Using Risk Assessment to Customize Periodontal Treatment

Copyright 1999 Journal of the California Dental Association.

In recent years, understanding of the multifactorial nature of periodontal disease has taken great strides. Periodontal disease is initiated and sustained by the presence of bacteria, but disease progression is significantly modified by the body's response to the bacteria. This article highlights the emerging evidence regarding which risk factors are predominant in influencing the disease process and how the incorporation of prognostic risk factors in overall diagnosis can help facilitate treatment planning. These factors appear to be smoking, genetic susceptibility, compliance, and diabetes. The first three factors mentioned are the focus of this article. Each is discussed with regard to their role in amplifying the disease process and how this information can be used in clinical practice. By acknowledging the importance of these factors, dentists can consider their patients' risk to allow for more cost-effective planning and treatment. The opportunity to identify high-risk patients and treat them more proactively is significant; the challenge rests with dentists' willingness and ability to embrace the change before them.

One of the most difficult challenges dentists face is how they can identify, treat, motivate, and sustain the oral health of a wide variety of patients in an increasingly complex practice environment. Dentists are faced with the need to develop appropriate treatment and maintenance plans based on what is often an uncertain prognosis and increasing pressure to deliver predictable, cost-effective outcomes. The explosion of knowledge in the past few years about periodontal disease in relation to other systemic disorders has added to the challenge of making these recommendations. As the mouth becomes increasingly important in connection to the overall systemic health of patients, the identification and treatment of periodontal disease early becomes even more critical.

With the emerging evidence of systemic interactions with the periodontal tissues comes a responsibility for dentists to provide better diagnoses and treatment outcomes for the whole patient. This requires improved techniques for assessing the presence or absence of periodontal disease and better classifications for the types of disease. It also demands more effective ways of identifying risk factors and understanding their impact on disease progression and on the treatments or procedures dentists recommend.

Figure 1. Decision making for high-risk patients with chronic gingivitis: Traditionally patients are placed into periodontal maintenance programs based only on the degree of anatomical destruction. With risk assessment, patients with generalized gingivitis may also enter periodontal maintenance if they are at high risk for periodontitis.

Research in this area has escalated in the past few years. This new scientific information has refined dentists' understanding of periodontal disease. Prominent bacteria associated with generalized, "garden variety" adult periodontitis have been identified in disease initiation and progression. These are Porphyromonas gingivalis, Bacteroides forsythus, and Actinobacillus actinomycetemcomitans.^1-3 At the same time, there is much confusion as to how the presence or absence of bacteria affects disease progression and severity, which can vary considerably from one individual to another. For example, a patient who does not have the suspected pathogens may present with periodontal lesions; or, conversely, the patient may have the suspected pathogens but present with no lesions. Clearly, there is more to the story than a simple infectious disease paradigm can explain.

Current evidence supports an interaction between the bacteria and the patient's systemic response to it. This interaction plays an essential role in the disease expression and progression.^4,5 Stated simply, bacteria are a necessary condition for initiation of disease but insufficient for predicting the progression of the disease or determining how severe the disease will become. Individual patient risk factors -- systemic, genetic, and behavioral -- play a critical role in the clinical manifestation and severity of the disease.^6,7 Knowing this makes assessing the risk of an individual patient an increasingly important step in the treatment planning process.

The primary reason to assess risk is to understand future disease progression so that appropriate treatment plans can be developed based on current disease status. Other diagnostic tools, such as radiographs or probes, are much more effective in looking backward at the damage that has occurred. Periodontal disease, like most common chronic diseases, is multifactorial. There are many pathways to severe disease. As such, risk assessment is not helpful in determining why patients have developed severe disease (looking backward). On the other hand, risk assessment can be very helpful in determining treatments that alter the future course of disease. Assessing risk is only of value "looking backward" if one wants to establish that a factor such as smoking or genotype may have contributed to the current disease status.

