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 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 . 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 after sion and ultimately failure of periodontal odontal therapy, 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 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 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 . 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 , 2Consultant in , 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 loss and . 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

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Presence of plaque days immature collagen fibres are current thinking is that not only is 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 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 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 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 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. where oral hygiene is inadequate. Such This interaction induces the production of patients should be given precise oral Pocket depth inflammatory mediators which in turn ini- hygiene advice and correction of the Periodontal pockets are a sign of previous tiate and propagate periodontal breakdown local factor considered. This may be as periodontal disease. However, the depth of (as well as complications in other tissues). simple as the extraction of a lingually the pockets per se is not a good predictor Thus it has been suggested that patients displaced lower premolar. Orthodontic of risk but when correlated to bleeding with uncontrolled diabetes mellitus may correction should be discussed if there is scores are of affirmative value in recog- be up to three times more likely to suffer an evident that cannot be nition of further periodontal destruction. from periodontal disease.20 simply managed. Pockets greater than 6 mm after active This risk appears to be similar for both Iatrogenic factors should always be treatment are predictive areas of future poorly controlled insulin dependent and assessed. Poor interproximal contacts, mar- periodontal disease.16 non-insulin dependent diabetes. Indeed the ginal discrepancies, orthodontic appliances

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Stress (fixed and removable), sub gingival mar- such nicotine is implicated in the reduced gins and over contoured restorations have functional ability of many aspects of the There is increasing evidence that emotional all been implicated in periodontal dis- host immune response. Thus the host has stress may influence the extent and severity ease aetiology and progression.23,24 Those a lowered response to a challenge from of chronic periodontitis. In one study indi- causative factors that can be addressed plaque bacteria. viduals with minimal negative life events should be and those that cannot should bacteria:There have been sug- suffered less periodontal breakdown.32 be regarded as risk factors and thus con- gestions that smokers harbour more spe- Stress increases circulating cortisol levels sidered when calculating recall intervals. cies associated with periodontal disease through stimulus of the adrenal glands. There is some limited evidence to impli- though this may be due to a simply inferior Such increases in endogenous cortisol may cate occlusal disharmony in the propaga- level of plaque control. impair/diminish the immune response to tion of periodontal disease. Occlusal forces Healing and response to treatment: periodontal pathogens. This isn’t a straight that exceed the adaptive capacity of the There is a marked reduced healing poten- linear relationship as the type of stress periodontal ligament may predispose to tial following both non-surgical and surgi- and the susceptibility of the individual are alveolar bone resorption and thus tooth cal treatment of periodontal disease. For thought to be factors: these can obviously mobility. Animal studies have shown this the former this is thought to be related vary greatly. There must of course be peri- process to be worse in subjects with exist- to the effects of nicotine upon the local odontal pathogens present also.33 ing periodontitis. In one study untreated inflammatory response, there being less As well as the cortisol effect, the lifestyle occlusal discrepancies had significantly oedema and more fibrosis within the gin- issues that lead to stress (nursing a sick increased probing depths compared to gival tissue of smokers. For the latter, in relative, unemployment, relationship prob- those teeth that were treated.25 Assessing addition to these there are the effects of lems etc) may be correlated to a patient’s the is an essential part of any nicotine upon vascularity, fibroblast activ- ability