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ID PMID Title PublicationDate abstract
27815799 CLA Has a Useful Effect on Bone Markers in Patients with Rheumatoid Arthritis. 2016 Dec Rheumatoid arthritis is a systemic, chronic disease which may increase the risk of osteoporosis. This study was carried out in order to examine the effect of conjugated linoleic acid (CLA) on bone markers in rheumatoid arthritis disease which is the most common autoimmune disease. The present study is a randomized double-blind clinical trial. Subjects included 52 patients with active rheumatoid arthritis who were divided into two groups. Group I received standard treatment plus 2 daily 1.25 g capsules (Containing about 2 g of 9-cis 11-trans isomer and 10-cis 12-trans isomer in ratio of 50 -50 CLA in glycerinated form), Group II received standard treatment plus 2 Placebo 1.25 g capsules containing sunflower oil with high oleic acid. Telopeptides C, osteocalcin, and MMP3 were analyzed by ELISA method, PGE(2) was done by competitive enzymatic immunoassay method, and IGF-1 was analyzed by the IRMA method based on the sandwich method and ALK-P of bone. Before and after the intervention, the questionnaires about general information, nutrition assessment and medical history were filled out by the subjects. Nutritional assessment was done by a 24-h record questionnaire for the three-day diet. The results were analyzed using SPSS software (version 18). FINDINGS: There was no significant difference between the groups in enzyme activity of ALK-P of bone, PGE(2) and MMP3 variables. However, differences between the two groups in terms of activity of telopeptides C, Osteocalcin, and IGF1 were significant (P < 0.05). CLA has a potentially beneficial effect on bone markers in patients with rheumatoid arthritis. Therefore, in order to study the effect of CLA on bone health in patients with RA and all patients with autoimmune and bone diseases more studies with longer duration and evaluation of bone mass density are required.
26535733 Lack of association between rare mutations of the SIAE gene and rheumatoid arthritis in a 2015 Oct 30 The function of rare genotypes encoding defective variants of sialic acid acetylesterase (SIAE) in some autoimmune diseases, including rheumatoid arthritis (RA), is ambiguous. We determined whether mutations in the SIAE gene are responsible for RA in a Han Chinese population.DNA was prepared from the venous leukocytes of 444 RA patients and 647 normal controls. The coding regions and adjacent intron sequences of SIAE were amplified by polymerase chain reaction. The products were then subjected to sequencing analysis. The detected variations were further evaluated in the normal controls and available family members by sequencing. Seven variants of RA were identified in this study, including four known single nucleotide polymorphisms SNPs (rs7941327, rs7941523, rs1942663, and rs12282107) and three novel SNPs. The genomic positions of the three novel SNPs are chr11:124013712, chr11:124023268, and chr11:124044505. No significant differences in the seven SNPs of SIAE were observed between patients with RA and controls in this cohort (P > 0.05). Three novel variations and four known SNPs in SIAE were detected in the Chinese RA patients and normal controls. Our results imply that SIAE does not play a major role in RA in this population.
27011180 Molecular Insight into Gut Microbiota and Rheumatoid Arthritis. 2016 Mar 22 Rheumatoid arthritis (RA) is a systemic, inflammatory, and autoimmune disorder. Gut microbiota play an important role in the etiology of RA. With the considerable progress made in next-generation sequencing techniques, the identified gut microbiota difference between RA patients and healthy individuals provides an updated overview of the association between gut microbiota and RA. We reviewed the reported correlation and underlying molecular mechanisms among gut microbiota, the immune system, and RA. It has become known that gut microbiota contribute to the pathogenesis of RA via multiple molecular mechanisms. The progressive understanding of the dynamic interaction between gut microbiota and their host will help in establishing a highly individualized management for each RA patient, and achieve a better efficacy in clinical practice, or even discovering new drugs for RA.
