Removal of the dental biofilm

14 October, 2010 / Infocus
 

The formation of a biofilm is ubiquitous when bacteria and a solid surface are concurrently present in a fluid environment. The oral cavity is no exception.

Soon after birth, the mucous membrane of the oral cavity is colonised by bacteria partly derived from the mother and partly from the new environment (food etc) with which it comes into contact. A biofilm (plaque) forms on the oral mucous membrane, the thickness of which is kept in check by shedding oral mucosal cells. Eruption of teeth presents a different surface where the dental biofilm (dental plaque) can become established.

The presence of a hard, non-shedding tooth surface facilitates the development of the dental biofilm. Within a few minutes of tooth eruption or cleaning of a tooth surface, an acquired salivary pellicle develops almost immediately on the enamel surface. Within hours of pellicle formation, bacterial colonisation ensues through the ability of bacterial cells to bind directly to the pellicle and also to each other. If the biofilm is left undisturbed for about two to three weeks after pellicle formation, an increase in the complexity (quantity and quality) of the bacterial community leads to the formation of a mature biofilm.

The tooth-gingiva junction is a unique area in the body – it is the only site where a hard surface penetrates the soft tissue integument. It is specifically at this junction that the prevention or treatment of periodontal diseases takes place.

It was the seminal work of the eminent Swedish periodontist Harald Löe1 which demonstrated very clearly that the accumulation of dental plaque at the tooth-gingiva interface led to the initiation of gingival inflammation (gingivitis) and that removal of dental plaque by instituting effective daily oral hygiene measures led to resolution of gingival inflammation and restitution of gingival health. This forms the basis of non-surgical periodontal therapy as we know it today.

Removal of dental biofilm – the patient’s role

Considering how quickly plaque forms on teeth after its removal, the effective daily removal of the dental biofilm by the patient is the most reliable way of preventing its build up. Practically all patients own a toothbrush, be it a mechanical or a powered one. However, whether it is used effectively is another matter. Most patients brush their teeth on average once or twice a day and this helps them maintain good dental health.

However, most are not aware of the importance of brushing the tooth-gingiva junction, i.e. the most crucial aspect in preventing or treating periodontal disease, and thus maintaining good periodontal health. In fact most patients withdraw from approaching the gingiva with a toothbrush when they experience gingival bleeding. Others think that it is normal for gums to bleed as “they have always done so”.

When asked whether they are aware of where the problem lies and how to follow effective daily tooth brushing regimes, most patients reply negatively. Most patients have never been given oral hygiene instructions. It is impossible to expect patients to perform such measures when they are unaware of where the problem lies or, more importantly, how to deal with it. What might seem common knowledge of dental anatomy to clinicians or dental care professionals might not be so obvious to our patients.

The first step in implementing an effective plaque control programme is by educating the patient on such measures. This is ideally done by performing an oral hygiene programme, which is individually tailored to each patient2. An assessment of the patient’s knowledge of the disease, expectations and long-term goals should be established. This should be followed by an assessment of the patient’s frequency of tooth brushing, motivation and assessment of manual dexterity.

The majority of clinicians, dental hygienists or therapists might be inclined to commence instrumentation at the first visit when patients attend for periodontal therapy. While this will lead to some improvement in the patient’s periodontal status, it is only a short-term measure if the patient does not achieve and maintain a strict supragingival plaque control regime. Instrumentation of a heavily inflamed periodontium will be particularly uncomfortable for the patient and bleeding will hamper proper instrumentation.

Furthermore, instrumentation at this stage will impart the notion to the patient that the onus of periodontal therapy (more specifically supragingival plaque control) lies with the dental professional rather than with the patient. The importance of the patient’s effective self-performed plaque control to a level compatible with periodontal health cannot be overemphasised.

Establishment of full mouth bleeding scores and plaque scores provides the patient with a tangible picture, and the clinician with documented evidence, of the level of plaque control. Demonstration of the periodontal status – plaque accumulation, periodontal pockets, bleeding on probing (BOP) etc – to the patient should be performed in the patient’s mouth and also by explanation of the dental chart.

Implementation of the appropriate oral hygiene techniques will help the patient attain and maintain periodontal health at the dento-gingival junction. The discussion at this stage should focus on the demonstration of effective tooth brushing techniques (Fig 1), including the use of interdental cleaning aids such as interspace brushes and dental floss (Figs 2, 3). Powered toothbrushes seem to offer additional benefit over manual toothbrushes3, while single tufted toothbrushes are particularly useful for entering periodontal pockets (Fig. 4).

Removal of the dental biofilm at the orifice of the periodontal pocket will deter microbial colonisation within the periodontal pocket. Several clinical studies have shown that, in the absence of strict supragingival plaque control, recolonisation of periodontal pockets can take place as early as three weeks following instrumentation4. Mouthwashes may be used as adjuncts in non-surgical periodontal therapy5; while they are capable of reducing the bacterial load supragingivally, they do not penetrate periodontal pockets6.

