Disrupting periodontal disease

This article considers why and how disruption of plaque biofilm is an important aspect of oral health.

Marsh (2005) wrote: ‘Dental plaque is the community of microorganisms found on a tooth surface as a biofilm, embedded in a matrix of polymers of host and bacterial origin’.1

We also know that plaque bacteria is considered a major cause of periodontal disease (PD).2 Put simply by Khan and colleagues (2015): ‘PD has been characterized as a microbial-shift disease owing to shift in the subgingival microbial communities that colonize the periodontal pockets from […] predominantly Gram-positive aerobic bacteria to a dominance of Gram-negative anaerobes during the transition from periodontal health to PD.’3

Adding practical, preventive context, when reporting back from Group B of the 5th European Workshop in Periodontology, Kinane and Attström (2005) stated: ‘Currently oral plaque biofilm disruption is the most effective way to treat and prevent both conditions [gingivitis and periodontitis].’4

A microbial community

As we have evolved, so too have the micro-organisms within the human body.5 The mouth is no exception, with a wide range of microbes flourishing within the oral cavity in the form of, ‘[…] structurally- and functionally-organised biofilms.’5

In fact, it was recently suggested that over 700 species of bacteria colonise on the hard surfaces of teeth and soft tissues in the oral mucosa.6

In addition, it is important to note that the teeth are the only surfaces in the human body that do not shed.6 Therefore, they, ‘[…] provide unique oppor¬tunities for extensive biofilm formation, and a secure haven for microbial persistence’, as do restorations.6

However, these plaque bacteria biofilms, when in balance with the rest of the body, have a beneficial effect on health, including an antibody response (an aspect of immunological priming) and suppressing any unwarranted inflammatory response.5

But, as Marsh and colleagues (2015) wrote: ‘On occasions, this symbiotic relationship breaks down, and previously minor components of the microbiota out-compete beneficial bacteria, thereby increasing the risk of disease.’5

They continued: ‘A delicate balance is needed […] to control the oral microbiota at levels compatible with health, without killing beneficial bacteria and losing the key benefits delivered by these resident microbes.5

Control versus elimination

To meet this need, over the years the ecological plaque hypothesis has been developed. In essence, it considers that disease may be controlled by targeting the factors that have brought about microbial disharmony, as well as by improving oral hygiene measures.7

In relation to periodontal disease, Marsh (2003) recorded: ‘[…] conventional treatment approaches involve mechanical removal of plaque or physical disruption of biofilm structure. […] From an ecological perspective, attempts could also be made to alter the local environment by reducing the flow of GCF [gingival crevicular fluid*] (e.g. by the use of anti-inflammatory agents; some antimicrobial agents in dental products also have anti-inflammatory properties) or the site could be made less anaerobic by the use of oxygenating or redox agents.’7

Focusing on the concept of mechanical plaque control alongside the use of an adjunctive anti-inflammatory agent, the idea is for patients to adopt preventive strategies to maintain plaque at a level compatible with health, rather than trying to eliminate it.8

The regimen needed may vary from patient to patient, since: ‘In peri¬odontitis, plaque control ‘thresholds’ that are compatible with a health-promoting biomass vary from patient-to-patient, with some requiring extremely good plaque control, while others manage with less stringent regimes.’8

What is clear, however, is that, for mechanical plaque control to be effective it, ‘[…] needs to be meticulous and patients have to be highly motivated and with an appropriate lifestyle (that is, an appropriate diet, avoid smoking, etc).’8

For some patients, ‘meticulous’ brushing and interdental cleaning is difficult to achieve,9 so a third step in the form of antiplaque or antimicrobial agent may be useful to help, ‘[…] interfere with biofilm composition and metabolism, especially at sites that are difficult to clean and are commonly missed during self-performed mechanical plaque control.’8

‘Antiplaque agents function by remov¬ing or disrupting biofilms, or by prevent¬ing the formation of new biofilm, without necessarily killing the component micro-organisms. In contrast, antimicrobial agents inhibit the growth of (bacteriostatic action) or kill (bactericidal action) micro-organisms in oral biofilms and are defined in terms of the minimum inhibitory con¬centration (MIC) or minimum bactericidal concentration (MBC) respectively. The activity of these agents can be against a limited (narrow spectrum) or wider (broad spectrum) target group of micro-organ¬isms.’8 Therefore, if appropriate, the recommendation of a well-chosen adjunct to mechanical cleaning may help to control biofilms without negatively affecting their contribution to the host’s overall health.8

Healthy levels

Placing the concept that oral plaque biofilm disruption is currently considered to be the most effective way to treat and prevent gingivitis and periodontitis in context, Marsh (2012) suggested: ‘Patients should be taught effective plaque control techniques that maintain dental biofilms at levels compatible with oral health so as to retain the beneficial properties of the resident microflora while reducing the risk of dental disease from excessive plaque accumulation. Antimicrobial and antiplaque agents in oral care products can augment mechanical plaque control by several direct and indirect mechanisms that not only involve reducing or removing dental biofilms but also include inhibiting bacterial metabolism when the agents are still present at sub-lethal concentrations.’8

* Gingival crevicular fluid increases as a result of inflammation and periodontal disease, supporting a more diverse bacterial community than found in individuals with healthy soft tissues.7,10


  1. Marsh PD. Dental plaque as a biofilm and a microbial community – implications for health and disease. BMC Oral Health 2006; 6 (Suppl 1): S14-S20
  2. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontology 2000 1997; 14: 9-11
  3. Khan SA. Periodontal diseases: bug induced, host promoted. PLoS Pathog 11(7): e1004952. doi:10.1371/journal.ppat.1004952
  4. Kinane DF, Attström R J. Group B consensus report of the fifth European Workshop in Periodontology. J Clin Periodontol 2005; 32(Suppl 6): 130-1
  5. Marsh PD et al. Ecological approaches to oral biofilms: control without killing. Caries Res. 2015; 49 (Suppl 1): 46-54
  6. Kilian M et al. The oral microbiome – an update for oral healthcare professionals. BDJ 2016; 221(10) 657-666
  7. Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology 2003; 149: 279-294
  8. Marsh PD. Contemporary perspective on plaque control. BDJ 2012; 212(12): 601-606
  9. Barnett ML. The rationale for the daily use of an antimicrobial mouthrinse. JADA 2006; 137: 16S-21S
  10. Gurenlian JR. The role of dental plaque biofilm in oral health. Journal of Dental Hygiene 2007; 81(5): 116-126