[Polymorphonuclear neutrophilic granulocytes and the defense and damage of periodontal tissues]. / I granulociti polimorfonucleati neutrofili nella difesa e nel danno dei tessuti parodontali.

The relationship of neutrophil to the periodontal tissue can be equated to the image of a double-edged blade. The role of the polymorphonuclear cells in the containment of gingival bacteria and their products must be weighed against the localized tissue destruction that may be due to the extracellular release of lysosomal enzymes and oxygen derived radicals. It seems reasonable to suggest that the role of neutrophils in the gingival tissue is primarily a defensive one. Therefore, several factors such as the entity of intrinsic activation, the quantity and quality of stimuli, as well as many physiological and/or pathological conditions can determine whether the response of polymorphonuclear leukocytes is more protective or destructive of the parodontium.

[Periodontal disease and crevicular neutrophils. Role of superoxide radicals]. / Parodontopatie e neutrofili crevicolari. Ruolo dei radicali superossido.

One early biochemical process in PMN activation is the stimulation of the NADPH oxidase membrane enzyme, which produces a flux of superoxide radicals, directed towards the extracellular place. These radicals initiate bacterial destruction; however they can react against the periodontal tissue and lead to its destruction, either when too many of them are produced, or when they are not adequately neutralized by the antioxidant activity of the gingival fluid. Striking a proper balance between the activation state of crevicular PMN and the antioxidant activity of the gingival fluid may be a critical factor in determining whether PMN response to plaque bacteria is either protective or destructive for the parodontium.

Effect of isoproterenol administration of rat heart glutathione status.

The intraperitoneal administration of 3, 10 and 80 mg/Kg isoproterenol produced in the cardiac muscle a dose dependent increase of GSH content and a slight elevation of GSSG content. In addition, the treatment with the catecholamine at the doses of 3 and 10 mg/Kg produced a slight decrease of the mixed glutathione disulfides level, whilst at the dose of 80 mg/Kg, this effect was more pronounced. These changes were not accompanied by modifications of the activities of the enzymes glutathione peroxidase, glutathione reductase and glutathione S-transferase.

Enhanced superoxide production with no change of the antioxidant activity in gingival fluid of patients with chronic adult periodontitis.

In the gingival crevicular fluid (GCF) of control and chronic adult periodontitis (CAP) patients there is a spontaneous release of O2- radicals from polymorphonuclear leukocytes (PMN). The addition of the exogenous stimuli phorbol myristate acetate (PMA) decreased the O2-. formation in control GCF, while in CAP patients produced a marked enhancement of O2-. generation. The circulating PMN of control subjects did not show a spontaneous O2-. formation, differently from CAP patients. On the contrary, a similar O2-. production was measured when the circulating PMN were stimulated with PMA. Moreover, the antioxidant activity measured in 10 microliters of cell free gingival supernatant (GS) of control and CAP patients had the same values by inhibiting 12.6% and 18.9% respectively of the O2- formation supported by a xanthine/xanthine oxidase system. Probably, the protective or destructive effect of PMN in GCF of CAP patients depends on the variations of the rate of O2- formation in respect to the intrinsic antioxidant property of GS.

Reduced oxidative activity of circulating neutrophils in patients after myocardial infarction.

Circulating neutrophils isolated from patients 3-4 h after a myocardial infarction produced less O2-. compared with controls, when stimulated with phorbol myristate acetate or formyl-methionine-leucine-phenylalanine. Three days after the infarction the O2-. generation elicited by both stimuli further decreased markedly. Seven and 15 days after infarction the O2-. stimulated production was only slightly lower than or similar to the control values. The neutrophils of infarcted patients showed an augmented latency period before O2-. production compared with controls in response to exogenous stimuli, particularly three days after infarction. Electron microscopy revealed that the neutrophils isolated from the infarcted patients displayed signs of cell exhaustion with few alterations of the plasma membranes when stimulated with phorbol ester. In contrast, control neutrophils displayed alterations of the plasma membranes characteristic of active neutrophils. The results of this study indicate that the circulating neutrophils appear exhausted and functionally inhibited immediately after myocardial infarction.