Joint Pain In Rheumatoid Arthritis Research Articles

Therapeutic Effect Of Warm Fragrant Lemongrass Foot Soak Against Changes In The Joint Pain Scale Of Rheumatoid Arthritis Patients

Uric acid is a natural antioxidant produced by the human body, but it can trigger rheumatoid arthritis if the amount exceeds the normal threshold with typical symptoms in the form of pain accompanied by swelling in the joint area, even in advanced conditions there is joint stiffness. Cymbopogon nardus (L.) Rendle or lemongrass is an effective plant to reduce joint pain and swelling. The purpose of this study was to describe the effect of warm lemongrass foot bath therapy on changes in the scale of joint pain in patients with rheumatoid arthritis. This study is a pre-experimental study with one group pre-test and post-test design without a control group, changes after two days of soaking warm lemongrass feet by observing changes in the pain scale of 23 respondents. The Wilcoxon test results showed that there was a change in the pain scale after intervention with a value of p = 0.01, which means that warm scented lemongrass foot soak affects reducing the pain scale of patients with rheumatoid arthritis. The warm sensation of the foot soaking intervention provides a peripheral vasodilation effect which causes a decrease in joint pain in inflamed tissues, the chemical effect of citronellal compounds is around 32-45%, geraniol 12-18%, and citronellol 12-25% in citronella plants are also proven to play a role in reducing pain. This study concluded that warm lemongrass foot soaking therapy affected the changes in the scale of joint pain in Rheumatoid Arthritis.

Repurposing of Pirfenidone (Anti-Pulmonary Fibrosis Drug) for Treatment of Rheumatoid Arthritis.

Clinical studies have shown that pirfenidone (PFD) effectively relieves joint pain in rheumatoid arthritis (RA) patients. However, the detailed mechanisms underlying the anti-RA effects of PFD have not been investigated. This study was undertaken to investigate the repurposing of PFD for the treatment of RA, and explore its anti-rheumatic mechanisms. A collagen-induced arthritis (CIA) rat model was used to observe joint pathological changes following PFD treatment. Based on bioinformatics to predict the mechanism of PFD anti-RA, using EA. hy926 and TNF-α-induced MH7A cells to establish in vitro model to explore its biological mechanism from the perspectives of synovial inflammation and angiogenesis. PFD significantly relieved pathological changes, including joint swelling, synovial hyperplasia, inflammatory cell infiltration and joint destruction. PFD was also associated with reduced expression of MMP-3 and VEGF in articular chondrocytes and synovial cells of CIA rats (p < 0.05). Using bioinformatic methods, we predicted that PFD inhibits cell inflammation and migration by interfering with the JAK2/STAT3 and Akt pathways. These results were verified using in vitro models. In particular, PFD effectively reduced the expression of pro-inflammatory, chondrogenic, and angiogenic cytokines, such as IL-1β, IL-6, IL-8, MMP-1/3/2/9 and VEGF (p < 0.05), in TNF-α-induced MH7A cells. In addition, PFD significantly reduced the production of MMP-2/9 and VEGF in EA. hy926 cells, thereby weakening migration and inhibiting angiogenesis (p < 0.05). These findings suggest that PFD may alleviate the pathological process in CIA rats, by inhibiting inflammation and angiogenesis through multiple pathways, and serve as a potential therapeutic drug for RA.

