RESUMO
Periodontal disease, a chronic disease caused by bacterial infection, eventually progresses to severe inflammation and bone loss. Regulating excessive inflammation of inflamed periodontal tissues is critical in treating periodontal diseases. The periodontal ligament (PDL) is primarily a connective tissue attachment between the root and alveolar bone. PDL fibroblasts (PDLFs) produce pro-inflammatory cytokines in response to bacterial infection, which could further adversely affect the tissue and cause bone loss. In this study, we determined the ability of Litsea japonica leaf extract (LJLE) to inhibit pro-inflammatory cytokine production in PDLFs in response to various stimulants. First, we found that LJLE treatment reduced lipopolysaccharide (LPS)-induced pro-inflammatory cytokine (interleukin-6 and interleukin-8) mRNA and protein expression in PDLFs without cytotoxicity. Next, we observed the anti-inflammatory effect of LJLE in PDLFs after infection with various oral bacteria, including Fusobacterium nucleatum, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. These anti-inflammatory effects of LJLE were dose-dependent, and the extract was effective following both pretreatment and posttreatment. Moreover, we found that LJLE suppressed the effect of interleukin-1 beta-induced pro-inflammatory cytokine production in PDLFs. Taken together, these results indicate that LJLE has anti-inflammatory activity that could be exploited to prevent and treat human periodontitis by controlling inflammation.
Assuntos
Anti-Inflamatórios/farmacologia , Fibroblastos/efeitos dos fármacos , Interleucina-1beta/antagonistas & inibidores , Lipopolissacarídeos/antagonistas & inibidores , Litsea/química , Extratos Vegetais/farmacologia , Adulto , Anti-Inflamatórios/química , Dente Pré-Molar/citologia , Dente Pré-Molar/cirurgia , Sobrevivência Celular/efeitos dos fármacos , Técnicas de Cocultura , Fibroblastos/citologia , Fibroblastos/imunologia , Fibroblastos/microbiologia , Fusobacterium nucleatum/química , Fusobacterium nucleatum/crescimento & desenvolvimento , Fusobacterium nucleatum/patogenicidade , Voluntários Saudáveis , Humanos , Interleucina-1beta/farmacologia , Interleucina-6/antagonistas & inibidores , Interleucina-6/biossíntese , Interleucina-6/imunologia , Interleucina-8/antagonistas & inibidores , Interleucina-8/biossíntese , Interleucina-8/imunologia , Lipopolissacarídeos/farmacologia , Dente Molar/citologia , Dente Molar/cirurgia , Ligamento Periodontal/citologia , Ligamento Periodontal/cirurgia , Extratos Vegetais/química , Folhas de Planta/química , Porphyromonas gingivalis/química , Porphyromonas gingivalis/crescimento & desenvolvimento , Porphyromonas gingivalis/patogenicidade , Cultura Primária de Células , Tannerella forsythia/química , Tannerella forsythia/crescimento & desenvolvimento , Tannerella forsythia/patogenicidade , Treponema denticola/química , Treponema denticola/crescimento & desenvolvimento , Treponema denticola/patogenicidadeRESUMO
Dental caries preventive agents, such as sodium fluoride (NaF) and bamboo salt (BS), are known to cause cellular growth that is characterized by morphological and gene expression changes. This study was designed to investigate the dual effect of NaF and BS on interleukin (IL)-1ß-induced gingival inflammation. Under in vitro experimental conditions, exposure to a subcytotoxic dose of IL-1ß enhanced human gingival fibroblast inflammation, as characterized by increased levels of inflammation-associated proteins. A combination of NaF and BS significantly protected fibroblasts from IL-1ß-induced cellular deterioration. Exposure to NaF and BS induced the cell growth and no changes in viability were found with the Lactate Dehydrogenase Assay (LDH) assay at the NaF and BS concentration analyzed. Molecular analysis demonstrated that NaF and BS increased resistance to inflammation by reduction of IL-1ß, IL-8, and tumor necrosis factor (TNF)-α production. In addition, NaF and BS decreased the expression of IL-1ß, IL-8, and TNF-α mRNA in IL-1ß-induced human gingival fibroblast cells. The study identifies a new role for NaF and BS in the IL-1ß-induced inflammation of gingival fibroblasts and provides a potential target for gingival protection.
Assuntos
Anti-Inflamatórios/farmacologia , Fibroblastos/metabolismo , Fluoreto de Sódio/farmacologia , Células Cultivadas , Avaliação Pré-Clínica de Medicamentos , Fibroblastos/efeitos dos fármacos , Expressão Gênica , Gengiva/citologia , Humanos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-8/genética , Interleucina-8/metabolismo , Cloreto de Sódio na Dieta , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
PURPOSE: To evaluate the laboratory remineralization effects of a dentifrice with bamboo salt and NaF on artificial caries-like enamel lesions, at both the surface and deep areas. METHODS: Early dental caries lesions were formed by treating bovine enamel samples for 48 hours at 37 degrees C with a demineralization solution (pH 5.0) containing 0.1 M lactic acid, 0.2% Carbopol 907, and 50% saturated calcium phosphate tribasic. pH cycling was then performed by immersing the samples in dentifrice slurry for 2 minutes every 8 hours per day, and in demineralization solution for 4 hours and mixed saliva for the remaining time period. The mixed saliva consisted of 50% human saliva and 50% artificial saliva. The surface hardness and the level of mineral surface alterations were analyzed using a hardness tester and transversal microradiography, among negative control (fluoride free), positive control (sodium fluoride 1100 ppm, Crest Cavity Protection), and test dentifrice (3.0% bamboo salt with sodium fluoride 1,000 ppm) groups. RESULTS: Test and positive control groups significantly increased the level of the surface hardness and decreased mineral loss of the artificial caries-like enamel lesions compared to the negative control (P<0.05). The test dentifrice also significantly decreased the lesion depth compared to the other two groups (P<0.05).