human rheumatoid arthritis (RA). TNF is thought to be a key mediator contributing to the formation of the arthritic lesion in RA. We studied this cytokine in goats suffering from chronic arthritis. TNF alpha expressing cells were detected by in situ hybridization in synovial membranes of arthritic carpal joints. Expression of TNF alpha did not correlate with the degree of viral replication as assessed by in situ hybridization for viral RNA. In line with the lack of correlation between the degree of viral replication and TNF expression in vivo, we failed to detect increased cytokine RNA in goat macrophages infected with CAE virus in vitro and no TNF protein was found in culture supernatants. In addition, virus infection failed to prime goat macrophages for enhanced TNF expression in response to lipopolysaccharide. Taken together, these findings argue against a direct role of CAE virus in increasing the expression of TNF alpha in caprine arthritis.

Animals↗

PubMed1983

Acute suppurative arthritis of the temporomandibular joint in a patient with rheumatoid arthritis.

Septic arthritis of the temporomandibular joint is a rare condition. A case of acute staphylococcal suppurative arthritis of the temporomandibular joint (TMJ) complicating rheumatoid arthritis (RA) in a 53 year old woman is reported. The aetiology of septic arthritis may be traced to several predisposing factors and many specific agents. It would appear that the case presented is the result of predisposition of patients known to have RA to the complication septic arthritis. Some treatment recommendations are given.

Acute Disease↗

PubMed1989

A specific HLA-DP beta allele is associated with pauciarticular juvenile rheumatoid arthritis but not adult rheumatoid arthritis.

Nonradioactive sequence-specific oligonucleotide probes specific for the HLA-DP beta locus have been used in a simple dot-blot format to type samples amplified by the polymerase chain reaction from 44 patients with pauciarticular juvenile rheumatoid arthritis, 32 patients with adult rheumatoid arthritis, and 50 random controls. The sequences of four new DP beta alleles derived from these patients and controls are reported, bringing the total number of alleles identified thus far to 19. The DPB2.1 allele is significantly increased in juvenile rheumatoid arthritis patients over controls; this allele is not increased in patients with adult rheumatoid arthritis. The association of juvenile rheumatoid arthritis with the DPB2.1 allele is independent of linkage with previously defined HLA-D region markers of disease. Analysis of the DPB2.1 sequence shows that it differs from the nonsusceptible DPB4.2 allele by only 1 amino acid at position 69 in the beta 1 domain.

Adolescent↗

PubMed2004

Role of major histocompatibility complex genes in murine collagen-induced arthritis: a model for human rheumatoid arthritis.

Collagen-induced arthritis is an animal model for rheumatoid arthritis that shares a number of clinical, hematologic, serologic, and radiographic features with human disease. Predisposition to rheumatoid arthritis has been associated with major histocompatibility complex (MHC) class II genes, HLA-DRB*0401/DQB1*0302 and resistance to DRB1*0402 and DQ6 genes. Animal models allow one to study the genetics and immunologic processes of individual genes involved in the complex human diseases. To study the interactions between class II molecules and to define their role in arthritis, the authors generated HLA-DR and -DQ transgenic mice. HLA transgenes are expressed on cell surface and can positively select CD4 cells. A peripheral tolerance is maintained to the trans-genes even though an efficient T cell response to immunodominant antigens similar to human T cells is observed. Using HLA-DQ/DR double transgenic mice, the studies show that complementation between DQ and DR molecules contributes to predisposition to and severity of, or protection from, arthritis. Thus, these mice provide a powerful tool to understand the role of HLA molecules in the predisposition to and immunotherapy for human disease.

Amino Acid Sequence↗

PubMed2004

Septic arthritis in a patient with juvenile rheumatoid arthritis.

The acute flare of joint inflammation in the child with known juvenile rheumatoid arthritis causes concern primarily regarding the need for additional or modified medical treatment. Acute joint inflammation in an otherwise healthy child creates concern regarding the existence of joint infection. In the early phase of disease, the clinical findings and symptoms of an inflamed joint attributable to juvenile rheumatoid arthritis or infection may be similar and difficult to differentiate from the other. Juvenile rheumatoid arthritis usually is well controlled by medical interventions, however, the initiation of specific treatment is more urgent in children with joint sepsis. The following case report is presented to emphasize the difficulty in evaluation of patients with known juvenile rheumatoid arthritis and coexistent septic arthritis, and to discuss the methods used to differentiate between the two conditions.

Adolescent↗

PubMed2006

Relapsing oligoarticular septic arthritis during etanercept treatment of rheumatoid arthritis.

Septic arthritis is a commonly reported complication of rheumatoid arthritis (RA). Tumor necrosis factor alpha (TNF-alpha) plays an important role in host defense against infection. Inhibition of its activity could therefore be anticipated to augment the risk of infection. Both opportunistic and bacterial infections have been described in patients with RA treated with anti-TNF-alpha therapy. We describe a patient who experienced 2 episodes of septic arthritis. Both occurred while the patient was on etanercept. Recurrence developed despite prolonged parenteral antibiotic. To our knowledge, this is the first report of relapsing oligoarticular methicillin-sensitive Staphylococcus aureus septic arthritis despite prolonged antibiotic treatment in a patient receiving etanercept therapy. Our case underscores the advisability of discontinuing TNF-alpha blockade in patients with septic arthritis during prolonged antimicrobial therapy.