RETRACTED: Artificial intelligence medical system and dexmedetomidine for postoperative analgesia in orthopedic surgery patients

An embedded device is an object in the creation of a unique computing system. An embedded device system, usually, will be executed as a single application. However, these devices can be connected via a network connection. It can communicate via the other network devices. Also used lower reported pain scores at rest and activity using the Principle Component Analysis (PCA) in the first 24 h after surgery, it is reduced compared to the control group. The author dexmedetomil is, there is an opioid-sparing effect; its use is considered to be able to promote the postoperative analgesia. Total Knee Arthroplasty (TKA) reduces the most common end-stage variant of the operation of joint disease and Knee of patients with rheumatoid arthritis joint pain. However, TKA is postoperative recovery, affecting patient satisfaction, and overall results have continued severe postoperative pain, from moderate. Generally, narcotics have been utilized for perioperative agony the executives in broadly TKA. In any case, drugs and the constraint of sickness in clinical practice, such as respiratory sadness and urinary maintenance, have been related to unwanted unfavorable impacts—the motivation behind to examine the recent decision of postoperative torment the executives for TKA. Multimodal analgesia, including preemptive analgesics, is the best solution for perioperative pain management through several delivery routes. Multimodal analgesia, to promote the recovery of providing knee excellent pain relief, reduces the side effects of patients receiving opioid consumption and TKA.

Neuronal FcγRI mediates acute and chronic joint pain.

Although joint pain in rheumatoid arthritis (RA) is conventionally thought to result from inflammation, arthritis pain and joint inflammation are at least partially uncoupled. This suggests that additional pain mechanisms in RA remain to be explored. Here we show that FcγRI, an immune receptor for IgG immune complex (IgG-IC), is expressed in a subpopulation of joint sensory neurons and that, under naïve conditions, FcγRI crosslinking by IgG-IC directly activates the somata and peripheral terminals of these neurons to evoke acute joint hypernociception without obvious concurrent joint inflammation. These effects were diminished in both global and sensory neuron-specific Fcgr1 knockout mice. In murine models of inflammatory arthritis, FcγRI signaling was upregulated in joint sensory neurons. Acute blockade or global genetic deletion of Fcgr1 significantly attenuated arthritis pain and hyperactivity of joint sensory neurons without measurably altering joint inflammation. Conditional deletion of Fcgr1 in sensory neurons produced similar analgesic effects in these models. We therefore suggest that FcγRI expressed in sensory neurons contributes to arthritis pain independently of its functions in inflammatory cells. These findings expand our understanding of the immunosensory capabilities of sensory neurons and imply that neuronal FcγRI merits consideration as a target for treating RA pain.

(213) IgG-Immune Complex Directly Activates Joint Sensory Neurons through Neuronal FcγRI to Induce Arthritis Pain

Joint pain in rheumatoid arthritis (RA) represents a significant health burden. Although RA pain is conventionally thought to result from inflammation, it often persists even after control of inflammation with available therapies, suggesting the additional involvements of non-inflammatory mechanisms. Yet, such mechanisms remain largely unexplored. Our in situ hybridization assays suggested that the immune complex receptor FcγRI was expressed in a subpopulation of joint sensory neurons. Consistent with this finding, the proportion of joint sensory neurons exhibiting a Ca2+ increase in response to IgG-immune complex (IgG-IC), assayed both in vitro and in vivo, was lower in global FcγRI−/− mice, compared with wildtype mice. Injection of IgG-IC but not monomeric IgG into one ankle of naive mice evoked joint pain-related behaviors without concurrent joint swelling. This effect was diminished in global FcγRI−/− mice. Ablation of T and B cells, mast cells or macrophages had no effect on IgG-IC evoked nocifensive behaviors. Under arthritic conditions, FcγRI mRNA expression and function were upregulated in dorsal root ganglion (DRG) in a mouse model of antigen-induced arthritis (AIA). In vivo extracellular electrophysiological recordings on intact DRG showed that genetic deletion of FcγRI reduced the incidence of abnormal activity and mechanical hypersensitivity of joint sensory neurons in the context of AIA. Acute blockade of FcγRI with neutralizing antibody and genetic knockout of FcγRI significantly attenuated pain-related behaviors in the AIA model. Conversely, no significant differences between treatments or genotypes were observed in the inflamed joint in the expression level of cytokines or in immune cell infiltration. These findings indicate that FcγRI may contribute to arthritis pain through a non-inflammatory mechanism that parallels inflammation and joint damage and point towards a promising therapeutic target to consider for RA pain that is resistant to current anti-inflammatory treatments. Supported by NIAMS 1R01AR072230 to L.Q.

