B cell depletion in patients with rheumatoid arthritis is associated with reduced IL-1β in GCF

Hatipoğlu, Mükerrem; Daltaban, Özlem; Uğur, Sevcan; Üstün, Kemal; Kaçar, Cahit; Tuncer, Tiraje; Kantarcı, Alpdoğan

doi:10.1007/s00784-022-04378-0

Cited by 5 publications

(7 citation statements)

References 30 publications

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“…Among the 35 included studies published until January 2023, 19 are cross‐sectional studies (Gamel et al., 2017; Hashimoto et al., 2021a, 2021b; Hatipoğlu et al., 2022; Jung et al., 2018; Kordtabar et al., 2019; Mayer et al., 2009, 2013; Mirrielees et al., 2010; Nik‐Azis et al., 2021; Ortiz et al., 2009; Pischon et al., 2008; Renvert et al., 2020; Romero‐Sanchez et al., 2017; Rovas et al., 2021; Schmalz et al., 2021; Wu et al., 2021; Yamashita et al., 2020; Ziebolz et al., 2018), 6 are case control studies (Äyräväinen et al., 2017, 2018a, 2018b; de Smit et al., 2021; Kobayashi et al., 2015; Kobayashi, Okada et al., 2014); 8 are longitudinal studies (Ancuta et al., 2017, 2020, 2021; Fabri et al., 2015; Kadkhoda et al., 2016; Kobayashi, Yokoyama et al., 2014; Savioli et al., 2012; Üstün et al., 2013), and 2 are cross‐sectional and longitudinal analyses in the one and the same article (Coat et al., 2015; Pers et al., 2008). All the studies were prospective except for one cross‐sectional study (Yamashita et al., 2020).…”

Section: Resultsmentioning

confidence: 99%

“…However, 10 cross-sectional studies found no significant association between the type of RA treatment and periodontal clinical measurements (Gamel et al, 2017;Hashimoto et al, 2021aHashimoto et al, , 2021bHatipo glu et al, 2022;Kordtabar et al, 2019;Mirrielees et al, 2010;Ortiz et al, 2009;Pischon et al, 2008;Renvert et al, 2020;Romero-Sanchez et al, 2017;Yamashita et al, 2020). Two cross-sectional studies that measured periodontal biomarkers in GCF or saliva found that IL-1β GCF level was decreased by B-cell depletion treatment, MMP-8 GCF level was lowered by DMARDs (Hatipo glu et al, 2022) and TNFI decreased IL-1β salivary level (Mirrielees et al, 2010). Nevertheless, although there were differences in biomarkers, these studies concluded there was negligible impact of the type of bDMARD on clinical measures of the periodontium (Romero-Sanchez et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

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

Petit,

Culshaw,

Weiger

et al. 2024

Molecular Oral Microbiology

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BackgroundNumerous 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.MethodsPubMed/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).ResultsA 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.ConclusionWithin 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.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Petit,

Culshaw,

Weiger

et al. 2024

Molecular Oral Microbiology

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“…Zhang et al (2022a) searched for key ferroptosis-related genes in periodontitis and constructed an mRNA-miRNA-lncRNA network to deeply explore the pathogenesis of periodontitis, and found the effect of IL1β on periodontitis. Hatipoglu et al (2022) assessed the effect of B-cell depletion on gingival canal fluid in patients with RA and found that host-regulated therapy in RA reduced local production of IL-1β and MMP-8, thereby alleviating periodontal tissue destruction. Yuan et al (2022) showed that IL1β, CCL3, and CLEC4E are promising therapeutic targets for peri-implantitis and that these key biological processes and identified genes contribute to the study of peri-implantitis specific to periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Identification of ferroptosis, necroptosis, and pyroptosis-associated genes in periodontitis-affected human periodontal tissue using integrated bioinformatic analysis

Pan

et al. 2023

Front. Pharmacol.