Risk factors do not explain the past, but they do help predict the future. For example, high cholesterol is well-established as an important risk factor for coronary artery disease. This understanding has directly and substantially affected clinical decision making by the physician and behavior changes by the patient; yet, not everyone with high cholesterol has coronary artery disease and not everyone who suffers from coronary artery disease has high cholesterol. The challenge for practitioners is to adopt the right mind-set when assessing risk and not to confuse risk assessment with the diagnostic phase. Both are important, but one looks back while the other looks forward.

This review will discuss the recent evidence regarding the factors influencing the individual patient's response to bacteria and its impact on the clinical severity of the disease. By being able to better diagnose the disease and understand how risk factors amplify its clinical manifestation, practicing clinicians can provide more proactive and targeted treatment. This should allow dentists to serve their patients better than they do when they adopt a reactive approach of "wait, see, react." Specific case examples will help to illustrate the value this approach can offer patients and clinicians. Dentists' challenge is to decide whether they will continue to treat the event only after the fact or manage the treatment process proactively.

The Importance of Bacteria

During the past 40 years, much of the research in periodontics has focused on refining the understanding of the role bacteria play in the onset and severity of disease. From this work, it has clearly been established that bacteria are essential in causing or initiating the disease process.^8,9 Plaque has been used to describe the general collection of bacteria found on the teeth, but the evidence has clearly shown that specific bacteria can be found in individual patients and result in different forms of the disease. This, in turn, has led to specific treatment recommendations such as antibiotics targeted at the pathogens involved.

Attempts have been made to identify different forms of periodontal disease based on the specific bacteria/etiology identified.³ In spite of these efforts, disease classification is not yet consistently applied. Obviously, the more unclear the diagnosis, the more generic the treatment plans tend to be, i.e., the shotgun approach as opposed to the rifle. As physicians who treat infectious diseases know, identifying the specific pathogens involved can be a key step in prescribing an appropriate antibiotic regimen or other treatment plan.

In general, however, knowing which bacteria are involved has not proved to be very helpful in predicting future clinical severity of the disease. As a result, leading researchers are now focused on understanding the role of systemic, genetic, and behavioral conditions on the progression of periodontitis.

Critical Risk Factors

During the past decade, periodontal research has focused on identifying risk factors for periodontal disease on a factor-by-factor basis. Eliminating the other variables from the analysis allows researchers to more fully examine the association of each factor with the disease process. From this work, strong evidence supports the negative impact of behavioral factors such as smoking and oral hygiene/compliance on the progression of disease.^10-12 Systemic conditions such as diabetes, HIV, and occupational or social stress have also emerged as strong contributors to disease progression.^13-19 In addition, one recent paper has identified local intraoral stress as a risk factor for periodontal breakdown. This author suggests that orthodontic trauma to the periodontium may increase the production of inflammatory mediators, such as IL-1, leading to periodontal breakdown. This suggestion may help explain why occlusal trauma leads to greater tissue destruction in some patients than in others.^20-22 And, most recently, the identification of a specific genetic marker has identified patients with a genetic predisposition to periodontal disease.²³

Since in the practice environment one rarely treats patients with isolated variables, recent clinical research has focused more on the interaction between these factors (such as smoking and genetics) and the potential synergy that may exist, leading to an even greater negative impact on the severity of disease.²⁴ Only by bringing these factors together can dentists fully appreciate the impact they have on the health of patients in clinical practice and treat them in ways most appropriate for them as individuals with a different history of disease and risk for future progression.

This review will focus on the three risk factors that appear to contribute most predominantly to the progression of periodontal disease: smoking, oral hygiene/compliance, and genetics. Diabetes is also established as a strong risk factor; but, as it applies to only a limited subset of the patient population, it will not be fully addressed here.

Smoking

Amplification Effect

Figure 2. Decision making for high-risk patients with periodontitis: These patients will benefit from a more thorough diagnostic evaluation, aggressive treatment approach, and more stringent recall program.

