Chronic Inflammatory Autoimmune Disease Research Articles

Comprehensive insights into rheumatoid arthritis: Pathophysiology, current therapies and herbal alternatives for effective disease management.

Rheumatoid arthritis is a chronic autoimmune inflammatory disease characterized by immune response overexpression, causing pain and swelling in the synovial joints. This condition is caused by auto-reactive antibodies that attack self-antigens due to their incapacity to distinguish between self and foreign molecules. Dysregulated activity within numerous signalling and immunological pathways supports the disease's development and progression, elevating its complexity. While current treatments provide some alleviation, their effectiveness is accompanied by a variety of adverse effects that are inherent in conventional medications. As a result, there is a deep-rooted necessity to investigate alternate therapeutic strategies capable of neutralizing these disadvantages. Medicinal herbs display a variety of potent bioactive phytochemicals that are effective in the complementary management of disease, thus generating an enormous potency for the researchers to delve deep into the development of novel phytomedicine against autoimmune diseases, although additional evidence and understanding are required in terms of their efficacy and pharmacodynamic mechanisms. This literature-based review highlights the dysregulation of immune tolerance in rheumatoid arthritis, analyses the pathophysiology, elucidates relevant signalling pathways involved, evaluates present and future therapy options and underscores the therapeutic attributes of a diverse array of medicinal herbs in addressing this severe disease.

The Role of H3K27me3-Mediated Th17 Differentiation in Ankylosing Spondylitis.

Ankylosing spondylitis (AS) is a common chronic progressive inflammatory autoimmune disease. T helper 17 (Th17) cells are the major effector cells mediating AS inflammation. Histone 3 Lys 27 trimethylation (H3K27me3) is an inhibitory histone modification that silences gene transcription and plays an important role in Th17 differentiation. The objective of this study was to investigate the expression of H3K27me3 in patients with AS and to explore its epigenetic regulation mechanism of Th17 differentiation during AS inflammation. We collected serum samples from 45 patients with AS at various stages and 10 healthy controls to measure their Interleukin-17 (IL-17) levels using ELISA. A quantitative polymerase chain reaction was used to quantify the mRNA levels of RORc and the signaling molecules of the JAK2/STAT3 pathway, JMJD3, and EZH2. Additionally, Western blot analysis was performed to quantify the protein levels of H3K27me3, RORγt, JAK2, STAT3, JMJD3, and EZH2 in cell protein extracts. The results showed that H3K27me3 expression in peripheral blood mononuclear cells (PBMCs) was significantly lower in patients with active AS compared to both the normal control groups and those with stable AS. Moreover, a significant negative correlation was observed between H3K27me3 expression and the characteristic transcription factor of Th17 differentiation, RORγt. We also discovered that patients with active AS exhibited significantly higher levels of JMJD3, an inhibitor of H3K27 demethylase, compared to the normal control group and patients with stable AS, while the expression of H3K27 methyltransferase (EZH2) was significantly lower. These findings suggest that H3K27me3 may be a dynamic and important epigenetic modification in AS inflammation, and JMJD3/EZH2 regulates the methylation level of H3K27me3, which may be one of the key regulatory factors in the pathogenesis of AS. These findings contribute to our understanding of the role of epigenetics in AS and may have implications for the development of novel therapeutic strategies for AS.

Full Guidelines—From the Medical Board of the National Psoriasis Foundation: Perioperative management of systemic immunomodulatory agents in patients with psoriasis and psoriatic arthritis

