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ID PMID Title PublicationDate abstract
27820156 Periodontal Disease as a Risk Factor for Rheumatoid Arthritis: A Systematic Review. 2012 REVIEW OBJECTIVE: The objective of this systematic review is to identify and synthesise the best available evidence to examine whether periodontal disease is a risk factor for rheumatoid arthritis. BACKGROUND: Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology and has a complex multifactorial pathogenesis affecting joints and other tissues. The natural history of rheumatoid arthritis is poorly defined; its clinical course fluctuates and the prognosis unpredictable. Rheumatoid arthritis affects up to 1-3% of the population, with a 3:1 female preponderance disappearing in older age. There is also evidence of a genetic predisposition to the disease. Rheumatoid arthritis is characterised by progressive and irreversible damage of the synovial-lined joints causing loss of joint space, bone and function, leading to deformity. Extracellular matrix degradation is a hallmark of rheumatoid arthritis which is responsible for the typical destruction of cartilage, ligaments, tendons, and bone.Rheumatoid arthritis is characteristically a symmetric arthritis (symmetrical swelling of the joints). Articular and periarticular manifestations include joint swelling and tenderness to palpation, with morning stiffness and severe motion impairment in the involved joints. Extra-articular signs can involve pulmonary, cardiovascular, nervous, and reticuloendothelial systems. The clinical presentation of rheumatoid arthritis rheumatoid arthritis varies, but an insidious onset of pain with symmetric swelling of the small joints is the most frequent finding. Rheumatoid arthritis onset is acute or subacute in about 25% of patients. Early rheumatoid arthritis is characterised by symmetric polyarthritis involving the small joints of the hands and feet with no radiologic changes. Rheumatoid arthritis most frequently affects the metacarpophalangeal, proximal interphalangeal and wrist joints. Although any joint, including the cricoarytenoid joint, can be affected, the distal interphalangeal, the sacroiliac and the lumbar spine joints are rarely involved, which is peculiar because these are some of the most typical targets of seronegative spondylarthropathies, such as psoriatic arthritis and ankylosing spondylitis. The clinical manifestations of rheumatoid arthritis vary, depending on the involved joints and the disease stage. The clinical features of synovitis are particularly apparent in the morning. Morning stiffness in and around the joints, lasting at least 1 hour before maximal improvement is a typical sign of rheumatoid arthritis. It is a subjective sign and the patient needs to be carefully informed as to the difference between pain and stiffness. Morning stiffness duration is related to disease activity. Progression of rheumatoid arthritis can be measured by laboratory tests and clinical evaluation (questionnaires of disease activity and physical examination). Laboratory tests include blood tests for Rheumatoid factor (RF) and Acute-phase reaction tests while clinical evaluation can be measured by the Disease activity using the Disease Activity Score (DAS). Periodontitis is a destructive inflammatory disease of the dental supporting tissues which leads to erosion of bone around teeth resulting in tooth loss. Severe periodontitis affects about 5-15% of the adult population. In periodontitis, the clinical findings of bone resorption and loss of clinical attachment level around tooth are a result of inflammatory mediated alterations to the bone remodelling balance. The inflammatory infiltrate present between the plaque biofilm, bone and connective tissues regulate the host immune response to the bacteria. The host produces proteases and substances that degrade the extracellular matrix, and lead to resorption of the alveolar bone, resulting in irreversible loss of tissue attachment.Bone is a dynamic tissue and bone homeostasis involves the opposing events of resorption and apposition; dissolution of the existing bone mineral, resorption of the extracellular matrix, and formation of a new matrix. Bone homeostasis mechanisms maintain bone integrity in the alveolar bone (regulates periodontal bone loss) and, elsewhere in the body. It also functions to regulate the calcium balance within the body; this is an important ion as it is involved in the clotting of blood, formation of glandular secretions and regulation of the cardiac pacemaker.Rheumatoid arthritis and periodontitis are arguably the most prevalent chronic inflammatory diseases in humans and associated with significant morbidities. rheumatoid arthritis and periodontitis share similar clinical and pathogenic characteristics. Both