Smoking has been established as a major risk factor in modifying a patient's response to bacterial plaque. In a recent publication by Salvi and colleagues, the role and adverse effect of smoking in periodontal disease has been thoroughly reviewed.⁴

Also, numerous reports have been published that substantiate the negative impact smoking has on the progression and severity of periodontal disease, as well as on predicting treatment responses and outcomes. Representative findings include:

* Smoking has a more dominant effect on attachment and tooth loss than poor compliance and severe gingival inflammation.²⁵

* Results from radiographic analysis of bone loss over 10 years in 350 patients showed that smokers lost bone at twice the rate of nonsmokers. Patients who quit smoking during the study fell in-between.²⁶

* Less favorable probing depth reduction, less clinical attachment gain, and increased levels of bleeding on probing have been found in smokers, treated both surgically and nonsurgically, when compared to nonsmokers.²⁷ A similar treatment response has been seen with dental implants.²⁸

The negative influence of smoking has been clearly documented even though the mechanisms of action are not yet well-understood. Most probably, the effects on vasculature, connective tissue, and immune cells compromise the repair and maintenance of the periodontium.

Clinical Risk Assessment

Figure 3. Decision making for high-risk patients with advanced periodontitis who are candidates for complex restorations: Patients at greater risk for losing critical abutments and costly restorations should be thoroughly evaluated diagnostically to assign a prognosis for critical teeth. This evaluation should be considered in conjunction with the predictability of the therapy options (e.g., periodontal or implant surgery) in recommending treatment. In high-risk cases, a more stringent recall regimen is warranted.

The negative effects of smoking appear to be directly related to the cumulative dosage over time, i.e., the number of cigarettes smoked per day and the number of years the individual has been a smoker. Evidence suggests that anything greater than 10 cigarettes per day substantially increases the risk for periodontal disease and will result in less favorable responses to treatment. Smoking cessation can help, as demonstrated by McDevitt and colleagues, whose findings indicated that risk for future disease was decreased by quitting smoking.²⁹ Of course, the effect is not clear-cut, since the cumulative effect of years of smoking can still impact bone loss and attachment levels. Studies related to other tobacco products, e.g., cigars and pipes, is virtually nonexistent; but it is reasonable to assume a similar effect.

Oral Hygiene/Compliance

Amplification Effect

As discussed previously, harmful bacterial plaque is the primary etiologic factor for initiating inflammation and periodontal disease. All plaque is not created equal. Unless routinely removed, the immature bacteria accumulate on the teeth; and the plaque continues to mature until it contains harmful pathogens contributing to the destruction of the tissue and supporting tooth structures. In a report recently presented by Socransky and colleagues, the authors concluded that patients with a positive genetic susceptibility present greater levels of harmful pathogens more frequently than those patients who do not have this genetic susceptibility.³⁰ This suggests a type of catch-22 effect for genetically susceptible patients, leading to increasingly severe periodontal involvement. This finding makes it all the more important to identify patients at genetic risk so dentists can better target their efforts at compliance modification and patient monitoring.

Oral hygiene and compliance are behavioral factors, which means that they can be controlled and/or modified. When niches around teeth are largely free of maturing bacteria and the plaque is removed on a regular basis, subsequent periodontal breakdown and tooth loss can be prevented. Research has clearly demonstrated that patients with periodontal disease and clinical breakdown who participate in a periodontal maintenance program as prescribed by their dentist present less attachment loss and tooth loss than patients who do not.^31,32 This is also true for patients who perform adequate oral hygiene home care as compared with those who do not.³³ So one of the opportunities to manage risk factors, and their amplifying effect on the progression of disease, is to place even greater emphasis on practicing regular home care and on professional supportive periodontal therapy.

