JournalTOCs

OA Arthritis
Number of Followers: 1

This is an Open Access Journal

Open Access journal
ISSN (Online) 2052-9554
Published by OA Publishing London

[37 journals]

Adult onset Still’s disease: Not so rare neither so benign.
- Abstract: The abstract will be provided by the corresponding author in due course.
  PubDate: 11/01/2014 07:17:06 am
Evidence on the effectiveness of interferential current therapy in the
treatment of knee osteoarthritis: A meta-analysis.
- Abstract: This study evaluated available evidence regarding the effectiveness of interferential therapy (IFC) on knee osteoarthritis (OA) in providing pain relief and improving physical function such as doing activities of daily living and its efficacy in reducing intake of analgesics, such as Paracetamol. An online database search for randomized controlled trials (RCTs) comparing IFC against control or sham IFC in knee OA was done and data from studies were pooled and analyzed using the Review Manager Software 5.2. Results revealed a significant difference between intervention group and control group in decreasing pain in the osteoarthritic knee using the Visual Analog Scale (VAS) and the Western Ontario and McMaster University (WOMAC) Osteoarthritis Index as objective measures, as well as in decreasing intake of paracetamol. However, there was no significant difference between intervention group and control group in improving function in the osteoarthritic knee with reference to the WOMAC subscale for physical function. Therefore, IFC is effective in reducing pain and likewise decreasing paracetamol intake in patients with knee OA. It is best to combine IFC with exercise in managing pain, reducing intake of pain medication and improving function in patients with knee OA.
  PubDate: 11/01/2014 07:17:06 am
The early stages of rheumatoid arthritis: New targets for the development
of combinational drug therapies.
- Abstract: The current methods of treating rheumatoid arthritis (RA) do not address the early phases of the disease progression and instead merely treat the symptoms. Whilst this approach may help to alleviate much of the pain and discomfort associated with RA, it does not stop the disease progression and the destruction of joint tissue still occurs. Furthermore, a number of serious side effects are associated with the current treatment modalities. A better strategy may be to eradicate the cause of the disease, thereby bypassing the later phase events. Until recently, this has not been possible due to a lack of understanding of the etiology of RA. However, recent advances have identified Proteus mirabilis as a trigger of the disease and have provided some understanding of the disease progression. An understanding of the early phases of the disease has identified a variety of new targets for anti-RA drug development which may allow for the development of new treatment regimes with increased efficacy and/or less serious side effects. The current report examines the P. mirabilis bacterial trigger of RA and how it results in self reactive antibody production. In so doing, the report highlights some targets for drug treatments aimed at blocking the early phases of RA before the more serious later phase events occur. Whilst it is unlikely that any single drug will be able to treat all aspects of this disease, resveratrol and other stilbenes are highlighted as a class of compounds which may have beneficial effects on several phases of RA disease progression.
  PubDate: 09/30/2014 10:15:09 pm
Positive psychological qualities and adjustment to arthritis.
- Abstract: The article has been forwarded to the production team. The processing may take few weeks. Then the proof will be forwarded to the corresponding author. The final PDF and HTML files will be uploaded when the corrections to the proof are returned by the corresponding author.
  PubDate: 07/28/2014 07:32:27 am
Digital ulcer management in patients with systemic sclerosis.
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  PubDate: 07/28/2014 07:32:27 am
Rhupus: A crosswalk between lupus and rheumatoid arthritis.
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  PubDate: 07/28/2014 07:32:27 am
The regulation of nerve and blood vessel ingrowth in aneural and avascular
intervertebral disc and articular cartilage.
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  PubDate: 07/28/2014 07:32:27 am
Superiority trials in osteoarthritis using glucosamine hydrochloride as
comparator: Overview of reviews and indirect comparison with Rosa canina
(a novel nutraceutical).