rheumatoid arthritis and periodontitis present an imbalance between pro-inflammatory and anti-inflammatory cytokines, which is thought to be responsible for the tissue damage. In this sense, both conditions are associated with destruction of bone, mediated by inflammatory cytokines such as interleukin-1, tumour necrosis factor and prostaglandin E2.Several studies have suggested a relationship between periodontitis and rheumatoid arthritis; rheumatoid arthritis may have a negative impact on periodontal condition and vice versa. Mercado et al. in 2001 reported a significantly high prevalence of moderate to severe periodontitis in individuals with rheumatoid arthritis. In addition, the converse is true: periodontitis patients have a higher prevalence of rheumatoid arthritis compared to the general population. One study found that induction of experimental arthritis in rats resulted in periodontal destruction and increased cytokines and matrix metalloproteinases in the periodontal tissues.Oral bacterial DNA (deoxyribonucleic acids) is detected in serum and synovial fluid of patients with rheumatoid arthritis. Patients with rheumatoid arthritis also have a significantly higher level of immunoglobulin G antibody against P. gingivalis, Prevotella intermedia, and Tannerella forsythia. Furthermore, two recent clinical trials suggested that the treatment of periodontal disease might have a significant impact on rheumatoid arthritis severity. Similarly, subjects with rheumatoid arthritis have significantly increased periodontal attachment loss.In a recent research article, Ogrendik et al. in 2009 concluded that antibodies formed against these oral bacteria could be important to the aetiopathogenesis of rheumatoid arthritis. They recommended that gingival tissue infections should be considered in rheumatoid arthritis pathogenesis and that periodontal infections should be treated and prevented from becoming chronic. If successful results are observed against periodontal infections in clinical, radiologic, and laboratory data of the rheumatoid arthritis patients, the essential role of these bacteria in the aetiology of rheumatoid arthritis can be proven. One hypothesis that links rheumatoid arthritis and periodontitis is the recently published "two-hit" model that attempts to link experimental evidence from animal models and is supported by evidence from human clinical studies. In this theory, the first "hit" involves the periodontopathic subgingival biofilm and its microbial products, such as endotoxin. The second "hit" involves a medical systemic disease, such as rheumatoid arthritis, which increases biomarkers of systemic inflammation in the circulation, including C reactive protein (CRP), cytokines (e.g. IL-6), prostanoids (e.g. PGE2), and matrix metalloproteinases (e.g. MMP-9), and tumour necrosis factor alpha (TNF- α). These cytokines are thought to stimulate resident cells in the synovium and the periodontium to produce MMPs mediating connective tissue destruction, and induce the differentiation and activity of osteoclasts to destroy bone In particular, TNF-α, also promotes bone resorption: (i) by up-regulating inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO); and (ii) by modulating the receptor activator of nuclear factor _B (NF_B) ligand (RANKL) in osteoblasts, and its antagonist osteoprotegerin (OPG), thus altering the RANKL/OPG ratio, which enhances osteoclast activity, and finally, lead to periodontal breakdown. Most recently Bartold et al, reported a series of experiments to examine the plausibility of the "two hit" theory investigated whether the onset and severity of experimental arthritis in a rodent model was influenced by the presence of a pre-existing extra-synovial chronic inflammatory reaction to P. gingivalis. They discovered that severe arthritis developed more rapidly in animals with a pre-existing P. gingivalis induced inflammatory lesion, thus providing further evidence for a relationship between the presence of periodontal pathogen-associated inflammation and the development of rheumatoid arthritis. Aggressive periodontitis is rapid progression of periodontal disease with severe periodontal breakdown. The amount and pattern of periodontal destruction is very aggressive indicating there may be other characteristics in addition that contribute to its rate of destruction, and hence is outside of the scope of this review.Before undertaking this review, the JBI Library of Systematic Reviews, Cochrane Library of Systematic Reviews, Medline and CINAHL were searched. As no systematic review has been identified as been either published or underway on this topic, the aim of this systematic review is to identify and synthesise the best available evidence of periodontal disease as a risk factor for rheumatoid arthritis.
