MRI characteristics of rheumatoid arthritis in the temporomandibular joint.
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ABSTRACT:
SUBMITTER: Kretapirom K
PROVIDER: S-EPMC3667508 | biostudies-other | 2013
REPOSITORIES: biostudies-other
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Project description:OBJECTIVES: The aim of this study was to determine the prevalence of incidental findings in MRI of the temporomandibular joint (TMJ). METHODS: MRI reports of 730 patients were assessed. The reports were analysed by one consultant and one clinical lecturer in dental and maxillofacial radiology. The prevalence of intracranial and extracranial incidental findings was recorded and categorized. RESULTS: There were 53 (7.3%) incidental findings, of which 11 (1.5%) were intracranial and 42 (5.7%) were extracranial (divided into paranasal sinuses, mastoid air cells, muscle hypertrophy, lymphadenopathy and salivary glands). A total number of eight intracranial findings needed further dedicated imaging and/or specialist clinical opinion. Only one tumour (a meningioma) was found and required surgical intervention. CONCLUSIONS: Incidental findings on TMJ MRI are rare but not unheard of. The clinical relevance of incidental findings can be significant, and it is therefore important to ensure that the full data set of images is inspected, including any scout slices. A close working relationship between the areas of dental and maxillofacial radiology and neuroradiology is essential in expediting a second opinion relating to intracranial findings. All incidental findings should be communicated to referring clinicians in a timely manner, based on their urgency and clinical significance.
| S-EPMC3853509 | biostudies-other
Project description:ObjectiveJuvenile idiopathic arthritis (JIA) frequently affects the temporomandibular joints (TMJs) and is often undetected by history, examination, and plain imaging. Qualitative assessment of gadolinium-enhanced magnetic resonance images (MRIs) is currently the standard for diagnosis of TMJ synovitis associated with JIA. The purpose of this study is to apply a quantitative analysis of synovial enhancement to MRIs of patients with and without JIA to establish a disease threshold and sensitivity and specificity for the technique.MethodsThis is a retrospective case-control study of children (age ≤16 years) who had MRIs with gadolinium including the TMJs. Subjects were divided into a JIA group and a control group. From a coronal T1-weighted image, a ratio (enhancement ratio [ER]) of the average pixel intensity within three 0.2-mm2 regions of interest (ROIs) in the TMJ synovium to that of a 50-mm2 ROI of the longus capitis muscle was calculated. Receiver operating characteristic curves were used to determine the sensitivity and specificity. The inter- and intraexaminer reliability was evaluated with Bland-Altman plots and 2-way mixed, absolute agreement intraclass correlation coefficients.ResultsThere were 187 and 142 TMJs included in the JIA and control groups, respectively. An ER threshold of 1.55 had a sensitivity and specificity for detecting synovitis of 91% and 96%, respectively. The inter- and intraexaminer reliability was excellent.ConclusionCalculating a ratio of pixel intensity between the TMJ synovium and the longus capitis muscle is a reliable way to quantify synovial enhancement. An ER of 1.55 differentiates normal TMJs from those affected by inflammatory arthritis.
| S-EPMC5573997 | biostudies-literature
Project description:To introduce a new approach to reconstruct a 3D model of the TMJ using magnetic resonance imaging (MRI) and cone-beam computed tomography (CBCT) registered images, and to evaluate the intra-examiner reproducibility values of reconstructing the 3D models of the TMJ.MRI and CBCT images of five patients (10 TMJs) were obtained. Multiple MRIs and CBCT images were registered using a mutual information based algorithm. The articular disc, condylar head and glenoid fossa were segmented at two different occasions, at least one-week apart, by one investigator, and 3D models were reconstructed. Differences between the segmentation at two occasions were automatically measured using the surface contours (Average Perpendicular Distance) and the volume overlap (Dice Similarity Index) of the 3D models. Descriptive analysis of the changes at 2 occasions, including means and standard deviation (SD) were reported to describe the intra-examiner reproducibility.The automatic segmentation of the condyle revealed maximum distance change of 1.9±0.93 mm, similarity index of 98% and root mean squared distance of 0.1±0.08 mm, and the glenoid fossa revealed maximum distance change of 2±0.52 mm, similarity index of 96% and root mean squared distance of 0.2±0.04 mm. The manual segmentation of the articular disc revealed maximum distance change of 3.6±0.32 mm, similarity index of 80% and root mean squared distance of 0.3±0.1 mm.The MRI-CBCT registration provides a reliable tool to reconstruct 3D models of the TMJ's soft and hard tissues, allows quantification of the articular disc morphology and position changes with associated differences of the condylar head and glenoid fossa, and facilitates measuring tissue changes over time.
