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Sjögren's Syndrome Patients (sjögren + syndrome_patient)

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Medical Sciences	100%

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Clinical and microbiological studies of periodontal disease in Sjögren's syndrome patients

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2 2002
B. Kuru
Abstract Background: Little is known about the periodontal status of patients with Sjögren's Syndrome (SS), a chronic inflammatory autoimmune disease characterized by xerophthalmia and xerostomia. The aim of the present study was to evaluate whether the periodontal status of SS patients, in terms of clinical and microbiological parameters, differs from systemically healthy age- and gender-matched controls. Methods: 8 primary SS and 10 secondary SS patients were examined in comparison with 11 control subjects. All patients were diagnosed by the European Community Criteria. Control subjects were systemically healthy and not undergoing periodontal treatment. The comparison of clinical status was made in terms of mean periodontal parameters (plaque index, gingival index, gingival recession, probing pocket depth, probing attachment level and bleeding on probing) as well as the frequency distribution of probing pocket depth and probing attachment level measurements. Microbiological assays of the subgingival dental plaque samples were carried out by both a chairside enzyme test (Periocheck®) for the detection of peptidase activity (PA) and a polymerase chain reaction (PCR) analysis for 9 selected periodontal micro-organisms (Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Prevotella intermedia, Treponema denticola, Porphyromonas gingivalis, Eikenella corrodens, Campylobacter rectus, Bacteroides forsythus, Streptococcus oralis). Results: The occurrence, severity and extent of periodontal lesions were not significantly different between the 3 patient groups for all periodontal parameters examined. No significant differences in the sub-gingival plaque samples from control, primary or secondary SS patients for the PA test, frequency or type of periodontal micro-organisms observed. Conclusion: No significant differences could be detected in either clinical or microbiological parameters of primary or secondary SS patients compared with that of control subjects. The results of the present study thus support the notion that the periodontal status of patients with SS do not differ from systemically healthy age- and gender-matched controls. Zusammenfassung Hintergrund: Es ist wenig über den parodontalen Status von Patienten mit Sjögren Syndrom (SS) bekannt, einer chronischen entzündlichen Autoimmunerkrankung, die durch Xerophtalmie und Xerostomie charakterisiert ist. Das Ziel der vorliegenden Studie war zu überprüfen, ob der parodontale Status der SS-Patienten bi Berücksichtigung der klinischen und mikrobiologischen Parameter von demjenigen bei systemisch gesunden alters- und geschlechtspassenden Kontrollen abweicht. Methoden: 8 primäre SS und 10 sekundäre SS Patienten wurden mit 11 Kontrollpersonen vergleichend untersucht. Alle Patienten waren durch Kriterien der EU diagnostiziert. Die Kontrollpersonen waren systemisch gesund und erhielten keine parodontale Behandlung. Der Vergleich des klinischen Status wurde auf der Basis von mittleren parodontalen Parametern (Plaque-Index, Gingivaindex, gingivale Rezession, Sondierungstiefe, Stützgewebeniveau, Provokationsblutung) sowie der Verteilungsmuster der Sondierungstiefe und des Stützgewebeniveaus vorgenommen. Mikrobiologische Assay's von subgingivalen Plaqueproben wurden sowohl mit einem chairside Enzymtest (Periocheck®) für die Feststellung der Peptidaseaktivität (PA) und einer Polymerasekettenreaktion (PCR) für 9 selektierte parodontale Mikroorganismen (Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Prevotella intermedia, Treponema denticola, Porphyromonas gingivalis, Eikenella corrodens, Campylobacter rectus, Bacteroides forsythus, Streptococcus oralis) durchgeführt. Ergebnisse: Das Vorkommen, die Schwere und die Ausdehnung von parodontalen Läsionen unterschied sich nicht signifikant zwischen den 3 Patientengruppen für alle geprüften parodontalen Parameter. Es gab auch keine signifikanten Differenzen in den subgingivalen Plaqueproben von den Kontrollen, den primären oder sekundären SS Patienten für die PA Teste und Frequenz oder Art von beobachteten parodontalen Mikroorganismen. Schlussfolgerung: Es konnten keine signifikanten Differenzen sowohl bei den klinischen oder mikrobiologischen Parametern von primären oder sekundären SS Patienten im Vergleich mit Kontrollpersonen entdeck werden. Die Ergebnisse der vorliegenden Studie unterstützen die Ansicht, dass sich der parodontale Status von Patienten mit SS nicht von demjenigen gesunder alters- und geschlechtspassender Kontrollen unterscheidet. Résumé Origine: On en sait peu sur l'état parodontal des patients atteints du syndrome de Sjögren (SS), une maladie chronique autoimmune inflammatoire caractérisée par une xérophtalmie et une xérostomie. Le but de cette étude était d'évaluer si l'état parodontal des patients SS, en terme de paramètres cliniques et microbiologiques était différent de sujets contrôles en bonne santé générale du même âge et du méme sexe. Méthodes: 8 patients atteints de SS primaires et 10 de SS secondaires furent examinés et comparés avec des sujets contrôles. Tous les patients étaient diagnostiqués selon les critères de la communauté européenne. Les sujets contrôles étaient en bonne santé générale et ne suivaient pas de traitement parodontal. La comparaison des états parodontaux fut réalisée pour les paramètres cliniques moyens (indice de plaque, gingival, récession gingivale, profondeur de poche au sondage, niveau d'attache et saignement au sondage) et aussi pour la frèquence de distribution des mesures des profondeurs de poche au sondage et des niveaux d'attache. Les tests microbiologiques des échantillons de plaque sous-gingivale ont été réalisés à la fois par un test enzymatique au fauteuil (Periocheck®) pour la détection de l'activité peptidase (PA) et par réaction de polymérase en chaine (PCR) pour 9 micro-organismes parodontaux sélectionnés (Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Prevotella intermedia, Treponema denticola, Porphyromonas gingivalis, Eikenella corrodens, Campylobacter rectus, Bacteroides forsythus, Streptococcus oralis). Résultats: La survenue, la sévérité et l'étendue de la maladie parodontale n'étaient pas significativement différente entre les 3 groupes de patients pour tous les paramètres parodontaux examinés. Aucune différence significative ne fut observée entre les échantillons de plaque sous-gingivale des contrôles et ceux des patients atteints de SS primaire et secondaire, pour PA, la frèquence ou le type de micro-organismes. Conclusions: Aucune différence significative ne put être détectée, ni pour les paramètres cliniques, ni pour les paramètres microbiologiques des patients atteints de SS primaire ou secondaire lorsque l'on comparait avec les sujets contrôles. Les résultats de cette étude corroborent ainsi l'idée suivant laquelle l'état parodontal des patients atteints de SS ne différe pas de celui des sujets en bonne santé du même âge et du même sexe. [source]

