See you in three months! IN BRIEF • Outlines the relevance of making recall plans individual to a patient’s needs GENERAL The rationale for the three and recognising the importance of compliance with these regimens. • Provides an understanding of the importance of risk assessment of monthly periodontal recall periodontal disease progression. • Enables an understanding of the concept of supportive periodontal therapy and the interval: a risk based approach integration of SPT with risk assessments. J. Darcey1 and M. Ashley2 VERIFIABLE CPD PAPER There is significant evidence to support the regular review of patients with chronic periodontitis. There is, however, com- paratively little evidence to demonstrate how often such reviews should take place. This paper looks at the periodontal healing period, the risks of periodontal progression and current thinking about maintenance programmes. It thus attempts to establish some guidelines that practitioners may use when calculating recall intervals. Clinical relevance The choice of individual, patient-focused recall intervals is essential to limit disease progression and maintain healthy periodontal tissues. These are so often the parting words as in turn give rise to further disease progres- Thus such combinations of active peri- a patient leaves the dental surgery after sion and ultimately failure of periodontal odontal therapy, oral hygiene advice and a course of periodontal treatment: ‘When treatment. The aim of this paper is to assess regular follow up have increasingly dem- would you like to see me again?’ It is the literature and discuss the rationale for onstrated improvements in periodontal then that the clinical auto-pilot engages such programmes. health.5-7 Thus we can begin to see a strong and a figure is reeled off: ‘Three months clinical argument for more regular peri- Mrs Jones.’ Years of education and clini- WHAT IS THE EVIDENCE FOR THE odontal maintenance therapy. IMPORTANCE OF MAINTENANCE? cal experience allow rapid processing of the information and we calculate a date. For obvious ethical reasons there are very WHAT IS THE CURRENT THINKING? Yet how? There is now a firm body of few studies that demonstrate the outcome Historically it is said that we should evidence supporting the prescription of of not treating or maintaining the peri- not undertake any form of periodontal recall intervals based upon caries risk odontal health of a population yet there treatment for three months after initial but when it comes to periodontal disease are some. In the seminal paper Loe et al.1 therapy so: and its follow up the literature becomes demonstrated significant progression of 1. There is sufficient time for more sparse. periodontal disease in a group of patients development and maturation of a long It is widely accepted that when a patient who had no periodontal therapy over 15 junctional epithelium with chronic periodontitis has come to years. This was also supported by Lindhe et 2. The sub-gingival flora can re-establish the end of a period of active periodontal al. in 1989 when a cohort of the Japanese and it is possible to assess whether treatment they should enter a maintenance population were observed for two years anaerobic periodontopathogens phase. The purpose of this is to allow the without any periodontal intervention: have re-colonised sites: In one study periodontal tissues to heal and for the although the extent of disease varied, there there was a marked reduction in clinical team to provide the appropri- was evident progression of periodontal spirochetes that continued up to ate support for the patient. Without such disease throughout the group.2 seven weeks after a course of root vigilance it is likely that the patient will Conversely for the last 50 years there planing and scaling.8 It has, however, not achieve an adequate standard of daily has been a growing body of evidence to also been noted that pathogens can dental hygiene and the tissues will become support the benefits of regular follow up. increase to pre-treatment levels in re-infected with dental plaque. This may In 1961 Lovdal et al. found that a com- 9-11 weeks9 bination of oral hygiene instruction and 3. Sufficient time has elapsed to assess 1*Specialist Registrar and Honorary Lecturer in Restora- cleaning performed 2-4×/annum for five the patient’s level of oral hygiene. tive Dentistry, 2Consultant in Restorative Dentistry, years dramatically reduced the incidence There is a tendency for this to plateau. University Dental Hospital of Manchester, Higher 3 Cambridge Street, Manchester, M15 6FH of tooth loss and inflammation. Axelsson Indeed it has been reported that *Correspondence to: Dr James Darcey and Lindhe in 1981 performed a similar without motivation patients’ oral Email: [email protected] study. The results indicated early follow- hygiene may deteriorate10 Refereed Paper up is linked to a reduction in disease and 4. Healing after non-surgical periodontal Accepted 21 July 2011 DOI: 10.1038/sj.bdj.2011.868 the progression of caries and periodontal therapy is complete. Although ©British Dental Journal 