Lang N, Suvan J, Tonetti M. Risk factor assessment tools for the prevention of periodontitis progression: a systematic review. J Clin Periodontol. 2014; 42:S59-S70
Persson R, Mancl L, Martin J, Page RC. Assessing periodontal disease risk: a comparison of clinicians' assessment versus a computerized tool. J Am Dent Assoc. 2003; 134:575-582
Löe H, Ånerud A, Boysen H, Morrison E. Natural history of periodontal disease in man, rapid, moderate and no loss of attachment of Sri Lankan laborers 14–46 years of age. J Clin Periodontol. 1986; 13:431-440
Frencken JE, Sharma P, Stenhouse L, Green D, Laverty D, Dietrich T. Global epidemiology of dental caries and severe periodontitis – a comprehensive review. J Clin Periodontol. 2017; 44:S94-S105
Chapple IL. Time to take periodontitis seriously. Br Med J. 2014; 348
Axelsson P. Periodontitis is preventable. J Periodontol. 2014; 85::1303-1307
Asimakopoulou K, Newton T, Daly B, Kutzer Y, Ide M. The effects of providing periodontal disease risk information on psychological and clinical outcomes: a randomized controlled trial. J Clin Periodontol. 2015; 42:350-355
Asimakopoulou K, Nolan M, McCarthy C, Newton T. The effects of goal-setting, planning and self-monitoring (GPS) on behavioural and periodontal outcomes: a randomised controlled trial.: IADR; 2017
Tonetti MS, Jepsen S, Jin L, Otomo-Corgel J. Impact of the global burden of periodontal diseases on health, nutrition and wellbeing of mankind: a call for global action. J Clin Periodontol. 2017; 44:456-462
Preparing for practice: Dental team learning outcomes for registration. 2015;
Steele J. NHS dental services in England: An independent review. 2009;
Meyle J, Chapple I. Molecular aspects of the pathogenesis of periodontitis. Periodontology 2000. 2015; 69:7-17
Loe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol. 1965; 36:177-187
Hillam D, Hull P. The influence of experimental gingivitis on plaque formation. J Clin Periodontol. 1977; 4:56-61
Needleman I, Nibali L, Di Iorio A. Professional mechanical plaque removal for prevention of periodontal diseases in adults – systemic review update. J Clin Periodontol. 2015; 42:S12-S35
Meyle J, Chapple I. Molecular aspects of the pathogenesis of periodontitis. Periodontology 2000. 2015; 69:7-9
Genco RJ, Borgnakke W. Risk factors for periodontal disease. Periodontology 2000. 2013; 62:59-94
Page RC, Martin J, Mancl L, Garcia R. Longitudinal validation of a risk calculator for periodontal disease. J Clin Periodontol. 2003; 30:819-827
Matuliene G, Studer R, Lang NP Significance of periodontal risk assessment in the recurrence of periodontitis and tooth loss. J Clin Periodontol. 2010; 37:191-199
Trombelli L, Farina R, Ferrari S, Pasetti P, Calura G. Comparison between two methods for periodontal risk assessment. Minerva Stomatol. 2009; 58:277-287
Lindskog S, Blomlöf J, Persson I Validation of an algorithm for chronic periodontitis risk assessment and prognostication: risk predictors, explanatory values, measures of quality and clinical use. J Periodontol. 2010; 81:584-593
Newton J, Asimakopoulou K. The perceived acceptability of the DEPPA patient assessment tool: a questionnaire survey of Denplan Excel patients. Br Dent J. 2016; 221:65-69
Risk assessment is vital for preventive dental care and validated technologies exist that enable the dental professional to assess a patient's risk of developing periodontal disease. Information personalized to individual patients can be presented in a simplified format, which patients can understand, enabling them to make informed decisions on, and start taking responsibility for, their oral health.
CPD/Clinical Relevance: This paper aims to explain the importance, purpose and impact of periodontal risk assessment in contemporary dental practice, where a focus on prevention and personalized biofeedback is an ethical and cost-effective way forward.
