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Cholinergic signalling mechanisms and early implant healing phases in healthy versus generalized aggressive periodontitis patients: A prospective, case–control study
Author(s) -
Meriç Pınar,
Buduneli Nurcan,
Kanmaz Burcu,
Gürlek Önder,
Çömlekoğlu Erhan,
Calvert Gareth,
Lappin David F.,
Nile Christopher
Publication year - 2019
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.13185
Subject(s) - osseointegration , aggressive periodontitis , cholinergic , implant , medicine , periodontitis , surgery
Abstract 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.