Cholinergic signalling mechanisms and early implant healing phases in healthy versus generalized aggressive periodontitis patients: A prospective, case–control study

Autor: Burcu Kanmaz, Christopher J. Nile, Nurcan Buduneli, Gareth Calvert, David F. Lappin, Erhan Çömlekoğlu, Pınar Meriç, Önder Gürlek
Přispěvatelé: Ege Üniversitesi
Rok vydání: 2019
Předmět:
Zdroj: Journal of Clinical Periodontology. 46:1155-1163
ISSN: 1600-051X
0303-6979
DOI: 10.1111/jcpe.13185
Popis: PubMed: 31444906
Aims: Periodontal diseases negatively affect implant osseointegration. Perturbations in non-neuronal cholinergic signalling mechanisms are associated with periodontitis; however, their role in generalized aggressive periodontitis (GAgP) is unknown. The aim of this prospective case–control study was to determine the relationship between non-neuronal cholinergic signalling mechanisms, secreted Ly-6/uPAR-related protein-1 (SLURP-1), interleukin-17 (IL-17) family cytokines and healing of dental implants in health and GAgP. Material and Methods: Thirteen GAgP patients and seven periodontally healthy individuals (PH) were recruited. Peri-implant crevicular fluid (PICF) was obtained at baseline and 1 month post-placement. Acetylcholine (ACh) levels and cholinesterase activity were determined biochemically. SLURP-1, IL-17A and IL-17E levels were determined by ELISA. Marginal bone loss (MBL) at 1 and 6 months post-placement was determined radiographically. Results: The concentration of ACh, cholinesterase activity and IL-17A levels was elevated in PICF of patients with GAgP compared to PH individuals at baseline and 1 month post-placement. The concentration of ACh and cholinesterase activity levels in PICF correlated with levels of IL-17A and MBL around implants 1 month post-placement in patients with GAgP. Conclusions: Non-neuronal cholinergic mechanisms may play a role in the aetiopathogenesis of GAgP and may directly or indirectly, through modulation of IL-17A, influence early implant osseointegration and potential long-term implant survival. © 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Databáze: OpenAIRE