27122121 Treatment of rheumatoid arthritis (RA) in India-how and by whom: results from a speciality 2016 Sep This study was conducted in order to study (a) seropositive RA patients for their prior caregivers, diagnosis makers, drugs and doses taken and (b) the disease status at the first visit and the last visit, from the standpoint of whether they received optimum or suboptimum DMARD treatment. Prospectively entered data were extracted from a rheumatology-specific electronic health record for demography, diagnostic delay, prior caregivers, diagnosis makers, intake of DMARDs and glucocorticoids and disease activity state at first presentation and at the last visit using structured query language. Among 316 patients, prior caregivers were orthopaedicians (73.4 %), alternative systems of medicine practitioners (62 %), internists (38 %), rheumatologists (35.8 %), general practitioners (17 %) and others (12 %). The diagnosis of RA was made by rheumatologists (55.6 %), orthopaedicians (21 %), internists (12.6 %), physiotherapists (3.5 %), homeopaths (2.8 %), general practitioner (2.1 %), neurologists (1.4 %) and Ayurvedic physicians (0.7 %). The mean and the median diagnostic delay among 142 patients where information was available were 18 and 8.5 months, respectively (SD +23.2). Thirty-two percent of the patients had early disease, 48 % established disease and 20 % late disease at presentation. Sixty-six percent of the patients had taken DMARDs-methotrexate (56 %), hydroxychloroquine (46.2 %), leflunomide (18.7 %) and sulfasalazine (20.6 %)-and often in combinations. Different preparations, doses and schedules of glucocorticoids were taken orally or parentally by 51 %. Only one (0.3 %) patient had taken biological DMARDs prior to visiting this clinic. High or moderate disease activity was present in 84 % at the first clinic visit that fell to 14 % at the last clinic visit. The majority of patients with RA were treated by orthopaedicians and practitioners of alternative systems of medicine with only a third by rheumatologists. In 80 % of patients, the diagnosis was made 18 months at the onset, yet in 84 %, the disease control was poor. Non-use or suboptimal use of methotrexate appeared to be the main reason.
27163292 The growth factor midkine may play a pathophysiological role in rheumatoid arthritis. 2017 Jan OBJECTIVES: Midkine (MK) is involved in cell proliferation, differentiation, migration, and survival. In this study, we measured serum MK levels in rheumatoid arthritis (RA) and investigated the correlation of serum MK with RA disease activity. Expression and effect of MK in RA synovial tissue were also examined. METHODS: Serum MK and production of inflammatory mediators by rheumatoid synovial fibroblasts (RSFs) were measured by enzyme-linked immunosorbent assay. MK expression in synovial tissue was examined by immunohistochemistry. MK receptor expression was analyzed by RT-PCR and Western blotting. RESULTS: RA patients had a significantly higher serum MK level than healthy controls. In RA patients, the MK level was correlated with DAS28-ESR, disability index of the Health Assessment Questionnaire, and rheumatoid factor level. The serum MK level tended to be decreased by anti-TNF therapy. MK was expressed by synovial lining cells in RA synovial tissues and it enhanced the production of IL-6, IL-8, and CCL2 by RSFs. RSFs expressed LDL receptor-related protein 1, candidate receptor for MK. CONCLUSIONS: The serum MK level could be a marker of disease activity in RA and an indicator of a poor prognosis. MK may have a role in the pathogenesis of RA via induction of inflammatory mediators.
27483042 Advanced oxidation protein products induce apoptosis of human chondrocyte through reactive 2017 Feb Advanced oxidation production products (AOPPs) have been confirmed to accumulate in patients with rheumatoid arthritis (RA). Previous study demonstrated that AOPPs could accelerate cartilage destruction in rabbit arthritis model. However, the effect of AOPP stimulation on apoptosis of human chondrocyte and the underlying mechanisms remains unclear. This study demonstrated that exposure of chondrocyte to AOPPs resulted in cell apoptosis. AOPP stimulation triggered reactive oxygen species (ROS) production, which induced mitochondrial dysfunction and endoplasmic reticulum stress (ER stress) resulted in caspase activation. Furthermore, an antioxidant, N-acetylcysteine, markedly blocked these signals. Our study demonstrated that AOPPs induce apoptosis via ROS-related mitochondria- and ER-dependent signals in human chondrocyte. Targeting AOPP-triggered ROS generation might be as a promising option for patients with RA.