to devote the necessary time to examination. One should be suspicious of ity and the matrix. In their oral health. Patients are therefore an occlusal correlation if there is: both cases it is also thought that contami- potentially less likely to spend the extra • Increased mobility nation of the root surfaces by products of five minutes in the bathroom required to • inhibits reattachment.26 achieve adequate plaque control every day. • Drifting Thus, significant correlations have Thus the role of stress on compliance must • Persistent discomfort on eating been demonstrated in smokers for clinical not be underestimated. • Thickening of lamina dura attachment loss, bone loss and . • Radiographic increased width of PDL - It is thought that this is related to most COMPILING RISK FACTORS funneling or saucerisation types of smoking including cigarettes, There is evidence to show that • Reduced bone height. pipes, cigars and of cannabis when smoked may underestimate the risk of periodon- with tobacco.27,28 The smoking status of all tal disease.34 Thus there have been many In these situations, after periodontal patients should be ascertained, appropri- suggestions as to how to correlate such treatment, one may consider occlusal ate and honest advice given about disease factors and calculate an overall risk of dis- equilibration and/or splinting. Consider risk and they should be referred to stop ease accurately. parafunction a risk factor and incor- smoking programmes. Some papers have porate it into the overall periodontal reported the risk attached to smoking may Periodontal Risk Calculator risk assessment. be dose dependent.29 Indeed as demon- In 2003 Page et al. devised an online web strated below, Lang and Tonetti differenti- based system for determining a patient’s Lifestyle influences ate risk associated upon smoking different risk of developing periodontal disease and Cigarette smoking quantities. These authors believe that in risk of progression of periodontal disease. the interests of long term success, complete This is a multiple-step process and records There is now an overwhelming body of and indefinite cessation should be sought data on: evidence to implicate smoking in the and patients should not be encouraged to • Patient age pathogenesis and progression of peri- simply cut down. • Smoking history odontal disease. The theories follow the • Diagnosis of diabetes effects upon: Nutrition • History of Host response: There are a variety of There may be an association between • Pocket depth effects. There is reduced blood supply to reduced Vitamin C & D and calcium con- • Bleeding on probing gingivae, thought to be due to the vaso- sumption and the risk of periodontal dis- • Furcation involvements constrictive effects of nicotine; indeed ease.30,31 Needless to say if it is apparent • Restorations or below the there may be simply fewer vessels too. a patient’s diet is poor (as recorded from Clinically, this often manifests as reduced dietary analysis) the dentist should advise • Radiographic bone height BOP, which is obviously misleading. them as such. It is not sufficient to dis- • Vertical bone lesions. Perhaps the more important aspect how- cuss cariogenic food stuffs alone; a holistic ever if the effect upon polymorphonucle- approach should be taken to the privilege This Periodontal Risk Calculator (PRC) ocytes, neutrophils and lymphoctyes. As of reviewing a diet sheet. gave strong predictions about disease risk

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and progression.35 This has been developed into the PreViser RiskCalculator and using mathematical algorithms this generates an age related risk score from 1 (low risk) to 5 (high risk). Once the risk has been calcu- lated the tool offers the most suitable treat- ment modalities and an appropriate recall interval. The system also re-calibrates itself as new sets of patients are added, thus it is an evolving risk assessment tool with new disease presentations and histories. Fig. 1 An example of a data collection Fig. 3 An example of a functional diagram screen using the PreViser software (images borrowed from Lang and Tonetti. BOP is 15%, In addition it offers treatment planning reproduced courtesy of Liz Chapple at OHI Ltd) four residual pockets ≥5 mm are diagnosed, alongside risk (Figs 1-2). two teeth had been lost, the bone factor in Professor Iain Chapple and colleagues at relation to the age is 0.25, no systemic factor is known and the patient is a non-smoker the University of Birmingham have been striving, in a joint venture with OHI Ltd, to increase awareness of this useful pro- Current periodontal status Bleeding on probing gramme within the United Kingdom. It is Pockets > freely available within dental universities Y N and practitioners