RESUMEN
BACKGROUND: Epidemiological studies support an association between obesity, metabolic syndrome (MetS), and periodontitis. Still, understanding of the effects of low-grade inflammation in obese subjects on periodontitis and influence of MetS remains incomplete. The aims of this cross-sectional study were to explore the association between obesity related variables and periodontitis, and assess if MetS is a risk indicator for periodontitis in a sample of obese adults. METHODS: The study sample comprised 52 adults with a body mass index (BMI) of ≥ 30 kg/m2 referred for obesity therapy at the Obesity Centre at Haukeland University Hospital (HUH), Bergen, Norway. The subjects had prior to enrolment completed a 5-month lifestyle intervention course as part of a 2-year managing program. According to the revised National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) classification of MetS, 38 subjects were recruited to the MetS group and 14 subjects to the non-MetS group. Medical data including peripheral blood samples were obtained from records at HUH at the time of enrolment. Probing depth, clinical attachment level, tooth mobility, furcation involvement, bleeding on probing (BoP) were recorded and intraoral bitewings evaluated at a full-mouth periodontal examination. Associations between risk variables for obesity/MetS and periodontitis were explored using linear and logistic regression models. RESULTS: In the present sample 79% of the subjects were diagnosed with periodontitis. The prevalence of stage III/IV periodontitis was 42.9% in the non-MetS group vs. 36.8% in the MetS group (p = 0.200). In the non-MetS group 29.8% of the sites displayed BoP vs. 23.5% in the MetS group (p = 0.048). For stage III/IV periodontitis, the effect of age appeared to be significant for obesity related variables and MetS (p = 0.006, p = 0.002, respectively). None of the other analyses showed significant association with the outcome variables. CONCLUSION: In the present sample of obese subjects, periodontitis occurred independently of MetS. Reaching a certain BMI level, suggested association between MetS and periodontitis might be non-significant due to the dominating impact of obesity related variables undermining the effect of other systemic factors. TRIAL REGISTRATION: The principal clinical trial, entitled "Obesity and Oral Diseases", was prospectively registered in ClinicalTrials.gov with registration NCT04602572 (20.10.2020).
Asunto(s)
Síndrome Metabólico , Periodontitis , Adulto , Humanos , Estudios Transversales , Síndrome Metabólico/complicaciones , Síndrome Metabólico/epidemiología , Obesidad/complicaciones , Obesidad/epidemiología , Periodontitis/complicaciones , Periodontitis/epidemiología , Factores de RiesgoRESUMEN
Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease characterized by infiltration of the exocrine glands and prominent B cell hyperactivity. Considering the key role of monocytes in promoting B cell hyperactivity, we performed RNA-sequencing analysis of CD14+ monocytes from patients with pSS, non-Sjögren's sicca (nSS), and healthy controls (HC). We demonstrated that the transcriptomic profile of pSS patients is enriched in intermediate and non-classical monocyte profiles, and confirmed the increased frequency of non-classical monocytes in pSS patients by flow-cytometry analysis. Weighted gene co-expression network analysis identified four molecular signatures in monocytes from pSS patients, functionally annotated for processes related with translation, IFN-signaling, and toll-like receptor signaling. Systemic and local inflammatory features significantly correlated with the expression of these signatures. Furthermore, genes highly associated with clinical features in pSS were identified as hub-genes for each signature. Unsupervised hierarchical cluster analysis of the hub-genes identified four clusters of nSS and pSS patients, each with distinct inflammatory and transcriptomic profiles. One cluster showed a significantly higher percentage of pSS patients with higher prevalence of anti-SSA autoantibodies, interferon-score, and erythrocyte sedimentation rate compared to the other clusters. Finally, we showed that the identified transcriptomic differences in pSS monocytes were induced in monocytes of healthy controls by exposure to serum of pSS patients. Representative hub-genes of all four signatures were partially inhibited by interferon-α/ß receptor blockade, indicating that the circulating inflammatory mediators, including type I interferons have a significant contribution to the altered transcriptional profile of pSS-monocytes. Our study suggests that targeting key circulating inflammatory mediators, such as type I interferons, could offer new insights into the important pathways and mechanisms driving pSS, and holds promise for halting immunopathology in Sjögren's Syndrome.