Objective: To evaluate a novel device for its efficacy in removing experimental biofilm from root surfaces and its potential for concomitantly removing/roughening the surface substance.
Methods And Materials: A novel acrylic rotary device (biofilm remover, BR) was tested in vitro in three experiments: surface loss, surface roughness [positive controls: Perioset (PS) and Proxoshape (PR)] and biofilm removal [positive controls: ultrasonic (US) and PS]. Surface loss/surface roughness was evaluated for dentin samples instrumented for three 20 s periods.
Objectives: To investigate the cleaning efficacy of a mechanical and a hydrodynamic homecare device on biofilm-coated titanium surfaces with and without chlorhexidine.
Material And Methods: Six-species biofilms were grown on 108 SLA-titanium discs, which were cleaned as follows: sonic toothbrush alone (i) or in combination with either a 0.2% chlorhexidine (ii) or a placebo gel (iii) and oral irrigator (hydrodynamic action) with water (iv) or combined with 0.
Objective: To investigate the microbial adherence and colonization of a polyspecies biofilm on 7 differently processed titanium surfaces.
Material And Methods: Six-species biofilms were formed anaerobically on 5-mm-diameter sterilized, saliva-preconditioned titanium discs. Material surfaces used were either machined, stained, acid-etched or sandblasted/acid-etched (SLA).
Recognition of pathogen-associated molecular patterns that activate IL-1β is regulated by inflammasomes, predominantly of the nucleotide-binding oligomerization domain-like receptor (NLR) family. NLRP3 inflammasome is involved in the innate immune responses in periodontal disease. This is an inflammatory condition that destroys the tooth-supporting (periodontal) tissues, initiated by the subgingival formation of multi-species biofilms, frequently including the Gram-negative species Porphyromonas gingivalis.
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December 2011
Polymicrobial oral biofilms attaching on tooth surfaces can trigger inflammatory responses by the neighbouring tooth-supporting periodontal tissues. An excessive inflammatory response can cause destruction of the periodontal tissues, including the alveolar bone, thus resulting in periodontitis. Mediators of inflammation, such as prostaglandin E(2) (PGE(2) ) and interleukin-6, are primary regulators of alveolar bone destruction in periodontitis.
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