BackgroundSystemic immunomodulatory agents are indicated in the treatment of moderate-to-severe plaque psoriasis and psoriatic arthritis. Perioperative use of these medications may increase the risk of surgical site infection and complication. ObjectiveTo evaluate the risk of surgical site infection and complication in patients with chronic autoimmune inflammatory disease receiving immunomodulatory agents (tumor necrosis factor-alpha inhibitors, interleukin [IL]-12/23 inhibitor, IL-17 inhibitors, IL-23 inhibitors, cytotoxic T-lymphocyte–associated antigen-4 co-stimulator, phosphodiesterase-4 inhibitor, Janus kinase inhibitors, tyrosine kinase 2 inhibitor, cyclosporine, and methotrexate) undergoing surgery. MethodsWe performed a search of the MEDLINE PubMed database of patients with chronic autoimmune inflammatory disease on immune therapy undergoing surgery. ResultsWe examined 48 new or previously unreviewed studies; the majority were retrospective studies in patients with rheumatoid arthritis and inflammatory bowel disease. ConclusionFor low-risk procedures, TNF-alpha inhibitors, IL-17 inhibitors, IL-23 inhibitors, ustekinumab, abatacept, methotrexate, cyclosporine, and apremilast can safely be continued. For intermediate- and high-risk surgery, methotrexate, cyclosporine, apremilast, abatacept, IL-17 inhibitors, IL-23 inhibitors, and ustekinumab are likely safe to continue; however, a case-by-case approach is advised. Acitretin can be continued for any surgery. There is insufficient evidence to make firm recommendations on tofacitinib, upadacitinib, and deucravacitinib.

Clinical safety and feasibility of a novel implantable neuroimmune modulation device for the treatment of rheumatoid arthritis: initial results from the randomized, double-blind, sham-controlled RESET-RA study.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that causes persistent synovitis, bone damage, and progressive joint destruction. Neuroimmune modulation through electrical stimulation of the vagus nerve activates the inflammatory reflex and has been shown to inhibit the production and release of inflammatory cytokines and decrease clinical signs and symptoms in RA. The RESET-RA study was designed to determine the safety and efficacy of an active implantable device for treating RA. The RESET-RA study is a randomized, double-blind, sham-controlled, multi-center, two-stage pivotal trial that enrolled patients with moderate-to-severe RA who were incomplete responders or intolerant to at least one biologic or targeted synthetic disease-modifying anti-rheumatic drug. A neuroimmune modulation device (SetPoint Medical, Valencia, CA) was implanted on the left cervical vagus nerve within the carotid sheath in all patients. Following post-surgical clearance, patients were randomly assigned (1:1) to active stimulation or non-active (control) stimulation for 1min once per day. A predefined blinded interim analysis was performed in patients enrolled in the study's initial stage (Stage 1) that included demographics, enrollment rates, device implantation rates, and safety of the surgical procedure, device, and stimulation over 12 weeks of treatment. Sixty patients were implanted during Stage 1 of the study. All device implant procedures were completed without intraoperative complications, infections, or surgical revisions. No unanticipated adverse events were reported during the perioperative period and at the end of 12 weeks of follow-up. No study discontinuations were due to adverse events, and no serious adverse events were related to the device or stimulation. Two serious adverse events were related to the implantation procedure: vocal cord paresis and prolonged hoarseness. These were reported in two patients and are known complications of surgical implantation procedures with vagus nerve stimulation devices. The adverse event of vocal cord paresis resolved after vocal cord augmentation injections with filler and speech therapy. The prolonged hoarseness had improved with speech therapy, but mild hoarseness persists. The surgical procedures for implantation of the novel neuroimmune modulation device for the treatment of RA were safe, and the device and its use were well tolerated. NCT04539964; August 31, 2020.

Integrative analysis and validation of necroptosis-related molecular signature for evaluating diagnosis and immune features in Rheumatoid arthritis

ObjectivesRheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that is characterized by persistent morning stiffness, joint pain, and swelling. However, there is a lack of reliable diagnostic markers and therapeutic targets that are both effective and trustworthy. MethodsIn this study, gene expression profiles (GSE89408, GSE55235, GSE55457, and GSE77298) were obtained from the Gene Expression Omnibus database. Differentially expressed necroptosis-related genes were attained from intersection of necroptosis-related gene set, differentially expressed genes, and weighted gene co-expression network analysis. The LASSO, random forest, and SVM-RFE machine learning algorithms were utilized to further screen potential diagnostic genes for RA. Immune cell infiltration was analyzed using the CIBERSORT method. The expressions of diagnostic genes were validated through quantitative real-time PCR, western blotting, immunohistochemistry, and immunofluorescence staining in synovial tissues collected from three trauma controls and three RA patients. ResultsFive core necroptosis-related genes (FAS, CYBB, TNFSF10, EIF2AK2, and BIRC2) were identified as potential biomarkers for RA. Two different necroptosis patterns based on these five genes were confirmed to significantly correlated with immune cells (especially macrophages). In vitro experiments showed significantly higher mRNA and protein expression levels of CYBB and EIF2AK2 in RA patients compared to normal controls, consistent with the bioinformatics analysis results. ConclusionOur study identified a novel necroptosis-related subtype and five diagnostic biomarkers of RA, revealed vital roles in the development and occurrence of RA, and offered potential targets for clinical diagnosis and immunotherapy.