28068286 Pathobiochemical Mechanisms Relating Iron Homeostasis to Parameters of Inflammatory Activi 2016 Dec 1 AIM: To find the correlations between the parameters of iron homeostasis, inflammatory activity and autoimmune disorders in rheumatoid arthritis (RA). MATERIALS AND METHODS: The present study included 114 patients with RA and 42 healthy controls. We determined the parameters of iron homeostasis: serum iron, total iron binding capacity (TIBC), ferritin and soluble transferrin receptor (sTfR), the parameters of inflammatory activity: C-reactive protein (CRP), interleukin-6 (IL-6) and prohepcidin, and the parameters of autoimmune disorders: rheumatoid factor (RF), anti-cyclic citrullinated peptide (antiCCP) antibodies, and DAS 28. RESULTS: The levels of sTfR, CRP, IL-6 and prohepcidin were significantly higher in RA patients than those in the controls and the level of serum iron was significantly lower in RA than that in the control group. Unlike the controls, in RA, there was a significant positive correlation of sTfR with the parameters of inflammatory activity (IL-6, prohepcidin, ESR) and with the parameters of autoimmune disorders (DAS 28, RF, antiCCP). A negative correlation of serum iron with sTfR was found only in RA patients. Prohepcidin positively correlated with the parameters of inflammation (CRP, ESR) and with the parameters for evaluation of autoimmune disorders (DAS 28 and RF) in the RA group. CONCLUSION: Our study shows that the simultaneous determination of the two parameters sTfR and prohepcidin is most informative in evaluating the changes in iron homeostasis in RA. The increase of both parameters provides information for tissue iron deficiency (assessed by the level of sTfR), caused by the inflammation when prohepcidin is expressed.
27252230 Emphysematous aortitis leading to esophagopleural fistula. 2016 Oct Emphysematous aortitis is a form of septic aortitis. It is a rare disease with a high mortality rate, necessitating prompt diagnosis and aggressive treatment. We present the computed tomography features of emphysematous aortitis leading to esophageal rupture and esophageal-pleural fistula in a 76-year-old female with rheumatoid arthritis.
27837340 Comorbidity of gout and rheumatoid arthritis in a large population database. 2017 Mar Coexistence of rheumatoid arthritis and gout is considered to be unusual. The current study was designed as a population-based cross-sectional study, utilizing the medical database of Clalit Health Services, the largest healthcare provider organization in Israel. Data of adult patients who were previously diagnosed with rheumatoid arthritis was retrieved. For each patient, five age- and sex-matched control patients were randomly selected. Different parameters including BMI, socioeconomic status, and existence of gout as well as smoking and hypertension were examined for both groups. The study included 11,540 patients with rheumatoid arthritis and 56,763 controls. The proportion of gout in the study group was high compared to controls (1.61 vs. 0.92%, P < 0.001). In a multivariate analysis, rheumatoid arthritis was associated with gout (OR = 1.72, 95% CI 1.45-2.05, P = 0.00). The proportion of gout in rheumatoid arthritis patients is not lower than in the general population.
26902805 Synovial fluid matrix metalloproteinase-2 and -9 activities in dogs suffering from joint d 2016 Jul 1 The activity of matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fluids (SF) sampled from dogs with joint disorders was investigated by gelatin zymography and densitometry. Pro-MMP-2 showed similar activity levels in dogs with idiopathic polyarthritis (IPA; n=17) or canine rheumatoid arthritis (cRA; n=4), and healthy controls (n=10). However, dogs with cranial cruciate ligament rupture (CCLR; n=5) presented significantly higher pro-MMP-2 activity than IPA and healthy dogs. Meanwhile, dogs with IPA exhibited significantly higher activity of pro- and active MMP-9 than other groups. Activity levels in pro- and active MMP-9 in cRA and CCLR dogs were not significantly different from those in healthy controls. Different patterns of MMP-2 and MMP-9 activity may reflect the differences in the underlying pathological processes.
