Saliva and Serum Levels of B-Cell Activating Factors and Tumor Necrosis Factor-a in Patients With Periodontitis

• Localización: Journal of periodontology, ISSN 0022-3492, Nº. 2, 2014, págs. 270-280
• Idioma: inglés
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• Resumen

  • Background: B-lymphocytes play a central and critical role in the adaptive immune response against invading pathogens. This study evaluates saliva and serum levels of APRIL (a proliferation-inducing ligand), B-cell activating factor (BAFF), tumor necrosis factor-a (TNF-a), interleukin (IL)-6, and IL-10 in patients with chronic periodontitis (CP) or aggressive periodontitis (AgP) and periodontally healthy individuals.

    Methods: Twenty-five patients with AgP, 20 patients with CP, and 20 periodontally healthy individuals were included. Smoking status was recorded, and all individuals were divided into non-smokers and smokers. Saliva and serum samples were collected before clinical periodontal measurements. APRIL, BAFF, TNF-a, IL-6, and IL-10 levels in serum and saliva samples were determined by enzyme-linked immunosorbent assay. Statistical analysis was performed using multivariate analysis of variance and bivariate correlation.

    Results: Serum and saliva levels of TNF-a, APRIL, BAFF, IL-6, and IL-10 were similar in CP and AgP groups. Serum levels of TNF-a, APRIL, and BAFF and saliva levels of BAFF were significantly higher in periodontitis groups than healthy controls (P <0.05). Non-smokers with CP or AgP had lower levels of saliva TNF-a and APRIL and serum APRIL and IL-6 than smokers with CP or AgP (P <0.05). Saliva APRIL and serum TNF-a and IL-6 levels were significantly higher in healthy smokers than healthy non-smokers (P <0.05). Clinical periodontal parameters correlated positively with TNF-family cytokines and negatively with IL-10 (P <0.05).

    Conclusions: Within the limits of this study, it may be suggested that elevated salivary and serum TNF-a, APRIL, and BAFF in patients with periodontitis may contribute to the dominance of B cells in periodontitis lesions. Moreover, higher levels in healthy smokers than non-smoking counterparts may play a role in detrimental effects of smoking on periodontal tissues.

    Periodontal diseases are a group of infectious/inflammatory diseases involving Gram-negative, anaerobic, and micro-aerophilic bacteria that colonize the subgingival area and cause local and systemic elevations of proinflammatory prostaglandins and cytokines, resulting in tissue breakdown. Periodontitis is characterized by gingival inflammation, alveolar bone resorption, and attachment loss.1 Immune responses are activated on stimulation by bacteria or their toxins present in the dental biofilm and eventually play a major role in the alveolar bone breakdown observed in periodontitis. However, the exact mechanisms of the molecular recognition and signaling transduction of host immune-inflammatory responses in periodontitis remain obscure.2 Periodontitis has been described as a B-cell lesion due to the presence of large numbers of plasma cells and B cells in periodontitis tissue biopsy specimens,3-5 and while the inflammatory infiltrate in aggressive periodontitis (AgP) and chronic periodontitis (CP) differs,6 factors that govern this process remain obscure. Together with a number of inflammatory and anti-inflammatory molecules such as interleukin (IL)-6 and IL-10, both APRIL (a proliferation-inducing ligand) and B-cell activating factor (BAFF) (also known as B lymphocyte stimulator [BLyS]) are likely to be involved. These molecules are members of the tumor necrosis factor (TNF) superfamily and are cytokines that regulate survival and proliferation of B lymphocytes.7 These molecules are homologs and are known to bind to a number TNF family receptors.8 B lymphocytes play a central and critical role in the adaptive immune response against invading pathogens. B cells have also long been considered to have a key role in the development and maintenance of many autoimmune diseases.9 BAFF and APRIL are expressed by monocytes, macrophages, and dendritic cells and at lower levels by T cells. BAFF expression has been associated with infection and inflammation, and excessive BAFF production has been shown in severe autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, and Sjögren syndrome.8,10,11 Liu et al.12 showed that elevated expression levels of BAFF and APRIL are associated with active pulmonary and extrapulmonary tuberculosis and that BAFF and APRIL are intimately correlated with the T helper 1 (Th1) response.

    Risk factors, including tobacco smoking, modify the periodontal response to microbial challenge. Smokers have been reported to be more susceptible to advanced and aggressive forms of periodontal disease than non-smokers.13-15 Smoking influences multiple aspects of leukocyte biology, including B-cell development and function.16-19 It has been suggested that smoking has an influence on host cytokine levels;20-23 however, the exact mechanisms by which smoking exerts detrimental effects on periodontal tissues remain unclear.

    Currently, there is no information on the relationship between BAFF and APRIL and periodontal tissue breakdown in periodontitis. The hypothesis is that salivary and/or serum levels of these novel cytokines may be different between patients with periodontitis and individuals with clinically healthy periodontium and that BAFF and APRIL may be helpful in understanding periodontitis pathogenesis. Thus, the aim of this study is two-fold: 1) to comparatively evaluate the concentrations of BAFF, APRIL, and TNF-a in saliva and serum samples of patients with periodontitis and periodontally healthy individuals; and 2) to investigate whether these parameters are affected by the smoking habits of the participants.