Effects of colchicine on gingival inflammation, apoptosis, and alveolar bone loss in experimental periodontitis

Aral, Cüneyt Asım; Aral, Kübra; Yay, Arzu; Özçoban, Özge; Berdelı, Afig; Saraymen, Recep

doi:10.1002/jper.17-0359

Cited by 24 publications

(20 citation statements)

References 50 publications

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“…Gingivomucosal tissues surrounding the left side of the mandibles were fixed for the analysis of apoptosis of periodontal cells, as previously described [13]. Cryostat sections (6 μ m thick) were obtained.…”

Section: Methodsmentioning

confidence: 99%

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Sun

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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Diabetes mellitus is a well-recognized risk factor for periodontitis. The goal of the present study was to elucidate whether oxidative stress and nuclear factor erythroid 2-related factor 2 (Nrf2) participate in the aggravation of periodontitis by diabetes. For this purpose, we assigned Wistar rats to control, periodontitis, diabetes, and diabetic periodontitis groups. Two weeks after induction of diabetes by streptozotocin, periodontitis was induced by ligation. Two weeks later, periodontal tissues and blood were harvested and analyzed by stereomicroscopy, immunohistochemistry, and real-time polymerase chain reaction. We found that ligation induced more severe bone loss and periodontal cell apoptosis in diabetic rats than in normal rats (p < 0.05). Compared with the control group, periodontitis significantly enhanced local oxidative damage (elevated expression of 3-nitrotyrosine, 4-hydroxy-2-nonenal, and 8-hydroxy-deoxyguanosine), whereas diabetes significantly increased systemic oxidative damage and suppressed antioxidant capacity (increased malondialdehyde expression and decreased superoxide dismutase activity) (p < 0.05). Simultaneous periodontitis and diabetes synergistically aggravated both local and systemic oxidative damage (p < 0.05); this finding was strongly correlated with the more severe periodontal destruction in diabetic periodontitis. Furthermore, gene and protein expression of Nrf2 was significantly downregulated in diabetic periodontitis (p < 0.05). Multiple regression analysis indicated that the reduced Nrf2 expression was strongly correlated with the aggravated periodontal destruction and oxidative damage in diabetic periodontitis. We conclude that enhanced local and systemic oxidative damage and Nrf2 downregulation contribute to the development and progression of diabetic periodontitis.

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Section: Methodsmentioning

confidence: 99%

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Sun

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…164 Preliminary evidence indicates that colchicine inhibited ligature-induced periodontitis in rats at both dosages tested (intraperitoneal injections, 30 and 100 μg/kg/d) when compared with vehicle control in an 11-day time course experiment. 164 Among the cytokines evaluated, gingival tissue interleukin-1β levels significantly decreased to half during colchicine treatment (~800 pg/mL in periodontitis and ~400 pg/mL at baseline and after providing both dosages of colchicine). The data indicate a general decrease in inflammation via the administration of colchicine that could be, in part, due to NLRP3 and/or pyrin inflammasomes.…”

Section: Nlrp3 and Pyrin Inflammasomesmentioning

confidence: 97%

“…Colchicine is used in the treatment of the inflammasome‐mediated diseases familial Mediterranean fever and gout, as well as cardiac disease (Table ) . The effects of colchicine as a therapeutic agent were recently evaluated in experimental periodontitis . Preliminary evidence indicates that colchicine inhibited ligature‐induced periodontitis in rats at both dosages tested (intraperitoneal injections, 30 and 100 μg/kg/d) when compared with vehicle control in an 11‐day time course experiment .…”

Section: Therapeutics Targeting the Inflammasomementioning

confidence: 99%

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Marchesan

Girnary

Moss

et al. 2019

Periodontology 2000

112

106

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Inflammasomes are a group of multimolecular intracellular complexes assembled around several innate immune proteins. Recognition of a diverse range of microbial, stress and damage signals by inflammasomes results in direct activation of caspase‐1, which subsequently induces the only known form of secretion of active interleukin‐1β and interleukin‐18. Although the importance of interleukin‐1β in the periodontium is not questioned, the impact of inflammasomes in periodontal disease and its potential for therapeutics in periodontology is still in its very early stages. Increasing evidence in preclinical models and human data strongly implicate the involvement of inflammasomes in a number of inflammatory, autoinflammatory and autoimmune disorders. Here we review: (a) the currently known inflammasome functions, (b) clinical/preclinical data supporting inflammasome involvement in the context of periodontal and comorbid diseases and (c) potential therapies targeting inflammasomes. To clarify further the inflammasome involvement in periodontitis, we present analyses of data from a large clinical study (n = 5809) that measured the gingival crevicular fluid‐interleukin‐1β and grouped the participants based on current periodontal disease classifications. We review data on 4910 European‐Americans that correlate 16 polymorphisms in the interleukin‐1B region with high gingival crevicular fluid‐interleukin‐1β levels. We show that inflammasome components are increased in diseased periodontal tissues and that the caspase‐1 inhibitor, VX‐765, inhibits ~50% of alveolar bone loss in experimental periodontitis. The literature review further supports that although patients clinically present with the same phenotype, the disease that develops probably has different underlying biological pathways. The current data indicate that inflammasomes have a role in periodontal disease pathogenesis. Understanding the contribution of different inflammasomes to disease development and distinct patient susceptibility will probably translate into improved, personalized therapies.

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“…During periodontitis development, hydrolytic enzymes, inflammatory cytokines and oxygen radicals were released by resident cells, such as tumor necrosis factor (TNF)-α, interleukin 1β (IL-1β) and IL-8 promoting the alveolar bone loss and periodontal tissue destruction, while IL-10 protecting against periodontitis. 4–6 Clinically, surgery and mechanical therapy were used for periodontitis treatment. 7 However, the effects are limited and unsatisfactory.…”

Section: Introductionmentioning

confidence: 99%

Implantable zoledronate-PLGA microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental periodontitis rat model

Yao

Zhang

et al. 2020

J Biomater Appl

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The effect of implantable Zoledronate-PLGA microcapsules (PLGA-ZOL) in periodontitis remains unclear. In this study, we aimed to explore the potential role of PLGA-ZOL in protecting periodontitis and elucidate the underlying mechanism. A rat model of periodontitis was established by ligation the mandibular first molars, then PLGA-ZOL was implanted. The healing volume was scanned by cone-beam computed tomography. Cytokine levels in the gingival tissues were determined by ELISA and RT-PCR. Oxidative stress was indicated by detecting superoxide dismutase concentration and catalase activity. After periodontitis model was successfully established in rats, PLGA-ZOL treatment significantly attenuated alveolar bone loss, as indicated by the increased total healing volume, bone volume/tissue volume and osteoprotegerin level, as well as decreased sRANKL level. PLGA-ZOL treatment also suppressed the inflammatory activities by inhibiting pro-inflammatory cytokine production (TNF-α, IL-1β) but increasing anti-inflammatory cytokine secretion (IL-10). Furthermore, PLGA-ZOL was found to ameliorate oxidative stress in gingival tissues. In conclusion, PLGA-ZOL microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental rat model of periodontitis.

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Effects of colchicine on gingival inflammation, apoptosis, and alveolar bone loss in experimental periodontitis

Abstract: 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.

Cited by 24 publications

References 50 publications

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics

Implantable zoledronate-PLGA microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental periodontitis rat model

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