Aged↗

PubMedDate not supplied

The effect of pregnancy on ankylosing spondylitis, psoriatic arthritis, and juvenile rheumatoid arthritis.

It has long been established that rheumatoid arthritis improves during pregnancy. The gestational course of other inflammatory arthritides like ankylosing spondylitis (AS), psoriatic arthritis (PsA), and juvenile rheumatoid arthritis (JRA) has been less well studied. The present review summarizes the results of our retrospective and prospective studies on the interaction between these diseases and pregnancy. The results showed clear differences for their gestational course. Patients with PsA improved or even remitted in 80% of the pregnancies, whereas 80% of the AS patients had unaltered or aggravated disease symptoms. The 20% of AS patients who markedly improved while pregnant all had AS with accompanying diseases like psoriasis, ulcerative arthritis, or small joint arthritis. Quiescent JRA was not reactivated by pregnancy, and active disease at conception ameliorated in about 60%. Fetal outcome was not adversely affected by AS, PsA, or JRA nor did there occur serious intercurrent diseases during pregnancy. In AS and PsA patients delivery was mainly uncomplicated. Sequelae of JRA were a frequent cause for cesarean section in JRA patients. A postpartum flare during the first 3 months after delivery occurred in about 90% of the AS pregnancies, 70% of the PsA pregnancies, and about 50% of the JRA pregnancies.

Arthritis, Juvenile↗

PubMed1978

Nitroblue tetrazolium test in psoriatic arthritis, rheumatoid arthritis, and osteoarthrosis.

Nitroblue tetrazolium test scores were obtained in 43 patients with psoriatic arthritis, 32 patients with rheumatoid arthritis, and 16 patients with osteoarthrosis. The mean score in all groups was similar and was higher than previously reported in patients awaiting heart surgery or with noninfective dermatoses. The test is not thought to be helpful in differentiating psoriatic arthritis from rheumatoid arthritis, and its usefulness in the diagnosis of septic arthritis superimposed on other forms of arthropathy is limited.

Arthritis↗

PubMed1989

Acute non-infectious arthritis of the hip in rheumatoid arthritis: synovial membrane findings.

A case of acute hip pain in rheumatoid arthritis is presented, with synovial membrane findings. A patient with classical rheumatoid arthritis suffered three unusual bouts of sudden, severe but transient hip pain. The hips were clinically normal between these episodes. The clinical picture on two of these occasions strongly suggested septic arthritis. Although the synovial fluid was highly inflammatory, cultures were negative. The synovial membrane showed mild lining cell hyperplasia, vascular congestion, and scattered inflammatory cells, predominantly lymphocytes. These findings were not compatible with either pyogenic infection or longstanding rheumatoid arthritis. The clinical and pathological features of acute non-infectious arthritis of the hip appear to delineate a distinct syndrome.

Acute Disease↗

PubMed2004

Collagen-induced arthritis as a model for rheumatoid arthritis.

Collagen-induced arthritis (CIA) is an animal model of rheumatoid arthritis (RA) that is widely used to address questions of disease pathogenesis and to validate therapeutic targets. Arthritis is normally induced in mice or rats by immunization with autologous or heterologous type II collagen in adjuvant. Susceptibility to collagen-induced arthritis is strongly associated with major histocompatibility complex class II genes, and the development of arthritis is accompanied by a robust T- and B-cell response to type II collagen. The chief pathological features of CIA include a proliferative synovitis with infiltration of polymorphonuclear and mononuclear cells, pannus formation, cartilage degradation, erosion of bone, and fibrosis. As in RA, pro-inflammatory cytokines, such as tumor necrosis factor alpha(TNFalpha) and interleukin (IL)-1beta, are abundantly expressed in the arthritic joints of mice with CIA, and blockade of these molecules results in a reduction of disease severity.

Animals↗

PubMed1998

AP-1 and NF-kappaB regulation in rheumatoid arthritis and murine collagen-induced arthritis.

OBJECTIVE: To determine the expression and regulation of nuclear transcription factors AP-1 and NF-kappaB in rheumatoid arthritis and in collagen-induced arthritis in mice. METHODS: AP-1 and NF-kappaB expression and function were determined in RA, OA and normal synovial tissue by electrophoretic mobility shift assay (EMSA) and immunohistochemistry. The kinetics of transcription factor expression were then examined in collagen-induced arthritis (CIA) in mice. EMSAs were performed with the nuclear extracts obtained from paws of CIA mice from 10 to 45d after immunization to determine AP-1 and NF-kappaB binding activity. The expression of collagenase-3 (MMP13) and stromelysin (MMP3) mRNA was examined by northern blot analysis. RESULTS: Immunohistochemistry showed that NF-kappaB expression was increased in both RA and OA synovial intimal lining. AP-1 components Jun and Fos were also present in the intimal lining and was significantly greater in RA than OA. The DNA binding activities of both AP-1 and NF-kappaB were significantly higher RA patients compared with OA. In CIA, AP-1 and NF-kappaB expression increased by day 20, which was 1-2 weeks before onset of clinical arthritis. However, collagenase and stromelysin gene expression did not increase until day 35. CONCLUSION: The DNA binding activity of AP-1 and NF-kappaB are markedly increased in both CIA and RA. In CIA, activation of AP-1 and NF-kappaB precede both clinical arthritis and metalloproteinase gene expression. NF-kappaB expression correlated better than AP-1 with metalloproteinase expression.

