Considering increasing number of pathogens resistant towards commonly used antibiotics as well as antiseptics, there is a pressing need for antimicrobial approaches that are capable of inactivating pathogens efficiently without the risk of inducing resistances. In this regard, an alternative approach is the antimicrobial photodynamic therapy (aPDT). The antimicrobial effect of aPDT is based on the principle that visible light activates a per se non-toxic molecule, the so-called photosensitizer (PS), resulting in generation of reactive oxygen species that kill bacteria unselectively via an oxidative burst. During the last 10-20 years, there has been extensive in vitro research on novel PS as well as light sources, which is now to be translated into clinics. In this review, we aim to provide an overview about the history of aPDT, its fundamental photochemical and photophysical mechanisms as well as photosensitizers and light sources that are currently applied for aPDT in vitro. Furthermore, the potential of resistances towards aPDT is extensively discussed and implications for proper comparison of in vitro studies regarding aPDT as well as for potential application fields in clinical practice are given. Overall, this review shall provide an outlook on future research directions needed for successful translation of promising in vitro results in aPDT towards clinical practice.
Tenuta LMA, van der Veen MH, Machiulskiene V. Prevention and control of dental caries and periodontal diseases at individual and population level: consensus report of group 3 of joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases. J Clin Periodontol 2017; 44 (Suppl. 18): S85-S93. doi: 10.1111/jcpe.12687.
AbstractBackground: The non-communicable diseases dental caries and periodontal diseases pose an enormous burden on mankind. The dental biofilm is a major biological determinant common to the development of both diseases, and they share common risk factors and social determinants, important for their prevention and control. The remit of this working group was to review the current state of knowledge on epidemiology, socio-behavioural aspects as well as plaque control with regard to dental caries and periodontal diseases. Methods: Discussions were informed by three systematic reviews on (i) the global burden of dental caries and periodontitis; (ii) socio-behavioural aspects in the prevention and control of dental caries and periodontal diseases at an individual and population level; and (iii) mechanical and chemical plaque control in the simultaneous management of gingivitis and dental caries. This consensus report is based on the outcomes of these systematic reviews and on expert opinion of the participants.
The threat of antibiotic resistance has attracted strong interest during the last two decades, thus stimulating stewardship programs and research on alternative antimicrobial therapies. Conversely, much less attention has been given to the directly related problem of resistance toward antiseptics and biocides. While bacterial resistances toward triclosan or quaternary ammonium compounds have been considered in this context, the bis-biguanide chlorhexidine (CHX) has been put into focus only very recently when its use was associated with emergence of stable resistance to the last-resort antibiotic colistin. The antimicrobial effect of CHX is based on damaging the bacterial cytoplasmic membrane and subsequent leakage of cytoplasmic material. Consequently, mechanisms conferring resistance toward CHX include multidrug efflux pumps and cell membrane changes. For instance, in staphylococci it has been shown that plasmid-borne
qac
(“quaternary ammonium compound”) genes encode Qac efflux proteins that recognize cationic antiseptics as substrates. In
Pseudomonas stutzeri
, changes in the outer membrane protein and lipopolysaccharide profiles have been implicated in CHX resistance. However, little is known about the risk of resistance toward CHX in oral bacteria and potential mechanisms conferring this resistance or even cross-resistances toward antibiotics. Interestingly, there is also little awareness about the risk of CHX resistance in the dental community even though CHX has been widely used in dental practice as the gold-standard antiseptic for more than 40 years and is also included in a wide range of oral care consumer products. This review provides an overview of general resistance mechanisms toward CHX and the evidence for CHX resistance in oral bacteria. Furthermore, this work aims to raise awareness among the dental community about the risk of resistance toward CHX and accompanying cross-resistance to antibiotics. We propose new research directions related to the effects of CHX on bacteria in oral biofilms.
The aim of the present in situ study was to evaluate the effect of different periods of intraoral remineralization to decrease the susceptibility of previously demineralized enamel against toothbrushing abrasion. Six human enamel specimens (A–F) were recessed in the buccal aspects of each of eight intraoral appliances which were worn for 21 days by 8 panelists. Demineralization of the samples was performed twice a day extraorally in the acidic beverage Sprite Light for 90 s. Subsequently, the enamel specimens were brushed at different times. Specimen A was brushed immediately after the demineralization. The remaining samples B–E were brushed after the intraoral appliances had been worn for various periods of remineralization: specimen B, 10 min; C, 20 min; D, 30 min and E, 60 min, respectively. Specimen F was only demineralized and remineralized, but not brushed. After 21 days, enamel wear was measured with a laser profilometer. The following values (mean ± standard deviation) were obtained: specimen A, 6.78±2.71 µm; B, 5.47±3.39 µm; C, 6.06±3.18 µm; D, 5.43±2.58 µm; E 4.78±2.57 µm, and F 0.66±1.11 µm. Analysis of variance revealed a significant influence of remineralization period on abrasive wear. However, even after a remineralization period of 60 min the wear was significantly increased as compared to the demineralized, but not brushed control. It is concluded that (1) abrasion resistance of softened enamel increases with remineralization period and (2) at least 60 min should elapse before toothbrushing after an erosive attack.
The objective of the study was to evaluate the period of remineralization needed to re–establish the resistance of eroded enamel against brushing abrasion. Enamel specimens were prepared from 84 polished bovine incisors. The samples were evenly distributed among 7 groups (A–G) and submitted to ten alternating de– and remineralization cycles which included abrasion by toothbrushing. Demineralization was accomplished by immersing the specimens in the erosive soft drink Sprite Light® for 1 min. Remineralization was performed by storing the samples in artificial saliva for either 0 min (A), 10 min (B), 60 min (C) or 240 min (D). After each remineralization, the specimens were brushed in an automatic brushing machine. Group E (erosion and 240 min remineralization, but no brushing) group F (erosion, but no remineralization and no brushing), and group G (brushing, but no erosion and no remineralization) served as controls. After performing the cycles, loss of enamel was determined by profilometry. The following values (mean ± SD) were obtained and statistically analyzed (p<0.05): group A (5.16±1.26 μm), B (2.47±0.68 μm), C (1.72±0.75 μm), D (1.11±0.42 μm), E (0.81±0.23 μm), F (1.04±0.31 μm), G (0.22±0.15 μm). Only the differences between groups D, E, and F were statistically not significant. Under the chosen in vitro conditions, it is concluded that abrasion resistance of eroded enamel continuously increases with remineralization time. However, even after a period of 1 h of remineralization, abrasion of previously eroded enamel is increased
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