Unfortunately, it has also been demonstrated that most patients do not comply with the suggestions provided by their dentist regarding the importance of these procedures. Dentists all recognize that the patient's compliance habits are well-established by the time clinical symptoms of the disease appear. Changing habits requires great and persistent motivation for the patient. Faced with this challenge, it has been reported that compliance can be improved; however, long-term behavioral changes do not usually occur. Most individuals find it difficult to modify their behavior when faced with a life-threatening disease; therefore, it is not surprising that for a non-life threatening disease, behavioral changes are that much more difficult to achieve.^32,34 However, this does not alleviate dentists from the responsibility to inform the patient of their risk for disease and the importance of compliance in managing the risk. It also does not mean that dentists shouldn't continue to treat the destruction caused by the disease process itself, often with the aim of making oral hygiene easier for the patient, especially in those individuals with increased susceptibility for severe disease and subsequent tooth loss.

Clinical Risk Assessment

Inadequate control of bacterial plaque is the principal cause of periodontitis. Although all patients should comply with professional plaque control procedures and be instructed continuously in home care, patients who present with additional risk factors -- e.g., smoking, genetic predisposition -- may need to be seen more frequently for follow-up care. Even patients presenting with very early signs of disease may benefit from increased care through a periodontal maintenance program if they are smokers or genetically predisposed to periodontal disease.

Furthermore, adult patients who have not satisfactorily responded to periodontal therapy and who are smokers or genetically susceptible to severe disease may require more careful attention. This may include aggressive plaque control and bacterial culturing; increased supportive periodontal treatment frequency including oral hygiene adjuncts; additional surgical intervention to reduce or eliminate niches; or localized modifiers of host response. These options should be considered and encouraged in the treatment/maintenance plan of high-risk patients.

Understanding the patient's oral hygiene compliance history is important in suggesting the most appropriate treatment options given his or her individual risk for severe disease and tooth loss.

Genetics

Amplification Effect

It has long been suspected and speculated that a patient's genetic makeup plays a role in the progression of common, chronic inflammatory diseases. A series of specific studies on identical twins confirmed this suspicion in the case of periodontal disease.^35,36 With the advent of the human genome project and explosion of knowledge in the area of human genetics, dentists are now beginning to understand the specific genetic factors involved in susceptibility to periodontal disease and how these factors interact with the environment to amplify the disease process.

Genetic research has documented the existence of common but slight variations that occur in human genetic makeup. These genetic variations, called polymorphisms, usually occur in a large percentage of the population and probably had some selective advantage in the past. This type of genetic variation often affects the host by regulating the body's response to environmental stimuli. This genetic effect is different than the genetic mutations that result in a more causal relationship with the onset and progression of disease. Examples of genetically inherited or genetically "caused" diseases include hemophilia and Huntington's Chorea. A person with the gene will manifest the trait, at least to some level of penetrance or extent. Polymorphisms do not cause the disease; they just influence the way the individual responds to a causative agent in the environment, often amplifying the response the individual with the polymorphism has to the trigger.

Genetic susceptibility to most common diseases, including periodontal disease, involves an interaction between the genetic response and the environmental stimuli necessary to manifest the condition. Examples include the role high cholesterol, poor diet, or lack of exercise play in heart disease in genetically susceptible individuals. Another example would be how lack of exercise, low calcium intake, and reduced hormonal secretion can lead to osteoporosis in some individuals, while having little to no effect in others. Periodontal disease appears also to involve an interaction between the genetic makeup of the host and the environment, with poor hygiene/compliance and smoking being more likely to lead to severe periodontal disease and tooth loss in genetically susceptible individuals than in those who are not.

Recent studies have shed new light on the genetics of periodontal disease and the functional significance of the variations. An important genetic discovery has identified the gene group (Interleukin 1" and Interleukin 1$ ) responsible for the production of inflammatory mediators. When these mediators are produced in high concentrations in response to a bacterial challenge, there is evidence that this leads to increased tissue destruction or more severe disease.^37,38 Some individuals have a common genetic variation or polymorphism that causes them to produce more Interleukin-1 than other individuals who do not have this polymorphism, even when faced with the same bacterial challenge.^39,40 This discovery has led to the development of a simple laboratory test that can identify those individuals who have the genotype ("positive") and are therefore at higher risk for periodontal disease.