2011; 211: 379-385 disease can be effectively halted.4 epithelialisation takes place after 2-7 BRITISH DENTAL JOURNAL VOLUME 211 NO. 8 OCT 22 2011 379 © 2011 Macmillan Publishers Limited. All rights reserved. GENERAL Presence of plaque days immature collagen fibres are current thinking is that not only is diabetes only laid down by 21 days. Complete We know that plaque is intimately related mellitus closely related to the aetiology of repair may take about seven weeks to periodontal disease.17,18 It is, however, periodontal disease but periodontal disease though collagen maturation may hard to correlate plaque levels to main- may be related to poor glycaemic control. take longer.11 tenance of periodontal health as host This, in turn has been demonstrated to lead inflammatory response to plaque is very to further bone destruction and progression Although these statements will be variable. Thus quantifying plaque levels, of periodontal disease.21 As such all patients known to most practitioners there is seem- though useful in terms of demonstrat- should be closely monitored. Conversely ingly little reference within the texts to the ing patient compliance, cannot so easily the dentist should be aware that progres- science behind them. Thus, although it is be used to quantify risk. It is the inflam- sive periodontitis in patients with otherwise useful to use these as a guide to selecting matory response to the plaque that is the controlled risk factors may be diabetic. It recall intervals, it would be more sensible crucial detail to correlate to plaques scores. is thought that approximately 30% of dia- to move away from generic statements and betic patients are undiagnosed. The dentist towards patient-focused decision making. Genetic influences certainly should screen and refer patients if To do this we can perform risk assessments In a study assessing 117 pairs of adult twins suspicions are aroused. for periodontal disease in the same way (monozygotic and dizygotic) Michalowicz we perform them for caries development et al. found statistically significant cor- Medication and progression. relations between these participants when There are several systemic medications compared to the general population for with the known side effect of gingival THE PERIODONTAL RISK adult periodontitis. Thus it has been sug- over growth. Though technically clas- ASSESSMENT gested genetic influences account for up to sified as a gingival disease modified by Risk is the likelihood of either developing 50% of the variance in disease across the medication, the ensuing overgrowth can a particular disease or of having a particu- population.19 This is thought to be related to present a risk for periodontal disease lar disease progress over a given period genetic differences in host response. Such through an interference to plaque con- of time. It depends on possession of and/ genetic polymorphisms include variants in trol. The most common enlargements or exposure to risk factors. Such risk fac- interleukin 1 (IL-1), tumour necrosis factor pertain to antihypertensive calcium chan- tors known to be involved in periodontal (TNF) and immunoglobulin G Fc (FcR). As nel blockers (nifedipine, amlodipine and disease include: such it is always wise to inquire as to fam- diltiazem), anti epileptics (phenytoin) ily history of gum disease or ‘pyorrhoea’ and immunosuppressants (cyclosporin). Current periodontal health and edentulousness in parents, grandpar- With such medications gingival enlarge- There is an ever increasing body of evi- ents and siblings. This may reveal a pre- ment is associated with plaque presence dence to suggest that the current disease disposition of which the patient needs to be and as such one can easily see a peri- status/severity is of paramount importance informed, so that preventive dental care can odontal condition deteriorating if plaque in calculating the future disease risk and be provided for younger family members. control is inhibited by gingival irregular- treatment planning for a patient.12 ity. Though the association has not been Systemic influences proven, as inadequate plaque control Bleeding on probing Diabetes mellitus is implicated in the aetiology of peri- The simplest measure of the absence of odontal disease, practitioners should be disease is the absence of bleeding on The strong relationship between diabe- vigilant nonetheless. probing. Bleeding is a marker of gingival tes mellitus and periodontal disease is inflammation and though not an indicator now recognised and being increasingly Local influences of attachment loss, it is a negative predic- understood. In such patients, chronically Mal-alignment, imbrications, drift- tor of future attachment loss.13 Bleeding elevated blood glucose levels speeds the ing and crowding have all been con- on probing can thus be regarded as a formation of advanced glycation end nected to loss of periodontal support.22 determinant of a higher risk of disease products (AGEs). These AGEs interact The risk of periodontal disease is greater progression.14,15 with endothelial cells and monocytes.