26043831 Associations Between PADI4 Gene Polymorphisms and Rheumatoid Arthritis: An Updated Meta-an 2015 May BACKGROUND AND AIMS: Studies investigating the association between the peptidylarginine deiminase 4 (PADI4) gene polymorphisms and rheumatoid arthritis (RA) reported conflicting results. The aim of this meta-analysis was to assess the association between PADI4 gene polymorphisms and RA. METHODS: A systematic literature search was conducted to identify relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of the association. RESULTS: A total of 34 studies from 28 articles involving 19859 patients with RA and 25771 healthy controls were included. Significant association of PADI4-94G/A polymorphism and RA was observed (OR = 0.891, 95% CI = 0.833-0.954, p = 0.001) in the overall study population and in the Asian populations (OR = 0.824, 95% CI = 0.759-0.894, p = 0.000) respectively. For the -92C/G polymorphism, a significant association was observed (OR = 1.481, 95% CI = 1.166-1.882, p = 0.001) in Africans. For the -90C/T polymorphism, a significant association was observed (OR = 0.576, 95% CI = 0.381-0.872, p = 0.009) in the Latin American population. The pooled estimates for the other polymorphisms were not statistically significantly associated with RA (PADI4-104C/T, -89A/G, -96T/C). CONCLUSIONS: This meta-analysis demonstrates that PADI4-94G/A polymorphism is associated with susceptibility to RA in the overall population and in the Asian population. The PADI4 -92C/G polymorphism confers susceptibility to RA in Africans and the PADI4-90C/T polymorphism was associated with RA in the Latin American population.
25499175 Association of Toll like receptor Asp299Gly with rheumatoid arthritis risk: a systematic r 2015 Mar OBJECTIVE: Rheumatoid arthritis (RA) is thought to be triggered by various genetic and environmental factors. Few human epidemiologic studies demonstrated that single nucleotide polymorphisms (SNPs) in Toll-like receptor (TLR) genes are associated with RA. We aimed to evaluate the effects of TLR polymorphisms on the risk of RA pathogenesis by using a meta-analysis approach. METHODS: Following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines, a systematic search and meta-analysis of the literature was conducted. We screened the medical literature based on keywords search in MEDLINE and EMBASE 'Toll-like receptor', 'polymorphism', and rheumatoid arthritis. Meta-analyses were performed under the random-effects model by using: (1) recessive, (2) homozygous, (3) dominant, (4) codominant and allele contrast models. RESULTS: A total of 3086 cases and 3756 controls in nine studies were included in the meta-analysis. Association between TLR4 Asp299Gly and RA risk was marginally significant [OR = 0.856 (95% CI, 0.716-1.022); P = 0.086] in the homozygous model. AA and GG homozygote genotypes tended to be significant protective factors against RA risk. CONCLUSION: Our overall analyses indicated that TLR4 Asp299Gly polymorphism might contribute to RA pathogenesis.