Nonopioid versus opioid agents for chronic neuropathic pain, rheumatoid arthritis pain, cancer pain and low back pain.

Chronic pain continues to be a major health issue throughout the world and a huge economic burden for nations around the world. While the use of opioids does have risks, they are still widely used by clinicians as a treatment option for various chronic pain conditions. This review explores and compares the efficacy and safety of opioid and nonopioid agents for the following commonly encountered chronic pain conditions: neuropathic pain, rheumatoid arthritis joint pain, cancer pain and low back pain. Our findings demonstrate that while there are several nonopioid pharmacologic options that are clinically effective, opioids maintain a role in the treatment of certain chronic pain conditions and should continue to have an important place in the armamentarium of clinicians.

Mechanisms for Joint Pain in Rheumatoid Arthritis (RA): from Cytokines to Central Sensitization.

Pain in rheumatoid arthritis (RA) may be due to different etiologies, ranging from peripheral inflammation to dysregulation of central nervous system (CNS) processing. This review evaluates relevant literature published on RA pain mechanisms in recent years. Despite successes of disease-modifying antirheumatic drugs (DMARDs), pain persists for many RA patients. Studies involving patient-reported outcomes, quantitative sensory testing, and neuroimaging indicate that, in addition to joint inflammation, abnormalities in CNS pain processing may contribute to pain. Some DMARDs (e.g., janus kinus inhibitors) may work via multiple pathways to decrease pain. Adjunctive treatments (e.g., antidepressants, antiepileptics) may also be useful in managing pain in RA patients with well-controlled disease. Both peripheral and central mechanisms play key roles in the expression of pain in RA. To effectively manage pain, physicians need accurate assessment tools to identify the pathways involved in each patient so that treatments may be appropriately targeted.

The effect of nerve mobilization exercise in patients with rheumatoid arthritis: a pilot study.

Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of the joints. The neurogenic inflammatory mechanism plays an important role in the inflammatory process of RA, and pathological changes in neural tissues in RA have also been noted. We aim to investigate treatment of the nervous system to relieve joint pain and inflammation in RA. Nerve mobilization, a nervous system-specific therapeutic exercise, was applied on RA patients to determine the effect of nerve mobilization on joint inflammation. Twelve RA patients were recruited from the community and were randomised into an experimental and a control group. In the experimental group, the subjects were taught a set of nerve mobilization exercises while the subjects in the control group were taught a set of gentle joint mobilization exercises. Both groups were instructed to practice the exercises daily. After a 4-week period, their RA pain scale (RAPS) and pain scores were examined, as well as the C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Subjects in the experimental group showed improvements in RAPS and pain scores after 4 weeks of nerve mobilization exercises, while CRP and ESR values remained unaffected. These preliminary data showed that nerve mobilization exercises might be beneficial in controlling joint pain in RA patients.

Do depression and anxiety reduce the likelihood of remission in rheumatoid arthritis and psoriatic arthritis? Data from the prospective multicentre NOR-DMARD study

ObjectiveTo investigate the predictive value of baseline depression/anxiety on the likelihood of achieving joint remission in rheumatoid arthritis (RA) and psoriatic arthritis (PsA) as well as the associations between baseline...