21698259 Shared epitope alleles remain a risk factor for anti-citrullinated proteins antibody (ACPA 2011 BACKGROUND: To investigate the associations between HLA-DRB1 shared epitope (SE) alleles and rheumatoid arthritis in subsets of rheumatoid arthritis defined by autoantibodies in three Asian populations from Malaysia. METHODS: 1,079 rheumatoid arthritis patients and 1,470 healthy controls were included in the study. Levels of antibodies to citrullinated proteins (ACPA) and rheumatoid factors were assessed and the PCR-SSO method was used for HLA-DRB1 genotyping. RESULTS: The proportion of ACPA positivity among Malay, Chinese and Indian rheumatoid arthritis patients were 62.9%, 65.2% and 68.6%, respectively. An increased frequency of SE alleles was observed in ACPA-positive rheumatoid arthritis among the three Asian ethnic groups. HLA-DRB1*10 was highly associated with rheumatoid arthritis susceptibility in these Asian populations. HLA-DRB1*0405 was significantly associated with susceptibility to rheumatoid arthritis in Malays and Chinese, but not in Indians. HLA-DRB1*01 did not show any independent effect as a risk factor for rheumatoid arthritis in this study and HLA-DRB1*1202 was protective in Malays and Chinese. There was no association between SE alleles and ACPA- negative rheumatoid arthritis in any of the three Asian ethnic groups. CONCLUSION: The HLA-DRB1 SE alleles increase the risk of ACPA-positive rheumatoid arthritis in all three Asian populations from Malaysia.
22423304 The future of rheumatoid arthritis and hand surgery - combining evolutionary pharmacology 2012 Rheumatoid arthritis is a systemic autoimmune disease of uncertain aetiology, which is characterized primarily by synovial inflammation with secondary skeletal destructions.Rheumatoid Arthritis is diagnosed by the presence of four of the seven diagnostic criteria, defined by The American College of Rheumatology.Approximately half a million adults in the United Kingdom suffer from rheumatoid arthritis with an age prevalence between the second and fourth decades of life; annually approximately 20,000 new cases are diagnosed.The management of Rheumatoid Arthritis is complex; in the initial phase of the disease it primarily depends on pharmacological management. With disease progression, surgical input to correct deformity comes to play an increasingly important role. The treatment of this condition is also intimately coupled with input from both the occupational therapists and physiotherapy.
22995442 The role of ectopic germinal centers in the immunopathology of primary Sjögren's syndrome 2013 Feb OBJECTIVES: To determine whether the presence of germinal centers (GCs) in salivary glands of patients with primary Sjögren's syndrome (pSS) is related to the severity of disease course and distinct immunopathology features. METHODS: A systematic search was performed in September 2011 for terms and synonyms of Sjögren's syndrome and germinal centers. A total of 80 articles were retrieved, of which 16 were included for (meta-) analysis. RESULTS: GC morphology was present in a mean ± SD 25.1 ± 5.0% of pSS patients. Mean lymphocyte focus scores were 1.25 points higher in patients with GCs as compared to those without GCs. Saliva production was reduced in patients with GCs, although this did not reach statistical significance. Percentages of patients positive for rheumatoid factor, anti-Sjögren's syndrome A (SSA), and anti-Sjögren's syndrome B (SSB) antibodies were significantly higher in patients with GCs (mean increase, 15%, 18%, and 18%, respectively). Additionally, patients with GCs were characterized by enhanced levels of local and systemic proinflammatory mediators. Importantly, these patients have a higher risk of lymphoma development (14% versus 1%). CONCLUSIONS: Patients with GCs are characterized by more severe disease, although the small number of studies and their design hamper generalizability of results. The precise mechanisms that contribute to the development and persistence of germinal centers in pSS are largely unknown. This and the strongly increased risk of lymphoma development warrant intensive studies for the role of germinal centers in the immunopathology of pSS.
