BACKGROUND: Neutrophils (PMNs) are critical components of the innate immune system and help to maintain oral health in the face of a constant bacterial challenge. However, along with protecting the periodontium from microbial invasion, these cells release potent lysosomal enzymes and oxygen radicals that can be destructive to periodontal tissues and lead to tooth loss. We examined neutrophil function in a unique population of patients diagnosed with refractory aggressive periodontitis (RAP). METHODS: Venous blood was obtained from 12 non-smoking patients who had been diagnosed with RAP, 10 patients with chronic periodontitis who had responded to periodontal therapy (CP), and 13 periodontally healthy controls (HCs). Peripheral blood PMNs were loaded with dihydrorhodamine 123 and stimulated with phorbol 12-myristate 13-acetate (PMA) to measure the receptor-independent respiratory burst of these key immune cells. Phagocytosis via the complement and Fc-gamma receptors was also assessed. RESULTS: PMNs from patients with RAP displayed significantly increased PMA-induced oxygen radical production compared to those from the HC and CP patients. PMNs from RAP patients also displayed increased phagocytosis compared to those from the CP group. CONCLUSIONS: Our findings demonstrated a larger receptor-independent respiratory burst and higher phagocytotic activity in PMNs derived from patients with RAP compared to PMNs derived from CP patients and periodontally HCs. We speculate that the higher intrinsic intracellular activity of the nicotinamide adenine dinucleotide phosphate oxidase system may account for the continued periodontal breakdown, despite ongoing periodontal therapy in these challenging patients.
BACKGROUND: Neutrophils (PMNs) are critical components of the innate immune system and help to maintain oral health in the face of a constant bacterial challenge. However, along with protecting the periodontium from microbial invasion, these cells release potent lysosomal enzymes and oxygen radicals that can be destructive to periodontal tissues and lead to tooth loss. We examined neutrophil function in a unique population of patients diagnosed with refractory aggressive periodontitis (RAP). METHODS: Venous blood was obtained from 12 non-smoking patients who had been diagnosed with RAP, 10 patients with chronic periodontitis who had responded to periodontal therapy (CP), and 13 periodontally healthy controls (HCs). Peripheral blood PMNs were loaded with dihydrorhodamine 123 and stimulated with phorbol 12-myristate 13-acetate (PMA) to measure the receptor-independent respiratory burst of these key immune cells. Phagocytosis via the complement and Fc-gamma receptors was also assessed. RESULTS: PMNs from patients with RAP displayed significantly increased PMA-induced oxygen radical production compared to those from the HC and CPpatients. PMNs from RAP patients also displayed increased phagocytosis compared to those from the CP group. CONCLUSIONS: Our findings demonstrated a larger receptor-independent respiratory burst and higher phagocytotic activity in PMNs derived from patients with RAP compared to PMNs derived from CPpatients and periodontally HCs. We speculate that the higher intrinsic intracellular activity of the nicotinamide adenine dinucleotide phosphate oxidase system may account for the continued periodontal breakdown, despite ongoing periodontal therapy in these challenging patients.