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Deposition of Immune Complexes in Gingival Tissues in the Presence of Periodontitis and Systemic Lupus Erythematosus.

ABSTRACT: Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease characterized by tissue damage and widespread inflammation in response to environmental challenges. Deposition of immune complexes in kidneys glomeruli are associated with lupus nephritis, determining SLE diagnosis. Periodontitis is a chronic inflammatory disease characterized by clinical attachment and bone loss, caused by a microbial challenge - host response interaction. Deposition of immune complex at gingival tissues is a common finding in the course of the disease. Considering that, the primary aim of this study is to investigate the deposition of immune complexes at gingival tissues of SLE patients compared to systemically healthy ones, correlating it to periodontal and systemic parameters. Twenty-five women diagnosed with SLE (SLE+) and 25 age-matched systemically healthy (SLE-) women were included in the study. Detailed information on overall patient's health were obtained from file records. Participants were screened for probing depth (PD), clinical attachment loss (CAL), gingival recession (REC), full-mouth bleeding score (FMBS) and plaque scores (FMPS). Bone loss was determined at panoramic X-ray images as the distance from cementenamel junction to alveolar crest (CEJ-AC). Gingival biopsies were obtained from the first 15 patients submitted to surgical periodontal therapy of each group, and were analyzed by optical microscopy and direct immunofluorescence to investigate the deposition of antigen-antibody complexes. Eleven (44%) patients were diagnosed with active SLE (SLE-A) and 14 (56%) with inactive SLE (LES-I). Mean PD, CAL and FMBS were significantly lower in SLE+ than SLE-(p < 0.05; Mann Whitney). The chronic use of low doses of immunosuppressants was associated with lower prevalence of CAL >3 mm. Immunofluorescence staining of markers of lupus nephritis and/or proteinuria was significantly increased in SLE+ compared to SLE-, even in the presence of periodontitis. These findings suggest that immunomodulatory drugs in SLE improves periodontal parameters. The greater deposition of antigen-antibody complexes in the gingival tissues of patients diagnosed with SLE may be a marker of disease activity, possibly complementing their diagnosis.

SUBMITTER: Pires JR

PROVIDER: S-EPMC8027066 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Systemic lupus erythematosus (SLE) is a potentially fatal complex autoimmune disease, that is characterized by widespread inflammation manifesting tissue damage and comorbidities across the human body including heart, blood vessels, joints, skin, liver, kidneys, and periodontal tissues. The etiology of SLE is partially attributed to a deregulated inflammatory response to microbial dysbiosis and environmental changes. In the mouth, periodontal environment provides an optimal niche for local and systemic inflammation. Our aim was to evaluate the reciprocal impact of periodontal subgingival microbiome on SLE systemic inflammation. Methods: Ninety-one female subjects were recruited, including healthy (n = 31), SLE-inactive (n = 29), and SLE-active (n = 31). Patients were screened for probing depth, bleeding on probing, clinical attachment level, and classified according to CDC/AAP criteria with or without periodontal dysbiosis. Serum inflammatory cytokines were measured by human cytokine panel and a targeted pathogenic subgingival biofilm panel was examined by DNA-DNA checkerboard from subgingival plaque samples. Results: The results showed significant upregulation of serum proinflammatory cytokines in individuals with SLE when compared to controls. Stratification of subject's into SLE-inactive (I) and SLE-active (A) phenotypes or periodontitis and non-periodontitis groups provided new insights into SLE pathophysiology. Ten proinflammatory cytokines were upregulated in serum of SLE-I only and one in SLE-A only. Four molecules overlapped in SLE-A and SLE-I. Anti-inflammatory cytokines included IL-4 IL-10, which were upregulated in SLE-I sera (but not SLE-A), controlling clinical phenotypes. Out of 24 significant differential oral microbial abundances found in SLE, 14 unique subgingival bacteria profiles were found to be elevated in SLE. The most severe oral pathogens (Treponema denticola and Tannerella forsythia) showed increase abundances on SLE-A periodontal sites when compared to SLE-I and healthy controls. Inflammation as measured by cytokine-microbial correlations showed that periodontal pathogens dominating the environment increased proinflammatory cytokines systemically. Conclusions: Altogether, low-grade systemic inflammation that influenced SLE disease activity and severity was correlated to dysbiotic changes of the oral microbiota present in periodontal diseases.

Project description:AimTo determine periodontitis prevalence in patients with systemic lupus erythematosus (SLE) and to assess whether periodontitis in SLE patients is associated with a greater subclinical atherosclerosis.MethodsAn observational case-control study was conducted in SLE (cases) and patients without any rheumatic diseases (controls), matched for sex. Sociodemographic and cardiometabolic variables were gathered, and SLE activity was assessed through several indexes. Periodontal examination registered probing pocket depth, clinical attachment level, bleeding on probing, plaque index, and tooth loss. Subclinical atherosclerosis was assessed by measuring the carotid-femoral pulse wave velocity (PWV) by Doppler velocimetry, homocysteine levels, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). Bivariate analyses and logistic regression were used to assess the association of any of the studied variables with SLE.ResultsSeventy-one cases and 72 controls were included in the study. Thirty-nine SLE patients (54.9%) were diagnosed with periodontitis, compared with 16 controls (22.2%). High levels of PWV (≥7.7 m/s, 75th percentile) were shown by 44.3% of the cases vs. 22.4% of the controls (p = .011). Among SLE patients, those with periodontitis showed higher PWV values (8.1 ± 1.52 vs. 7.16 ± 1.11 m/s, p = .006) and higher homeostasis model assessment index (indicative of insulin resistance) (1.7 ± 0.73 vs. 2.92 ± 3.05, p = .028) compared to those with periodontal health. Logistic regression showed that waist circumference (OR 1.06, 95% CI 1.01-1.12, p = .015); ESR (OR 1.09, 95% CI 1.03-1.16, p = .003); and bleeding on probing (OR 1.1, 95% CI 1.01-1.19, p = .018) were associated with the risk of SLE.ConclusionSystemic lupus erythematosus patients showed a higher periodontitis percentage than controls. Higher PWV values were found in SLE patients with periodontitis, indicating a higher prevalence of subclinical atherosclerosis. Patients with higher gingival bleeding showed a higher risk of SLE.

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Deposition of Immune Complexes in Gingival Tissues in the Presence of Periodontitis and Systemic Lupus Erythematosus.

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