Use of an oxygen planar optode to assess the effect of high velocity microsprays on oxygen penetration in a human dental biofilms in-vitro

• Main Authors: Yalda Khosravi, Raja Durga Prasad Kandukuri, Sara Palmer, Erin S. Gloag, Sergey M. Borisov, E. Michelle Starke, Marilyn T. Ward, Purnima Kumar, Dirk de Beer, Arjun Chennu, Paul Stoodley
• Format: Article
• Language: English
• Published: BMC 2020-08-01
• Series: BMC Oral Health
• Subjects: Mechanical disruption; Microspray; Oral; Biofilm; Planar optodes; Dissolved oxygen
• Online Access: http://link.springer.com/article/10.1186/s12903-020-01217-0

Abstract Background Dental plaque biofilms are the causative agents of caries, gingivitis and periodontitis. Both mechanical and chemical strategies are used in routine oral hygiene strategies to reduce plaque build-up. If allowed to mature biofilms can create anoxic microenvironments leading to communities which harbor pathogenic Gram-negative anaerobes. When subjected to high velocity fluid jets and sprays biofilms can be fluidized which disrupts the biofilm structure and allows the more efficient delivery of antimicrobial agents. Methods To investigate how such jets may disrupt anoxic niches in the biofilm, we used planar optodes to measure the dissolved oxygen (DO) concentration at the base of in-vitro biofilms grown from human saliva and dental plaque. These biofilms were subject to “shooting” treatments with a commercial high velocity microspray (HVM) device. Results HVM treatment resulted in removal of much of the biofilm and a concurrent rapid shift from anoxic to oxic conditions at the base of the surrounding biofilm. We also assessed the impact of HVM treatment on the microbial community by tracking 7 target species by qPCR. There was a general reduction in copy numbers of the universal 16S RNA by approximately 95%, and changes of individual species in the target region ranged from approximately 1 to 4 log reductions. Conclusion We concluded that high velocity microsprays removed a sufficient amount of biofilm to disrupt the anoxic region at the biofilm-surface interface.