22563590 American College of Rheumatology classification criteria for Sjögren's syndrome: a data-d 2012 Apr OBJECTIVE: We propose new classification criteria for Sjögren's syndrome (SS), which are needed considering the emergence of biologic agents as potential treatments and their associated comorbidity. These criteria target individuals with signs/symptoms suggestive of SS. METHODS: Criteria are based on expert opinion elicited using the nominal group technique and analyses of data from the Sjögren's International Collaborative Clinical Alliance. Preliminary criteria validation included comparisons with classifications based on the American–European Consensus Group (AECG) criteria, a model-based “gold standard”obtained from latent class analysis (LCA) of data from a range of diagnostic tests, and a comparison with cases and controls collected from sources external to the population used for criteria development. RESULTS: Validation results indicate high levels of sensitivity and specificity for the criteria. Case definition requires at least 2 of the following 3: 1) positive serum anti-SSA and/or anti-SSB or (positive rheumatoid factor and antinuclear antibody titer >1:320), 2) ocular staining score >3, or 3) presence of focal lymphocytic sialadenitis with a focus score >1 focus/4 mm2 in labial salivary gland biopsy samples. Observed agreement with the AECG criteria is high when these are applied using all objective tests. However, AECG classification based on allowable substitutions of symptoms for objective tests results in poor agreement with the proposed and LCA-derived classifications. CONCLUSION: These classification criteria developed from registry data collected using standardized measures are based on objective tests. Validation indicates improved classification performance relative to existing alternatives, making them more suitable for application in situations where misclassification may present health risks.
22289719 Genetics of Sjögren's syndrome in the genome-wide association era. 2012 Aug While Sjögren's syndrome (SS) is more common than related autoimmune disorders, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), scientific and medical research in SS has lagged behind significantly. This is especially true in the field of SS genetics, where efforts to date have relied heavily on candidate gene approaches. Within the last decade, the advent of the genome-wide association (GWA) scan has altered our understanding of disease pathogenesis in hundreds of disorders through the successful identification of novel risk loci. With strong evidence for a genetic component in SS as evidenced by familial aggregation of SS as well as similarities between SS and SLE and RA, the application of GWA approaches would likely yield numerous novel risk loci in SS. Here we review the fundamental scientific principles employed in GWA scans as well as the limitations of this tool, and we discuss the application of GWA scans in determining genetic variants at play in complex disease. We also examine the successful application of GWA scans in SLE, which now has more than 40 confirmed risk loci, and consider the possibility for a similar trajectory of SS genetic discovery in the era of GWA scans. Ultimately, the GWA studies that will be performed in SS have the potential to identify a myriad of novel genetic loci that will allow scientists to begin filling in the gaps in our understanding of the SS pathogenesis.
30533107 A case of effusive-constrictive pericarditis accompanying rheumatoid arthritis: The possib 2013 Jan A 68-year-old female, suffering from rheumatoid arthritis, was admitted to our institution for right heart failure with massive pericardial effusion. Her pericardial effusion had increased after starting infliximab, tumor necrosis factor (TNF)-inhibitor therapy, despite improvement in arthralgia. Hemodynamic findings demonstrated effusive-constrictive pericarditis. Because association between exacerbation of pericarditis and infliximab was highly suspected through her clinical course, its administration was stopped. We should pay much attention to pericardial effusion and symptoms of right heart failure after starting TNF-inhibitor therapy in patients with rheumatoid arthritis. .
