Die Handzahnbürste gilt seit Jahrhunderten als das Instrument zur mechanischen Reinigung von Zähnen. Sie kommt mehrmals täglich mit der Mundflora in Kontakt und ist somit potenzieller Träger verschiedenster humanpathogener Mikroorganismen. In einer In-vitro-Studie kontaminierten wir zwei Handzahnbürsten mit unterschiedlicher Borstenhärte (Dr. BEST Flex Plus mittel und hart) mit zwei etablierten Leitkeimen (Streptococcus mutans und Staphylococcus aureus). Vier verschiedene Dekontaminationsmethoden (24 -stündige Lufttrocknung, 0,2%ige CHX-Lösung, 0,2%iges CHX-Spray, UV-Ofen VIOlight) wurden anschließend verglichen und statistisch ausgewertet. Wir konnten nachweisen, dass die Borstenhärte nur je nach untersuchtem Bakterium einen signifikanten Einfluss auf die Keimbesiedlung des Borstenfeldes hat (nur bei Staphylococcus aureus). Eine zusätzliche Anwendung einer Dekontaminationsmethode zur reinen Lufttrocknung führte immer zu einer weiteren Bakterienreduktion auf dem Borstenfeld. Die Bestrahlung mit UV-Licht zeigte den größten Einfluss auf die Keimbesiedlung bei Zahnbürsten (mittel und hart), welche mit dem Bakterium Streptococcus mutans kontaminiert wurden, sowie bei den mit Streptococcus aureus kontaminierten Zahnbürsten mit harten Borsten. Die Methoden mit dem Wirkstoff CHX führten bei den Zahnbürsten mit mittlerer Borstanhärte und der Kontamination mit Straphylococcus aureus zur stärksten Bakterienreduzierung.

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L'apoptosi pot ser induïda a través de nombrosos estímuls, entre els quals hi ha elsreceptors de mort. Per induir apoptosi TNFα necessita la participació d'inhibidors de latranscripció d'ARN o de la síntesi proteica, com són ActD i CHX. En aquest estudidemostrem com la citotoxicitat de TNFα en cèl·lules PC12 i en neurones corticalssensibilitzades amb ActD es dóna a través de l'activació de la caspasa iniciadora 8, dela generació de tBid i de la conseqüent activació de les pro-caspases-9 i -3. A més, eltractament amb TNFα/ActD no indueix diferències detectables en l'expressió deproteïnes involucrades en el complex de senyalització de TNFα. L'anàlisi de lesprincipals proteïnes antiapoptòtiques, com són FLIP, IAPs i els membres de la famíliade Bcl-2, demostra que Bcl-xL endogen és capaç de regular l'apoptosi induïda perTNFα, sense afectar l'activació de la via del factor de transcripció NF-κB. Lasobreexpressió de Bcl-xL dóna resistència a la mort promoguda per TNFα i ActD, i lareducció dels seus nivells indueix mort cel·lular per mitjà de TNFα, a través del'activació de JNK. Per confirmar la rellevància de Bcl-xL en el senyal promogut perTNFα, es va avaluar l'efecte de la reducció dels nivells basals de proteïnesantiapoptòtiques com Bcl-2, Bcl-xL, Bcl-w i Mcl-1, en el model cel·lular HeLa, onaquestes s'hi troben expressades de forma fisiològica, contràriament al que passa enles cèl·lules PC12, demostrant que Bcl-xL és la proteïna antiapoptòtica més rellevanten la protecció de la mort induïda per TNFα.Per altra banda, l'apoptosi induïda per TNFα pot ser deguda a l'acumulació d'elevatsnivells de hemo lliure. El grup hemo sensibilitza les cèl·lules Hepa a l'acció citotòxicade TNFα a través de la inducció d'estrès oxidatiu, que provoca un dany cel·lular queporta a l'activació de la via de JNK y de pro-caspasa-3. La producció de ROS i el danyinduït per estrès oxidatiu, així com la mort induïda per TNFα, conjuntament ambelevats nivells del grup hemo lliure, poden inhibir-se amb l'expressió de proteïnesprotectores com HO-1 y H-Ferritina. / La apoptosis puede ser inducida a través de numerosos estímulos, entre los cuales losreceptores de muerte. Para promover la apoptosis, TNFα necesita la colaboración deinhibidores de la trascripción del RNA o de la síntesis proteica, como ActD y CHX. Eneste estudio demostramos como la citotoxicidad de TNFα en células PC12 y enneuronas corticales sensibilizadas con ActD ocurre a través de la activación de lacaspasa iniciadora 8, la generación de tBid y la activación de las pro-caspasas-9 y -3.Además no se detectan diferencias de expresión, inducidas por