The results suggested that increased serum proinflammatory cytokine production may be a complication of dHPT, and this may affect healthy and diseased periodontia by increasing gingival proinflammatory cytokine levels.
Background: The present study aimed to investigate the local peptidergic innervation of diseased and healthy periodontia in smokers and non‐smokers.
Methods: Fifteen smokers and 12 non‐smokers, all with localized chronic periodontitis, participated in the study. Periodontally diseased and healthy tooth sites were selected in smokers (groups 1 and 2, respectively) and non‐smokers (groups 3 and 4, respectively). Local peptidergic innervation was assessed by the concentrations of two neuropeptides, substance P (SP) and calcitonin gene‐related peptide (CGRP), in the gingival biopsies obtained from the groups. Clinical data and biopsies were collected from the same two tooth sites in each group. SP and CGRP levels were measured by enzyme immunosorbent assay in the supernatants of gingival samples.
Results: Increased probing depth and attachment loss were found in group 1 compared to group 3 (P <0.05). SP was higher in group 1 compared to groups 2, 3, and 4, and it was higher in group 3 compared to groups 2 and 4 (P <0.05). CGRP was higher in group 1 than in groups 2, 3, and 4, but it was lower in group 3 than in groups 2 and 4 (P <0.05).
Conclusion: The study results suggested that 1) although smoking may affect the neurogenic inflammation in the presence of periodontitis by increasing local peptidergic innervation, this effect may not be seen in periodontal health, and 2) SP may be regarded as an indicator of periodontitis, whereas CGRP may be important in the acute and/or initial periodontal inflammation.
In patients with ACSs, reactive local enzyme activity increases for the scavenging to myocardial-free radicals during PCI. Administration of a solution of GIK as a metabolic support agent might prevent oxidative stress in the myocardial level, in these patients.
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