can purchase the package 6mm Y 2/12 3-6/12 at various subscription rates depending N 3-6/12 >6/12 upon a practice’s circumstances and need. Hopefully, with increased professional Major risk factors Smoker awareness of PreViser more patients will Unstable Y N benefit from it in the future. Type II Y 2/12 3-6/12 Periodontal risk assessment with Diabetic functional diagram (Fig. 3)36 N 3-6/12 >6/12 This proposes the observation of six factors Fig. 2 An example of a completed periodontal evaluation using the PreViser Modifying factors that contribute to a patient’s risk and the software (images reproduced courtesy of Liz Family history production of a ‘functional diagram’. The Chapple at OHI Ltd) History of periodontal treatment six factors are: Local risk factors • Percentage of sites with bleeding Medications on probing This is not only helpful to the clinical team Parafunctional habits • Prevalence of residual pockets greater but to patient education and motivation. Stress than 4 mm Quite simply, if a patient can reduce a risk • Loss of teeth from a total of 28 teeth factor the image produced on the diagram Fig. 4 Algorithm for determining risk • Loss of periodontal support in relation changes. This immediate feedback can be to the patient’s age very tangible to patients. • Low-risk: green, recall greater than six • Systemic and genetic conditions months (dependent upon other oral • Environmental factors, such as An alternative and simplified disease risks). approach to risk assessment cigarette smoking. This simple method of risk assessment is Once a risk assessment has been made Each parameter has its own scale and as to construct 2 × 2 tables for known fac- this should be incorporated in the patient’s such for patients a diagram can be created tors (Fig. 4). treatment plan and form the foundations to demonstrate the risk.36 Further examples One should be guided by the lowest recall of their future supportive care. The risk of functional diagrams can be found in time; ie, if a patient has pocketing >6 mm assessment may also be a screening tool Lang and Tonetti’s paper.36 The extent of and bleeding but neither smokes nor drinks for patients. Though it is not within the the functional diagram represents risk, and then they should still visit every two months. remit of this paper to discuss treatment the larger the risk, the more often a patient If a patient has any modifying factors one regimens it is worth reiterating how this should be recalled and the more active the should consider recalling them more often risk assessment and recall decision should treatment may need to be at recall. if they are not already within a high risk fit into the patient’s future care plan. One need not actually construct the dia- recall. Once a risk assessment has been made These authors also believe it essen- gram to make the risk assessment but they patients may be given simple colour-codes: tial to discuss the recall intervals with are certainly a useful tool to demonstrate • High-risk: red, recall every two months patients and the outcome of this discus- risk and if performed regularly, demon- • Medium-risk: amber, recall every sion recorded within the patient’s notes. strate the variable and fluid nature of risk. 3-6 months Only after a discussion has taken place

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should the precise recall be agreed. It of such review/treatment and may be that patients of a high risk choose modification of treatment rationale not, for whatever reason, to follow that as required. prescription. Conversely many patients like attending more often than may be Whether one adopts the name or not, clinically necessary were one to follow this concept should be the fundamental such recall proposals. Such flexibility is paradigm of periodontal disease manage- 5 essential when managing people but those ment and prevention. Using this model patients who choose not to adhere to recall therefore we can be more confident of programmes must be made aware of the achieving success with patients and there risks involved and this must be reflected is an increasingly sound body of evidence in clinical record keeping. to support this.40-42

