Cholinergic signalling mechanisms and early implant healing phases in healthy versus generalized aggressive periodontitis patients: A prospective, case-control study
JOURNAL OF CLINICAL PERIODONTOLOGY, cilt.46, sa.11, ss.1155-1163, 2019 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 46 Sayı: 11
- Basım Tarihi: 2019
- Doi Numarası: 10.1111/jcpe.13185
- Dergi Adı: JOURNAL OF CLINICAL PERIODONTOLOGY
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.1155-1163
- Anahtar Kelimeler: acetylcholine, esterases, implants, periodontitis, SLURP-1
- Dokuz Eylül Üniversitesi Adresli: Hayır
Özet
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.