Gut-Brain Interactions and Their Impact on Astrocytes in the Context of Multiple Sclerosis and Beyond.

Multiple Sclerosis (MS) is a chronic autoimmune inflammatory disease of the central nervous system (CNS) that leads to physical and cognitive impairment in young adults. The increasing prevalence of MS underscores the critical need for innovative therapeutic approaches. Recent advances in neuroimmunology have highlighted the significant role of the gut microbiome in MS pathology, unveiling distinct alterations in patients' gut microbiota. Dysbiosis not only impacts gut-intrinsic processes but also influences the production of bacterial metabolites and hormones, which can regulate processes in remote tissues, such as the CNS. Central to this paradigm is the gut-brain axis, a bidirectional communication network linking the gastrointestinal tract to the brain and spinal cord. Via specific routes, bacterial metabolites and hormones can influence CNS-resident cells and processes both directly and indirectly. Exploiting this axis, novel therapeutic interventions, including pro- and prebiotic treatments, have emerged as promising avenues with the aim of mitigating the severity of MS. This review delves into the complex interplay between the gut microbiome and the brain in the context of MS, summarizing current knowledge on the key signals of cross-organ crosstalk, routes of communication, and potential therapeutic relevance of the gut microbiome. Moreover, this review places particular emphasis on elucidating the influence of these interactions on astrocyte functions within the CNS, offering insights into their role in MS pathophysiology and potential therapeutic interventions.

Single-cell RNA-seq reveals keratinocyte and fibroblast heterogeneity and their crosstalk via epithelial-mesenchymal transition in psoriasis

The pathogenesis of psoriasis, a chronic inflammatory autoimmune skin disease with a high global prevalence, remains unclear. We performed a high-resolution single-cell RNA sequencing analysis of 94,759 cells from 13 samples, including those from psoriasis model mice and wild-type mice. We presented a single-cell atlas of the skin of imiquimod-induced mice with psoriasis and WT mice, especially the heterogeneity of keratinocytes and fibroblasts. More interestingly, we discovered that special keratinocyte subtypes and fibroblast subtypes could interact with each other through epithelial–mesenchymal transition and validated the results with drug verification. Moreover, we conducted a tentative exploration of the potential pathways involved and revealed that the IL-17 signalling pathway may be the most relevant pathway. Collectively, we revealed the full-cycle landscape of key cells associated with psoriasis and provided a more comprehensive understanding of the pathogenesis of psoriasis.

Expression of Inflammatory Mediators in Biofilm Samples and Clinical Association in Multiple Sclerosis Patients in Remission-A Pilot Study.

Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of unknown etiology that affects the central nervous system and can lead to neurological impairment. Our aim was to determine whether MS patients also show inflammatory changes in the oral cavity more frequently than healthy individuals. For this purpose, we examined plaque samples for various mediators and their correlation with clinical findings. A study group (MS) and a control group were examined and compared. The plaque samples were analyzed for the expression of interleukins (IL-2, -6, -10), matrix metalloproteinases (MMP-7, MMP-9), and a surface antigen CD90 by quantitative real-time PCR. The clinical parameters examined were the Mombelli plaque index; bleeding on probing (BOP) index; periodontal pocket depth; and decayed, missing, and filled tooth (DMFT) index. The expression of MMP9 was significantly (p = 0.035) higher in the control group. The expression of IL-2 was increased four-fold in the MS group; however, this difference was not statistically significant. The mean PD (p < 0.001) and BOP index (p = 0.029) values were increased in the study group. The clinical parameters of the BOP index and PD were significantly amplified in the MS patients. However, no causal relationship between the investigated inflammatory mediators and the clinical findings could be established in this case series.