AGGRESSIVE PERIODONTAL WHEN SHOULD MAINTENANCE DISEASE COME TO AN END? Although the focus of most evidence con- It needs to be stressed that patients can 6 cerning periodontal recall is related to modify their own disease risk. As with car- chronic disease, similar principles can be ies prevention, those patients that reduce applied to patients with aggressive disease. their risk factors ie by stopping smoking Such patients have non-contributory medi- and improving their oral hygiene, need cal histories but often have a familial his- not be recalled as frequently. In those tory of the disease. Thus to a degree they patients with un-avoidable risk factors lie outside the normal diagnostic pattern such as family histories of periodontal 7 of chronic disease. Given aggressive perio- disease, it would still be wise to see them dontitis is associated with episodic destruc- more often. An open dialogue should be tive bone loss it is essential to have a strict present with the patient about their peri- recall protocol to allow close monitoring odontal health and a recall interval should of the disease activity. These patients need be set that is satisfactory to both patient to be informed they are susceptible to the and professional. One must also remember same risk factors associated with chronic that periodontal disease is often refractory disease. One study, yet to be published has in nature as is the compliance of patients. stressed the importance of close support- It may be that patients placed upon a 12 8 ive therapy and in the month recall interval should have their Figs 5-8 A high risk case of chronic successful outcome of disease stability. As recall interval cut to every three months periodontitis such these patients should be placed in a if the disease presents, progresses or their high risk and have a frequent recall.37 risk factors change for the worse. One must also be influenced by a the most important factors in the suc- SUPPORTIVE PERIODONTAL patient’s other oral disease risks. Consider cess of periodontal maintenance therapy. THERAPY OR SUPPORTIVE PERIODONTAL CARE38,39 those patients who smoke and drink alco- Unfortunately it has also been demon- hol frequently and heavily. Given the syn- strated that the majority of patients fail In 1989 the 3rd World Workshop of the ergistic influence of smoking and alcohol to comply with maintenance regimens.45,46 American Academy of intake upon risk of oral carcinoma these Thus treatment may not be successful termed the maintenance phase ‘support- patients must be recalled at least every six irrespective of a proposed and attended ive periodontal therapy’. This term encom- months. Likewise those patients with no recall interval. All patients must be passes a holistic approach to individual periodontal disease or risk factors should informed of this. As healthcare profession- patient management of those with peri- still be seen every 3-6 months if they are als we can only help the patient directly odontal disease including: caries active. A periodontal risk assess- in the surgery setting by service provision • A risk assessment of the individual ment should be just part of the holistic and education. Patient responsibility and • Regular clinical re-evaluations based approach to preventive management and compliance is essential if they are to ben- upon this risk disease modification in patients. efit from treatment. • Implementation of regular oral hygiene practices PATIENT COMPLIANCE EXAMPLES • Continual motivation of patients with It is unequivocal: the disease prognosis Patient A positive reinforcement in those patients who comply with regu- • Re-treatment of sites demonstrating lar periodontal therapy is better than in A 62-year-old female. Non-insulin depend- inflammation and/or disease progression those that do not.43,44 Thorough and dedi- ent diabetes: poorly controlled. Smokes • Continual reappraisal of the outcome cated oral hygiene measures are arguably 15/day and has done so for 40 years.

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Infrequent attender. Poor oral hygiene. patients limits the progression of disease She has no family history of periodontal and thus the need for further more costly disease (Figs 5-8). intervention.48 In secondary care, however, This is a classic case of severe generalised this argument is not so persuasive.49 chronic periodontitis. Using the 2 × 2 tables we can see this patient has a risk of peri- CONCLUSION odontal disease. There is pocketing >5 mm The management of those patients diag- 9 and BOP. She both smokes and has poorly nosed with chronic periodontitis does not controlled diabetes. We can also see that end after a course of mechanical debride- there is bone loss beyond the furcation on ment. To promote long-term stabilisation several teeth: this is a further local factor and success patients need to be enrolled that increases risk of disease progression. upon a life-long regime of regular moni- This patient needs to be placed in a high risk toring and support. Dentists and dental category. Once active treatment has been care professionals (DCPs) should con- completed she needs to be reviewed every struct risk assessments to determine the

