Evidence for the expression of cyclooxygenase-2 enzyme in periodontitis

Lohinai, Zsolt; Stachlewitz, Robert F.; Székely, Andrea; Fehér, Erzsébet; Dézsi, László; Szabó, Csaba

doi:10.1016/s0024-3205(01)01391-1

Cited by 49 publications

(51 citation statements)

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“…It has been suggested that the therapeutic activities of nonsteroidal anti-inflammatory drugs (NSAIDs) are derived from COX-2 blockade, whereas unwanted side effects such as gastrointestinal ulceration and bleeding, renal damage and platelet dysfunction are due to inhibition of COX-1 (11,12). Thus, a selective blockade of the COX-2 isoform should lead to the inhibition of inflammation and pain without causing the COX-1-dependent side effects in gastric tissue and kidney (13,14).…”

Section: Introductionmentioning

confidence: 99%

Comparison of etoricoxib and indomethacin for the treatment of experimental periodontitis in rats

Azoubel¹,

Menezes²,

Bezerra³

et al. 2007

Braz J Med Biol Res

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We investigated the effect of etoricoxib, a selective cyclooxygenase-2 inhibitor, and indomethacin, a non-selective cyclooxygenase inhibitor, on experimental periodontitis, and compared their gastrointestinal side effects. A ligature was placed around the second upper left molars of female Wistar rats (160 to 200 g). Animals (6 per group) were treated daily with oral doses of 3 or 9 mg/kg etoricoxib, 5 mg/kg indomethacin, or 0.2 mL saline, starting 5 days after the induction of periodontitis, when bone resorption was detected, until the sacrifice on the 11th day. The weight and survival rate were monitored. Alveolar bone loss (ABL) was measured as the sum of distances between the cusp tips and the alveolar bone. The gastric mucosa was examined macroscopically and the periodontium and gastric and intestinal mucosa were examined by histopathology. The ongoing ABL was significantly inhibited (P < 0.05) by 3 and 9 mg/kg etoricoxib and by indomethacin: control = 4.08 ± 0.47 mm; etoricoxib (3 mg/kg) = 1.89 ± 0.26 mm; etoricoxib (9 mg/kg) = 1.02 ± 0.14 mm; indomethacin = 0.64 ± 0.15 mm. Histopathology of periodontium showed that etoricoxib and indomethacin reduced inflammatory cell infiltration, ABL, and cementum and collagen fiber destruction. Macroscopic and histopathological analysis of gastric and intestinal mucosa demonstrated that etoricoxib induces less damage than indomethacin. Animals that received indomethacin presented weight loss starting on the 7th day, and higher mortality rate (58.3%) compared to etoricoxib (0%). Treatment with etoricoxib, even starting when ABL is detected, reduces inflammation and cementum and bone resorption, with fewer gastrointestinal side effects.

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Section: Introductionmentioning

confidence: 99%

Comparison of etoricoxib and indomethacin for the treatment of experimental periodontitis in rats

Azoubel¹,

Menezes²,

Bezerra³

et al. 2007

Braz J Med Biol Res

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“…A COX2 pertence à família de enzimas que convertem o ácido araquidônico em prostaglandina (PG). A forma induzível desta enzima é estimulada por citocinas inflamatórias, lipopolissacarídeos (LPS) e fatores de crescimento (FC) 34,35 . O presente estudo evidenciou maior quantidade de vasos sanguíneos nas lesões no grupo tratado quando comparado ao grupo controle.…”

Section: Discussionunclassified

Inibição da expressão de ciclooxigenase 2 em feridas cutâneas de camundongos NOD submetidos à terapia a laser de baixa intensidade