22174698 A comprehensive analysis of shared loci between systemic lupus erythematosus (SLE) and six 2011 Dec In spite of the well-known clustering of multiple autoimmune disorders in families, analyses of specific shared genes and polymorphisms between systemic lupus erythematosus (SLE) and other autoimmune diseases (ADs) have been limited. Therefore, we comprehensively tested autoimmune variants for association with SLE, aiming to identify pleiotropic genetic associations between these diseases. We compiled a list of 446 non-Major Histocompatibility Complex (MHC) variants identified in genome-wide association studies (GWAS) of populations of European ancestry across 17 ADs. We then tested these variants in our combined Caucasian SLE cohorts of 1,500 cases and 5,706 controls. We tested a subset of these polymorphisms in an independent Caucasian replication cohort of 2,085 SLE cases and 2,854 controls, allowing the computation of a meta-analysis between all cohorts. We have uncovered novel shared SLE loci that passed multiple comparisons adjustment, including the VTCN1 (rs12046117, P = 2.02×10(-06)) region. We observed that the loci shared among the most ADs include IL23R, OLIG3/TNFAIP3, and IL2RA. Given the lack of a universal autoimmune risk locus outside of the MHC and variable specificities for different diseases, our data suggests partial pleiotropy among ADs. Hierarchical clustering of ADs suggested that the most genetically related ADs appear to be type 1 diabetes with rheumatoid arthritis and Crohn's disease with ulcerative colitis. These findings support a relatively distinct genetic susceptibility for SLE. For many of the shared GWAS autoimmune loci, we found no evidence for association with SLE, including IL23R. Also, several established SLE loci are apparently not associated with other ADs, including the ITGAM-ITGAX and TNFSF4 regions. This study represents the most comprehensive evaluation of shared autoimmune loci to date, supports a relatively distinct non-MHC genetic susceptibility for SLE, provides further evidence for previously and newly identified shared genes in SLE, and highlights the value of studies of potentially pleiotropic genes in autoimmune diseases.
22208654 Biologic therapies in primary Sjögren's syndrome. 2012 Aug Primary Sjögren's Syndrome (PSS) is characterized by dryness of the eyes and mouth due to lymphocytic infiltration of secretory exocrine glands. As well as disabling dryness, patients commonly have fatigue and arthralgia and an associated reduction in quality of life. The condition principally affects adult women and is relatively common--approximately 1:1000 to 1:250 adult women are estimated to have the condition in European/North American studies. Current therapy is principally symptomatic with the use of artificial tears and oral gels, pastilles and sprays. Medications to stimulate residual glandular secretion can be helpful for appropriate individuals. A proportion of patients also develop extraglandular features such as skin vasculitis, or lung, neurological, haematological or other systemic involvement. Conventional general immunosuppressive therapies such as corticosteroids or disease-modifying drugs, have been used in some patients with these clinical features. Biologic therapies specifically directed against molecules involved in disease pathogenesis represent a potentially more effective approach to therapeutic intervention in rheumatic diseases including PSS. The greatest experience in PSS is with rituximab, an anti-B-cell monoclonal antibody already in use for the treatment of B-cell lymphoma and rheumatoid arthritis. A randomised placebo controlled study is currently recruiting in France and a further study is planned in the UK. This review discusses the utility of biologic therapies in PSS, potential challenges for their use, the available data on rituximab and the potential role for other biologic therapies currently in development, or in clinical trials, in other autoimmune conditions.
22570845 Total knee arthroplasty in rheumatoid arthritis. 2012 Mar The course of rheumatoid arthritis varies from mild disease to severe joint destructive variant that progresses rapidly, eventually leading to unremitting pain and joint deformity. In advanced disease, total knee arthroplasty has proven to be the most successful intervention that reduces knee pain and improves physical function in rheumatoid arthritis patients. However, as rheumatoid arthritis patients carry additional potential for late complications, many important considerations regarding preoperative evaluation and surgical technique must be taken into account in order to improve the results of total knee arthroplasty in this subgroup of patients.