| S-EPMC5241008 | biostudies-literature
Project description:ObjectiveAlbuminuria is a marker for subclinical cardiovascular disease (CVD) in the general population. It is uncertain whether this association is present in patients with rheumatoid arthritis (RA), a population with increased atherosclerosis and CVD events.MethodsUrine albumin from a spot morning collection was measured, and the urine albumin-to-creatinine ratio (uACR) was calculated for RA patients and a population-based sample of demographically matched non-RA controls. Associations of elevated uACR (?25 mg/gm for women and ?17 mg/gm for men) with CVD risk factors and measures of atherosclerosis (coronary artery calcification, ultrasound-determined maximal intima-media thickness of the common carotid artery and internal carotid artery [ICA], and the presence of focal plaque in the ICA) were compared cross-sectionally according to RA status.ResultsWe compared 196 RA patients with 271 non-RA controls. Elevated uACR was found in 18% of the RA patients compared with 17% of the controls (P = 0.89). After adjustment, RA was associated with 57% lower odds of elevated uACR (P = 0.016). Higher serum creatinine levels and hypertension were both strongly and significantly associated with elevated uACR in the control group but not in the RA group (both P for interaction < 0.05). Among RA characteristics, the adjusted prevalence of elevated uACR among those treated with tumor necrosis factor inhibitors was less than half that among those not so treated (9% versus 20%, respectively; P = 0.047).ConclusionThere was no association in the RA group of elevated uACR with measures of atherosclerosis or with several key cardiometabolic risk factors, which suggests a lower usefulness of elevated uACR as an indicator of subclinical CVD in RA.
| S-EPMC5899611 | biostudies-literature
Project description:Stratifying patients on the basis of molecular signatures could facilitate development of therapeutics that target pathways specific to a particular disease or tissue location. Previous studies suggest that pathogenesis of rheumatoid arthritis (RA) is similar in all affected joints. Here we show that distinct DNA methylation and transcriptome signatures not only discriminate RA fibroblast-like synoviocytes (FLS) from osteoarthritis FLS, but also distinguish RA FLS isolated from knees and hips. Using genome-wide methods, we show differences between RA knee and hip FLS in the methylation of genes encoding biological pathways, such as IL-6 signaling via JAK-STAT pathway. Furthermore, differentially expressed genes are identified between knee and hip FLS using RNA-seq. Double-evidenced genes that are both differentially methylated and expressed include multiple HOX genes. Joint-specific DNA signatures suggest that RA disease mechanisms might vary from joint to joint, thus potentially explaining some of the diversity of drug responses in RA patients.
2016-06-09 | GSE80072 | GEO
Project description:Stratifying patients on the basis of molecular signatures could facilitate development of therapeutics that target pathways specific to a particular disease or tissue location. Previous studies suggest that pathogenesis of rheumatoid arthritis (RA) is similar in all affected joints. Here we show that distinct DNA methylation and transcriptome signatures not only discriminate RA fibroblast-like synoviocytes (FLS) from osteoarthritis FLS, but also distinguish RA FLS isolated from knees and hips. Using genome-wide methods, we show differences between RA knee and hip FLS in the methylation of genes encoding biological pathways, such as IL-6 signaling via JAK-STAT pathway. Furthermore, differentially expressed genes are identified between knee and hip FLS using RNA-seq. Double-evidenced genes that are both differentially methylated and expressed include multiple HOX genes. Joint-specific DNA signatures suggest that RA disease mechanisms might vary from joint to joint, thus potentially explaining some of the diversity of drug responses in RA patients.
2016-06-09 | GSE80071 | GEO
Project description:ObjectiveSubclinical joint inflammation in patients with arthralgia is predictive for progression to rheumatoid arthritis (RA). However, the time course of progression for bone marrow edema (osteitis), synovitis, and/or tenosynovitis is unsettled. This longitudinal study assessed the course of magnetic resonance imaging (MRI)-detected subclinical joint inflammation during progression to RA.MethodsPatients that progressed from clinically suspect arthralgia (CSA) to RA underwent 1.5-T MRI of the metacarpophalangeal (MCP), wrist, and metatarsophalangeal (MTP) joints at presentation with arthralgia and at first identification of synovitis assessed through physical examination (n?=?31). MRIs were evaluated for osteitis, synovitis, tenosynovitis, and erosions by two readers, blinded for clinical data and order in time. To estimate changes in MRI scores between the asymptomatic state and CSA onset, scores of MRI features at CSA baseline were compared with scores from age-matched symptom-free persons.ResultsAt presentation with CSA, synovitis and tenosynovitis scores were higher than scores from age-matched symptom-free persons (p?=?0.004 and p?=?0.001, respectively). Anti-citrullinated protein antibody (ACPA)-positive arthralgia patients also had increased osteitis scores (p?=?0.04). Median duration between presentation with arthralgia and RA development was 17 weeks. During progression to RA, synovitis and osteitis increased significantly (p?=?0.001 and p?=?0.036, respectively) in contrast to tenosynovitis and erosion scores. This pattern was similar in both ACPA subsets, although statistical significance was reached for synovitis and osteitis in ACPA-negative but not ACPA-positive RA.ConclusionIncreased tenosynovitis and synovitis scores at CSA onset and the increase in synovitis and osteitis during progression to RA suggest an 'outside-in' temporal relationship of arthritis development, in particular for ACPA-negative RA. For ACPA-positive RA, further studies are needed.
