Abstract
Aim: The primary objective of this pilot study was to evaluate the effect of non-surgical periodontal treatment. The secondary aim was to evaluate the effect of dietary therapy on both parameters of oxidative stress in leukocytes and leukocyte-endothelial cell interactions in an obese population. Methods: This was a pilot study with a before-and-after design. Forty-nine obese subjects with periodontitis were randomized by means of the minimization method and assigned to one of two groups, one of which underwent dietary therapy while the other did not. All the subjects underwent non-surgical periodontal treatment. We determined periodontal, inflammatory and oxidative stress parameters—total reactive oxygen species (ROS), superoxide production, intracellular Ca2+, mitochondrial membrane potential and superoxide dismutase (SOD) activity. We also evaluated interactions between leukocytes and endothelium cells—velocity, rolling flux and adhesion—at baseline and 12 weeks after intervention. Results: Periodontal treatment improved the periodontal health of all the patients, with a reduction in serum retinol-binding protein 4 (RBP4), total superoxide production and cytosolic Ca2+ in leukocytes. In the patients undergoing dietary therapy, there were less leukocyte adhesion to the endothelium, an effect that was accompanied by a decrease in TNFα, P-selectin and total ROS and an increase in SOD activity. Conclusions: Whereas non-surgical periodontal treatment induces an improvement in leukocyte homeostasis, dietary therapy as an adjuvant reduces systemic inflammation and increases antioxidant status which, in turn, modulates leukocyte-endothelium dynamics.
Highlights
Obesity is a chronic inflammatory disease associated with a series of comorbidities, including dyslipidemia, arterial hypertension, diabetes mellitus and periodontitis [1,2]
We have shown in a previous study that the release of reactive oxygen species (ROS) from leukocytes is exacerbated in a proinflammatory state, contributing to oxidative stress and endothelial dysfunction in obesity and periodontitis [8,22]
A total of 52 patients with grade II-III obesity (BMI ≥ 35 kg/m2) and periodontitis were recruited for the study, three of whom eventually dropped out
Summary
Obesity is a chronic inflammatory disease associated with a series of comorbidities, including dyslipidemia, arterial hypertension, diabetes mellitus and periodontitis [1,2]. Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by host-mediated inflammation that results in the progressive destruction of periodontal attachment [3]. The host cells’ first defense strategy against periodontal pathogens is to release proinflammatory cytokines, which stimulates infiltration of polymorphonuclear leukocytes (PMNs). Together with disrupted antioxidant defenses, this leads to oxidative stress and apoptosis in the periodontal tissue [4,5], suggesting there are shared mechanisms in periodontitis and systemic inflammatory diseases. Very little research has centered on the production of ROS by PMNs under unstimulated conditions [7,8,9]. Diminished mitochondrial biogenesis, altered membrane potential, genetic factors and aging simultaneously contribute to mitochondrial dysfunction, which appears to be a central cause of insulin resistance and cardiovascular complications [11], though little is known about its role in periodontal disease
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