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Effects of colchicine on gingival inflammation, apoptosis, and alveolar bone loss in experimental periodontitis
Author(s) -
Aral Cüneyt Asım,
Aral Kübra,
Yay Arzu,
Özçoban Özge,
Berdeli Afig,
Saraymen Recep
Publication year - 2018
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1002/jper.17-0359
Subject(s) - rankl , periodontitis , osteoprotegerin , tunel assay , dental alveolus , oxidative stress , colchicine , medicine , terminal deoxynucleotidyl transferase , inflammation , apoptosis , endocrinology , chemistry , receptor , dentistry , activator (genetics) , immunohistochemistry , biochemistry
Background The aim of the study was to investigate the effects of colchicine on cytokine production, apoptosis, alveolar bone loss, and oxidative stress in an experimental model of periodontitis in rats. Methods Forty‐eight rats were divided equally into four groups: healthy (H); periodontitis (P); periodontitis+colchicine low dose (CL, 30 μg/kg/day), and periodontitis+colchicine high dose (CH, 100 μg/kg/day). After 11 days, interleukin (IL) ‐1β, IL‐8, and IL‐10 were analyzed in gingival samples using Enzyme‐Linked ImmunoSorbent Assay. Receptor activator of nuclear factor kappa‐B ligand (RANKL), osteoprotegerin (OPG), total oxidative stress (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured in gingiva and serum. Alveolar bone volume was evaluated via micro‐CT. Apoptotic cells were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay in histological sections. Results Colchicine treatment significantly reduced IL‐1β, IL‐8, RANKL, RANKL/OPG, TOS, OSI, and bone volume ratio levels, and increased TAS levels compared to group P (p < 0.05). High dose colchicine treatment (CH) significantly decreased TUNEL+ cell counts compared to group P (p < 0.05). Conclusions These finding suggest that colchicine has a prophylactic potential for the prevention of periodontal tissue destruction through anti‐inflammatory, anti‐oxidative, anti‐apoptotic, and bone‐protective effects.