2-3 months until her periodontal health has recall interval time appropriate to each 10 stabilised. It would be sensible to maintain individual patient. It may be necessary to that recall interval for life. review some patients every two months or indeed every month. Such visits should Patient B review oral hygiene, assess disease activity, A 45-year-old male. Medically healthy. include therapy of disease active areas and Non-smoker, nor has he ever smoked. re-emphasise through constructive criti- No family history of periodontal disease. cism the importance of the patient’s role Historical periods of poor oral hygiene. in their therapy. 11 Currently has some supra-gingival depos- Current estimates suggest that the preva- Figs 9-11 A low risk patient for future its and staining. No periodontal disease lence of moderate to severe periodontal disease progression (Figs 9-11). disease affects up to 79% of the world Using the 2 × 2 tables we can see this population (WHO 2004). In the UK one effect of sub-gingival scaling and controlled oral patient has a low risk current periodontal survey showed 54% of dentate adults had hygiene on the incidence of . Acta Odontol status and no major or minor risk factors. pocketing of 4 mm or more.50 There are Scand 1961; 19: 537–555. 4. Axelsson P, Lindhe J, Nystrom B. On the prevention Thus once an initial course of supra-gin- neither the staff nor facilities to manage of caries and periodontal disease. J Clin Periodontol gival and oral hygiene advice such numbers in secondary care. It is also 1991; 18: 182–189. 5. Suomi J, Green J, Vermillion J. The effect of con- has been completed it would be prudent more cost efficient to provide maintenance trolled oral hygiene procedures on the progression to review this patient in approximately in primary care.49 Primary Care Trusts (or of periodontal disease in adults: results after third and final year.J Periodontol 1971; 42: 152–160. six months given his oral hygiene is inad- whatever body replaces their function) 6. Axelsson P, Lindhe J. Effect of controlled oral equate. If on review this has improved should recognise that periodontal disease hygiene procedures on caries ad periodontal dis- eases in adults. J Clin Periodontol 1978; 5: 133–151. he may be recalled up to 24 months later demands flexible management. It is known 7. Morrison E, Ramford S, Hill R. Short-term effects of assuming he is controlled for other dental that the UDA system does not accom- initial, non-surgical periodontal treatment (hygiene phase). J Clin Periodontol 1980; 7: 199–211. disease risks. modate the complexities and temporal 8. Mousques T, Listgarten M. Effect of scaling and root demands of many dental treatments. It is planing on the composition of human sub gingival micro flora.J Periodontal Res 1980; 15: 144. COST OF PERIODONTAL also inadequate to place rigid restrictions 9. Cohen R E, American Academy of Periodontology. FOLLOW-UP on minimum time periods before further Position paper: periodontal maintenance. J Periodontol 2003; 74: 1395-1401. There is also a strong economic argu- treatment can be claimed under the NHS 10. Axelsson P, Lindhe J. The significance of mainte- ment for good maintenance programmes terms of care. Those concerned with mod- nance care in the treatment of periodontal disease. J Periodontol 1981; 8: 281-294. in periodontally susceptible individuals. ernising and planning the future deliv- 11. Stanton G, Levy M, Stahl S. Collagen restoration in Historically oral disease accounts for the ery of dental care should accept that if a healing human gingiva. J Dent Res 1969; 48: 27-31. 12. Martin J A, Page R C, Loeb C F, Levi P A Jr. Tooth loss fourth highest healthcare cost in indus- high standard of periodontal care is to be in 776 treated periodontal patients. J Periodontol 47 2010; 81: 244–250. trialised countries. Traditional treatment provided for within the remits of primary 13. Lang N, Adler R, Joss A, Nyman S. Absence of bleed- of symptomatic disease is costly and thus health care the system will have to change. ing on probing: an indicator of periodontal stability. J Clin Periodontol 1990; 17: 714–721. in some countries, including the United 14. Claffey N, Nylund K, Kiger R, Garrett S, Egelberg J. Kingdom, preventive oral care and oral 1. Loe H, Anerud A, Boysen H, Morrison E. Natural Diagnostic predicability of scores of plaque, bleed- history of periodontal disease in man. Rapid, ing, suppuration and probing depth for attachment public health have been increasingly moderate and no loss of attachment in Sri Lankan loss. J Clin Periodontol 1990; 17: 108–114. used. This has significantly reduced the laborers 14 to 46 years of age. J Clin Periodontol 15. Badersten A, Nilveus R, Egelberg J. Scores of plaque, 1986; 13: 431–445. bleeding, suppuration and probing depth to predict cost burden of oral health care. The same 2. Lindhe J, Okamoto H, Yoneyama T, Haffajee A, probing attachment loss. J Clin Periodontol 1990; model can be directly applied to periodon- Sockransky S. Periodontal loser sites in untreated 17: 102–107. adult subjects. J Clin Periodontol 1989; 16. Haffajee A, Sockransky S, Lindhe J, Kent R, Okamoto tal disease as a separate health care entity. 16: 671–678. H, Yoneyama T. Clinical risk indicators for periodon- Regular recall and follow-up of periodontal 3. Lovdal A, Arno A, Schei O, Waerhaug J. Combined tal attachment loss. J Clin Periodontol 1991;