Gene expression profile in the salivary glands of primary Sjögren's syndrome patients before and after treatment with rituximab

ARTHRITIS & RHEUMATISM, Issue 8 2010
Valérie Devauchelle-Pensec
Objective Primary Sjögren's syndrome (SS) is a complex disorder, in part due to B cell abnormalities. Although anti,B cell therapy is promising in primary SS, no treatment has yet been demonstrated to modify the disease course. This open-label study was undertaken to evaluate the efficacy of rituximab in primary SS and to investigate whether expression of specific genes is associated with efficacy of this treatment. Methods Fifteen patients with primary SS were treated in an open-label trial. Salivary gland biopsy specimens were obtained, and total RNA was extracted and amplified. Microarray analysis with the Affymetrix Human Genome U133 Plus 2.0 Array was used to analyze >54,000 transcripts, and potential pathways were identified. Results With gene expression data obtained before treatment, patients could be correctly classified in terms of whether they would be responders or nonresponders to rituximab. Gene pathway analysis demonstrated that the B cell signaling pathway was the most profoundly differentially expressed before treatment in the responders compared with nonresponders. Subclassification of patients based on the level of infiltration also demonstrated differential expression of genes belonging to the interferon (IFN) pathway between responders and nonresponders. Furthermore, unsupervised analysis based on gene expression modification before and after treatment allowed identification of 8 genes that were differentially expressed between responders and nonresponders, with the difference remaining significant after Bonferroni correction. Conclusion Our results demonstrate the ability to elaborate a set of genes predictive of rituximab efficacy and highlight the importance of studying the differential expression of B cell and IFN pathway signaling molecules in relation to the response to anti-CD20 treatment. A randomized controlled study is currently ongoing to confirm these results. [source]