Article
Risk assessment in periodontal disease
Risk assessment is the foundation stone for prevention, employing the latest evidence base to identify those patients who have a higher likelihood of developing a specific disease, then providing them with enhanced preventive care pathways. A key aspect involves persuading at risk people that they differ from the rest of the population and therefore have to work harder, both with their clinician and in their personal behaviours and home care strategies, if they wish to lower their risk of that disease developing.
Within the field of oral health, of the available risk assessment systems, periodontal risk assessment holds pride of place. This is because:
Validated systems have been shown to predict the likely risk of tooth loss through periodontal disease with a degree of accuracy.1
Assessment of periodontal risk is complex involving genetic, environmental and lifestyle exposures, and individual clinician assessment of risk has been shown to be highly variable.2
Susceptibility to periodontal disease varies across a broad spectrum. Some people are disease resistant and others exhibit high risk even prior to accounting for lifestyle and behavioural risk factors.3
Periodontal disease matters. Periodontitis affects 45–50% of the adult population and severe periodontitis affects 10% of adults.4 Despite substantial efforts being made in oral health education and associated oral health improvements, the prevalence of severe disease is reported to be increasing.5 A healthy periodontium is an essential foundation for one's natural dentition and for successful restorative dentistry, which is increasingly important given the ageing population. Effects of periodontitis within the mouth include tooth loss, pain, halitosis, aesthetic compromise and reduced masticatory ability, all of which impact negatively upon self-confidence and quality of life. Beyond the mouth, periodontitis is significantly and independently associated with chronic inflammatory non-communicable diseases of ageing, including cardiovascular disease, diabetes mellitus, rheumatoid arthritis and chronic kidney disease.6
Periodontitis is preventable7 but it is essential to identify it early before irreversible damage occurs.
Evidence is emerging for positive outcomes on both psychological and clinical markers of health that can be achieved through periodontal risk assessment.8,9
Aims
In 2002, the American Academy of Periodontology stated that risk assessment ‘should be part of every comprehensive dental and periodontal assessment’. A green paper calling for global action on periodontal disease endorsed by professional periodontal organizations throughout the world states ‘A critical element is that prevention needs to be tailored to the individual's needs through diagnosis and risk profiling’.10 The General Dental Council (GDC) places periodontal risk assessment firmly in its training requirements for undergraduates.11 Steele's review of National Health Service (NHS) dental care services in 200912 stated that ‘For new patients there should be a formal oral health assessment to evaluate the risks of all major dental disease (decay, gum disease and oral cancer) and the need for treatment. Personalised prevention should be started’.
The aim of this paper is to discuss the logic behind this approach, and why risk-driven prevention is critical if NHS dental care for an increasingly ageing population, with multi-morbidity, is to survive.
The aims of this narrative review are:
To review current understanding of the roles of the dental plaque biofilm and the host's immune response in the pathogenesis of periodontitis.13
To revisit the evidence that demonstrates how risk-targeted prevention can improve health and wellbeing.
To introduce the key technologies available to assess periodontal disease risk and explain how they support clinicians in decision-making.
To consider the frequently ignored intent of risk assessment and the element we would deem the most important: providing patients with simple, personalized information to empower them to make decisions about their current and future health.
Aetiology and pathogenesis of periodontitis
Periodontitis is a complex disease. Once considered to be a simple bacterial infection, triggered by plaque, we now know that it requires a series of complex interactions between the host's inflammatory and immune responses which are influenced by genetic, environmental and lifestyle factors.
In health, the commensal oral flora exists in a state of symbiosis with each other and with our immune system. When inflammation of the periodontal tissues occurs due to biofilm accumulation, this balance in the microbiota is upset (dysbiosis) and an overgrowth of pathogenic bacterial phylotypes results. Experimental gingivitis studies by Löe et al in 196514 clearly demonstrated that plaque triggers gingival inflammation, and also that removal of that plaque biofilm triggers resolution of the inflammatory process. Subsequent research, however, demonstrated that the causal association between plaque and gingivitis was not quite that simple. Hillam and Hull demonstrated, in 1977, that gingival tissues which were inflamed accumulated more plaque than healthy non-inflamed sites in the same people.15 Therefore, plaque causes gingivitis but gingivitis also causes plaque accumulation because of the additional nutrients supplied within gingival crevicular fluid exudates from inflamed sites (eg iron from haem), providing periodontal pathogens like P. gingivalis with essential nutrition. This circular process limits the effectiveness of professional mechanical plaque removal (PMPR) if patients do not implement good oral hygiene practices at home. Indeed, the latest results from the European Federation of Periodontology (EFP) consensus review16 states that ‘in relation to gingival health, there is little benefit to PMPR without oral hygiene instruction (OHI) and indeed that repeated thorough OHI can achieve a similar benefit to repeated PMPR’.