24291654 Mortality in rheumatoid arthritis: the impact of disease activity, treatment with glucocor 2015 Feb OBJECTIVES: To investigate the impact of disease activity, the course of the disease, its treatment over time, comorbidities and traditional risk factors on survival. METHODS: Data of the German biologics register RABBIT were used. Cox regression was applied to investigate the impact of time-varying covariates (disease activity as measured by the DAS28, functional capacity, treatment with glucocorticoids, biologic or synthetic disease modifying antirheumatic drugs (DMARDs)) on mortality after adjustment for age, sex, comorbid conditions and smoking. RESULTS: During 31 378 patient-years of follow-up, 463 of 8908 patients died (standardised mortality ratio: 1.49 (95% CI 1.36 to 1.63)). Patients with persistent, highly active disease (mean DAS28  > 5.1) had a significantly higher mortality risk (adjusted HR (HRadj)=2.43; (95% CI 1.64 to 3.61)) than patients with persistently low disease activity (mean DAS28 < 3.2). Poor function and treatment with glucocorticoids > 5 mg/d was significantly associated with an increased mortality, independent of disease activity. Significantly lower mortality was observed in patients treated with tumour necrosis factor α (TNFα) inhibitors (HRadj=0.64 (95% CI 0.50 to 0.81), rituximab (HRadj=0.57 (95% CI 0.39 to 0.84), or other biologics (HRadj=0.64 (95% CI 0.42 to 0.99), compared to those receiving methotrexate. To account for treatment termination in patients at risk, an HRadj for patients ever exposed to TNFα inhibitors or rituximab was calculated. This resulted in an HRadj of 0.77 (95% CI 0.60 to 0.97). CONCLUSIONS: Patients with long-standing high disease activity are at substantially increased risk of mortality. Effective control of disease activity decreases mortality. TNFα inhibitors and rituximab seem to be superior to conventional DMARDs in reducing this risk.
27912794 A genetic risk score composed of rheumatoid arthritis risk alleles, HLA-DRB1 haplotypes, a 2016 Dec 3 BACKGROUND: To prevent debilitating and irreversible joint damage, rheumatoid arthritis (RA) is often treated with tumor necrosis factor inhibitor (TNFi), but many patients do not respond to this costly therapy. Few predictors for response are known, and it has been proposed that genetic factors which influence the development of RA may also influence disease severity and response to therapy. Several previous studies have attempted to confirm this but results remain inconclusive. We expand on previous studies by including more RA risk alleles, and maximize power by combining them into a genetic risk score. METHOD: We linked genotyped RA patients from the Epidemiological Investigation of Rheumatoid Arthritis study to the Swedish Rheumatology Quality Register, identifying patients who started a TNFi as their first biological disease-modifying anti-rheumatic drug, with a return visit within 2-8 months after treatment start (N = 867). We calculated risk scores from 76 established RA risk SNPs, and four HLA-DRB1 amino acid positions, and tested whether risk scores or individual genetic risk factors could predict the European League Against Rheumatism (EULAR) response. RESULTS: We found no association between any of the risk scores or HLA-DRB1 haplotypes and EULAR response, neither overall nor stratified by anti-citrullinated protein/peptide antibody (ACPA) status. When evaluating each of the 76 SNPs, we found that the number of SNPs presenting significant associations was not higher than expected by chance (5/76 SNPs had p < 0.05 in ACPA-positive RA, 4/76 in ACPA-negative RA). CONCLUSION: Overall, known RA risk SNPs do not predict response to TNFi, either individually or when combined into a risk score. This does not support the hypothesis that genes influencing RA onset would also influence its prognosis and treatment response.