TNFα/ActD, deproteínas involucradas en la formación del complejo de señalización de TNFα. Elanálisis de las principales proteínas antiapoptóticas, como FLIP, IAPs y miembros dela familia de Bcl-2, demuestra que Bcl-xL es la molécula endógena capaz de regular laapoptosis promovida por TNFα, sin afectar la activación de la vía del factor detrascripción NF-κB. La sobre-expresión de Bcl-xL confiere resistencia a la muerteapoptótica mediada por TNFα y ActD, y su disminución forzada es capaz de inducirmuerte celular únicamente tratando con TNFα por activación de JNK. Para confirmar larelevancia de Bcl-xL en la señal promovida por TNFα, la represión de proteínas antiapoptóticascomo Bcl-2, Bcl-xL, Bcl-w y Mcl-1 ha sido evaluada en el modelo de célulasHeLa, donde estas se expresan fisiológicamente al contrario que en las células PC12,demostrando que Bcl-xL es la proteína anti-apoptótica más importante en la protecciónde la muerte inducida por TNFα.Por otra parte, la apoptosis mediada por TNFα puede ser promovida por laacumulación de elevados niveles del grupo hemo libre. El grupo hemo sensibiliza lascélulas Hepa a la acción citotóxica de la citoquina TNFα a través de la inducción deestrés oxidativo, cuyo daño resulta en la activación de la vía de JNK y de pro-caspasa-3. La producción de ROS y el daño inducido por estrés oxidativo, así como la muerteinducida por elevados niveles del grupo hemo libre y de TNFα, pueden inhibirse por lasobre-expresión de proteínas protectoras como HO-1 y H-Ferritina. / Apoptotic cell death is triggered by several different stimuli, among which deathreceptors. To induce apoptosis, TNFα needs the cooperation of RNA transcription orprotein synthesis inhibitor, i.e. ActD and CHX. In this study we demonstrate that ActDrenders rat PC12 cells and primary mouse cortical neurons susceptible to the cytotoxiceffect of TNFα by the activation of the initiator caspase 8, generation of tBid andactivation of pro-caspase-9 and -3. Proteins involved in TNFα receptor signalingcomplex are not affected by TNFα/ActD stimulation. However, the analysis of antiapoptoticproteins, e.g. FLIP, IAPs and Bcl-2 family members, demonstrates that Bcl-xLis the endogenous regulator of neuronal sensitivity to TNFα-induced apoptosis and thatit operates in a NF-κB-independent manner. Bcl-xL overexpression completely protectsagainst TNFα/ActD-induced apoptosis, whereas its endogenous decrease sensitizes toTNFα cytotoxic effect promoting JNK-dependent cell death. To point out the relevanceof Bcl-xL in TNFα signaling pathway, endogenous decrease of the main anti-apoptoticBcl-2 family members, e.g. Bcl-2, Bcl-xL, Bcl-w and Mcl-1, was performed in HeLa cellline in which, contrarily to PC12, these proteins are expressed. The results obtaineddemonstrate that Bcl-xL is the most important Bcl-2-cytoprotective protein in regulatingTNFα cytotoxicity.Moreover, TNFα-induced cell death is promoted by high levels of free hemeaccumulation. Heme sensitizes Hepa cell line to TNFα-triggered apoptosis enhancingROS production and ROS-mediated damage. This results in JNK and pro-caspase-3activation. Oxidative stress-promoted apoptosis induced by heme/TNFα treatment isinhibited by the overexpression of HO-1 and H-Ferritin cytoprotective proteins.

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Magister Chirurgiae Dentium - MChD (Oral Medicine and Periodontics) / The aim of this study was to assess whether a mouthwash containing carbohydrate derived fulvic acid, is effective in reducing the salivary microbial count pre-operatively. Endeavours have been made to reduce the risk of infection, bacteraemia and cross-contamination during dental procedures by the application of topical antimicrobial agents. To date chlorhexidine is the most widely evaluated and efficacious agent against oral biofilms but there have been reports of adverse effects ranging from contact dermatitis to severe anaphylactic shock. A new mouth rinse containing carbohydrate derived fulvic acid are reported to have broad spectrum antimicrobial activity against specific oral microbes and Candida albicans with no side effects.