21933593 Serum IgA against type 3 muscarinic acetylcholine receptor is a novel marker in diagnosis 2011 Aug BACKGROUND: Antibodies against type 3 muscarinic acetylcholine receptor (M3R) are involved in the pathogenesis of Sjögren's syndrome (SS), but the clinical value of them in SS patients has been controversial. The aims of this study were to: (1) establish an improved enzyme-linked immunosorbent assay (ELISA) to detect IgA antibodies against M3R; (2) evaluate the value of IgA antibodies against the second extracellular loop of M3R205-220 (c2M3RP) in diagnosis of SS. METHODS: To increase the ELISA sensitivity, c2M3RP was coupled to bovine serum albumin (BSA) by the glutaraldehyde method and a 96-well microplate was treated by ultraviolet rays before coated. Concentrations of anti-c2M3RP, anti-SSA, and anti-SSB were measured in the sera of 240 individuals: 91 patients with primary SS and 149 controls (16 secondary SS, 27 systemic lupus erythematosus, 40 rheumatoid arthritis and 66 healthy controls). Diagnostic properties of anti-c2M3RP were determined by receiver-operating characteristic curve analysis. RESULTS: The prevalence of serum IgA anti-c2M3RP antibodies in patients with pSS (46%, 42/91) was significantly higher than that in patients with systemic lupus erythematosus (19%, 5/27), in rheumatoid arthritis (15%, 6/40) and in healthy controls (5%, 3/66). However, there was no significant difference between the two SS groups (P = 0.727). The diagnostic performance of IgA anti-M3RP antibodies was similar to anti-SSA assay, but had 22% higher sensitivity than anti-SSB. By analyzing of IgA anti-c2M3RP antibodies, combination of anti-SSA and anti-SSB resulted in increased sensitivity, whereas their specificity was not significantly changed. CONCLUSIONS: The improved anti-c2M3RP ELISA is a novel, sensitive, and specific serological test for the diagnosis of SS. The combined application of anti-c2M3RP, anti-SSA and anti-SSB tests can improve the laboratory diagnosis of SS. The IgA anti-c2M3RP antibodies may serve as a novel diagnostic marker for SS.
24198591 Is yoga a suitable treatment for rheumatoid arthritis: current opinion. 2012 Aug 8 We reviewed published literature regarding the use of yoga for managing rheumatoid arthritis to determine whether adequate evidence exists to suggest its usefulness as a therapy. A search for previous studies involving yoga and rheumatoid arthritis in PubMed yielded eight reports. These studies reported the benefits of yoga in the physical and mental health of patients with rheumatoid arthritis (RA), suggesting that yoga is a useful add-on therapy for RA patients. However, all studies showed limitations with respect to sample size, study design, description and duration of yoga intervention, and assessment tools and statistical methods used. Additionally, the studies did not attempt to understand the mechanisms underlying observed benefits. Hence, evidence suggests a definite role of yoga in RA improvement, reducing pain, improving function, and creating a positive mental state. However, detailed analysis and additional studies are necessary to verify these observations.
22091296 Pamidronate infusion improved two cases of intractable seronegative rheumatoid arthritise. 2011 May Pamidronate is a bisphosphonate derivative that can inhibit bone resorption by actions on osteoclasts and increase bone density in spite of treatment with steroids. This drug has the anti-inflammatory effect by increase apoptosis of monocytes. 5-10 percent of rheumatoid arthritis patients is seronegative and may be resistant to conventional disease modifying anti rheumatic drugs (DMARDs). Intravenous (IV) pamidronate can be effective in disease control in seronegative rheumatoid arthritis. We report two cases of seronegative and drug resistant rheumatoid arthritis that favorably responds to pamidronate.