27887639 Prevalence, sensitivity and specificity of antibodies against carbamylated proteins in a m 2016 Nov 25 BACKGROUND: Antibodies against carbamylated proteins (anti-CarP) have been recently identified in the sera of patients with rheumatoid arthritis (RA). The objective of the study was to evaluate the prevalence, sensitivity and specificity of anti-CarP compared to anti-citrullinated peptide antibodies (ACPA) and rheumatoid factor (RF), replicating the existing data in a large cohort of Italian patients with RA and extending the evaluation to other autoimmune rheumatic diseases (AIRDs). METHODS: Serum samples (n = 607) from 309 patients with RA, 200 disease controls and 98 normal healthy subjects (NHS) were evaluated. Anti-CarP were detected using carbamylated fetal calf serum as the antigen. ACPAs were detected using second-generation ELISA and IgM RF was assessed as part of routine analysis. RESULTS: Anti-CarP antibodies were detected in 117 patients with RA (34.4%), ACPA in 190 patients (61.4%) and RF in 202 patients (65.3%). Two (2.04%) of the NHS were positive for anti-CarP, one NHS (1.02%) was positive for ACPA and three NHS were positive for RF (3.06%). Among disease controls, anti-CarP antibodies were detected in 33 patients (16.5%), ACPA in 29 patients (14.5%) and RF in 64 patients (32%). In particular, 16.8% of patients with systemic lupus erythematosus and 31.1% of patients with Sjögren syndrome were positive for anti-CarP. The sensitivity of anti-CarP, ACPA and RF was 46.8%, 61.8% and 64.4%, respectively and specificity was 91.95%, 89.93% and 76.51%, respectively. CONCLUSIONS: The present study extends the knowledge of anti-CarP antibodies, confirming previous data on the diagnostic accuracy of anti-CarP in RA in a large cohort of Italian patients. Anti-CarP antibodies demonstrated relatively low sensitivity and slightly higher specificity compared to ACPA and RF. Even if predominantly present in RA, anti-CarP was detected in a variable percentage of patients with other autoimmune rheumatic diseases and their generation could be attributed to the inflammatory status; the clinical relevance of anti-CarP antibodies in these latter patients should be further determined.
27796523 Adaptation and validation of the Rheumatoid Arthritis Quality of Life (RAQoL) questionnair 2017 Apr Rheumatoid arthritis (RA) is one of the most prevalent inflammatory rheumatic diseases. As it is a chronic and a lifelong destructive disease, the aim of the treatment is to reduce disability and improve quality of life. The Rheumatoid Arthritis Quality of Life (RAQoL) questionnaire is a patient-reported outcome measure, specific to RA. To adapt and validate the RAQoL for use in Serbia, two translation panels were involved to produce the Serbian RAQoL. After successful translation, face and content validity was determined via cognitive debriefing interviews. The psychometric properties of the questionnaire were examined, including reliability and construct validity, by using the Nottingham Health Profile (NHP) as a comparator scale. The RAQoL was translated successfully and rated as applicable, relevant and comprehensive by respondents. The questionnaire had high internal consistency (alpha = 0.94 at both time points) and test-retest reliability (r = 0.92). Moderately high correlations were found between the RAQoL and physical mobility, pain and energy level sections of the NHP, providing evidence of convergent validity. The RAQoL was able to distinguish between patients grouped by perceived general health, incidence of flare-up and disease severity. The Serbian language version of the RAQoL showed strong evidence of reliability and validity and is recommended for use in clinical trials and routine general practice in RA.
26273599 Inhibitory Effect of a Novel Antirheumatic Drug T-614 on the IL-6-Induced RANKL/OPG, IL-17 2015 T-614 (also named as iguratimod), a novel antirheumatic drug, could attenuate joint inflammation and articular damage in rheumatoid arthritis (RA) patients, providing a new therapy for RA. Here, we tested the role T-614 on the IL-6-induced receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG), IL-17, and MMP-3 expression in synovial fibroblasts from rheumatoid arthritis (RASFs) patients. T-614 decreased RANKL expression and RANKL/OPG ratio in IL-6-induced RASFs. We confirmed this effect by a decrease of the mRNA and protein RANKL and mRNA RANKL/OPG in RASFs exposed in vitro to T-614 or MTX. Markedly decreased levels of IL-17, retinoid-related orphan receptor C (RORc), and MMP-3 mRNA expression were also observed in IL-6-induced RASFs in the presence of T-614 or MTX compared with those in its absence. Furthermore, T-614 blocked expression of p-ERK1/2 protein without affecting ERK1/2 expression, indicating that the way that T-614 regulated RANKL expression might be ERK1/2 pathway. Our results suggest that T-614 yields a strong improvement in arthritis via exact suppression of RANKL/OPG, IL-17, and MMP-3 expression in RASFs.
