Periodontal disease has been associated with rheumatic diseases; however, few studies have evaluated the association with systemic lupus erythematosus (SLE), and its impact on the local inflammatory and microbial profiles. Therefore, this study evaluated the levels of several cytokines in gingival crevicular fluid (GCF) and serum from juvenile SLE (jSLE) patients with gingival inflammation, compared with controls. In addition, we assessed their subgingival microbial profile. Thirty jSLE patients and 29 systemically healthy individuals were recruited. Participants were rheumatologically and periodontally examined, and GCF, serum and intrasulcular biofilm were collected. Cytokines were analysed by bead-based multiplex assays and the bacterial profile by checkerboard DNA–DNA hybridization. jSLE patients presented higher percentages of dental plaque and bleeding than controls, as well as increased mean probing depth and attachment loss. After adjustment for multiple comparisons, GCF levels of interleukin (IL)-1β, IL-8, granulocyte colony-stimulating factor (G-CSF), interferon-γ and monocyte chemoattractant protein-1 were significantly higher, whereas the levels of granulocyte–macrophage colony-stimulating factor were significantly lower in jSLE patients. In serum, G-CSF levels tended to be higher in jSLE patients (adjusted p-value = 0.06). Intrasulcular counts of Aggregatibacter actinomycetemcomitans were significantly higher in jSLE patients as compared with controls. We conclude that patients with jSLE present a worse periodontal condition associated with altered levels of pro-inflammatory cytokines in GCF and increased counts of A. actinomycetemcomitans in the intrasulcular biofilm.

A large number of studies have shown a potential association between periodontal and autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus (SLE). Similar mechanisms of tissue destruction concerning periodontitis and other autoimmune diseases have stimulated the study of a possible relationship between these conditions. This study aims to review the literature about this potential association and their different pathogenic mechanisms. Considering that periodontal disease is a disease characterized by inflammation influenced by infectious factors, such as SLE, it is plausible to suggest that SLE would influence periodontal disease and vice versa. However, this issue is not yet fully elucidated and several mechanisms have been proposed to explain this association, as deregulation mainly in innate immune system, with action of phagocytic cells and proinflammatory cytokines such as IL-1β and IL-18 in both conditions' pathogenesis, leading to tissue destruction. However, studies assessing the relationship between these diseases are scarce, and more studies focused on common immunological mechanisms should be conducted to further understanding.

Adipokines are present in inflammatory processes and may be directly related to periodontal disease. Moreover, their activities may be regulated by fatty acids. The goal of this study was to quantify the concentrations of the main adipokines, leptin, adiponectin and resistin, and the docosahexaenoic (DHA), docosapentaenoic (DPA), eicosapentaenoic (EPA) and arachidonic (AA) fatty acids, in patients with generalized chronic periodontitis. As a secondary objective, the ratios of these substances in the blood of these patients were evaluated. The study included 15 systemically healthy patients with generalized chronic periodontitis (test group) and 15 patients with gingivitis (control group). Medical and periodontal parameters and blood samples were collected. Serum concentrations of fatty acids were analyzed by gas chromatography and adipokines by multiplex bead immunoassay. There was no significant difference in adipokines between groups. However, there was a tendency for lower values of adiponectin in periodontitis patients. Regarding the fatty acids, they were significantly higher in the test group compared with controls. The res/DHA, res/AA, adipon/DHA, adipon/AA and adipon/DPA ratios were significantly lower in the test group. There was no significant correlation between adipokines and clinical parameters and between adipokines and fatty acids levels. It was concluded that generalized chronic periodontitis patients showed significantly higher levels of fatty acids in comparison to gingivitis; adiponectin revealed a trend to lower values in the periodontitis group, even after Ancova correction. The ratios suggest a minor proportion of adiponectin and resistin in relation to the fatty acids in patients with generalized chronic periodontitis.

The use of a standardized punch of 2 mm diameter for periodontal tissue biopsies seems to be suitable for immunohistochemistry analysis and showed that the GCF may not express all the markers in the same proportion at the corresponding tissue.

The aim of this study was to characterize the salivary metabolomic profile in adolescents with juvenile systemic lupus erythematosus (jSLE). A total of 24 adolescents with jSLE (15.92 ± 2.06 years) and 12 systemically healthy controls (15.25 ± 2.7 years) were included in the study. Participants underwent rheumatologic testing and periodontal examination, with the recording of plaque index (PI), probing depth (PD), clinical attachment level (CAL), and bleeding on probing index (BPI). Unstimulated whole saliva was collected from both groups and stored at -80 ºC. The salivary proton nuclear magnetic resonance ( 1 H-NMR) spectra were acquired in a spectrometer operating at 500 MHz. Partial least squared discriminant analysis (PLS-DA) and orthogonal PLS-DA (O-PLS-DA) were used for statistical analysis. Mean CAL and PI were significantly increased in the group with jSLE (p < 0.01). Patients with jSLE presented a significantly different salivary metabolic profile (accuracy = 0.54; R² = 0.86; Q² = -0.293), significantly higher salivary levels of N-acetyl sugars, and significantly reduced levels of phenylalanine, glycine, taurine, hydroxybutyrate, and valerate compared with healthy controls (p < 0.05). It is suggested that the salivary metabolomic profile analyzed by ¹H NMR in patients with jSLE presents a different fingerprint that the systemically healthy subjects. Integrating the variation of metabolites with the identification of the metabolic pathways involved seems to provide a better understanding of the influence of systemic disease on salivary metabolites.