A narrative review on scientific evidence of mechanisms of naturopathy and yoga interventions for rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune systemic inflammatory disease, which has serious physical, psychological, and social consequences. Many RA patients continue to experience intolerable side effects from their treatments or an inadequate response, which leads to the disease progressing despite advancements in targeted biological and pharmacologic interventions. Examining the multi-modular, drugless approach of yoga and naturopathy to this autoimmune disease is equally important as it enables physicians to provide better care. Hence, the current review was undertaken to present an overview of the available scientific evidence on the mechanism of naturopathy and yoga therapeutic modalities in the management of RA. We searched PubMed and PubMed Central for pertinent English-language articles about the impact of yoga and naturopathy on RA. The results in this review are presented based on the therapeutic effect of yoga and various naturopathy treatment modalities with their mechanisms on RA. It shows naturopathy and yoga was effective in the management of RA due to its analgesic, anti-inflammatory, immunomodulatory and antioxidant effect.

A Comprehensive Ayurvedic Management of Amavata

Amavata is an Ama pradoshaja vikara, caused by Agnimandya, which leads to accumulation of Ama in Shleshmasthana and Prakopa of Vata dosha, resulting in pain, stiffness and swelling of joints, which closely resembles the chronic inflammatory autoimmune disorder called Rheumatoid arthritis. Prevalence of rheumatoid arthritis is approximately 0.8% worldwide and 0.5-0.75% in India. Materials and Methods: A 44 years female presented with pain in multiple joints associated with swelling and stiffness since 2 years was diagnosed as Amavata. The patient was treated with Kottamachukkadi lepa, Dashamoola kashaya and Dhanyamla Kayaseka, Vaitarana basti followed by Guduchyadi kashaya basti along with Rasayana and oral medications. Results: There was a significant improvement in overall symptoms. Conclusion: Contemporary medicine offers DMARDS and steroid medications for very long time as it is Auto immune condition. Whereas on other hand Panchakarma therapies can target on root cause of the Vyadhi and provide more promising results.

GAMBARAN RHEMATOID FACTOR (RF) PADA PETANI USIA 50-60 TAHUN

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, in which a person's immune system can be damaged and disrupted leading to the destruction of joint organs and layers on the sinoval, especially in the joints of the hands, legs, and knees. The most influential factors for rheumatoid arthritis (RA) are age, genetics, gender, immunity and lifestyle. One of the autoimmune diseases is rheumatoid arthritis with a presence of 49%. (RF). The study aims to find out the picture of Rheumatoid Factor in farmers aged 50-60 years in Pallangga district, Gowa district. The sample collection method in this study is accidental sampling. While the test method in this study is using the qualitative test of latex agglutination. The sample number in this research is 10 samples of serum with results showing that 1 positive sample occurred agglutinization, while 9 negative samples did not occur agglutination. Thus, it can be concluded that the results of the Rheumatoid Factor examination are mostly negative for rheumatic arthritis.

A rare case of childhood-onset systemic lupus erythematosus associated end-stage renal disease with cerebral abscess and hemorrhage

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease that affects multiple organs. More than half of the patients with SLE have kidney involvement, and up to 10% of patients with lupus nephritis develop end-stage renal disease (ESRD). Central nervous system (CNS) involvement in SLE occurs in 21% to 95% of patients. Severe neurological manifestations such as seizures, cerebrovascular disease, meningitis, and cerebrovascular accidents can develop in childhood-onset SLE, but cerebral infections, such as brain abscess and hemorrhage, are seldom reported in lupus nephritis, even in adults. Here, we report a rare case of childhood-onset SLE with ESRD, a cerebral abscess, and hemorrhage. A 9-year-old girl diagnosed with lupus nephritis was administered high-dose steroids and immunosuppressant therapy to treat acute kidney injury (AKI) and massive proteinuria. The AKI deteriorated, and after 3 months, she developed ESRD. She received hemodialysis three times a week along with daily peritoneal dialysis to control edema. She developed seizures, and imaging showed a brain abscess. This was complicated by spontaneous cerebral hemorrhage, and she became unstable. She died shortly after the hemorrhage was discovered. In conclusion, CNS complications should always be considered in clinical practice because they increase mortality, especially in those with risk factors for infection.