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18: 117–125. 29. Haber J, Wattles J, Crowley M, Mandell R, Joshipura of patients with advanced periodontal disease. 17. Loe H, Theilade E, Jensen S. Experimental gingivitis K, Kent R. Evidence for cigarette smoking as a major J Periodontol 1979; 50: 163–169. in man. J Periodontol 1965; 36: 177–187. risk factor for periodontitis. J Periodontol 1993; 41. Valderhaug J. Periodontal conditions and carious 18. Lindhe J, Hamp S, Loe H. Plaque induced peri- 64: 16–23. lesions following the insertion of fixed prosthesis: odontal disease in beagle dogs. A 4-year clinical, 30. Nishida M, Grossi S, Dunford R, Ho A, Trevisan M, a 10 year follow-up study. Int Dent J 1980; roentgenographical and histometrical study. Genco R. Dietary vitamin C and the risk for peri- 30: 296–304. J Periodontal Res 1975; 10: 243–253. odontal disease. J Periodontol 2000; 42. Ramfjord S, Morrison E, Burgett F, Nissle R, Shick 19. Michalowicz B, Diehl S, Gunsolley J et al. Evidence 71: 1215–1223. R, Zann G et al. 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RESEARCH

CONCLUSIONS recorded working length. The radiographic 17. Goldberg F, Marroquin B B, Frajlich S, Dreyer C. In vitro evaluation of the ability of three apex assessment is only capable of determin- In general dental practice, no signifi- locators to determine the working length during ing the relationship of the master cone cant difference was observed in working retreatment. J Endod 2005; 31: 676–678. 18. Dental Practice Board. DPB digest of statistics. to the radiographic apex and not to the lengths when determined using an apex Eastbourne, UK: Dental Practice Board, 2004. anatomical apical foramen or constric- locator combined with a master cone GP 19. Molyneux L, Mccullough C, Preston A J, Jarad F D. Apex locator use by general dental practitioners tion. However, this method of radiographic radiograph or using the conventional in Merseyside. J Dent Res 2008; 87(Spec Iss C): assessment is widely used in clinical studies method. There is a need for further stud- Abstract number 0166 (PEF IADR). Available from: http://iadr.confex.com/iadr/pef08/techprogram/ in the literature as a method of determin- ies to assess the effectiveness of different abstract_111422.htm. ing satisfactory .1–3,26 methods of working length determination 20. Faculty of General Dental Practice (UK) of the Royal College of Surgeon of England. Selection criteria for If the outcome measure is deemed and their effect on the clinical outcome . London: FGDP(UK), 2004. acceptable, this does not necessarily mean of root canal treated teeth in general 21. European Society of Endodontology. Quality guidelines for endodontic treatment: consensus that the root canal filling is actually within dental practice. report of the European Society of Endodontology. the root canal system, because the ana- Int Endod J 2006; 39: 921–930. This study was funded by the NHS Research and 22. Saad A Y, al-Nazhan S. 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Farzaneh M, Abitbol S, Lawrence H P, Friedman S. endodontic case difficulty assessment form and that 2 mm) but in fact it is at or close to Treatment outcome in – the Toronto guidelines. Endodontics: Colleagues for Excellence the apical foramen. The available assess- Study. Phase II: initial treatment. J Endod 2004; 2005; Spring/Summer: 6–7. Available from: http:// 30: 302–309. www.aae.org/uploadedFiles/Publications_and_ ment technique does not allow the opera- 3. Schaeffer M A, White R R, Walton R E. Determining Research/Endodontics_Colleagues_for_Excellence_ tor to assess if the root filling is confined the optimal obturation length: a meta-analysis of Newsletter/ss05ecfe.pdf. literature. J Endod 2005; 31: 271–274. 25. Williams C B, Joyce A P, Roberts S. A comparison to the root canal system. Cone beam CT 4. Kuttler Y. 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‘See you in three months! The rationale for the three monthly periodontal recall interval: a risk based approach’ In the above general article, the caption for Figure 3 should have read: BOP is 9%, six residual pockets ≥5 mm, four teeth had been lost, the bone factor in relation to the age is 0.75 and there are genetic influences.

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