In the early stages of plaque formation Streptococci
, such as
S. oralis and
S. gordonii, attach, followed by a succession of organisms, which attach to the streptococci through a process known as coaggregation [
5,
6]. As these organisms metabolize dietary sugars they consume oxygen to lower the local dissolved oxygen (DO) concentration at the base of the biofilm, produce acids, and metabolites that may favor or antagonize other community members. As the biofilm matures, anaerobic bacteria such as
Veillonella parvula,
Fusobacterium nucleatum and
Porphyromonas gingivalis proliferate [
7].
For those on a high- sugar diet acid fermentation by the cariogenic pathogen,
S. mutans results in lowering the pH within the biofilm, as well as the production of an extracellular insoluble glucans which provides volume, structure and mechanical stability to the developing biofilm. As the thickness of the biofilm increases diffusion limitation of oxygen into the biofilm and metabolites out of the biofilm results in the build-up of steep gradients from physiological conditions to acidic and anoxic within 100 μm [
8]. The oral cavity and especially the periodontal pocket provides a unique eco-system for microbial organisms and harbors a diverse microbiota with up to 700 prokaryote species [
9]. One model for pathogenesis of periodontitis suggests that periodontal microbial communities can be clustered into complexes that are associated with disease severity [
10‐
12]. Seminal work, at that time based on culture dependent techniques, of Socransky identified a “red complex” harboring
Porphyromonas gingivalis,
Tannerella forsythia, and
Treponema denticola, associated with the severe form of periodontitis. Further complexes included an intermediate orange complex with, e.g.,
Fusobacterium nucleatum and a yellow and green complex dominated by
Streptococcus spp., the latter being associated with health. Support for a classical role for the red complex as direct pathogens came from the observation by Holt showing induction of periodontitis upon oral implantation of these bacteria in non-human primates [
13]. However, more recent concepts suggest that keystone pathogens can disrupt tissue homeostasis and change the composition of the commensal microbiota thereby generating host immune modulation and dysbiosis, that is responsible for periodontitis [
14,
15]. Such a concept takes into account observations that periodontal pathogens often are low abundant and can be present in healthy people [
16]. Periodontitis resembles the process of microbial succession with an increase of periodontitis-associated taxa while health-associated species remain but decrease in number. In turn, the microbial community structure changes significantly, and biomass typically increases [
10]..
P. gingivalis can also occur in the saliva and supragingival plaque both in healthy patients (≈10%) and those with chronic periodontitis (≈60%) [
17], presumably protected in the microaerophilic or anoxic environment of attached biofilm or detached biofilm aggregates.
Dental biofilms, are recalcitrant to antimicrobial agents as well as to complete mechanical removal, when growing in places difficult to reach with tooth-brush bristles. High velocity microspray (HVM) is a new technology which provides an alternative to string flossing for interproximal plaque management, and has been shown in clinical trials to reduce plaque and gingival index when used in combination with manual and electric toothbrushes and mouthwashes [
18‐
20]. However, the precise mechanism(s) of action are not known. In a recent in vitro study we reported that a commercial HVM device designed for interproximal cleaning removed significant amounts of a
S. mutans biofilm, but intriguingly caused the small amount of remaining biofilm to flow, forming interfacial instabilities between the air/water spray and the biofilm [
21]. This effect allowed much deeper penetration of particles and antimicrobial agents into the biofilm than could be achieved by shaking at 200 rpm for 30 s alone [
22]. We hypothesized that a combination of removal and mixing might disrupt the pathogenic anoxic environment at the base of the biofilm, thus potentially directing the biofilm community from pathogenic to commensal by modifying the environment, rather than purely trying to kill the biofilm bacteria with antimicrobial agents.
To test our hypotheses biofilms grown from saliva and toothbrush recovered plaque from healthy volunteers were grown on oxygen planar optodes [
23,
24]. The oxygen concentration was measured prior to and after two daily shootings with a high velocity water spray. Reduction in the amount of total bacteria and 7 species representing early and late colonizers of various Socransky microbial complexes [
10] was quantified by qPCR.