22567181 Comparison of adenosine deaminase levels in serum and synovial fluid between patients with 2012 OBJECTIVES: Adenosine deaminase (ADA) is an enzyme being involved in purine metabolism and plays a significant role in the immune system. The aim of this study was to investigate the use of adenosine deaminase levels in differentiating between rheumatoid arthritis and osteoarthritis. MATERIAL AND METHODS: Thirty patients with rheumatoid arthritis and 30 osteoarthritis patients enrolled the study. They were matched in sex and age. Using the ROC curve, we determined the optimal serum and synovial cutoff for rheumatoid effusion. RESULTS: The results showed a statistically significant difference between ADA levels in joint effusion and serum of patients with rheumatoid arthritis and osteoarthritis (p<0.001). Synovial fluid cutoff value for diagnosing rheumatoid arthritis was 20 with a sensitivity of 90% and specificity of 80% and the serum cutoff value was 15 with a sensitivity of 93% and specificity of 53.3%. Area under ROC curve for synovial ADA, ESR and CRP co-linearity was 99%. CONCLUSION: We concluded that synovial total ADA assay can be a sensitive and specific test, being suitable for rapid diagnosis of rheumatoid effusions.
26673660 The pathogenesis of rheumatoid arthritis in radiological studies. Part I: Formation of inf 2012 Jun Rheumatoid arthritis is a chronic inflammatory disease with a multifactorial etiology and varied course, which in the majority of patients leads to partial disability or to permanent handicap. Its characteristic trait is a persistent inflammation of the synovial membrane and the formation of an invasive synovial tissue, called the pannus, which in time leads to destruction of the cartilage, subchondral bone tissue, and the soft tissue of the affected joint(s). The pathogenesis of rheumatoid arthritis is complex and involves cells of both innate and adaptive immunity, a network of various cytokines and an immunoregulatory dysfunction. An important role in the discovery of rheumatoid arthritis pathogenesis was played by magnetic resonance imaging, which showed the disease process to extend beyond the synovium into the bone marrow. Many studies have shown a strict correlation between the vascularity of the synovium (assessed through the power Doppler ultrasound and magnetic resonance examinations), bone marrow edema and the clinical, laboratory and histopathological parameters of rheumatoid arthritis. From the current understanding of rheumatoid arthritis, bone erosions could occur from two directions: from the joint cavity and from the bone marrow. With power Doppler ultrasound, as well as in magnetic resonance imaging, it is possible to visualize the well-vascularized pannus and its destructive effects on joint structures and ligaments. In addition, the magnetic resonance study shows inflammatory and destructive changes within the bone marrow (bone marrow edema, inflammatory cysts, and erosions). Bone marrow edema occurs in 68-75% of patients with early rheumatoid arthritis and is considered to be a predictor of rapid disease progression.
22628958 Is there a relationship between periodontitis and rheumatoid arthritis? 2012 Jan BACKGROUND: Growth of scientific evidence suggests an exquisite association between oral infection and systemic diseases. Though etiologies of periodontitis and rheumatoid arthritis (RA) are separate, their underlying pathological processes are sufficient to warrant consideration of hypothesis that individuals at risk of developing RA may also be at the risk of developing periodontitis and vice versa. MATERIALS AND METHODS: To test their relationship, a study was carried out on 80 individuals. Part A: Forty subjects having rheumatoid arthritis (RA group) were compared to 40 controls without arthritis (NRA group). Their periodontal indices rheumatoid arthritis clinical laboratory parameters were also correlated with periodontitis in group. Part B: Omplete periodontal treatment was done for 10 patients of group suffering from periodontitis. All parameters of periodontal indices were measured pre-operatively and weeks after completion of periodontal treatment. RESULTS: (1) There was high prevalence of mild (12.5%) to moderate (75%) periodontitis in group. (2) Extent severity of periodontal disease rheumatoid arthritis were positively correlated. (3) Statistically significant differences were present in periodontal parameters of RA group compared to NRA group. (4) There was statistically, significant reduction in parameters postoperatively with concomitant decrease in periodontal parameters in RA group. CONCLUSION: Thus, an association exists between periodontal disease with an underlying dysregulation of the molecular pathways in the inflammatory response. Also, there are significant management implications in the future as new host modifying medications are developed.