- Abstract: Background: In the absence of randomized trials making head-to-head comparisons, we wanted to evaluate the pain-reducing effect of glucosamine hydrochloride (GH) and the use of the hip powder, Rosa canina (RP) therapy in osteoarthritis (OA) patients by using an indirect comparison meta-analysis. Methods: Randomized controlled trials included in published meta-analyses were eligible for inclusion. The standardized mean difference (SMD) was used as effect measure, and the difference between GH and RP, was calculated using the Bucher approach. Results: There was no heterogeneity for any of the nutraceuticals. GH studies were consistently located around an effect size of zero (SMD= -0.01 [-0.14 ; 0.12]) whereas the RP studies consistently pointed towards an effect size of 0.4 (SMD = -0.37 [-0.60 ; -0.13]). Testing whether there was any significant difference between GH and RP (both in contrast to placebo), we applied the Bucher approach, resulting in an effect size of 0.36 in favour of RP (SMD = 0.36 [0.09 ; 0.62], Z = 2.65; P = .0082). Conclusion: GH should not be used in clinical practice. However, we see no harm in having patients continue GH therapy as long as they perceive a benefit and cover the costs of treatment themselves. GH may be used as an ethical ineffective active comparator in OA trials.
  PubDate: 04/14/2014 12:15:02 pm
The role of AQP1 in knee Osteoarthritis (OA): A contemporary review.
- Abstract: Introduction The aim of this issue is to review literature about AQP1 and its involvement in joint disease. In particular we focused our research on Osteoarthritis (OA) of the knee. Materials and methods We reviewed the literature regarding AQP1 role in joint cavity disease. We examined the current literature searching on PubMed and Scopus using appropriate keywords in relation to AQP1 and OA. Main research articles were selected for review. Results AQP1 is an integral membrane protein expressed in different normal and pathologicaltissues, e.g.erythrocytes, renal tubule cells andin knee tissues (synoviocytes, articular chondrocytes and fibrochondrocytes). In knee tissue AQP1 is also espressed in human synovitis andin chondrocytes of patients with rheumatoid arthritis (RA) and Osteoarthritis (OA). The process of development and aging of articular cartilage is related with its nutrition and function, which depend mainly on the water molecular transmembrane transport. Water transport is taken by aquaporins. The regulation of the water and solute content of chondrocytes will profoundly aﬀect their anabolic and catabolic functions. The chondrocytes are supplied by diffusion, helped by the pumping action generated by compression of the articular cartilage or flexion of the elastic cartilage.The water content of cells is eﬀectively inﬂuenced by the abundance of aquaporin (AQP) water channels. Conclusion This review reports recent findings about the involvement of AQP1 in the function of the articular cartilage and its possible role in knee Osteoarthritis.
  PubDate: 04/14/2014 12:15:02 pm
Predicting response to anti-tumour necrosis factor therapy in rheumatoid
arthritis patients: what has genetics taught us so far'
- Abstract: Although Tumor necrosis factor alpha (TNFα) blocking strategies are very effective for the treatment of Rheumatoid arthritis (RA), prolonged response is seen only in about 70% of the patients. Inefficacy of anti-TNF therapy together with reported adverse events and the high costs of anti-TNF blocking agents have driven the search for markers able to predict treatment response. The exact causes for non-response are unknown but it is expected that genetic variation is (partly) responsible for these differences in treatment response. Pharmacogenetic research has put much effort into the identification of genetic markers predicting anti-TNF treatment outcome, using both hypothesis driven (candidate gene) and non-hypothesis driven (whole-genome) approaches. However, both approaches did not yet identified a genetic marker that can predict anti-TNF treatment outcome with high sensitivity and specificity.This review gives an overview of current literature concerning the search for genetic markers able to predict anti-TNF response in RA patients. In addition, several possible explanations are put forward why these studies were unsuccessful in identifying these markers for therapy response.
  PubDate: 04/14/2014 12:15:02 pm
Intrinsic joint tissue repair by joint distraction.
- Abstract: In this systematic review we described the effect of joint distraction treatment. Joint distraction is a surgical technique that has been used to treat a variety of joint diseases, including degenerative arthropathies such as osteoarthritis and chondrolysis. The systematic search was specifically aimed at pre-clinical and clinical publications about joint distraction in subjects with degenerative cartilage damage. After literature screening, 30 publications were included reporting on treatment of degenerative arthropathies of hip, ankle, and knee. Joint distraction has been found to reduce pain and improve joint function in both pre-clinical and clinical studies. Furthermore, structural tissue repair is shown and improved joint motion, using a hinged distractor. Although well documented the clinical studies are of limited quality. Only two randomized controlled trials, both on ankle joint distraction and both with limited number of patients were included. Furthermore, most studies have modest follow-up periods of 1 and 2 years. Nonetheless, the promising results on structural repair induced by this treatment may lead to a better understanding of the regeneration capacity of joint tissues in degenerative joint diseases.