Foot orthoses in the management of chronic subtalar and talo crural joint pain in rheumatoid arthritis

BackgroundThis pilot study investigated whether semi-rigid and soft orthoses had an effect on pain, disability and functional limitation in participants with chronic rheumatoid hindfoot involvement. MethodsParticipants with chronic hindfoot pain were randomly assigned to 2 groups, commencing either with semi-rigid Subortholene orthoses or soft EVA orthoses. The Foot Function Index and the Ritchie Articular Index were administered pre- and post-intervention, which lasted for 3 months. Following a 2 week washout period, each group was switched over to the other type of orthoses. ResultsNine female participants (mean age 52.2years (SD 9.1); mean weight 71kg (SD 12.64); mean height 160cm (SD 5.18)) with a mean RA duration of 11.7years (SD 7.83), and a mean ankle/subtalar joint pain duration of 5.7years (SD 2.62), completed the programme. Mean improvement in FFI score for both orthoses resulted in the same statistical significance (p=0.001). Statistically significant reduction in pain, disability and functional limitation was observed for both interventions, together with improvement in the Ritchie Articular Index score. ConclusionBoth Subortholene and EVA orthoses significantly reduced pain, disability and functional limitations in participants with chronic ankle/subtalar joint pain in rheumatoid arthritis.

Low level light effects on inflammatory cytokine production by rheumatoid arthritis synoviocytes

Low level light therapy (LLLT) is being evaluated for treating chronic and acute pain associated with rheumatoid arthritis (RA) and other inflammatory diseases. The mechanisms underlying the effectiveness of LLLT for pain relief in RA are not clear. The objectives of this study were to determine whether LLLT decreased production of pro-inflammatory cytokines by cells from RA joints, and, if so, to identify cellular mechanisms. Synoviocytes from RA patients were treated with 810 nm radiation before or after addition of tumor necrosis factor-alpha (TNF-alpha). mRNA for TNF-alpha, interleukin (IL)-1beta, IL-6, and IL-8 was measured after 30, 60, and 180 minutes using RT-PCR. Intracellular and extracellular protein levels for 12 cytokines/chemokines were measured at 4, 8, and 24 hours using multiplexed ELISA. NF-kappaB activation was detected using Western blotting to follow degradation of IkappaBalpha and nuclear localization of the p65 subunit of NF-kappaB. Radiation at 810 nm (5 J/cm(2)) given before or after TNF-alpha decreases the mRNA level of TNF-alpha and IL-1beta in RA synoviocytes. This treatment using 25 J/cm(2) also decreases the intracellular levels of TNF-alpha, IL-1beta, and IL-8 protein but did not affect the levels of seven other cytokines/chemokines. TNF-alpha-induced activation of NF-kappaB is not altered by 810 nm radiation using 25 J/cm(2). The mechanism for relieving joint pain in RA by LLLT may involve reducing the level of pro-inflammatory cytokines/chemokines produced by synoviocytes. This mechanism may be more general and underlie the beneficial effects of LLLT on other inflammatory conditions.

Custom-made foot orthoses for the treatment of foot pain

Custom foot orthoses are commonly recommended for the treatment of foot pain. To evaluate the effectiveness of custom foot orthoses for different types of foot pain. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2007, Issue 2), MEDLINE (from January 1966), EMBASE (from January 1980), CINAHL (from January 1982) and the Physiotherapy Evidence Database (PEDro) (to June 2007). We also contacted authors of included trials and known researchers in the field and checked the reference lists of included trials to identify trials. No language or publication restrictions were applied. Randomised controlled trials and controlled clinical trials evaluating custom-made foot orthoses for any type of foot pain. Outcomes included quantifiable levels of foot pain, function, disability, health-related quality of life, participant satisfaction, adverse effects and compliance. Two authors independently selected trials, rated methodological quality and cross checked data extraction. Data were analysed separately for different diagnoses of foot pain and follow-up time points. Eleven trials involving 1332 participants were included: five trials evaluated custom-made foot orthoses for plantar fasciitis (691 participants); three for foot pain in rheumatoid arthritis (231 participants); and one each for foot pain in pes cavus (154 participants), hallux valgus (209 participants) and juvenile idiopathic arthritis (JIA) (47 participants). Comparisons to custom-made foot orthoses included sham orthoses; no intervention; standardised interventions given to all participants; non-custom (prefabricated) foot orthoses; combined manipulation, mobilisation or stretching; night splints; and surgery. Follow up ranged from one week to three years. Custom-made foot orthoses were effective for painful pes cavus (NNTB:5), rearfoot pain in rheumatoid arthritis (NNTB:4), foot pain in JIA (NNTB:3) and painful hallux valgus (NNTB:6); however, surgery was even more effective for hallux valgus and non-custom foot orthoses appeared just as effective for JIA but the analysis may have lacked sufficient power to detect a difference in effect. It is unclear if custom-made foot orthoses were effective for plantar fasciitis or metatarsophalangeal joint pain in rheumatoid arthritis. Custom-made foot orthoses were a safe intervention in all studies. There is limited evidence on which to base clinical decisions regarding the prescription of custom-made foot orthoses for the treatment of foot pain. Currently, there is gold level evidence for painful pes cavus and silver level evidence for foot pain in JIA, rheumatoid arthritis, plantar fasciitis and hallux valgus.