Patients with this positive genotype produce substantially more (two to four times more) inflammatory mediators in response to the same bacterial challenge as patients who are negative for the genotype.⁴¹ This exaggerated response leads to greater and more rapid tissue destruction. In the study that first identified this factor, it was found that 67 percent of the patients with severe disease were also genotype-positive for the gene marker and more than 80 percent of the severe periodontitis could be explained by the presence of two risk factors: IL-1 genotype or smoking.²³ In another recently published study, it was reported that there might be a synergistic effect between these two risk factors resulting in an even greater risk for disease and tooth loss. McGuire and colleagues reported that patients who were either genotype-positive or smokers were almost three times more likely to lose their teeth due to periodontal disease. They went on to report that when the two risk factors are combined, there is a multiplicative effect, resulting in a genotype-positive smoker having an almost eight times greater likelihood of losing teeth due to the periodontal disease than a negative nonsmoker.²⁴

Emerging evidence is also identifying the role genetics may play in treatment response and maintaining treatment outcomes.^42-45 The challenge for dentists is to find meaningful ways to use risk factor assessment in their clinical practices for the benefit of patients and their long-term health.

Clinical Risk Assessment

The presence of the IL-1 genetic marker does not cause periodontal disease, it amplifies the response to bacterial stimuli resulting in more severe tissue destruction and an increased risk of tooth loss. The genetic test offers an alternative to the use of the unreliable self-reported family history by directly identifying the genetic predisposition for that individual. Performing the test is straightforward, requiring a fingerstick drop of blood to be collected and sent to a specific laboratory for analysis.

Using the test effectively, however, is a bigger obstacle. The key resides with clinicians' ability to connect genetic information to an overall risk assessment for each individual patient, and then to consider risk in specific decisions they make (such as when to refer and which restorative options to select) in the treatment planning process. Using genetic information in everyday practice will take time; but, just as in medicine, it is clearly an approach whose time has come and one that will be commonplace in the clinical practice of the future.

The PST Genetic Susceptibility Test (Medical Science Systems, Inc., San Antonio, Texas) is a targeted DNA test, identifying only the designated locations in the gene to evaluate the presence or absence of this polymorphism. This analysis is conducted through a specifically approved laboratory. The results are reported simply as "PST positive," indicating an increased risk for periodontitis, or "PST negative," indicating a normal risk for periodontitis. Because a person's genetic makeup doesn't change, the test is required only once and provides information that can be used in treating that patient for a lifetime.

Importance of Risk Factor Assessment

Periodontal risk factors may be assessed for all or selected patients. For example, risk assessment and genetic testing may be used with existing or new patients. Patients who already present with severe disease may want family members tested prior to the onset of clinical symptoms to allow for more preventive procedures or earlier intervention. Since risk is commonly assessed and considered in treatment planning for other multifactorial diseases such as coronary artery disease, to patients this may not seem as "new" as it may to dentists.

The identification of periodontal risk factors can provide many advantages and valuable information to clinicians in creating or modifying patients' treatment plans. If patients can be identified as "high risk" at an earlier stage of the disease process, the clinician may want to see the patient more frequently for periodontal maintenance rather than waiting for advanced symptoms to occur. For patients who do not respond favorably to treatments, it can be helpful to understand what risk factors may be interfering with the desired treatment outcome. If a patient is a smoker, it may be important to know if he or she is also genetically susceptible to periodontal disease prior to moving forward with periodontal therapy.

In addition, many patients with periodontal disease require complex and costly restorative work. Smoking and genotype have recently been identified as two important prognostic factors in providing a more accurate prognosis for periodontally involved teeth. If a patient presents with either or both of these risk factors, they should be considered in the treatment/restorative plan and in assigning a prognosis for the remaining teeth involved. In some cases, the restorative plan may need to call for additional abutments as a result, or possibly moving forward with implant therapy sooner where questionable teeth are involved and the patient is clearly high risk.

Minimizing the bacterial niches is just one consideration. In high-risk patients who have teeth with a poor prognosis, advanced periodontal or implant surgery is often clearly justified. In all cases, compliance to a maintenance program is critical to managing and sustaining the desired clinical outcomes.