  PubDate: 04/14/2014 12:15:02 pm
The interleukin-23/interleukin-17 axis and the role of Treg/Th17 cells in
rheumatoid arthritis and joint destruction.
- Abstract: Rheumatoid arthritis(RA) is caused by a complex mechanism involving synoviocytes, osteoclasts, and immune cells interconnected via cytokines and other signalling molecules. Effective medical treatment for joint destruction in RA is lacking because the molecular mechanisms leading to joint destruction are incompletely understood. However, it is known that cytokine-mediated immunity and perturbations in the balance of effector cells at the disease site play a crucial role in RA pathogenesis. Cellular and cytokine inhibitors have been used for treatment purposes. Increasing evidence has revealed the importance of IL-17, an activated T cell-derived inflammatory cytokine, and IL-23 in the pathogenesis of RA. The role of IL-17 has been of particular interest, as IL-17 affects the differentiation and activation of pathogenic osteoclasts. Cellularly, disturbance of the Th17/Treg balance and plasticity, dysregulated Th17 responses, and the reduction or absence of Treg cells are key features of RA. Recent developments in the area of CD4+ T-cell differentiation, together with experimental and preclinical findings on inhibitors of the IL-17 pathway and the use of Treg cell-based therapy, indicate that CD4+ effector cells, TH17 and Treg, could be an effective target for restoring immune tolerance. In this review, we will summarise the progress in our understanding of the role of IL-23, IL-17 and CD4+ T-cell differentiation into specialised effectors, focusing on Th17 and Treg cells, in the pathogenesis of RA.
  PubDate: 04/14/2014 12:15:02 pm
The pro-inflammatory niche: how the extracellular matrix drives rheumatoid
arthritis'
- Abstract: The extracellular matrix is a complex, three-dimensional network of secreted molecules that provides structural support to tissues and environmental cues to the cells within. One particular subset of matrix molecules is specifically expressed upon tissue damage. These molecules contribute to effective tissue repair by orchestrating the behaviour of cells that mediate this process and, once repair is complete, the expression of this matrix is down regulated. Here, we focus on recent data highlighting a direct role for these injury induced molecules in driving inflammation upon tissue damage and propose that this matrix creates a specific microenviroment or ‘pro-inflammatory niche’ that is permissive for localized inflammation during repair. We also examine evidence indicating that this niche exists, and persists, in the damaged joint of rheumatoid arthritis patients. We assess the data which demonstrate that these matrix molecules actively contribute to maintaining chronic inflammation during disease progression and we discuss the implications of these findings in developing new ways to treat rheumatoid arthritis.
  PubDate: 04/14/2014 12:15:02 pm
Bone formation in ankylosing spondylitis.
- Abstract: Introduction. Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disorder with unclear pathogenesis. Bone formation is a hallmark feature of AS, precise mechanisms of which are unknown. The aim of this review is to summarize the current knowledge regarding both clinical significance and pathogenesis of bone formation in AS. Methods. Articles, published in the medical literature and chapters in textbooks related to the discussed topic were critically reviewed, relevant data selected, collated and organized for the purpose of this manuscript. Results. Conventional radiography is the most valuable classical tool for identification of structural changes in AS. The typical manifestations of bone formation in AS usually involve the axial skeleton, including spine, sacroiliac and hip joints, and, if properly recognized, have an important role in diagnosing, classifying and monitoring patients. Molecular pathways leading to bone formation in AS have not been elucidated sufficiently. Abnormally active signaling by wingless-type (wnt)-like and bone morphogenic proteins (BMPs)-mediated pathways have been suggested as major contributors to disease-related ossification in AS. The only medicines, shown currently to delay the process of bone formation in AS patients, are non-steroidal anti-inflammatory drugs. Conclusions. Better understanding and prediction of structural damage would help to improve and individualize management of patients suffering from AS.