27044368 CTGF promotes articular damage by increased proliferation of fibroblast-like synoviocytes 2016 Jul OBJECTIVES: Fibroblast-like synoviocytes (FLS) are a major component of the hyperplastic synovial pannus, which aggressively invades cartilage and bone during the course of rheumatoid arthritis (RA). Connective tissue growth factor (CTGF or CCN2) is a product of a growth factor-inducible immediate early gene and is involved in cell adhesion, proliferation, and differentiation. However, the role that CTGF plays in FLS proliferation has remained undetermined. The aim of this study was to identify the role of CTGF in regulating the proliferation of FLS derived from patients with RA. METHOD: CTGF levels in serum and synovial fluid (SF) were determined by enzyme-linked immunosorbent assay (ELISA). Expression of CTGF in FLS was determined using reverse transcription polymerase chain reaction (RT-PCR). FLS proliferation stimulated by CTGF was measured by thymidine incorporation. The influence of CTGF small interfering RNA (siRNA) on FLS apoptosis was detected by flow cytometry. RESULTS: CTGF was overexpressed in serum and SF samples from RA patients compared with samples from normal controls. Elevated levels of CTGF in RA SF promoted the proliferation of FLS. Furthermore, in samples from RA patients, CTGF was found to protect FLS from apoptosis and to sustain the expression of survivin in FLS. The expression of CTGF in FLS can be up-regulated by tumour necrosis factor (TNF)-α. CONCLUSIONS: Our findings indicate that CTGF plays a crucial role in the proliferation of FLS in RA and probably contributes to synovial lining cell hyperplasia and eventually to joint destruction in patients with RA.
27989011 Temporomandibular joint findings in patients with rheumatoid arthritis, ankylosing spondyl 2017 Nov AIM: The aim of the present study was to investigate the prevalence of temporomandibular joint (TMJ) symptoms in rheumatoid arthritis (RA), primary Sjögren's syndrome (pSS), and ankylosing spondylitis (AS) patients. METHODS: The present study consisted of 79 individuals with various rheumatic disease (study group: 39 with RA, 17 with AS, 23 with pSS) and 79 age- and sex-matched healthy controls (control group). Subjective symptoms of the TMJ were recorded by means of a questionnaire. And stomatognathic examination was then performed. RESULTS: The prevalence of subjective symptoms in patients with rheumatic disease (73.4%) were significantly higher than that of the controls (22.8%; P<.05). The most common objective symptoms were pain during lateral TMJ palpation (29.1% of patients overall, 8.9% of controls) and mandibular movements (19% of patients overall, 2.5% of controls), and muscle pain during palpation (38% of patients overall, 3.8% of controls). They were significantly higher in all of the rheumatic patients than the controls (P<.05). There was not a statistically-significant difference in the values for mandibular movements between the study and control groups (P>.05, Mann-Whitney U test). CONCLUSIONS: TMJ symptoms were observed to be higher in the patients with RA, AS and pSS than the control group. Dentists and rheumatologists should be aware of TMJ symptoms in patients with rheumatic diseases.
27396567 Metagenome-wide association studies: fine-mining the microbiome. 2016 Aug Metagenome-wide association studies (MWAS) have enabled the high-resolution investigation of associations between the human microbiome and several complex diseases, including type 2 diabetes, obesity, liver cirrhosis, colorectal cancer and rheumatoid arthritis. The associations that can be identified by MWAS are not limited to the identification of taxa that are more or less abundant, as is the case with taxonomic approaches, but additionally include the identification of microbial functions that are enriched or depleted. In this Review, we summarize recent findings from MWAS and discuss how these findings might inform the prevention, diagnosis and treatment of human disease in the future. Furthermore, we highlight the need to better characterize the biology of many of the bacteria that are found in the human microbiota as an essential step in understanding how bacterial strains that have been identified by MWAS are associated with disease.