Constitutionally Hyperreactive Neutrophils in Periodontitis

Abstract

Our findings suggest that the increased CL from peripheral neutrophils in periodontitis may be related to a constitutionally greater responsiveness of the Fcgamma-receptor.

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

“…In the present study, we found a significant rise in the level of LPO in Group 1 and Group 2 in comparison with healthy controls (Group 4). This result is in agreement with other studies [8,42,45]. In the study by Tsai et al [8], increased concentration of LPO was found in GCF and whole saliva.…”

“…An increased LPO level following periodontitis has been noted in many studies [6,8,42]. In addition to oxygen-derived free radicals, glycated collagen has also been shown to raise the oxidative breakdown of lipids compared to normal collagen which causes increased MDA in serum and tissues of diabetic subjects [24].…”

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

“…By using microarrays not tailored for the disease we were able to elucidate transcriptional changes that were previously not part of current understanding. These studies have identified several functional groups of genes up-regulated in periodontitis patients' neutrophils compared with healthy controls, providing a better understanding of the molecular processes underpinning this highly prevalent disease in which peripheral neutrophils generate increased levels of ROS in the presence and absence of stimulation (7)(8)(9)(10).…”

“…The resultant collateral host tissue damage to the supporting periodontal tissues leads to progressive periodontitis and ultimately culminates in tooth loss (6). Several studies have demonstrated that PBN from chronic periodontitis patients are not only hyperreactive, in response to Fc␥R stimulation by periodontal pathogens, but also hyperactive, with respect to baseline unstimulated ROS production (7)(8)(9)(10). Although a host molecular defect in intracellular lipid signaling may explain peripheral neutrophil ROS hyperreactivity in the relatively rare form of the disease, localized aggressive periodontitis (11), this mechanism does not explain the patient predisposition observed in chronic periodontitis.…”

“…Although a host molecular defect in intracellular lipid signaling may explain peripheral neutrophil ROS hyperreactivity in the relatively rare form of the disease, localized aggressive periodontitis (11), this mechanism does not explain the patient predisposition observed in chronic periodontitis. The underlying mechanism(s) responsible for the hyperinflammatory neutrophil phenotype seen in chronic periodontitis (the commonest form of the disease) is currently unknown, although analyses indicate that it is not a result of altered adhesion molecule (7) or Phox gene (10) expression, polymorphisms in Fc␥R (8,12), or in vitro priming by cytokines or LPS (13,14). Furthermore, the association of periodontitis with increased relative risk for cardiovascular disease, fatal coronary events (15), and ischemic stroke (16), and the demonstrable medium-term reductions in vascular endothelial dysfunction following aggressive periodontal therapies (17), emphasize the potential impact of inflammatory periodontitis on peripheral macrovascular disease.…”