  PubDate: 04/14/2014 12:15:02 pm
How obesity links with osteoarthritis: mechanic or metabolic'
- Abstract: Osteoarthritis (OA) is highly prevalent joint disease. Obesity is one of the most important risk factors of new-onset and deterioration of OA.Obesity was once considered to cause OA simply by added mechanical force. Yet, more recent studies have shown that metabolic factors produced by fat tissue can also initiate inflammatory cascade that consequently can lead to OA. This is a narrative review of recent literature about how obesity lead to OA. Mechanical loading, metabolic factors, and other related issues are discussed. Knowledge on how obesity links with OA will help to identify targets for modifying the metabolic effect for treatment of osteoarthritis.
  PubDate: 04/14/2014 12:15:02 pm
The early spondyloarthritis (ESPA): Concept, role of new imaging
techniques, therapeutic opportunities and research agenda.
- Abstract: INTRODUCTION The interest on early Spondyloarthtiris (eSpA) is born in the last ten years for the acknowledgment of the “evidence based” utility of the rapid diagnostic and therapeutic approach in this disease. METHODS We discussed the definition of eSpA (chronological and classification criteria), the role of new imaging techniques in diagnosis, and the therapeutic approach in early disease. RESULTS The chronological definition of eSpA is notuniform in literature. ASAS criteria, together with the use of MRI and US in early diagnosis have increased the diagnostic power and the capacity to classify eSpA. Few issues investigated and codified the use of DMARDs and antiTNFalpha in early phases. CONCLUSION: Future studies must be conducted in the future to better clarify MRI and US findings and the role of other imaging techniques in early phase. Furthermore, an intensified research on efficacy of treatments in early phase with prospective studies are needed in the future.
  PubDate: 04/14/2014 12:15:02 pm
Osteoarthritis: rationale for a new paradigm shift involving transforming
growth factor-β1.
- Abstract: Osteoarthritis (OA) in no longer considered a disease of the articular cartilage alone and in recent years we considered OA as a disease of the joint. Clinical and basic studies now question this notion. Indeed, current evidence is now indicating that OA may be a disease involving abnormal bone tissue modeling or remodeling based on alterations in mesenchymal stem cell (MSC) recruitment and differentiation. Biological factors produced by OA osteoblasts, which have been shown to affect chondrocyte function, may now be involved in the alteration of MSC recruitment/differentiation. One such factor may be transforming growth factor-b1 (TFG-b1).
  PubDate: 04/14/2014 12:15:02 pm
The potential role of resveratrol in ameliorating osteoarthritis and
resultant joint damage.
- Abstract: Introduction Articular cartilage is critical to the normal function of human joints. Articular cartilage provides lubrication and load bearing to permit friction-free locomotion and movement. It is a uniquely avascular, aneural, and alymphatic tissue and consists of an extensive extracellular matrix (ECM) with relatively few chondrocytes. Articular cartilage has a limited capacity to repair itself because of its avascular nature. Cartilage repair is dependent on the production of extracellular matrix by chondrocytes, and is stimulated by anabolic morphogenetic proteins, such as bone morphogenetic proteins (BMPs), transforming growth factor (TGF-β), and growth factors such as insulin-like growth factor (IGF-1). Catabolic cytokines such as interleukin-1 beta (IL-1β), and tumour necrosis factor alpha (TNFα) degrade the cartilage extracellular matrix. A dynamic change in the cartilage homeostasis precedes the initiation and progression of osteoarthritis. Osteoarthritis is an unmet clinical challenge. Osteoarthritis is the most common form of arthritis and occurs in a large segment of aging individuals. There is no effective treatment for osteoarthritis, other than pain-amelioration by non-steroidal anti-inflammatory drugs. These drugs are notorious for their deleterious side effects. Therefore the drug of choice for treating osteoarthritis should be one that has anti-inflammatory properties with no side effects. Resveratrol, a component of red wine, has potent anti-inflammatory properties. In this critical review we summarize the potential actions of resveratrol in articular cartilage. Conclusion The anti-inflammatory effects of resveratrol have been shown in several animal model studies. Resveratrol might be the relevant compound for potential use in osteoarthritis therapy.
