Επίπεδα ακετυλοχολίνης στο σάλιο και το υγρό ουλοδοντικής σχισμής ασθενών με περιοδοντική νόσο
Creators: name: Ισκάς, Αχιλλέας Στέφανου
Publisher: name: Aristotle University of Thessaloniki
Year: 2018
Subjects: Ακετυλοχολίνη
Περιοδοντική φλεγμονή
Χολινεργική αντιφλεγμονώδης οδός
Acetylcholine
Periodontal inflammation
Cholinergic anti-inflammatory pathway

description: Η ακετυλοχολίνη εκτός από νευροδιαβιβαστής έχει βρεθεί ότι συμμετέχει και στην ρύθμιση της φλεγμονής, μέσω της χολινεργικής αντιφλεγμονώδους οδού. Στόχος της παρούσας έρευνας ήταν να συγκριθούν τα επίπεδα της ακετυλοχολίνης και των ενζύμων που τη διασπούν στο σάλιο και το υγρό της ουλοδοντικής σχισμής ατόμων με περιοδοντική φλεγμονή και ατόμων με περιοδοντική υγεία. Παράλληλα, τα επίπεδα αυτά συσχετίστηκαν με μικροβιολογικές και ανοσολογικές παραμέτρους. Το δείγμα της μελέτης αποτελούταν από 151 άτομα, 52 με ουλίτιδα, 49 με χρόνια περιοδοντίτιδα και 50 περιοδοντικά υγιή. Ανιχνεύθηκαν στατιστικά αυξημένα επίπεδα ακετυλοχολίνης στο σάλιο και το υγρό ουλοδοντικής σχισμής της ομάδας της περιοδοντίτιδας σε σύγκριση με την ομάδα της ουλίτιδας και της υγείας. Συμπερασματικά, φαίνεται να υπάρχει μια αύξηση των επιπέδων της ακετυλοχολίνης στα άτομα με περιοδοντίτιδα λόγω της ύπαρξης φλεγμονής, χωρίς όμως τα επίπεδα της ακετυλοχολίνης να συσχετίζονται με κάποια κλινική ή βιοχημική παράμετρο
description: Acetylcholine is the main neurotransmitter acting in the central nervous system. Apart from this role, acetylcholine has been found to be able to influence the immune system via the cholinergic anti-inflammatory pathway. This pathway is mediated by the vagus nerve which releases acetylcholine to interact predominantly with the a7 subunit of the nicotinic acetylcholine receptor (a7nAChR) on proximate immuno-regulatory cells. Activation of the a7nAChR on these cells leads to down-regulated expression of pro-inflammatory mediators and thus regulates localized inflammatory responses. Acetylcholine, the enzymes that act upon its synthesis and its degradation and its receptors are being expressed in periodontal and immune cells. Gingivitis is the presence of gingival inflammation without loss of connective tissue attachment. Periodontitis can be defined as the presence of gingival inflammation at sites where there has been a pathological detachment of collagen fibers from cementum and the junctional epithelium has migrated apically. In addition, inflammatory events associated with connective tissue attachment loss also lead to the resorption of coronal portion of tooth supporting alveolar bone. So far, to our knowledge there has been no study in vivo concerning the effects of cholinergic system in the periodontal inflammation. The aim of this study was to compare the levels of acetylcholine and the enzymes hydrolyze its degradation in individuals with periodontal inflammation and in healthy individuals. Additionally, these levels were correlated with clinical and microbiological parameters. A total of 151 individuals all of Caucasian origin were recruited for the study from patients attending The Lab of Preventive Dentistry, Periodontology and Implant Biology, Aristotle University of Thessaloniki. Of this cohort 50 were determined to be periodontally healthy, 52 were diagnosed with generalized chronic gingivitis and 49 with generalized chronic periodontitis. To these subjects a full mouth periodontal chart was obtained. Additionally, specimens of saliva and gingival crevicular fluid (GCF) were obtained from the sites that were the deepest in each quadrant (PD&gt;5 mm). The specimens were laboratory analyzed to examine the levels of acetylcholine, acetylcholinesterase (AChE), butyrylcholinesterase (BChE), IL-17A, IL-17F, IL-17A/F, IL-17E, IL-17A:IL-17E, IL-4, IL-6, IL-23, IL-23R, TNF-α, TGF-β, as well as the levels of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans. There were found statistically significant differences among groups regarding almost all the cytokine levels in GCF. In saliva the differences were not so profound and were predominantly observed between periodontitis and gingivitis, periodontitis and health groups. Regarding the levels of acetylcholine, there were found statistically significantly elevated in the group of periodontitis in compare with the group of gingivitis and health both in saliva and in GCF. Regarding GCF levels of BChE, there were found statistically significant differences between periodontal health and periodontal inflammation. The highest levels were found in the health group. Regarding saliva levels of BChE, there were found statistically significantly elevated in the periodontitis group in comparison with the health group. Regarding the AChE levels, there were not found any statistically significant differences among groups. Regarding the AChE:BChE ratio, there were found statistically significant differences between periodontal health and periodontal inflammation groups. The highest levels were observed in the periodontitis group. Regarding the two periodontal pathogens, P. gingivalis was found to be statistically significantly elevated in the groups of periodontitis and gingivitis in comparison with health. There were found no statistically significant differences among groups regarding A. actinomycetemcomitans. No statistically significant correlations of acetylcholine with any clinical or biochemical parameters were observed. In conclusion, acetylcholine synthesis seems to be elevated in sites were periodontal inflammation is present. Acetylcholine is proven to down regulate inflammation. So the increased synthesis of acetylcholine could be a mechanism to control inflammation. The fact that BChE synthesis is down regulated in sites were periodontal inflammation is present could be a mechanism to prevent acetylcholine degradation. This could allow acetylcholine perform its anti-inflammatory properties