Investigation into the neural correlates of emotional augmentation of clinical pain

Although depressive mood is an important psychological determinate of chronic pain, the neural circuitry that mediates its influence on the pain experience is largely unknown. We used functional magnetic resonance imaging (FMRI) to investigate the neurophysiological interactions between depressive symptoms and disease-relevant pain in rheumatoid arthritis (RA) patients. RA is associated with chronic joint pain and swelling, but peripheral joint pathology often does not fully explain the amount of pain a patient experiences. We investigated the neural circuitry that relates joint pain and depressive symptoms and contrasted this with experimental heat pain. We hypothesized that (1) depressive symptoms influence the cerebral processing of provoked joint pain in RA, and (2) the interaction of depressive symptoms with pain processing contributes to the pain RA patients experience on a daily basis. Twenty patients underwent whole brain FMRI during which disease-relevant joint pain was provoked. Depressive symptoms were assessed using the Beck Depression Inventory (BDI). The tender-to-swollen joint ratio (T/S) was assessed as one component of the patients' clinical pain. BDI scores correlated significantly with T/S and medial prefrontal cortex (MPFC) activation during provoked joint pain. The association between BDI scores and T/S was partly mediated by the MPFC activation. Furthermore, the MPFC activation co-varied significantly with the FMRI signal in limbic areas and in areas that process self-relevant information. These results suggest that the MPFC may play an important role in mediating the relationship between depressive symptoms and clinical pain severity in RA, possibly by engaging brain areas important for affective and self-relevant processing.

Interleukin‐1β influences the effect of infliximab on temporomandibular joint pain in rheumatoid arthritis

Objectives: The aim of this study was to investigate the influence of plasma and synovial fluid tumour necrosis factor alpha (TNFα), interleukin‐1beta (IL‐1β), IL‐6, soluble TNF receptor II (TNF‐sRII), IL‐1 receptor antagonist (IL‐1ra), soluble IL‐1 receptor II (IL‐1sRII) and IL‐10 on the effect of the TNFα antibody infliximab on temporomandibular joint (TMJ) pain in patients with active rheumatoid arthritis (RA).Methods: Fifteen patients with TMJ pain taking methotrexate were included in the study. The effect of intravenous infusions of infliximab was assessed after 14 or 22 weeks. TMJ resting and movement pain was assessed by a visual analogue scale (VAS) (0–100 mm) and samples of venous blood and TMJ synovial fluid were collected before and after treatment.Results: The effect of infliximab on TMJ pain was influenced by pretreatment plasma levels of IL‐1β, IL‐1ra, and IL‐10 as well as pretreatment levels of TMJ synovial fluid IL‐1sRII. High pretreatment levels of these cytokines and receptors as well as the presence of rheumatoid factor (RF) were associated with no or minor reduction in TMJ pain after treatment.Conclusions: Systemic treatment of RA with a combination of infliximab and methotrexate seems to be insufficient to alleviate TMJ pain in patients with RF or high pretreatment plasma levels of IL‐1β.