Increased plasma TNF-superfamily cytokines in periodontitis patients undergoing supportive therapy

OBJECTIVES: B cells are arguably the most prominent immune cell in chronic periodontitis lesions. To investigate the influence of periodontal disease and cigarette smoking on plasma levels of B cell activating cytokines in particular the tumour necrosis factor super family cytokines., a proliferation-inducing ligand (APRIL/ TNFSF13/TALL-2), B cell activating factor (BAFF TNFSF13b/TALL-1) and TNFα MATERIALS & METHODS: Plasma concentrations of TNFα, APRIL and BAFF were evaluated by ELISA in 189 systemically healthy subjects (61 smokers and 128 non-smokers) divided into four groups: non-smokers with periodontitis (n=101), smokers with periodontitis (n=55), healthy non smokers (n=27) and healthy smokers (n=6). RESULTS: Clinical probing depth of smokers with periodontitis were significantly greater than those of non-smoking patients (p<0.05). Although clinical attachment loss and the number of deep sites affected were greater in the smokers with periodontitis, these differences were not significant. In the non-smoker groups periodontitis patients had significantly higher plasma TNFα APRIL and BAFF than healthy subjects (p<0.01). Although TNFα levels were higher in the smokers with periodontitis than in non-smokers with this disease (p=0.011) there was no significant difference in APRIL or BAFF between smokers and non-smokers with periodontitis. In addition, TNFα, APRIL and BAFF concentrations were significantly greater in non-smoker patients with periodontitis than in healthy non-smokers (p=0.009 and p=0.002, respectively). In addition, TNFα and BAFF concentrations were significantly higher in the smokers with periodontitis than in the healthy smokers (p=0.001) Plasma APRIL and BAFF correlated with and TNFα (p= 0.010) and all three cytokines correlated with clinical probing depth and clinical attachment loss (p<0.001). CONCLUSION: Plasma concentrations of the B cell activating cytokines and TNFα appear to mirror the severity of chronic periodontitis but show that cigarette smoking had little effect on the circulating levels of these molecules despite increasing circulating TNFα concentrations