Phase Angle as a Marker of Physical Function in Non-Sarcopenic Rheumatoid Arthritis.

Background: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease. Most patients with RA face a barrier to participation in social activities or exercise due to joint pain, despite the beneficial effects of exercise and physical activity. Thus, RA may be a risk factor for sarcopenia in the clinical field. Bioelectrical impedance analysis-derived phase angle (PhA) reflects cellular health and is correlated with the prognosis of various diseases. However, its association with physical function in non-sarcopenic RA female patients remains unclear. We evaluated the association between PhA values and various physical function measures in female patients with non-sarcopenic RA. Methods: Thirty-five participants with RA were screened. One met the criteria for sarcopenia. Finally, 34 patients with non-sarcopenic RA were enrolled. This cross-sectional retrospective study evaluated upper- and lower-extremity strengths, cross-sectional area of rectus femoris, 6 min walking test, Borg scale score, sit-to-stand test, and physical function and mental health from 36-Item Short Form Health Survey scores. Results: In total, 34 female participants (mean age = 49.74 ± 8.15 years) were enrolled. In non-sarcopenic RA patients, PhA was significantly correlated with BMI and ASM/(height)2. Multicollinearity was not detected among the independent variables (VIF < 5). The final multivariable regression model identified ASM/height2 as a significant predictor of PhA among non-sarcopenic RA patients. Conclusion: Multivariable linear regression analyses identified appendicular skeletal muscle mass as a significant predictor of PhA. Bioelectrical impedance analysis-derived PhA is a valuable guidance tool for RA management. PhA can be a useful clinical biomarker of muscle status in non-sarcopenic RA patients.

NGF facilitates ICAM-1-dependent monocyte adhesion and M1 macrophage polarization in rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder in which monocytes adhering to synovial tissue differentiate into the pro-inflammatory M1 macrophage phenotype. Nerve growth factors (NGF) referred to as neurotrophins have been associated with inflammatory events; however, researchers have yet to elucidate the role of NGF in RA. Our examination of clinical tissue samples and analysis of data sourced from the Gene Expression Omnibus dataset unveiled elevated expression levels of M1 macrophage markers in human RA synovial tissue samples compared to normal tissue, with no such distinction observed for M2 markers. Furthermore, immunofluorescence data depicted increased expression levels of NGF and M1 macrophages in RA mice in contrast to normal mice. It appears that NGF stimulation facilitates macrophage polarization from the M0 to the M1 phenotype. It also appears that NGF promotes ICAM-1 production in human RA synovial fibroblasts, which enhances monocyte adhesion through the TrkA, MEK/ERK, and AP-1 signaling cascades. Our findings indicate NGF/TrkA axis as a novel target for the treatment of RA.

LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast-like synoviocyte in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, and the role of HOXA transcript at the distal tip (HOTTIP) in its pathogenesis remains underexplored. This study investigates the mechanism by which HOTTIP influences apoptosis and the inflammatory response of fibroblast-like synoviocytes (FLS). An RA mouse model was established, and clinical scores were analyzed. Pathological changes in synovial tissues, bone mineral density (BMD) of the paws, serum tartrate-resistant acid phosphatase (TRAP) activity, and TNF-α and IL-1β levels were assessed. FLS were transfected, and cell proliferation and apoptosis were examined. The RNA-pull-down assay determined HOTTIP's interaction with mixed-lineage leukemia 1 (MLL1), while RNA immunoprecipitation assay measured HOTTIP expression pulled down by MLL1. The levels of MLL1 and toll-like receptor 4 (TLR4) after MLL1 overexpression based on HOTTIP silencing were determined. Chromatin immunoprecipitation (ChIP) was performed with H3K4me3 as an antibody, followed by the evaluation of TLR4 expression. HOTTIP expression was elevated in RA mouse synovial tissues. Inhibition of HOTTIP led to reduced clinical scores, inflammatory infiltration, synovial hyperplasia, TRAP activity, and TNF-α and IL-1β levels, along with increased BMD. In vitro Interference with HOTTIP suppressed RA-FLS apoptosis and inflammation. HOTTIP upregulated TLR4 expression by recruiting MLL1 to facilitate TLR4 promoter methylation. MLL1 overexpression reversed HOTTIP silencing-mediated repression of RA-FLS apoptosis. Activation of H3K4 methylation counteracted HOTTIP knockout, ameliorating the inflammatory response. HOTTIP regulates TLR4 expression by recruiting MLL1, leading to TLR4 promoter methylation, thereby suppressing RA-FLS proliferation and inducing cell apoptosis and inflammatory response in RA.

