Background: Recent epidemiologic studies suggest that inflammation is the link between periodontal diseases and cardiovascular complications. This study aimed to evaluate the effects of non‐surgical periodontal treatment on plasma levels of inflammatory markers (interleukin [IL]‐6, C‐reactive protein [CRP], and fibrinogen) in patients with severe periodontitis and refractory arterial hypertension.Methods: Twenty‐two patients were examined and randomly divided into two groups. The test group was composed of 11 patients (mean age, 48.9 ± 3.9 years) who received periodontal treatment, whereas the control group had 11 patients (mean age, 49.7 ± 6.0 years) whose treatment was delayed for 3 months. Demographic and clinical periodontal data were collected, and blood tests were performed to measure the levels of IL‐6, CRP, and fibrinogen at baseline and 3 months later.Results: The clinical results showed that the mean percentages of sites with bleeding on probing, probing depth (PD) 4 to 5 mm, PD ≥6 mm, clinical attachment loss (CAL) 4 to 5 mm, and CAL ≥6 mm were significantly reduced in the test group 3 months after periodontal treatment. There were no significant differences between the data at baseline and 3 months in the control group. Periodontal treatment significantly reduced the blood levels of fibrinogen, CRP, and IL‐6 in the test group.Conclusion: Non‐surgical periodontal therapy was effective in improving periodontal clinical data and in reducing the plasma levels of IL‐6, CRP, and fibrinogen in hypertensive patients with severe periodontitis.

Periodontal disease is characterised by a dense inflammatory infiltrate in the connective tissue. When the resolution is not achieved, the activation of T and B cells is crucial in controlling chronic inflammation through constitutive cytokine secretion and modulation of osteoclastogenesis. The present narrative review aims to overview the recent findings of the importance of T and B cell subsets, as well as their cytokine expression, in the pathogenesis of the periodontal disease. T regulatory (Treg), CD8⁺ T, and tissue-resident γδ T cells are important to the maintenance of gingival homeostasis. In inflamed gingiva, however, the secretion of IL-17 and secreted osteoclastogenic factor of activated T cells (SOFAT) by activated T cells is crucial to induce osteoclastogenesis via RANKL activation. Moreover, the capacity of mucosal-associated invariant T cells (MAIT cells) to produce cytokines, such as IFN-γ, TNF-α, and IL-17, might indicate a critical role of such cells in the disease pathogenesis. Regarding B cells, low levels of memory B cells in clinically healthy periodontium seem to be important to avoid bone loss due to the subclinical inflammation that occurs. On the other hand, they can exacerbate alveolar bone loss in a receptor activator of nuclear factor kappa-B ligand (RANKL)-dependent manner and affect the severity of periodontitis. In conclusion, several new functions have been discovered and added to the complex knowledge about T and B cells, such as possible new functions for Tregs, the role of SOFAT, and MAIT cells, as well as B cells activating RANKL. The activation of distinct T and B cell subtypes is decisive in defining whether the inflammatory lesion will stabilise as chronic gingivitis or will progress to a tissue destructive periodontitis.

Background: We have previously found hyperreactive neutrophils, intrinsic or induced, in periodontitis patients by in vitro quantitation of free oxygen radicals. The effects of periodontitis and cigarette smoking on blood parameters have generally been described separately. Our aim was to compare these systemic effects of periodontitis and cigarette smoking, separately and in combination, in order to study the hyperreactivity in peripheral neutrophils.Methods: Blood cells and acute‐phase proteins were studied in 40 periodontitis patients and 43 healthy controls. The generation of free oxygen radicals from neutrophils was measured as luminolenhanced chemiluminescence (CL) after activation of their Fcγ receptors with opsonized Staphylococcus aureus.Results: An increase in CL in peripheral neutrophils from periodontitis patients was confirmed. Smoking had no significant effect on CL. The periodontitis patients had higher concentrations of C‐reactive protein (CRP) than the controls. ANOVA analysis showed that the increase in neutrophil count, haptoglobin, and α‐1 antitrypsin levels was significantly influenced by cigarette smoking. IgG₂ was lower in patients than in controls (P <0.017, ANOVA), and there was an interaction between periodontitis and smoking (P <0.047, ANOVA). The lower concentration of IgG₂ in patients who smoke may impair neutrophil function and be a mechanism by which smoking aggravates periodontitis.Conclusions: In general, the combination of periodontitis and cigarette smoking alters the parameters studied. The effects of periodontitis on CRP and IgG₂ means that periodontal lesions may also leak agents, priming the peripheral neutrophils to increased CL. J Periodontol 1999;70:1355‐1360.