It is unequivocal that gingivitis is the precursor to periodontitis and that plaque accumulation is also a prerequisite: periodontitis will not develop in a pristine mouth or in someone who lacks the necessary risk factors. However, it is apparent to any clinician that some patients with abundant plaque do not develop periodontal attachment or bone loss, whilst other patients with apparently excellent oral hygiene may suffer from severe periodontitis. Löe et al's longitudinal study on the Sri Lankan tea workers,3 a seemingly homogeneous cohort, aged between 14 and 31 at baseline, who had poor plaque control and generalized gingival inflammation but received no dental care or treatment, provides evidence for the spectrum of periodontal risk. Over a 15-year period, approximately 8% demonstrated rapid progression of periodontal disease (high risk), 11% no progression (resistant) and 81% moderate progression (variable positive risk).
Whilst bacteria are a necessary requirement to initiate and potentially propagate periodontitis, the majority of tissue damage is host-mediated,17 yet existing management protocols do not address host susceptibility; rather they focus almost entirely on plaque removal. An everyday analogy is that of driving a car: the bacteria are the key that turns the ignition, but it is the host response that moves the car forward by forming the gearing and accelerator control system. Factors known to increase periodontitis risk are cigarette smoking, poorly controlled diabetes mellitus, poor oral hygiene and local plaque retention factors, which intensify the bacterial challenge. Genco and Borgnakke also review the evidence for obesity, osteoporosis, low dietary calcium and vitamin D and stress as systemic risk factors in their 2013 paper.18
Assessing risk
The risk factors for periodontitis carry different weights and interactions. Assessing periodontal disease is not a simple process. Persson et al2 demonstrated that dentists who examined the same sets of patient data came to widely differing conclusions on the grading of risk. When benchmarked against a standardized risk scoring method (the PreViser™ risk assessment algorithms), they consistently under-estimated the level of risk for high susceptibility patients.19 A further study by the same group20 demonstrated that, in their assessment of risk, dentist scoring was mainly influenced by the presence of existing disease. Disease and risk are, however, very different entities, the former representing current status and the latter the likelihood of disease occurring or developing in the future. A patient with severe disease is logically at high risk of future disease, but a young patient, for example with a large number of unmanaged risk factors, but limited clinical or radiographic evidence of disease, could also be at elevated risk.
Periodontal disease risk assessment systems
In a recent consensus meeting by the EFP, based upon underpinning systematic reviews,1 two systems were reported as having evidence of validity: PreViser™18 (also provided through DEPPA, the Denplan PreViser™ Patient Assessment in the UK) and the Periodontal Risk Assessment (PRA) tool.21 The predictive ability of these tools has been demonstrated in a number of studies.22,23 PreViser™ technology is widely used in general dental practice in both the UK and USA. It is an online assessment, which evaluates 11 factors: patient age, smoking, diabetes, history of perio surgery, pocket depth, BOP, furcation involvements, sub-gingival restorations, root calculus, radiographic bone height and the presence of vertical bone lesions. A fundamental element of the tool is its patient report, which is designed as a patient biofeedback and communication tool. The report (Figure 1) includes numeric and traffic light coded representations of periodontal disease risk (on a scale of 1–5) and severity (on a scale of 1–100). A graph is produced which tracks change (improvement/deterioration) since the previous assessment. Suggested treatment options, based on the clinical inputs, are also provided to discuss with the patient.