  PubDate: 04/14/2014 12:15:02 pm
No littering: The clearance of dead cells and leaking cellular contents
and possible pathological complications.
- Abstract: Apoptosis and necrosis differ in morphological, biochemical and immunological aspects, but both eventually result in engulfment of the dead cell or its remnants by a phagocyte. Apoptotic cells can be swallowed in one gulp due to the preserved impermeability of the plasma membrane. If clearance does not occur fast enough, the cells may undergo secondary necrosis and lose plasma membrane integrity. (Secondary) necrotic cells pose several problems for the body: a) Necrotic cell clearance is pro-inflammatory due to danger signals leaking out of the cell. This is in strong contrast to the anti-inflammatory clearance of apoptotic cells. Exaggerated inflammation may cause tissue damage and exacerbate the course of various diseases. b) Chronic deficiencies in apoptotic cell clearance lead to an accumulation of late apoptotic and secondary necrotic cells. The persistent accessibility of otherwise occult intracellular antigens may challenge auto-tolerance and is a hallmark of systemic lupus erythematosus. c) Intracellular macromolecules that leaks out of necrotic cells have to be cleared individually. Here we summarize the knowledge on clearance mechanisms for chromatin, neutrophil extracellular traps (NETs), RNA and uric acid and the possible implications if their clearance is insufficient. A potentially fatal outcome of massive leakage is the tumor lysis syndrome.
  PubDate: 04/14/2014 12:15:02 pm
Adamantiades-Behcet’s disease: the past, the present and the future.
- Abstract: Background:Adamantiades-Behcet’s disease is more common along the “Silky Road” and among young adults with HLA-B51 allele. Discussion:It is a chronic relapsing vasculitis characterized by recurrent oral and genital ulcers, cutaneous and ocular manifestations. It. Visual loss may occur in up to 20% of the affected patients. Arthritis, gastrointestinal and nervous involvement may occur. This vasculitis has a tendency for superficial and deep vein thrombosis. Corticosteroids remain the mainstay of treatment, while other immunosuppressive agents, such as azathioprine, cyclophosphamide, anti-TNF-a, colchicine and thalidomide have been used successfully for its treatment. Anti-TNF-a agents seem to be very promising for severe CNS, ocular and gastrointestinal involvement. Conclusion:Morbidity is mainly due to ocular lesions, while mortality is low and is due to CNS involvement, bowel perforation, pulmonary symptoms or thrombosis.
  PubDate: 04/14/2014 12:15:02 pm
A role for anti-HSP60 antibodies in arthritis: a critical review.
- Abstract: Introduction As a result of the high sequence similarity between HSP60 proteins, found in both prokaryotic and eukaryotic cells, it has been suggested, but never concluded, that anti-HSP60 antibodies could be of importance in the pathology of arthritis diseases explained by a concept named molecular mimicry. In a number of clinical studies antibodies to both human and bacterial HSP60 have been detected in serum from patients with different inflammatory diseases, but divergent results have been published. Recent progress, however, has increased the specificity in tests used to determine the humoral response to HSP60. In this review, these new findings are compared with old questioning the durability of molecular mimicry as a hypothesis for arthritis pathogenesis. The current literature was examined through a thorough search using PubMed with appropriate keywords in relation to anti-HSP60 antibodies and arthritis-related disease. Main research articles were selected for review. Discussion Recent reports have added new information to the interpretation of the humoral immune response to HSP60 proteins. By introducing determination of IgG subclasses by the ELISA HSP60 specific antibodies were shown to be predominantly of the IgG1 and IgG3 isotypes for bacterial and human HSP60, respectively, thereby improving the strategy to test the hypothesis of cross-reaction. Conclusion The hypothesis of molecular mimicry comes from attempts to link bacteria to the development of arthritis. However, based on a critical investigation on the literature, it is here argued that investigation on the role of HSP60 in the development of arthritis in addition to anti-HSP60 serology should include a more functional study on how HSP60 can reach the extracellular locations and whether it is tolerogenic. Secondly, studies are needed on how the different subclasses of IgG specific human HSP60 may stimulate the immune environment into an anti- or pro-inflammatory state.