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Introduction: Periodontitis is a chronic inflammatory oral disease that destroys soft and hard periodontal support tissues. Multiple cell death modes including apoptosis, necroptosis, pyroptosis, and ferroptosis play a crucial role in the pathogenicity of inflammatory diseases. This study aimed to identify genes associated with ferroptosis, necroptosis, and pyroptosis in different cells present in the periodontium of periodontitis patients.Methods: Gingival tissues’ mRNA sequencing dataset GSE173078 of 12 healthy control and 12 periodontitis patients’ and the microarray dataset GSE10334 of 63 healthy controls and 64 periodontitis patients’ were obtained from Gene Expression Omnibus (GEO) database. A total of 910 differentially expressed genes (DEGs) obtained in GSE173078 were intersected with necroptosis, pyroptosis, and ferroptosis-related genes to obtain the differential genes associated with cell death (DCDEGs), and the expression levels of 21 differential genes associated with cell death were verified with dataset GSE10334.Results: Bioinformatic analysis revealed 21 differential genes associated with cell death attributed to ferroptosis, pyroptosis, and necroptosis in periodontitis patients compared with healthy controls. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that 21 differential genes associated with cell death were related to various cellular and immunological pathways including inflammatory responses, necroptosis, and osteoclast differentiation. Additionally, the single-cell RNA (scRNA) sequencing data GSE171213 of 4 healthy controls and 5 periodontitis patients’ periodontal tissue was analyzed to obtain cell clustering and cell types attributed to differential genes associated with cell death. We found that among 21 DCDEGs, SLC2A3, FPR2, TREM1, and IL1B were mainly upregulated in neutrophils present in the periodontium of periodontitis patients. Gene overlapping analysis revealed that IL-1B is related to necroptosis and pyroptosis, TREM1 and FPR2 are related to pyroptosis, and SLC2A3 is related to ferroptosis. Finally, we utilized the CIBERSORT algorithm to assess the association between DCDEGs and immune infiltration phenotypes, based on the gene expression profile of GSE10334. The results revealed that the upregulated SLC2A3, FPR2, TREM1, and IL1B were positively correlated with neutrophil infiltration in the periodontium.Discussion: The findings provide upregulated SLC2A3, FPR2, TREM1, and IL1B in neutrophils as a future research direction on the mode and mechanism of cell death in periodontitis and their role in disease pathogenicity.

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“… 62 , 63 Therefore, B-cell deletion therapy in RA (rituximab) induced a reduction in IL-1β levels in gingival crevicular fluid in patients with periodontitis. 64 In contrast to proinflammatory B-cell responses, regulatory B cells (Breg) exert immunosuppressive functions by producing anti-inflammatory cytokines such as IL-10. 62 In RA patients, Bregs can inhibit disease progression by inducing the production of IFN-γ and IL-21 by T cells while reducing the production of ACPAs.…”

Section: Part I Similarities Between Rheumatoid Arthritis and Periodo...mentioning

confidence: 99%

New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis

et al. 2023

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Rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases leading to increased bone resorption. Preventing this inflammatory bone resorption is a major health challenge. Both diseases share immunopathogenic similarities and a common inflammatory environment. The autoimmune response or periodontal infection stimulates certain immune actors, leading in both cases to chronic inflammation that perpetuates bone resorption. Moreover, RA and periodontitis have a strong epidemiological association that could be explained by periodontal microbial dysbiosis. This dysbiosis is believed to be involved in the initiation of RA via three mechanisms. (i) The dissemination of periodontal pathogens triggers systemic inflammation. (ii) Periodontal pathogens can induce the generation of citrullinated neoepitopes, leading to the generation of anti-citrullinated peptide autoantibodies. (iii) Intracellular danger-associated molecular patterns accelerate local and systemic inflammation. Therefore, periodontal dysbiosis could promote or sustain bone resorption in distant inflamed joints. Interestingly, in inflammatory conditions, the existence of osteoclasts distinct from “classical osteoclasts” has recently been reported. They have proinflammatory origins and functions. Several populations of osteoclast precursors have been described in RA, such as classical monocytes, a dendritic cell subtype, and arthritis-associated osteoclastogenic macrophages. The aim of this review is to synthesize knowledge on osteoclasts and their precursors in inflammatory conditions, especially in RA and periodontitis. Special attention will be given to recent data related to RA that could be of potential value in periodontitis due to the immunopathogenic similarities between the two diseases. Improving our understanding of these pathogenic mechanisms should lead to the identification of new therapeutic targets involved in the pathological inflammatory bone resorption associated with these diseases.

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B cell depletion in patients with rheumatoid arthritis is associated with reduced IL-1β in GCF

Cited by 5 publications

References 30 publications

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

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

Identification of ferroptosis, necroptosis, and pyroptosis-associated genes in periodontitis-affected human periodontal tissue using integrated bioinformatic analysis

New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis

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