| S-EPMC6249752 | biostudies-literature
Project description:BackgroundOsteoblasts participating in the inflammation regulation gradually obtain concerns. However, its role in joint inflammation of rheumatoid arthritis (RA) is largely unknown. Here, we investigated the role of osteoblastic pleckstrin homology domain-containing family O member 1 (PLEKHO1), a negative regulator of osteogenic lineage activity, in regulating joint inflammation in RA.MethodsThe level of osteoblastic PLEKHO1 in RA patients and collagen-induced arthritis (CIA) mice was examined. The role of osteoblastic PLEKHO1 in joint inflammation was evaluated by a CIA model and a K/BxN serum-transfer arthritis (STA) model which were induced in osteoblast-specific Plekho1 conditional knockout mice and mice expressing high Plekho1 exclusively in osteoblasts, respectively. The effect of osteoblastic PLEKHO1 inhibition was explored in a CIA mice model and a non-human primate arthritis model. The mechanism of osteoblastic PLEKHO1 in regulating joint inflammation were performed by a series of in vitro studies.ResultsPLEKHO1 was highly expressed in osteoblasts from RA patients and CIA mice. Osteoblastic Plekho1 deletion ameliorated joint inflammation, whereas overexpressing Plekho1 only within osteoblasts exacerbated local inflammation in CIA mice and STA mice. PLEKHO1 was required for TRAF2-mediated RIP1 ubiquitination to activate NF-κB for inducing inflammatory cytokines production in osteoblasts. Moreover, osteoblastic PLEKHO1 inhibition diminished joint inflammation and promoted bone formation in CIA mice and non-human primate arthritis model.ConclusionsThese data strongly suggest that the highly expressed PLEKHO1 in osteoblasts contributes to joint inflammation in RA. Targeting osteoblastic PLEKHO1 may exert dual therapeutic action of alleviating joint inflammation and promoting bone formation in RA.
| S-EPMC6442230 | biostudies-literature
Project description:We conducted a genetic analysis of the developing temporo-mandibular joint (TMJ), a highly specialized synovial joint that permits movement and function of the mammalian jaw. First, we used laser capture microdissection to perform a genome-wide expression analysis of each of its developing components. The expression patterns of genes identified in this screen were examined in the TMJ and compared to other synovial joints including the shoulder joint and the hip joint. Striking differences were noted, indicating that the TMJ forms via a distinct molecular program. Several components of the Hedgehog (Hh) signaling pathway are among the genes identified in the screen, including Gli2, which is expressed specifically in the condyle and in the disk of the developing TMJ. We found that mice deficient in Gli2 display aberrant TMJ development such that the condyle loses its growth plate-like cellular organization and no disk is formed. In addition, we utilized a conditional strategy to remove activity of the Hh co-receptor encoded by Smo from chondrocyte progenitors. This cell autonomous loss of Hh signaling allows for disk formation, but the resulting structure fails to separate from the condyle. Thus, these experiments establish that Hh signaling acts at two distinct steps in disk morphogenesis, condyle initiation and disk-condyle separation, and provide a molecular framework for future studies of the TMJ. Experiment Overall Design: Mouse embryos fresh frozen and TMJ tissue captured by LCM. 3 samples in biological triplicate.
2009-10-23 | E-GEOD-17473 | biostudies-arrayexpress
Project description:Objective:To characterize the expression of malondialdehdye-acetaldehyde (MAA) adducts and anti-MAA antibody in articular tissues and serum of patients with RA. Methods:Paired sera and SF were examined from 29 RA and 13 OA patients. Anti-MAA antibody, RF, ACPA and total immunoglobulin were quantified. SF-serum measures were compared within and between disease groups. The presence and co-localization of MAA, citrulline and select leukocyte antigens in RA and OA synovial tissues were examined using immunohistochemistry. Results:Circulating and SF anti-MAA antibody concentrations were higher in RA vs OA by 1.5- to 5-fold. IgG (P < 0.001), IgM (P = 0.006) and IgA (P = 0.036) anti-MAA antibodies were higher in paired RA SF than serum, differences not observed for total immunoglobulin, RF or ACPA. In RA synovial tissues, co-localization of MAA with citrulline and CD19+ or CD27+ B cells was demonstrated and was much higher in magnitude than MAA or citrulline co-localization with T cells, monocytes, macrophages or dendritic cells (P < 0.01). Conclusion:Anti-MAA antibodies are present in higher concentrations in the RA joint compared with sera, a finding not observed for other disease-related autoantibodies. Co-localization of MAA and citrulline with mature B cells, coupled with the local enrichment of anti-MAA immune responses, implicates MAA-adduct formation in local autoantibody production.
| S-EPMC5850833 | biostudies-other