Martin R Ling1, Iain L C Chapple1, John B Matthews1. 1. Periodontal Research Group and MRC Centre for Immune Regulation, College of Medical and Dental Sciences, The University of Birmingham, Birmingham, UK.
Abstract
AIM: To determine peripheral blood neutrophil superoxide release and C-reactive protein (CRP) concentration in chronic periodontitis patients, before and after non-surgical periodontal treatment. MATERIALS AND METHODS: Neutrophils were isolated from patient and control volunteers (n = 20) and superoxide measured by lucigenin-enhanced chemiluminescence with and without stimulation with unopsonized Porphyromonas gingivalis, unopsonized Fusobacterium nucleatum and phorbol 12-myristate 13-acetate (PMA) before and 2-months following non-surgical therapy. Corresponding high-sensitivity plasma CRP concentrations were also determined. RESULTS: At pre-treatment baseline, patient neutrophils released more superoxide in the absence (p ≤ 0.032) and presence of periodontal bacteria (p ≤ 0.013) and after PMA stimulation (p = 0.041) compared to control cells. Post-therapy, patient neutrophil superoxide release was reduced to control cell levels. Median patient plasma CRP concentrations were non-significantly higher than control values and were reduced after therapy (1.80-1.36 mg/l). Patient pre-treatment baseline, unstimulated neutrophil superoxide release showed a significant, positive correlation with plasma CRP concentration (p = 0.01). CONCLUSIONS: Chronic periodontitis is characterized by peripheral neutrophils exhibiting superoxide hyperactivity and hyper-reactivity to periodontal pathogens that is not a constitutive feature of periodontitis patients. The positive, pre-therapy relationship between unstimulated neutrophil superoxide release and plasma CRP is consistent with a protective role for CRP in reducing oxidative stress and systemic inflammation in vivo.
AIM: To determine peripheral blood neutrophil superoxide release and C-reactive protein (CRP) concentration in chronic periodontitispatients, before and after non-surgical periodontal treatment. MATERIALS AND METHODS: Neutrophils were isolated from patient and control volunteers (n = 20) and superoxide measured by lucigenin-enhanced chemiluminescence with and without stimulation with unopsonized Porphyromonas gingivalis, unopsonized Fusobacterium nucleatum and phorbol 12-myristate 13-acetate (PMA) before and 2-months following non-surgical therapy. Corresponding high-sensitivity plasma CRP concentrations were also determined. RESULTS: At pre-treatment baseline, patient neutrophils released more superoxide in the absence (p ≤ 0.032) and presence of periodontal bacteria (p ≤ 0.013) and after PMA stimulation (p = 0.041) compared to control cells. Post-therapy, patient neutrophil superoxide release was reduced to control cell levels. Median patient plasma CRP concentrations were non-significantly higher than control values and were reduced after therapy (1.80-1.36 mg/l). Patient pre-treatment baseline, unstimulated neutrophil superoxide release showed a significant, positive correlation with plasma CRP concentration (p = 0.01). CONCLUSIONS:Chronic periodontitis is characterized by peripheral neutrophils exhibiting superoxidehyperactivity and hyper-reactivity to periodontal pathogens that is not a constitutive feature of periodontitispatients. The positive, pre-therapy relationship between unstimulated neutrophil superoxide release and plasma CRP is consistent with a protective role for CRP in reducing oxidative stress and systemic inflammation in vivo.
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