Juvenile idiopathic arthritis and rheumatoid arthritis: bacterial diversity in temporomandibular joint synovial fluid in comparison with immunological and clinical findings

Olsen‐Bergem, Heming; Kristoffersen, Anne Karin; Bjørnland, Tore; Reseland, Janne Elin; Aas, J.A.

doi:10.1016/j.ijom.2015.08.986

Cited by 13 publications

(16 citation statements)

References 139 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These inconsistent findings may have arisen because of differing study design, patients’ ethnicity or some causative agents that were not taken into account. Infections, including those caused by Yersiniae , have been regarded as possible triggering factors in JIA 4 , 19 , 20 , 21 , 22 , 23 . We have addressed this consideration to some extent by dividing the patients into those with suspected Yersinia infection and those without.…”

Section: Discussionmentioning

confidence: 99%

“…Several bacteria have been implicated in the etiology of JIA and one of the commonest associations is with Yersinia enterocolitica. 4 , 19 , 20 , 21 , 22 , 23 …”

mentioning

confidence: 99%

“…Several bacteria have been implicated in the etiology of JIA and one of the commonest associations is with Yersinia enterocolitica. 4,[19][20][21][22][23] Yersiniae are able to survive in synovial cells up to 6 weeks in vitro, after experimental infection. After that, antigen aggregates containing lipopolysaccharide (endotoxin) and 'bacterial ghosts' (rod-shaped forms possessing lipopolysaccharide but not DNA) are still detectable.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

et al. 2017

View full text Add to dashboard Cite

Both complement activation and certain infections (including those with Yersinia sp.) may contribute to the pathogenesis of juvenile idiopathic arthritis (JIA). We investigated factors specific for the lectin pathway of complement: mannose-binding lectin (MBL), ficolins and MBL-associated serine protease-2 (MASP-2), in 144 patients and 98 controls. One hundred and six patients had oligoarticular disease and 38 had polyarticular disease. In 51 patients (out of 133 tested), Yersinia-reactive antibodies were found (JIA Ye group). MBL deficiency was significantly more frequent in the JIA Ye group than in patients without Yersinia-reactive antibodies or in controls. Median serum ficolin-2 level was significantly lower (and proportion of values deemed ficolin-2 insufficient greater) in JIA patients irrespective of their Yersinia antibody status. The minority (C) allele at -64 of the FCN2 gene was less frequent among JIA patients than among control subjects. No differences were found in the frequency of FCN3 gene +1637delC or MASP2 +359 A>G mutations nor for median values of serum ficolin-1, ficolin-3 or MASP-2. However, high levels of serum ficolin-3 were under-represented in patients, in contrast to MBL. MBL, ficolin-1, ficolin-2, ficolin-3 and MASP-2 were also readily detectable in synovial fluid samples but at a considerably lower level than in serum. Our findings suggest a possible role for the lectin pathway in the pathogenesis of JIA, perhaps secondary to a role in host defence, and indicate that investigations on the specificity of lectin pathway recognition molecules towards specific infectious agents in JIA might be fruitful.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Several bacteria have been implicated in the etiology of JIA and one of the commonest associations is with Yersinia enterocolitica. 4 , 19 , 20 , 21 , 22 , 23 …”

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In view of these findings, both null hypotheses were rejected. The aetiology of TMJ DJD is complex and multifactorial in nature, and includes immunological and bacterial factors for joint inflammation . Biomechanical overload has been commonly assumed to be an important pre‐disposing factor for degenerative changes in TMJs .…”

Section: Discussionmentioning

confidence: 99%

Condylar repair and regeneration in adolescents/young adults with early‐stage degenerative temporomandibular joint disease: A randomised controlled study