Disruption of tight junction structure in salivary glands from Sjögren's syndrome patients is linked to proinflammatory cytokine exposure

ARTHRITIS & RHEUMATISM, Issue 5 2010
Patricia Ewert
Objective Disorganization of acinar cell apical microvilli and the presence of stromal collagen in the acinar lumen suggest that the labial salivary gland (LSG) barrier function is impaired in patients with Sjögren's syndrome. Tight junctions define cell polarity and regulate the paracellular flow of ions and water, crucial functions of acinar cells. This study was undertaken to evaluate the expression and localization of tight junction proteins in LSGs from patients with SS and to determine in vitro the effects of tumor necrosis factor , (TNF,) and interferon-, (IFN,) on tight junction integrity of isolated acini from control subjects. Methods Twenty-two patients and 15 controls were studied. The messenger RNA and protein levels of tight junction components (claudin-1, claudin-3, claudin-4, occludin, and ZO-1) were determined by semiquantitative reverse transcriptase,polymerase chain reaction and Western blotting. Tight junction protein localization was determined by immunohistochemistry. Tight junction ultrastructure was examined by transmission electron microscopy. Isolated acini from control subjects were treated with TNF, and IFN,. Results Significant differences in tight junction protein levels were detected in patients with SS. ZO-1 and occludin were strongly down-regulated, while claudin-1 and claudin-4 were overexpressed. Tight junction proteins localized exclusively to apical domains in acini and ducts of LSGs from controls. In SS patients, the ZO-1 and occludin the apical domain presence of decreased, while claudin-3 and claudin-4 was redistributed to the basolateral plasma membrane. Exposure of isolated control acini to TNF, and IFN, reproduced these alterations in vitro. Ultrastructural analysis associated tight junction disorganization with the presence of endocytic vesicles containing electron-dense material that may represent tight junction components. Conclusion Our findings indicate that local cytokine production in LSGs from SS patients may contribute to the secretory gland dysfunction observed in SS patients by altering tight junction integrity of epithelial cells, thereby decreasing the quality and quantity of saliva. [source]

Expansion of circulating T cells resembling follicular helper T cells is a fixed phenotype that identifies a subset of severe systemic lupus erythematosus

ARTHRITIS & RHEUMATISM, Issue 1 2010
Nicholas Simpson
Objective In the sanroque mouse model of lupus, pathologic germinal centers (GCs) arise due to increased numbers of follicular helper T (Tfh) cells, resulting in high-affinity anti,double-stranded DNA antibodies that cause end-organ inflammation, such as glomerulonephritis. The purpose of this study was to examine the hypothesis that this pathway could account for a subset of patients with systemic lupus erythematosus (SLE). Methods An expansion of Tfh cells is a causal, and therefore consistent, component of the sanroque mouse phenotype. We validated the enumeration of circulating T cells resembling Tfh cells as a biomarker of this expansion in sanroque mice, and we performed a comprehensive comparison of the surface phenotype of circulating and tonsillar Tfh cells in humans. This circulating biomarker was enumerated in SLE patients (n = 46), Sjögren's syndrome patients (n = 17), and healthy controls (n = 48) and was correlated with disease activity and end-organ involvement. Results In sanroque mice, circulating Tfh cells increased in proportion to their GC counterparts, making circulating Tfh cells a feasible human biomarker of this novel mechanism of breakdown in GC tolerance. In a subset of SLE patients (14 of 46), but in none of the controls, the levels of circulating Tfh cells (defined as circulating CXCR5+CD4+ cells with high expression of Tfh-associated molecules, such as inducible T cell costimulator or programmed death 1) were increased. This cellular phenotype did not vary with time, disease activity, or treatment, but it did correlate with the diversity and titers of autoantibodies and with the severity of end-organ involvement. Conclusion These findings in SLE patients are consistent with the autoimmune mechanism in sanroque mice and identify Tfh effector molecules as possible therapeutic targets in a recognizable subset of patients with SLE. [source]