PSORIATICUM: Topical Hypericum Perforatum for Moderate Plaque Psoriasis: Study Protocol for a Randomized Controlled Trial

Introduction: Psoriasis is an autoimmune chronic inflammatory disorder in which an increased amount of Tumor Necrosis Factor Alpha (TNF-α) leads to the formation of psoriatic plaques. Hypericum perforatum (HP) is a flowering plant used as an herbal medication due to its antimicrobial, wound-healing, and anti-inflammatory properties. Pilot studies have reported its ability to decrease the levels of TNF-α and severity of psoriatic plaques in moderate forms of psoriasis with fewer side effects and lower costs compared to standard treatment. More extensive studies are needed to confirm this. Objectives: To assess the effectiveness of topical HP in decreasing the mean total PASI score at the end of 12 weeks in patients with moderate plaque psoriasis. Methods: PSORIATICUM is a phase II, single-center, two-arm parallel, double-blinded randomized clinical trial that has the purpose of evaluating the efficacy of HP versus a control vehicle based on the decrease of the PASI score. The primary outcome is the total PASI score in the treatment group, compared to the control group at the end of the 12 weeks of testing. Normality will be evaluated using Kolmogorv-Smirnov, having the statistical significance of the findings tested using a two-tail Student’s T test for independent means or Mann-Whitney-Wilcoxon test. The secondary outcomes include the mean PASI change at weeks 4 and 8. Discussion: PSORIATICUM will provide information about the usefulness of Hypericum perforatum to treat psoriasis, allowing for future trials to study a safe and accessible alternative treatment for the condition.

Impact of treatment of rheumatoid arthritis on periodontal disease: A review.

Numerous studies support a bidirectional association between rheumatoid arthritis (RA), a chronic autoimmune degenerative inflammatory joint disease, and periodontitis, a chronic inflammatory disease caused by the immune reaction to bacteria organized in biofilms. RA and periodontitis are both multifactorial chronic inflammatory diseases that share common modifiable and non-modifiable risk factors. There is no cure for RA; treatment is based on lifestyle modifications and a variety of medications: nonsteroidal anti-inflammatory drugs (NSAID), glucocorticoids, and disease-modifying antirheumatic drugs (DMARDs, e.g., conventional synthetic DMARDs [csDMARDs]; biological DMARDs [bDMARD] and targeted synthetic DMARDs). There are molecular pathways of inflammation that are common to both RA and periodontitis. Thus, there is a potential effect of RA treatments on periodontitis. This systematic review aims to assess the impact of antirheumatic agents on periodontal conditions of patients suffering from both RA and periodontitis. PubMed/MEDLINE, Cochrane Library, and Embase online databases were systematically explored, and a manual search was performed to identify relevant studies published until January 2023. This review is registered in the PROSPERO database (CRD42023409006). A total of 2827 articles were identified, and 35 fulfilled the inclusion criteria. The included studies generally show a consensus that, at normal dosage, NSAID and corticosteroids have negligible impact on periodontium. Similarly, csDMARD alone or in combination with other csDMARD demonstrated no adverse effect on periodontium. Monotherapy with bDMARD had a positive effect on periodontal pocket depths and gingival inflammation in the longitudinal studies up to 6 months but showed negligible effect on the periodontium in interventional studies with a longer follow-up (9 months and 15.1 months). However, the combination of tumor necrosis factor (TNF)-α inhibitors+methotrexate (MTX) was associated with a rise in gingival inflammation. Due to the considerable heterogeneity of the study designs, a meta-analysis could not reasonably be performed. Within the limitations of the available studies, there is evidence to suggest that bDMARD monotherapy may improve the periodontal condition of RA patients with periodontal disease to a certain extent; the concomitant medication of TNF inhibitor+MTX could worsen gingival inflammation. More data are required to understand the impact of RA therapies on periodontal health.

