Cameron A Stewart1, Jenny H Hong2, Benjamin D Hatton3, Yoav Finer4. 1. Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada; Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada. 2. Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada. 3. Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada; Department of Materials Science and Engineering, University of Toronto, Toronto, Ontario, Canada. 4. Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada; Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada. Electronic address: yoav.finer@dentistry.utoronto.ca.
Abstract
OBJECTIVE: Assess the ability of an antimicrobial drug-releasing resin adhesive, containing octenidine dihydrochloride (OCT)-silica co-assembled particles (DSPs), to enhance the biostability and preserve the interfacial fracture toughness (FT) of composite restorations bonded to dentin. Enzyme-catalyzed degradation compromises the dental restoration-tooth interface, increasing cariogenic bacterial infiltration. In addition to bacterial ingress inhibition, antimicrobial-releasing adhesives may exhibit direct interfacial biodegradation inhibition as an additional benefit. METHODS: Mini short-rod restoration bonding specimens with total-etch adhesive with/without 10% wt. DSPs were made. Interfacial fracture toughness (FT) was measured as-manufactured or post-incubation in simulated human salivary esterase (SHSE) for up to 6-months. Effect of OCT on SHSE and whole saliva/bacterial enzyme activity was assessed. Release of OCT outside the restoration interface was assessed. RESULTS: No deleterious effect of DSPs on initial bonding capacity was observed. Aging specimens in SHSE reduced FT of control but not DSP-adhesive-bonded specimens. OCT inhibited SHSE degradation of adhesive monomer and may inhibit endogenous proteases. OCT inhibited bacterial esterase and collagenase. No endogenous collagen breakdown was detected in the present study. OCT increased human saliva degradative esterase activity below its minimum inhibitory concentration towards S. mutans (MIC), but inhibited degradation above MIC. OCT release outside restoration margins was below detection. SIGNIFICANCE: DSP-adhesive preserves the restoration bond through a secondary enzyme-inhibitory effect of released OCT, which is virtually confined to the restoration interface microgap. Enzyme activity modulation may produce a positive-to-negative feedback switch, by increasing OCT concentration via biodegradation-triggered release to an effective dose, then subsequently slowing degradation and degradation-triggered release.
OBJECTIVE: Assess the ability of an antimicrobial drug-releasing resin adhesive, containing octenidine dihydrochloride (OCT)-silica co-assembled particles (DSPs), to enhance the biostability and preserve the interfacial fracture toughness (FT) of composite restorations bonded to dentin. Enzyme-catalyzed degradation compromises the dental restoration-tooth interface, increasing cariogenic bacterial infiltration. In addition to bacterial ingress inhibition, antimicrobial-releasing adhesives may exhibit direct interfacial biodegradation inhibition as an additional benefit. METHODS: Mini short-rod restoration bonding specimens with total-etch adhesive with/without 10% wt. DSPs were made. Interfacial fracture toughness (FT) was measured as-manufactured or post-incubation in simulated human salivary esterase (SHSE) for up to 6-months. Effect of OCT on SHSE and whole saliva/bacterial enzyme activity was assessed. Release of OCT outside the restoration interface was assessed. RESULTS: No deleterious effect of DSPs on initial bonding capacity was observed. Aging specimens in SHSE reduced FT of control but not DSP-adhesive-bonded specimens. OCT inhibited SHSE degradation of adhesive monomer and may inhibit endogenous proteases. OCT inhibited bacterial esterase and collagenase. No endogenous collagen breakdown was detected in the present study. OCT increased human saliva degradative esterase activity below its minimum inhibitory concentration towards S. mutans (MIC), but inhibited degradation above MIC. OCT release outside restoration margins was below detection. SIGNIFICANCE: DSP-adhesive preserves the restoration bond through a secondary enzyme-inhibitory effect of released OCT, which is virtually confined to the restoration interface microgap. Enzyme activity modulation may produce a positive-to-negative feedback switch, by increasing OCT concentration via biodegradation-triggered release to an effective dose, then subsequently slowing degradation and degradation-triggered release.
Authors: P M C Scaffa; C M P Vidal; N Barros; T F Gesteira; A K Carmona; L Breschi; D H Pashley; L Tjäderhane; I L S Tersariol; F D Nascimento; M R Carrilho Journal: J Dent Res Date: 2012-01-19 Impact factor: 6.116
Authors: Tryfon Beazoglou; Stephen Eklund; Dennis Heffley; Jonathan Meiers; L Jackson Brown; Howard Bailit Journal: Public Health Rep Date: 2007 Sep-Oct Impact factor: 2.792
Authors: Walter G Renné; Amanda Lindner; Anthony S Mennito; Kelli A Agee; David H Pashley; Daniel Willett; David Sentelle; Michael Defee; Michael Schmidt; Camila Sabatini Journal: Clin Oral Investig Date: 2016-03-28 Impact factor: 3.573
Authors: R Seseogullari-Dirihan; F Apollonio; A Mazzoni; L Tjaderhane; D Pashley; L Breschi; A Tezvergil-Mutluay Journal: Dent Mater Date: 2016-01-04 Impact factor: 5.304
Authors: Dhiraj Kumar; Debarati Ghose; Isha Mutreja; Robert D Bolskar; Conrado Aparicio; Robert S Jones Journal: Dent Mater Date: 2021-12-18 Impact factor: 5.304