Individual and Combined Effects of Selective Cyclooxygenase‐2 Inhibitor and Omega‐3 Fatty Acid on Endotoxin‐Induced Periodontitis in Rats

Vardar, Saynur; Buduneli, Eralp; Baylas, Haluk; Berdelı, Afig; Buduneli, Nurcan; Atilla, Gül

doi:10.1902/jop.2005.76.1.99

Cited by 50 publications

(47 citation statements)

References 38 publications

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“…Biosynthesis of PGE 2 involves the translocation of NF-B (9) and expression of COX and PGE synthase (16). Historically, blocking agents have been used to counteract PGE 2 production (57,59). Most of these agents were found to abolish PGE 2 production through complete blockage of COX (33).…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 protects periodontal ligament

Mustafa

Zarrough²,

Bolstad

et al. 2013

American Journal of Physiology-Cell Physiology

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Resolution agonists are endogenous mediators that drive inflammation to homeostasis. We earlier demonstrated in vivo activity of resolvins and lipoxins on regenerative periodontal wound healing. The goal of this study was to determine the impact of resolvin D1 (RvD1) on the function of human periodontal ligament (PDL) fibroblasts, which are critical for wound healing during regeneration of the soft and hard tissues around teeth. Primary cells were cultured from biopsies obtained from three individuals free of periodontal diseases. Peripheral blood mononuclear cells were isolated by density gradient centrifugation from whole blood of healthy volunteers. PGE2, leukotriene B4 (LTB4), and lipoxin A4 (LXA4) in culture supernatants were measured by ELISA. The direct impact of RvD1 on PDL fibroblast proliferation was measured and wound closure was analyzed in vitro using a fibroblast culture "scratch assay." PDL fibroblast function in response to RvD1 was further characterized by basic FGF production by ELISA. IL-1β and TNF-α enhanced the production of PGE2. Treatment of PDL cells and monocytes with 0.1-10 ng/ml RvD1 (0.27-27 M) reduced cytokine induced production of PGE2 and upregulated LXA4 production by both PDL cells and monocytes. RvD1 significantly enhanced PDL fibroblast proliferation and wound closure as well as basic FGF release. The results demonstrate that anti-inflammatory and proresolution actions of RvD1 with upregulation of arachidonic acid-derived endogenous resolution pathways (LXA4) and suggest resolution pathway synergy establishing a novel mechanism for the proresolution activity of the ω-3 docosahexaenoic acid-derived resolution agonist RvD1.

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Section: Discussionmentioning

confidence: 99%

Resolvin D1 protects periodontal ligament

Mustafa

Zarrough²,

Bolstad

et al. 2013

American Journal of Physiology-Cell Physiology

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“…The effects of NSAIDs on PGE 2 levels (2,13), gingival inflammation (17) and alveolar bone loss (16,18,19) have been widely examined in human, animal and in vitro experiments (6,20). In general, the results have shown beneficial effect the early phase of periodontal treatment, gingivitis and prevention of bone loss.…”

Section: Discussionmentioning

confidence: 99%

Short-Term effect of COX-2 selective inhibitor as an adjunct for the treatment of periodontal disease: a clinical double-blind study in humans

et al. 2008

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Adjunctive therapeutic strategies that modulate the inflammatory mediators can play a significant role in periodontal therapy. In this double-blind, placebo-controlled study, 60 subjects diagnosed as periodontitis patients were evaluated for 28 days after periodontal treatment combined with selective cyclooxygenase-2 (COX-2) inhibitor. The experimental group received scaling and root planning (SRP) combined with the Loxoprofen antiinflammatory drug (SRP+Loxoprofen). The control group received SRP combined with placebo (SRP+placebo). Plaque index (PI), probing pocket depth (PD) and bleeding on probing (BOP) were monitored with an electronic probe at baseline and after 14 and 28 days. Both groups displayed clinical improvement in PD, PI and BOP. They also showed statistically similar values (p>0.05) of PD reduction on day 14 (0.4 mm) and on day 28 (0.6 mm). At the baseline, few deeper sites (7 mm) from SRP+Loxoprofen group were responsible and most PD reduction was observed after 14 days (p<0.05). The percentage of remaining deep pockets 7 mm) after 14 days in the SRP+Loxoprofen group was significantly lower (p<0.05) than in the SRP+placebo group. Loxoprofen presents potential effect as an adjunct of periodontal disease treatment, but long-term clinical trials are necessary to confirm its efficacy.

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“…In short-term studies (14 days), using a LPS-induced experimental periodontitis rat model, omega-3 fatty acid significantly reduced the gingival tissue levels of prostaglandin E2 (PGE 2 ), PGF 2α , leukotriene B4 (LTB 4 ), platelet-activating factor (PAF) [72] and matrix metalloproteinase 8 (MMP-8) expression and increased tissue inhibitor of metalloproteinases (TIMP) expression levels [73], but this supplement was not effective in preventing alveolar bone loss [74]. The combination of omega-3 fatty acid and celecoxib showed a synergistic effect and yielded significant reductions in the gingival tissue levels of PGE 2 , PGF 2α , LTB 4 and PAF in this animal model [75]. In long-term studies (22 weeks), an omega-3 fatty acid-supplemented diet in rats infected with P. gingivalis was related to significantly reduced alveolar bone resorption [76] and decreased proinflammatory cytokine gene expression, such as for interleukin-1 beta (IL-1β) or tumour necrosis factor alpha (TNF-α) and enhanced interferon gamma (IFN-γ), catalase and superoxide dismutase mRNA expression in gingival tissues [77].…”

Section: Dietetic Intervention and Periodontitismentioning

confidence: 95%

Nutrition-linked chronic disease and periodontitis: are they the two faces of the same coin?

Morillo

Bullón

Ramírez-Tortosa

et al. 2009

Mediterr J Nutr Metab

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There is increasing evidence of a relationship between periodontitis and several nutrition-linked chronic conditions, such as obesity, dyslipidaemia and metabolic syndrome, with a putative bidirectional influence between periodontal disease and each condition. An association between several dietary factors and the progression of periodontitis is relevant to this relationship. Thus, omega-3 fatty acids, vitamin C, lactic acid foods, soy products and a diet rich in vegetables and fresh food appear to be favourable for better periodontal health, whereas a lipid-rich diet may be detrimental to periodontal tissues.

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Individual and Combined Effects of Selective Cyclooxygenase‐2 Inhibitor and Omega‐3 Fatty Acid on Endotoxin‐Induced Periodontitis in Rats

Cited by 50 publications

References 38 publications

Resolvin D1 protects periodontal ligament

Resolvin D1 protects periodontal ligament

Short-Term effect of COX-2 selective inhibitor as an adjunct for the treatment of periodontal disease: a clinical double-blind study in humans

Nutrition-linked chronic disease and periodontitis: are they the two faces of the same coin?

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