Removal of dental biofilm – the clinician’s role

Periodontal pockets provide the ideal ecological environment for harbouring periodontal pathogens that migrate subgingivally from the supragingival microflora. The accumulation of sub-gingival microflora leads to the formation of a subgingival biofilm on the root surface. In contrast with the supragingival bacteria, the predominant subgingival bacteria are anaerobic and Gram-negative. These bacteria release various toxins including lipoplysaccharide (LPS, released by Gram-negative bacteria), which are capable of eliciting an inflammatory response by the host. The subgingival biofilm might also calcify to form subgingival calculus.

The removal of the subgingival biofilm, especially in moderately deep (4-5mm) or deep (>6mm) pockets is equally as important as removal of its supragingival counterpart by the patient. Subgingival instrumentation is the remit of the dental surgeon, hygienist or therapist and should corroborate the patients’ efforts.

Mechanical removal of the subgingival biofilm can take place either via hand, sonic or ultrasonic instrumentation. Several studies have confirmed that the different subgingival modalities yield similar clinical improvements in therapeutic outcomes in both moderately deep7,8 and deep9,10 periodontal pockets. The use of ultrasonic debridement might have the added benefits of its cavitational effect and of being kinder to the clinician and patient. Recent clinical studies have shown that one episode of full mouth ultrasonic debridement is as effective as the more time-consuming (and possibly more painful) quadrant by quadrant scaling and root planing11,12.

Traditional periodontal instrumentation has been based on scaling i.e. the removal of supragingival calculus and/or root planing i.e. the instrumentation aimed at removing the microbial flora on the root surface or lying free in the pocket, all flecks of calculus and all contaminated cementum and dentin13. The emphasis was on removal of ‘contaminated’ and ‘infected’ cementum and thus sharp (hand) instruments were used to remove cementum until a smooth root surface was established.

The removal of cementum invariably leads to the removal of the notorious subgingival biofilm associated with its surface and hence leads to improvement in clinical symptoms i.e. probing depths, bleeding and suppuration14. The removal of cementum per se has been questioned as soft tissue healing via a long junctional epithelium has been observed if the cementum is kept plaque free 15,16.

Furthermore, in vitro studies have shown that the bacterial endotoxin (lipopolysaccharide) and other bacterial toxins are very superficially bound by cementum and these can be relatively easily removed by brushing or a conservative regime of ultrasonic root debridement17,18. Smart et al (1990)18 proposed the use of the term root surface debridement (RSD), defined as ultrasonic instrumentation of the root surface using overlapping strokes and assuming light pressure and limited time. This is distinct from the more traditional root surface planing (RSP) which involved the deliberate removal of root cementum13.

The presence of a smooth surface after RSP was considered to be the therapeutic goal; however, clinical success should be judged by the resolution of clinical periodontal symptoms (BOP, reduction in pockets depths, etc) upon clinical re-evaluation at a subsequent visit rather than on the smoothness of the root surface.

Maintenance of periodontal health – patient’s and clinician’s role

Once the active phase of periodontal therapy is over, each patient’s periodontal status is re-evaluated in order to ascertain the effect of non-surgical periodontal therapy. In some patients, periodontal pockets might persist and these pockets would warrant surgical elimination. At re-examination, some patients’ manifest complete resolution of periodontal pocketing and these proceed directly to the maintenance phase of periodontal therapy, also known as supportive periodontal therapy (SPT). SPT is defined as “the essential need for therapeutic measures to support the patient’s own efforts to control periodontal infections and to avoid recontamination”19.

Two integral components of SPT are:

  • Regular visits by the patient – these should yield positive feedback, encouraging the patient to maintain as plaque-free a dentition as possible
  • Continuous diagnostic monitoring of the patient by the clinician in order to intercept with adequate therapy at the optimal time.

Continuous monitoring should include recording of plaque and bleeding scores. It has been clearly established that plaque-free dentitions which are under regular supportive care maintain periodontal stability for many years, while plaque-infected dentitions will manifest recurrence of periodontal breakdown20,21,22. The frequency of recall visits should be based on each patient’s needs as assessed by the individual’s periodontal risk assessment (PRA), which should be established at the end of active treatment. Based on the PRA, some high-risk patients might need to be seen every three months for continuous monitoring and possibly for further treatment as determined by the clinical findings.

Some patients might continue to have good periodontal health at the three-month recall visit and, if low risk, would not need any further instrumentation, but a review visit possibly at a longer time interval than three months. Instrumentation at healthy, i.e. non-inflamed, periodontal sites will actually induce loss of attachment 23,24.

Thus, not all patients require three-monthly visits to the dentist or hygienist; some benefit from six-monthly (medium risk) or annual visits (low-risk cases).

The frequency of recall is determined by consideration of previous disease predisposition as well as general factors (systemic/environmental/genetic) and local factors (BOP, pocket probing depths >5mm, tooth loss, bone loss)25.

Conclusions

  1. Removal of the bacterial biofilm remains the cornerstone of non-surgical periodontal therapy.
  2. The importance of the patient’s self-performed plaque control cannot be over emphasised.
  3. Mechanical disruption of the sub-gingival biofilm, in addition to strict supragingival plaque control, is crucially important and leads to improved clinical outcomes.
  4. Removal of cementum is unwarranted.
  5. Maintenance of periodontal health should be jointly established by the patient’s continued supragingival plaque control and the clinician’s subgingival instrumentation when indicated.
  6. The frequency of recall visits should be tailored according to patient’s needs.