Rocha

Júnior²,

Aarestrup

et al. 2012

J. vasc. bras.

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ResumoContexto: A terapia a laser de baixa intensidade (LLLT) tem sido relatada como importante moduladora da cicatrização de feridas cutâneas aumentando a proliferação fibroblástica associada ao aumento da expressão da citocina fator transformador de crescimento-β2 (TGF-βB2). Objetivo: No presente estudo foram avaliados os efeitos da LLLT sobre a expressão da enzima ciclooxigenase 2 (COX2) no sítio do reparo tecidual utilizando o modelo experimental com camundongos diabéticos não obesos (NOD) para estudar a cicatrização de feridas cutâneas. Métodos: Foram utilizados 30 camundongos NOD, destes 14 ficaram diabéticos e foram divididos em dois grupos: o grupo I (n=7) foi submetido a um procedimento cirúrgico de feridas cutâneas e o grupo II (n=7) foi submetido a um procedimento cirúrgico de feridas cutâneas e tratados com LLLT. O grupo II foi submetido à LLLT nos seguintes parâmetros: 15 mW de potência, dose de 3,8 J/cm 2 e tempo de aplicação de 20 segundos. Após sete dias do ato cirúrgico e após aplicação do laser, os animais foram eutanasiados com sobredose de anestesia e amostras das feridas foram colhidas para posterior análise histopatológica, histomorfométrica e imuno-histoquímica. Resultados: A LLLT promoveu a inibição da expressão da COX2 em feridas cutâneas de camundongos diabéticos. Conclusão: Em conjunto, os resultados sugeriram que a LLLT é capaz de modular negativamente a expressão da enzima COX2 contribuindo para o controle da resposta inflamatória em feridas cutâneas de camundongos NOD.Palavras-chave: camundongos endogâmicos NOD; ciclooxigenase 2; terapia a laser de baixa intensidade. AbstractBackground: Low-level laser therapy (LLLT) has been reported to modulate the healing of wounds by inducing an increase in fibroblast number associated with increased expression of the cytokine transforming growth factor-β 2 (TGF-β 2 ). Objective: In the present study, the effect of LLLT on expression of COX2 at the site of tissue repair was evaluated, using an experimental model with non obese diabetic mice (NOD) to study cutaneous wound healing. Methods: Thirty NOD mice were used, of which 14 were diabetic and were divided into two groups: group I (n=7) underwent a surgical procedure of skin wounds and group II (n=7) underwent a surgical procedure of skin wounds and treated with LLLT. Group II was submitted to LLLT in the following parameters: 15 mW of power, dose of 3.8 J/cm 2 and exposure time of 20 seconds. Seven days after surgery and after laser application, animals were euthanized with an overdose of anesthesia and tissue samples were collected for subsequent histological analysis, histomorphometry and immunohistochemistry. Results: The LLLT has promoted the inhibition of COX2 expression in skin wounds in mice diabetic. Taken together the results suggest that LLLT modulate the expression of COX2 improved the control of inflammatory reaction in cutaneous wound lesions in NOD mice. Conclusion: Taken together, the results suggested that LLLT is able to negatively modulate the expression of COX2 enzyme contri...

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“…ÇANAKÇI, DOĞAN J Dent Fac Atatürk Uni Supplement: 9, Yıl: 2014, Sayfa : [74][75][76][77][78][79][80][81][82][83][84] via direct effects including reaction with metal complex, interaction with metal-oxygen and oxo complex, and reaction with radical species, or indirect effects including reaction with oxygen molecule (O 2 ) and reaction with superoxide radicals (O 2 ). 50 NO has reversibly activity on soluble guanylate cyclase 52 and inhibitor effect on cytochrome c oxidase 53 in nanomolar concentrations.…”

Section: The Properties Of No or No Derived Molecules;mentioning

confidence: 99%

“…Derg. ÇANAKÇI, DOĞAN J Dent Fac Atatürk Uni Supplement: 9, Yıl: 2014, Sayfa : [74][75][76][77][78][79][80][81][82][83][84] Porphyromonas gingivalis and Fusobacterium nucleatum in composition of dental plaque play major role via invading gingival tissue. The iNOS-generated NO is an important element of the host defenses against these pathogens, because experimental studies shown that, the iNOS-generated NO is able to kill Porphyromonas gingivalis 68 and Fusobacterium nucleatum.…”

Section: 66mentioning

confidence: 99%

“…Expression of COX-2 is increased predominantly in fibroblasts, and in resident and free macrophages, but not in PMN in periodontitis, and also these cell types are the source of the prostaglandins (PGs) produced by COX-2. 75 Recently, in vitro studies shown that, COX-2 founds in periodontal ligament cells in response to mechanical stress of abnormal forces 76 and in the oral keratinocytes. 77 In the healthy gingivomucosal tissues, low COX-2 activity and low or non-detectable prostaglandin E 2 (PGE 2 ) levels are found in periodontal tissues and crevicular fluid of normal healthy subjects.…”

Section: Host Tissue Damaging Effect;mentioning

confidence: 99%

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Role of Nitric Oxide in Inflammatory Periodontal Diseases:

Çanakçı¹,

Doğan²

2015

Atatürk Üniversitesi Diş Hekimliği Fakültesi Dergisi

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Nitric oxide (NO) is a unique molecule for biological organisms, and has also very important effects on various pathologic and physiologic mechanisms. Many cell types can generate NO during different pathological and physiologic conditions. Recently, many authors have been reported the connections between NO and inflammatory diseases. Periodontal pathologies are characterized with specific periodontal inflammation and host tissues damage around the teeth, and additional factors such as force application on teeth. However, the production of NO and the role of NO in the development of periodontal pathologies are unclear. On the other hand, many evidences from previous studies indicates a close relationship between NO and periodontal pathologies. In this review, we want to discuss; overproduction of NO during inflammation and mechanical stress of force application on teeth, which directly cause progression of periodontal pathologies, and the possible effects of NO overproduction in periodontal diseases.

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Evidence for the expression of cyclooxygenase-2 enzyme in periodontitis

Cited by 49 publications

References 0 publications

Comparison of etoricoxib and indomethacin for the treatment of experimental periodontitis in rats

Comparison of etoricoxib and indomethacin for the treatment of experimental periodontitis in rats

Inibição da expressão de ciclooxigenase 2 em feridas cutâneas de camundongos NOD submetidos à terapia a laser de baixa intensidade

Role of Nitric Oxide in Inflammatory Periodontal Diseases:

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