Lei

Yap

Liu

et al. 2019

J of Oral Rehabilitation

View full text Add to dashboard Cite

Background Anterior repositioning splint (ARS) can facilitate regenerative condylar remodelling. Objective To determine the effect of ARS on osseous condylar changes in adolescents/young adults with early‐stage degenerative joint disease (DJD). Methods Sixty‐nine patients with early‐stage temporomandibular joint (TMJ) DJD based on the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) and cone beam computed tomography (CBCT) imaging were recruited and randomly allocated to two treatment groups: (a) conservative therapy with ARS and (b) conservative therapy without ARS. Subjects with acute TMJ closed‐lock had their displaced discs physically reduced by mandibular manipulation prior to ARS therapy. Clinical and CBCT data of 59 patients (86.4% females, mean age 17.95 ± 4.53 years, 67 joints) were attained pre‐ and at 6 or 12 months post‐treatment. Osseous changes after treatment were categorised into (a) progressed, (b) unchanged, (c) repaired (remodelled without new bone formation) and (d) regenerated (remodelled with new bone formation). Statistical analysis including chi‐square test, independent samples t test or Mann‐Whitney U test was conducted. Results About 85.5% of patients (59/69) completed the study, with 28 subjects (32 joints) in the splint group and 31 (35 joints) in the control group. The occurrence of condylar repair and regeneration was significantly higher with ARS (78.1%/[25/32] of joints) when compared to control group (48.6%/[17/35]) (P < 0.05). Moreover, condylar regeneration was exclusively observed in 50%/(16/32) of joints with ARS. For the 14 joints in splint group that received physical TMJ closed‐lock reduction, 85.7%/(12/14) exhibited condylar regeneration. The splint group (3.1%/[1/32]) also had significantly lower incidence of progressive TMJ degeneration than the control (37.1%/[13/35]) (P < 0.001). Conclusion Condylar repair and regeneration in early‐stage TMJ DJD are possible, and ideal spatial disc‐condyle relationship appears important. The possibility of restoring TMJ form/structure by ARS therapy presents an attractive area of new basic science and clinical research (Bone defect repair in early osteoarthrosis of temporomandibular joint by joint distraction therapy: A randomized controlled trial/ChiCTR‐TRC‐14005172).

show abstract

“…Patients with reactive arthritis and RA often have a combined etiology of hereditary and microenvironmental factors such as altered microbial flora in the gastrointestinal system (Toivanen, 2003). Bacterial degradation products, their cell walls and DNA, have been identified in synovial fluids from patients with TMD, RA, and reactive arthritis (Klineberg et al, 1998; Toivanen, 2001; Chen et al, 2002; Olsen-Bergem et al, 2016). Multiple experimental studies have demonstrated dysregulated TNFα and malfunctioning TNFR1 and TNFR2 caused by inflammation (Peschon et al, 1998; Kagari et al, 2002; Choi et al, 2010), or neuropathy (Sommer and Kress, 2004), as well as by “double-hit” inflammatory insults that can cause chronic inflammation not only in joints (Hains et al, 2010; Westlund et al, 2012; Traub et al, 2014) but also in other organs (Mariotti et al, 2002; Ilievski and Hirsch, 2010).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory ‘double hit’ model of temporomandibular joint disorder with elevated CCL2, CXCL9, CXCL10, RANTES and behavioural hypersensitivity in TNFR1/R2−/− mice

McIlwrath

Nesemeier

et al. 2017

European Journal of Pain

View full text Add to dashboard Cite

Background Patients with temporomandibular joint disorders (TMD), reactive arthritis, and rheumatoid arthritis often have combined etiology of hereditary and microenvironmental factors contributing to joint pain. Multiple clinical and animal studies indicate “double-hit” inflammatory insults can cause chronic inflammation. The first inflammatory insult primes the immune system and subsequent insults elicit amplified responses. The present “double hit” study produced a chronic orofacial pain model in mice with genetic deletion of both TNFα receptors (TNFR1/R2−/−), investigating the main nociceptive signaling pathways in comparisons to wild type mice. Methods An initial inflammatory insult was given unilaterally into the temporomandibular joint (TMJ). Secondary hypersensitivity was tested on the skin over the TMJ throughout the experiment. Three weeks later after complete reversal of hypersensitivity, a second inflammatory insult was imposed on the colon. Pharmacological interventions were tested for efficacy after week 10 when hypersensitivity was chronic in TNFR1/R2−/− mice. Serum cytokines were analyzed Days 1, 14, and Week 18. Results The double hit insult produced chronic hypersensitivity continuing through the four month experimental timeline in the absence of TNFα signaling. P2X7 and NMDA receptor antagonists temporarily attenuated chronic hypersensitivity. Serum cytokine/chemokine analysis on Day 14 when CFA induced hypersensitivity was resolved identified increased levels of pro-inflammatory cytokines CCL2, CXCL9, CXCL10, RANTES and decreased levels of anti-inflammatory cytokines IL-1ra and IL-4 in TNFR1/R2−/− compared to WT mice. Conclusions These data suggest a causal feed-forward signaling cascade of these little studied cytokines have the potential to cause recrudescence in this orofacial inflammatory pain model in the absence of TNFα signaling.

show abstract

Juvenile idiopathic arthritis and rheumatoid arthritis: bacterial diversity in temporomandibular joint synovial fluid in comparison with immunological and clinical findings

Cited by 13 publications

References 139 publications

Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

Condylar repair and regeneration in adolescents/young adults with early‐stage degenerative temporomandibular joint disease: A randomised controlled study

Inflammatory ‘double hit’ model of temporomandibular joint disorder with elevated CCL2, CXCL9, CXCL10, RANTES and behavioural hypersensitivity in TNFR1/R2−/− mice

Contact Info

Product

Resources

About