Animals↗

PubMed2003

Soluble IL-6 receptor governs IL-6 activity in experimental arthritis: blockade of arthritis severity by soluble glycoprotein 130.

Studies in IL-6-deficient (IL-6(-/-)) mice highlight that IL-6 contributes to arthritis progression. However, the molecular mechanism controlling its activity in vivo remains unclear. Using an experimental arthritis model in IL-6(-/-) mice, we have established a critical role for the soluble IL-6R in joint inflammation. Although intra-articular administration of IL-6 itself was insufficient to reconstitute arthritis within these mice, a soluble IL-6R-IL-6 fusion protein (HYPER-IL-6) restored disease activity. Histopathological assessment of joint sections demonstrated that HYPER-IL-6 increased arthritis severity and controlled intrasynovial mononuclear leukocyte recruitment through the CC-chemokine CCL2. Activation of synovial fibroblasts by soluble IL-6R and IL-6 emphasized that these cells may represent the source of CCL2 in vivo. Specific blockade of soluble IL-6R signaling in wild-type mice using soluble gp130 ameliorated disease. Consequently, soluble IL-6R-mediated signaling represents a promising therapeutic target for the treatment of rheumatoid arthritis.

Animals↗

PubMed1979

Chronic Lyme arthritis. Clinical and immunogenetic differentiation from rheumatoid arthritis.

Ten patients with Lyme arthritis have developed chronic involvement of one or both knees. Lyme arthritis was diagnosed by onset with erythema chronicum migrans (six patients); residence in Lyme, Connecticut (eight); seasonal onset in summer and early fall (nine); early periods of short recurrent attacks (nine); absence of rheumatoid factor (nine); and absence of symmetrical polyarthritis, morning stiffness, subcutaneous nodules, or antinuclear antibodies (in all). Five patients had synovectomies; pannus formation and underlying cartilage erosion were present in all. Seven of the 10 patients had the same B-cell alloantigen, DRw2 (frequency in normal control subjects, 22% [P less than 0.005]), but did not have an increased frequency of the alloantigens associated with rheumatoid arthritis. Chronic Lyme arthritis, the result of an apparent tick-transmitted infection, resembles rheumatoid arthritis pathologically but generally differs from it in both prearticular and immunogenetic characteristics.

Adolescent↗

PubMed2002

[Immunopathogenesis of inflammatory arthritis: lesson from Lyme and rheumatoid arthritis].

Arthritis is a common manifestation of late Lyme disease and can develop into an erosive arthritis with histopathologic similarities to rheumatoid arthritis (RA). The development of persistent arthritis and in some cases cartilage and bone erosion is the result of autoimmune phenomena that develop after contact with Borrelia burgdorferi. Analysis of the host-pathogen interaction and immunopathogenic factors in Lyme arthritis are presented in this study.

Antibodies, Bacterial↗

PubMed2005

[Cricoarytenoid arthritis diagnosed after tracheostomy in a rheumatoid arthritis patient].

A 65-year-old woman was scheduled for total knee replacement. She had been suffering from rheumatoid arthritis for 22 years. She also had a history of occasional acute dyspnea, which had been diagnosed as asthmatic bronchitis. Preoperative examinations of the airway revealed limited neck flexion, a small jaw, and normal mouth opening. After epidural catheterization, anesthesia was induced with propofol, and a #3 laryngeal mask airway (LMA) was inserted. However, her lungs could not be ventilated through the LMA. Despite repeated attempts, proper placement of the LMA could not be achieved. Hence, a 7.0 mm ID armored endotracheal tube was inserted through an intubating LMA. Anesthesia was maintained with nitrous oxide and sevoflurane in oxygen. The surgery proceeded uneventfully. Five minutes after extubation, inspiratory dyspnea occurred. The patient's trachea was re-intubated nasally with a bronchofiberscope. Since the bronchofiberscopy revealed remarkable laryngeal edema, percutaneous tracheostomy was performed. On the 3 rd postoperative day, cricoarytenoid arthritis that had caused occasional airway obstruction was diagnosed, although her laryngeal edema disappeared. She went home with a permanent tracheostomy. Although cricoarytenoid arthritis is a common occurrence in patients with rheumatoid arthritis, the diagnosis can be difficult. A scrupulous preoperative evaluation and awareness of cricoarytenoid arthritis are necessary for optimal anesthetic management.

Aged↗