Indiana University-Purdue University Indianapolis (IUPUI) / Purpose: This in vitro study aims to analyze the effect of combining two ADA-recommended professionally applied 1:1 Chlorhexidine/Thymol varnish ((Cervitec Plus)) and professionally prescribed 5,000 ppm fluoride toothpaste ((PreviDent 5000 Plus)) on reducing lesion depth and increasing mineral content Materials & Methods: Forty-eight dentin specimens were randomly distributed into four treatment groups (n=12 per treatment). Biofilms of Streptococcus mutans and Candida albicans were created on the polished surfaces of bovine root dentin specimens (n=12 per treatment). 1:1 Chlorhexidine/Thymol varnish was applied once then the tested 5,000 ppm fluoride toothpaste was applied for 120 seconds twice daily over the course of 2 days. Tested groups were: (1) 1:1 Chlorhexidine/Thymol varnish ((Cervitec Plus)) (C/T). (2) 5,000 ppm F toothpaste ((PreviDent 5000 Plus)) (F). (3) Combination of 1:1 Chlorhexidine/Thymol varnish ((Cervitec Plus)) & 5000 ppm F toothpaste ((PreviDent 5000 Plus)) (C/T+F). (4) Deionized water (DIW) as control group. Biofilms were analyzed for biofilm dry weight. Dentin specimens were analyzed using transversal microradiography (TMR) for mineral content change and lesion depth. PH data was analyzed using two-way ANOVA. Total biofilm dry weight data was analyzed using one-way ANOVA. Integrated mineral loss and lesion depth data was analyzed using two-way ANOVA All pair-wise comparisons from ANOVA analysis were made using Fisher’s Protected Least Significant Differences to control the overall significance level at 5%. Results: Treatment with (C/T+F) resulted in higher mean pH values compared to the control group (DIW) and (F) group. The average pH values of group (C/T) were not statistically different than group (C/T+F). the biomass of the combined S. mutans & C. albicans biofilm among all the groups were not significantly different. (DIW) presented significantly deeper lesions for both surfaces (sound &demineralized) when compared to (F) (P=0.0118), (C/T) (P=0.0002), and (C/T+F) (P<.0001). The sound surfaces for the specimens for group (C/T) and Group (F) showed superficial lesion depth. However, the sound surfaces of specimens treated with (C/T+F) showed the most superficial depth. Due to mineral gain, the demineralized surfaces of the specimens of both (C/T) & (C/T+F) showed a decrease in the lesion depth. Conclusion: Within the limitations of our study. The combination of 5,000 ppm fluoride toothpaste and CHX/Thymol had no significant effect on mineral content. However, the combination had a considerable effect on lesion depth reduction.

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Indiana University-Purdue University Indianapolis (IUPUI) / The purpose of this study was to investigate the antibacterial efficacy of 0.12-percent and 2.0-percent chlorhexidine gluconate (CHX) on eliminating Enterococcus faecalis from dentinal tubules, and whether this antibacterial effect was enhanced by heat. To date there have been no published articles that describe the heating of 2.0-percent CHX and its antimicrobial efficacy and clinical relevance towards E. faecalis within dentinal tubules in root canal systems. Ninety-five human extracted, single rooted, maxillary, anterior teeth were used to prepare dentin disk specimens. After proper sterilization, a 2.5-mm ISO-sized diameter lumen was prepared, and then the canals were filled with brain-heart infusion (BHI) broth infected with E. faecalis. The BHI was removed and the specimens in equally divided groups were rinsed with sterile saline and filled with saline, or 0.12 percent CHX or 2.0 percent CHX at ambient temperature (24°C) or experimental temperature (46°C) and incubated at oral temperature (37°C) or the experimental temperature (46°C), respectively. The specimens were frozen to -70˚C and pulverized in liquid nitrogen. Serial dilutions were prepared of 1:100 and 1:1000 and spiral plated on BHI agar plates in duplicate. They were incubated, and the number of bacterial colonies was recorded 24 hours later for data analysis. A two-way analysis of variance (ANOVA), with factors for solution, solution temperature, and the solution-by-temperature interaction was used to determine antibacterial efficacy. Pair-wise comparisons between groups were examined for significance using the Fisher’s Protected Least Significant Differences Method. The E. faecalis CFU were log-transformed to satisfy the assumptions required for the ANOVA. The results of this investigation demonstrated no statistically significant difference with the addition of heat to either test irrigation solution regarding the elimination of E. faecalis from dentinal tubules within the root canal system. There was a statistically significant difference in the antibacterial efficacy of CHX against E. faecalis in comparison with the concentration tested. A higher concentration of 2.0-percent CHX demonstrated a significantly higher antibacterial efficacy against E. faecalis compared with 0.12-percent CHX, and likewise with the saline control. It can be concluded that the use of a higher concentration of 2.0-percent CHX is advantageous as a final irrigation solution after copious amounts of NaOCl and EDTA have been utilized for effective antimicrobial efficacy and substantivity.