23626923 Role of TH-17 cells in rheumatic and other autoimmune diseases. 2011 Oct 20 In humans multiple pathways can induce TH-17 cell differentiation, whereas in mice this process is mostly modulated by IL-6 and TGF-β. IL-17 produced by TH-17 cells has been associated with a number of inflammatory autoimmune diseases including psoriasis, systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, and rheumatoid arthritis. In this review, we have primarily focused on the role of TH-17 cells/IL-17 in the pathogenesis of rheumatoid arthritis and experimental arthritis. The potential role of TH-17 cells in rheumatoid arthritis progression has been demonstrated by correlating the percent TH-17 cells or levels of IL-17 with rheumatoid arthritis disease activity score and C-reactive protein levels. Further, previous studies suggest that IL-17 mediated vascularization may lay the foundation for rheumatoid arthritis joint neutrophil and monocyte recruitment as well as cartilage and bone destruction. The profound role of IL-17 in the pathogenesis of experimental arthritis may be due to its synergistic effect with TNF-α and IL-1β. Although the initial clinical trial employing anti-IL-17 antibody has been promising for rheumatoid arthritis, future studies in humans will shed more light on how anti-IL-17 therapy affects rheumatoid arthritis and other autoimmune disease pathogenesis.
21941451 Hepatotoxicity due to tocilizumab and anakinra in rheumatoid arthritis: two case reports. 2011 Elevation of liver enzymes in patients with rheumatoid arthritis treated with the biological agents, tocilizumab and anakinra, is now well documented. However, histological characterization of these effects and outcomes has not been defined. Here we report toxic liver effects in two women with rheumatoid arthritis, refractory to all nonbiological therapies, following treatment with anakinra and tocilizumab. Liver biopsy in both cases showed focal necrosis of hepatocytes as a hallmark of drug toxicity, along with steatosis and early fibrosis. In addition, the patient treated with anakinra demonstrated inflammatory changes. Tocilizumab was continued with no further deterioration in liver function. Withdrawal of anakinra led to rapid normalization of liver function. The biological agents, tocilizumab and anakinra, may result in significant histological hepatic changes, including necrosis, but despite this, the outcome appears to be good.
22275906 Rheumatoid meningitis. 2011 An 80-year-old woman with rheumatoid arthritis had gait difficulties and frequent falls. MRI of the brain showed an extra-axial enhancing lesion overlying the right frontal-parietal cortex, that progressively extended to the contralateral side. This was accompanied by further decline in her functional status. We discuss the diagnostic and therapeutic approach of a pachy-leptomeningeal process in a rheumatoid patient.
22383918 Rheumatoid arthritis: refractory to infliximab, a tumor necrosis factor inhibitor. 2011 Oct Rheumatoid arthritis is one of the commonest autoimmune diseases. It is a chronic, progressive, systemic inflammatory disorder affecting the synovial joints and typically producing symmetrical arthritis. If left untreated, it leads to joint destruction and thus deformity and disability.In the recent years, advances in molecular biology have led to a variety of new treatment approaches to rheumatoid arthritis and other systemic inflammatory diseases associated with autoimmunity. Anti tumor necrosis factor (TNF) agents are emerging in the frontline management of rheumatoid arthritis (RA) in the current era of biological treatment. We presented a 46-year-old Chinese female with a history of seropositive RA for the past 22 years refractory and intolerant to multiple medications including sulphasalazine (SSZ), leflunomide, hydroxychloroquine (HCQ) and methotrexate (MTX), thus infliximab, a tumor necrosis factor (TNF) inhibitor was initiated. However, despite receiving 6 cycles of infliximab therapy, she still complained of persistent disabled multiple joint pain and swelling. This report will discuss about rheumatoid arthritis, which is refractory to infliximab (a TNF inhibitor) and its alternative. KEYWORDS: Rheumatoid arthritis; Biologics treatment; Tumor-necrosis factor inhibitor; Infliximab.