About the author

Marilou Ciantar is a specialist periodontist and oral surgeon based at Blackhills Clinic in Aberuthven. She welcomes referrals for any aspect of periodontal therapy, oral surgery or implant surgery, with conscious sedation if required. http://www.blackhillsclinic.com


References

1. Löe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol. May-Jun; 36: 177-87.

2. Jönsson B, Öhrn K, Oscarson N, Lindberg P. The effectiveness of an individually tailored oral health educational programme on oral hygiene behaviour in patients with periodontal disease: a blinded randomised-controlled clinical trial (one-year follow up). J Clin Periodontol 2009; 36: 1025-1034.

3. Robinson PG, Deacon SA, Deery C, et al. Manual versus powered tooth brushing for oral health. Cochrane Database Syst Rev 2005; Apr 18:CD002281 (revised from 2003).

4. Sbordone L, Ramaglia L, Gulletta E, Iacono V. Recolonisation of the subgingival microflora after scaling and root planing in human periodontitis. J Periodontol 1990; 61: 579-584.

5. Ciantar M. Chemical agents in periodontal therapy: use or misuse? Dental Update 1995: Jul/Aug; 238-242.

6. Pitcher GR, Newman HN, Strahan JD. Access to subgingival plaque by disclosing agents using mouth rinsing and direct irrigation. J Clin Periodontol 1980; 7: 300-308.

7. Torfasen T, Kiger R, Selvig KA, Egelberg J. Clinical improvement of gingival conditions following ultrasonic versus hand instrumentation of periodontal pockets. J Clin Periodontol 1979; 6: 165-176.

8. Badersten A, Nilveus R, Egelberg J. Effect of nonsurgical periodontal therapy (I). Moderately advanced periodontitis. J Clin Periodontol 1981; 8: 57-72.

9. Badersten A, Nilveus R, Egelberg J. Effect of nonsurgical periodontal therapy (II). Severely advanced periodontitis. J Clin Periodontol 1984; 11: 63-76.

10. Oosterwaal PJM, Matee MI, Mikx FHM, et al. The effect of subgingival debridement with hand and ultrasonic instruments on the subgingival microflora. J Clin Periodontol 1987; 4: 528-533.

11. Zanatta GM, Bittencourt S, Nociti FH Jr, et al. Periodontal debridement with povidone-iodine in periodontal treatment: short-term clinical and biochemical observations. J Periodontol. 2006; 77: 498-505.

12. Del Peloso Ribiero E, Bittencourt S, Sallum EA et al. Periodontal debridement as a therapeutic approach for severe chronic periodontitis: a clinical, microbiological and immunological study. J Clin Periodontol 2008; 35: 789-798.

13. O’Leary T. The impact of research on scaling and root planing. J Periodontol 1986; 57: 69-75.

14. Slots J, Mashimo P, Levine MJ, Genco RJ. Periodontal therapy in humans.I. Microbiological and clinical effects of a single course of periodontal scaling and root planing and of adjunctive tetracycline therapy. J Periodontol 1979; 50: 495-509.

15. Listgarten MA, Ellegard B. Electron microscopic evidence of a cellular attachment between junctional epithelium and dental calculus. J Periodontal Res. 1973; 8: 143-50.

16. Nyman S, Sarhed G, Ericsson I, Gottlow J, Karring T. Role of “diseased” root cementum in healing following treatment of periodontal disease. An experimental study in the dog. J Periodontal Res 1986 Sep; 21: 496-503.

17. Moore J, Wilson M, Kieser JB. The distribution of bacterial lipoplysaccharide (endotoxin) in relation to periodontally involved root surfaces. J Clin Periodontol 1986; 13: 748-751.

18. Smart GJ, Wilson M, Davies EH, Kieser JB. Assessment of ultrasonic root surface debridement by determination of residual endotoxin levels. J Clin Periodontol 1990: 17; 174-178.

19. Lang NP, Bragger U, Salvi G, Tonetti MS. Supportive periodontal therapy. In: Clinical periodontology and implant dentistry. Ed: Lang NP, Lindhe J. 2008; Chapter 59; p 1257.

20. Rosling B, Nyman S, Lindhe J, Jern B. The healing potential of the periodontal tissues following different techniques of periodontal surgery in plaque-free dentitions. J Clin Periodontol 1976; 3: 233-250.

21. Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures on caries and periodontal disease in adults. Results after 6 years. J Clin Periodontol 1981a; 8: 239-248.

22. Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol 1981b; 8: 281-294.

23. Lindhe J, Nyman S, Karring T. Scaling and root planing in shallow pockets. J Clin Periodontol 1982; 9: 415-418.

24. Cobb CM. Non surgical pocket therapy: mechanical. Ann Periodontol 1996: 1 :443-490.

25. Lang NP, Tonetti MS. Periodontal risk assessment for patients in supportive periodontal therapy (SPT). Oral Health Prev Dent 2003; 1: 7-16.

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