Management of Patients with Oral Lesions Associated Systemic Lupus Erythematous (SLE) Nephritis: A Case Report

Introduction: Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease involving multi-organ such as mucocutaneous, musculoskeletal, and blood vessels with varied extraoral and intraoral clinical manifestations that require treatment from many medical specialists including dentists. The purpose of writing a case report is to describe how to manage oral lesions in patients with SLE Nephritis.&#x0D; Case report: A female 17 years old patient was referred to the oral medicine department of Dr. Hasan Sadikin General Hospital from the pediatrics department and was diagnosed with SLE nephritis due to complaints of ulcers on almost the entire oral mucosa. Extraoral examination revealed a moon face, malar rash, and erythematous rash on the palms of the hands. Intraoral examination revealed multiple ulcers, on labial mucosa, buccal mucosa, lateral right of the tongue, palate, and white plaque on the dorsum of the tongue. The therapy provided was non-pharmacological and pharmacological. Non-pharmacological therapies include oral hygiene instruction and communication, information, education. Pharmacological therapy is a solution containing sucralfate and prednisone which is gargled for one minute, then followed by nystatin oral suspension drug that discards after one minute, then followed by chlorhexidine digluconate 0,12% mouthwash, gargle for one minute, as an antiseptic (each drug is applied in 0,5 – 1 hours). The patient has received a systemic corticosteroid drug (methylprednisolone), but the treatment of oral lesions requires additional topical corticosteroids to accelerate the healing process because of its direct effect on the mucosa.&#x0D; Conclusion: The management of oral lesions using topical corticosteroids in patients with SLE nephritis can help accelerate the healing process.&#x0D; Keywords: Management, Oral Lesions, SLE nephritis

Rethinking Sjögren Beyond Inflammation: Considering the Role of Nerves in Driving Disease Manifestations.

Sjögren syndrome (SS) is a chronic inflammatory autoimmune disease characterized by destruction of mucosal glands resulting in dry eye and dry mouth. Ocular presentations can be heterogenous in SS with corneal nerves abnormalities that are structural, functional, or both. Some individuals present with corneal hyposensitivity, with a phenotype of decreased tear production and epithelial disruption. Others present with corneal hypersensitivity, with a phenotype of neuropathic pain including light sensitivity and pain out of proportion to signs of tear dysfunction. A similar correlate can be found outside the eye, with dry mouth predominating in some individuals while pain conditions predominate in others. Understanding how nerve status affects SS phenotype is an important first step to improving disease management by targeting nerve abnormalities, as well as inflammation.

Influence of periodontal treatment on rheumatoid arthritis clinical parameters

Periodontitis is a common chronic inflammatory disease characterized by destruction of tooth-supporting tissues, including alveolar bone, periodontal ligament, and cementum. It is the leading cause of dental loss and is considered one of the two biggest threats to oral health (Zhao et al., 2018). Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by swelling of the joints, joint tenderness, and destruction of the synovial joints, leading to severe incapacitation and premature mortality as it involves systemic effects. Both have been related, because the severity of RA is greater in patients with the first disease (Mercado et al., 2001) and Porphyromonas gingivalis, is also identified in synovial fluid and not only in damaged periodontal tissue. The proposed research was a prospective clinical trial with a quantitative approach carried out in the dental clinic of UNIOESTE in 90 days with 20 patients suffering from the autoimmune disease. Improvements in the disease were noted by means of analysis by the T, DAS 28 and VAS tests when the periodontal suitability was chosen.