The PRA is often referred to as the spider diagram (Figure 2) and is widely known from specialist teaching programmes. Available online it produces a functional graphical representation of a patient's risk based on six clinical, systemic and environmental factors being:
Percentage BOP;
Number of residual periodontal pockets ≥5 mm;
Number of lost teeth;
Alveolar bone loss in relation to patient age;
Systemic and/or genetic predispositions;
Environmental factors such as tobacco use.
This tool is designed to be used after periodontal therapy has been completed.
Other systems include a simplified risk assessment proposed by Trombelli et al,24 which has been validated against PreViser™, and DentoRisk®, developed by Lindskog et al,25 where patients' risk is first determined for their whole dentition and is combined with a skin test for inflammatory reactivity. Where DentoRisk® identifies a patient as high risk, tooth-based risk assessments can then be calculated.
How should/does risk assessment change patient care plans?
The aim of risk assessment is to identify patients who are at risk before irreversible damage occurs. By assessing periodontal risk in addition to disease, the clinician is able to determine the high risk patient's care plan in terms of recall periods, reduction of risk factors, intensity of treatment and referral to specialists more effectively. Conversely, risk-based prevention also prevents over treatment. As stated in the Steele report,12 ‘Longer recall intervals are a marker of success, not an abdication of duty, and the recall interval is integral to a continuing care arrangement. A move away from the six-month interval should be the prize of a preventively led service, releasing resources for other services’.
Quantifying risk and disease by means of scores enables the success of care plans to be objectively measured, which is valuable on an individual, practice and population level. The incorporation of periodontal risk and disease markers into capitation banding calculations can ensure that sufficient time is allowed for periodontal treatment. Periodontal disease risk levels are employed by public and private health providers and insurers to focus resources on those who need them most for prevention.
How is risk assessment received by patients?
Evidence from the NHS pilots is that, funding methodology aside, the oral health assessment is welcomed by patients and dentists for its preventive approach. Patients now expect more information, and thus control, of their own oral health. More importantly, empowering patients to play a stronger role in the maintenance of their own health requires their understanding of their specific risk factors for periodontitis, eg oral hygiene, smoking, losing weight or acceptance of treatment. Without such knowledge of their own risk status, the preventive care plan provided by their clinician will not be effective in the longer term. The information patients receive from a dentist can be confusing. Risk assessment systems aim to present this information in a way that patients can understand, placing knowledge and control in their hands, so that they can make appropriate decisions. Risk assessment can also highlight to patients how they differ from the rest of the population through numerical comparison.
In a questionnaire-based survey published by Newton and Asimakopoulou in 2016,26 participants expressed a high level of acceptability of the DEPPA tool. In particular, the tool was seen as enhancing the relationship between the patient and practitioner and providing information to support behaviour change.
A further randomized controlled trial8 considered the psychological impact of including PreViser™'s individualized periodontal risk assessment in consultations. The study demonstrated that, relative to those who just had a routine consultation, patients who had a periodontal risk assessment saw periodontal disease treatment as more effective, were more confident in their ability to follow a periodontal treatment regimen, and reported higher intentions of adhering to periodontal disease instructions.8
Does risk-targeted prevention improve clinical markers of periodontal health?
Axelsson's7 30-year study began in 1971 and demonstrated that, by using a risk-based approach to determine intensity of treatment, it is possible to maintain a population with almost no loss of periodontal support.
More recently, a randomized controlled trial (RCT) presented by Asimakopoulou at the IADR 2017, and submitted for publication, showed how, over a 12-month period, a simple behavioural intervention using PreViser™'s individualized periodontal disease risk communication significantly improved clinical outcomes (bleeding and plaque) and self-reported interdental cleaning vs a routine periodontal assessment at 3 months.8
Conclusion
In spite of efforts by the dental profession in oral hygiene instruction and general overall improvements in oral hygiene levels in the population, the prevalence of severe periodontitis is increasing.
The focus of modern healthcare systems must move towards patients taking personal responsibility for their own wellbeing. Health messages delivered to all people are an important part of this process, but evidence is emerging that personalizing data to the patient and presenting it in a simple format so that patients can understand their unique health and risk status, carries both psychological and clinical impact. Moreover, it sits well with the new era of precision medicine, where patients are treated as individuals and the ‘one size fits all’ philosophy is becoming an approach from a bygone era.