To quantitatively assess gingival crevicular fluid (GCF), periodontal condition, and clinical parameters of Rheumatoid Arthritis (RA) and verify the correspondence between systemic and dental aspects. Investigating the influence of systemic inflammation, polypharmacy, and anticholinergic load on GCF may help to better understand the exacerbation of periodontal destruction in patients with RA.
A cross-sectional study evaluated 33 participants (18 RA, 15 controls). Demographic data, RA activity, functional capacity, anticholinergic burden, polypharmacy (PP), orofacial physical examination, and complete periodontal evaluation were assessed. GCF volume was measured using a Periotron (Oralflow Inc., New York, NY, USA). Statistical analysis included parametric and non-parametric tests, as well as multiple correspondence analysis (p < 0.05).
RA patients exhibited worse periodontal status, with 50% having periodontitis, while 80% of controls had gingivitis, despite similar GCF levels between groups. Multiple correspondence analysis revealed strong associations between advanced periodontitis (stages III/IV grade B), high biofilm (> 20%), bleeding index (> 10%), pocket depth > 4 mm, severe gingival inflammation, higher RA activity, severe functional impairment, PP, and elevated anticholinergic activity. Periodontal health and RA remission were associated with low inflammatory markers, less medication use and absence of immunosuppressive therapy.
RA patients had greater periodontal impairment despite similar GCF volumes. Strong associations were observed between periodontal severity, RA activity, PP, and anticholinergic burden, suggesting GCF involvement in periodontal disease progression in RA, highlighting underexplored clinical connections.
In systemic lupus erythematosus (SLE), thrombocytopenia is a common hematological complication associated with severe disease manifestations and increased mortality.
The study aimed to investigate the prevalence of thrombocytopenia in the Oman lupus cohort and explore its correlation with clinical, immunological, and epidemiological characteristics, as well as mortality and survival outcomes.
The study forms a section of the Oman Lupus Study, which is a longitudinal research initiative that includes 1 160 patients diagnosed with SLE between January 2006 and February 2020. The patients were evaluated for the prevalence of thrombocytopenia, which was further analyzed in relation to epidemiological and clinical characteristics, laboratory profile, survival, and mortality outcomes.
Thrombocytopenia was found in 22.5% of patients (262/1 160), with no significant difference between males (12%) and females (88%, p = 0.642). There were significant correlations between thrombocytopenia and antiphospholipid antibodies, as well as organ involvement, such as renal (5.3% vs. 0.6%, p = 0.000), neuropsychiatric (30.9% vs. 17.9%, p = 0.000), and respiratory complications (25.6% vs. 16.4%, p = 0.001). A similar prevalence rate was identified between pediatric and adult patients (20.2% vs. 22.8%, p = 0.490). It has been demonstrated that the mortality rate in thrombocytopenia patients was significantly higher (11.1% vs. 2.9%, p = 0.000), translating to a nearly fourfold increased risk. The Kaplan–Meier curve indicated that patients with thrombocytopenia had a reduced survival rate.
Thrombocytopenia impacts nearly a quarter of lupus patients and is strongly associated with organ involvement and increased mortality risk, irrespective of gender or age. These findings underscore the necessity for additional research and specialized guidelines to enhance outcomes in this high-risk group.
Rheumatoid arthritis (RA) is a complex autoimmune disease influenced by genetic and immune dysregulation. The causal roles of specific immune-related genes in RA pathogenesis remain incompletely understood.
We conducted a large-scale genome-wide association study (GWAS) meta-analysis across three RA cohorts to identify genome-wide significant risk loci. Causal genes and proteins were prioritized by integrating these results with cis-eQTL and pQTL datasets using two-sample Mendelian randomization (MR) and summary-data-based MR (SMR). Cell-type-specific expression was assessed using single-cell RNA sequencing (scRNA-seq), and gene expression in RA synovial tissue was validated via bulk RNA-seq.
We identified 29 independent RA-associated loci, including 7 novel associations. Integrated MR and SMR analyses classified ERAP2 as a high-confidence causal gene, while SWAP70 and LTBR were deemed moderate-confidence causal genes. SWAP70 showed a protective association, whereas ERAP2 and LTBR were positively associated with RA risk. Single-cell transcriptomic analysis revealed cell-type-specific enrichment, with SWAP70 prevalent in B cells and LTBR in dendritic cells. Bulk RNA-seq confirmed the upregulation of SWAP70, RASGRP1, and RHOH in RA patients.
Our integrative multi-omics framework reveals immune regulatory genes with potential causal roles in RA pathogenesis, highlighting ERAP2, SWAP70, LTBR, and other candidates as promising therapeutic targets.
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