  PubDate: 04/14/2014 12:15:02 pm
Free radical biology in cellular inflammation related to rheumatoid
arthritis.
- Abstract: Introduction: Chronic inflammation is a prolonged pathological condition characterized by mononuclear cell infiltration, tissue destruction and fibrosis due to excess production of free radicals. Where rheumatoid arthritis is systemic autoimmune diseases characterized by synovial cell infiltration as well as destruction of tissues. The main aim of this review is to analyze the role of free radicals in cellular inflammation, related to rheumatoid arthritis. Discussion: Free radicals are defined as molecules or any chemical species having an unpaired electron in the outer orbit and are capable of independent existence. In biological systems, the most common source of free radicals is oxygen which in term reacts with nitrogen and produces nitrogen intermediates. Under certain stress conditions, Oxygen becomes much more active and forming superoxide anion radicals (O2-) and hydroxyl radical (OH-). The important nitrogen species are nitric oxide (NO) and peroxynitrite anion (ONOO-). NADPH oxidation by NADPH oxidase is considered as the major source of O2- where the antioxidant enzyme superoxide dismutase (SOD) converts O2- to less toxic hydrogen peroxide (H2O2). Nitric oxides (NO) is formed from L-arginine by one of the three nitric oxide synthase and react with O2- and produce highly toxic ONOO-. Collectively all reactive oxygen and nitrogen species ultimately responsible for creating oxidative stress during inflammation by producing different cytotoxic cytokines through the phosphorylation of nuclear factor kappa-B (NFκB). Conclusion: DNA damage caused by reactive radicals as well as cytokines may lead to abnormal functioning of the cells. Although cellular repair system corrects much of these damages, but the free radicals induced DNA lesion can be an important etiology of inflammatory autoimmune diseases like rheumatoid arthritis. Thus it should be recommended that management of oxidative stress by antioxidant therapies in combination with modulator of cytokines and other inflammatory pathways are the therapeutic weapon to fight against rheumatoid arthritis.
  PubDate: 04/14/2014 12:15:02 pm
Fibromyalgia syndrome: An approach to pathogenesis, current and novel
treatments.
- Abstract: Understanding the pathophysiology of fibromyalgia and therefore the establishment of effective treatments have been complex arguments. The findings of recent studies related with central pain processing, genetic abnormalities, and external factors have led to the use of new therapies that have shown beneficial effects on symptoms. This review discusses ideas that have become accepted as well as novel associations under consideration regarding the pathogenesis of fibromyalgia and the current and emerging therapeutics for its treatment.
  PubDate: 04/14/2014 12:15:02 pm
B-cell kinase inhibitors in rheumatoid arthritis.
- Abstract: The pathogenesis of rheumatoid arthritis (RA) involves systemic dysregulation of T and B lymphocytes resulting in immune responses against self-antigens, and ultimately leading to downstream effects such as cartilage destruction, pannus formation, and bone erosion. Clinical evidence for the role of B cells in RA includes the effectiveness of rituximab, an antibody designed to deplete autoreactive B cells. A separate and newer approach to RA treatment involves interference with key intracellular signaling kinases present in B cells, notably spleen tyrosine kinase (SYK) and Bruton’s tyrosine kinase (BTK). Inhibition of SYK, a non-receptor tyrosine kinase predominantly expressed in hematopoietic cells that is involved in the activation of immune cells critical to RA, has proven effective in animal models of inflammation and inflammatory arthritis. BTK is a Tec-family kinase prominently expressed in B cells, with well-established function in B-cell receptor–mediated activation and survival. Ibrutinib, a first-in-class BTK inhibitor recently approved in mantle cell lymphoma and currently in clinical trials for B-cell malignancies, potently and dose-dependently reverses clinical arthritis, preventing cartilage and bone erosion in animal models of arthritis. Here we briefly review available data for SYK and BTK inhibitors in RA and other inflammatory diseases and outline their current clinical status.
  PubDate: 04/14/2014 12:15:02 pm