Potential Effect of Neutrophil Functional Disorders on Pathogenesis of Aggressive Periodontitis

Abstract

Leukocytes play a key role in maintaining the balance between an effective host defence response to microorganisms and periodontal tissue destruction. Neutrophil dysfunction has been associated with increased susceptibility to periodontal diseases. We undertook this study to determine to what extent neutrophil dysfunction constitutes to the pathogenesis of aggressive periodontitis (AgP) in tropical country like ours. Age- and sex-matched groups consisting of 20 subjects each of generalized aggressive periodontitis (GAP)-cases and nonperiodontitis (NP)-controls. diabetes mellitus, HIV infection, prolonged antibiotic use and smoking were excluded. Each neutrophil function was assessed using the chemotactic assay using case in, phagocytosis assay, candidacidal assay (for intracellular killing) and NBT assay (for respiratory burst failure). Student's t-test, Fisher's exact test and Chi-square test. In the study 17 out of 20 subjects (85%) had at least one abnormal neutrophil assay either hypofunctional or hyperfunctional of which 16 (80%) had hypofunctional assays and 8 (40%) had hyperfunctional assays. Defective phagocytosis was the commonest (50%) followed by chemotactic defect (45%), defective respiratory burst (40%) and defective intracellular killing (30%). Mean of chemotaxis assay was significantly less in AgP when compared to controls (103 vs 129 µm, p=0.002), similarly for phagocytic defect (3.45 vs 4.65, p≤0.001) and with candidacidal assay (26.80 vs 37.35, p<0.001). The prevalence of neutrophil dysfunction, predominantly hypofunctional, was significantly very high in GAP patients with few even having hyperactive respiratory burst function. Multiple level neutrophil defects could account for the aggressive nature of AgP even in apparently healthy subjects.