Specific risk factors (smoking, compliance) have been associated with a less favorable postsurgical healing response.^27,46 Although specific data on the surgical healing response in PST-positive patients is not yet available, it is expected that these patients will require extremely good plaque control prior to surgery and throughout the healing phase.

Following are suggestions regarding how risk assessment could be incorporated into the treatment planning process:

1. A traditional examination is performed.

2. A clinical diagnosis is made. There are three possible general designations: health (no signs of inflammation, no attachment loss); gingivitis (signs of inflammation, no attachment loss); or periodontitis (signs of inflammation, attachment loss).⁴⁷

3. Risk factors are assessed.

a. Systemic, including genetic factors and diabetes.

b. Behavioral, including smoking habit and history, oral hygiene habits, and compliance history.

c. Local, including bacterial niches resulting from overhanging restorations or periodontal pockets, signs of occlusal trauma, and other factors.

4. Based on this information, the patient is provided with a suggested treatment plan. A few examples of how this may direct clinical decision making are provided.

Case Examples

Case 1

A patient with a diagnosis of chronic gingivitis who is risk-factor positive.

1. Inform the patient of the potential problems associated with being positive for the IL-1 gene and of the fact that he or she will need to be in good compliance with suggested oral hygiene and maintenance procedures.

2. Reduce or eliminate any additional risk factors, such as smoking.

3. Suggest testing family members.

4. Treat the patient using the traditional approaches of oral hygiene instruction and mechanical removal of bacteria and their products from the teeth.

5. Re-evaluate at 30 to 45 days. If the clinical signs of inflammation are absent, then place the patient in maintenance and see him or her in three months. The patient is re-probed at each maintenance visit.

6. If the clinical signs of disease are still present, then find the genesis of the problem and eliminate it, if possible.

7. When the clinical signs of inflammation are eliminated, place the patient on a maintenance schedule (an average of three months) and do periodontal probing at each maintenance visit.

Case 2

A patient with a diagnosis of adult periodontitis who is risk-factor positive.

1. Inform the patient of the potential problems associated with being positive for the IL-1 gene and of the fact that he or she will need to be in good compliance with suggested oral hygiene and maintenance procedures.

2. Reduce or eliminate any additional risk factors, such as smoking, where possible.

3. Suggest testing family members.

4. Consider sampling bacteria and have antibiotic specificity testing done if the patient is compliant and is not responding to conventional periodontal therapy.

5. Such patients are much more likely to be candidates for periodontal surgery than those individuals with adult periodontitis who are genotype-negative.

6. Short maintenance intervals (every two months is often needed) after therapy has eliminated as many of the risk factors as possible. The patient is re-probed at each maintenance visit.

Case 3

A patient diagnosed with advanced adult periodontitis who is risk-factor positive.

1. Inform the patient of the potential problems associated with being positive for the IL-1 gene and of the fact that he or she will need to be in good compliance with suggested oral hygiene and maintenance procedures.

2. Reduce or eliminate any additional risk factors, such as smoking.

3. Suggest testing family members.

4. Consider sampling bacteria and have antibiotic specificity testing done, especially if the patient is compliant and is not responding to conventional periodontal therapy.

5. Teeth intended as critical abutments in a complex restoration with moderate to poor prognosis are likely candidates for periodontal surgery. Depending on the tooth location and defect severity, e.g., Class 2 or 3 furcations, where the periodontal procedure is unpredictable (for that clinician), dental implant therapy should be considered.⁴²

Summary

While evidence continues to reinforce the role of bacteria in causing periodontal disease, recent studies support the importance of individual patient risk factors in the amplification and progression of the disease, leading to tooth loss. This information, when taken together, provides the dental professional with important direction on how to plan, treat, and maintain periodontal patients, especially by identifying and monitoring high-risk patients more frequently before advanced clinical symptoms appear. Smoking, compliance, diabetes, and genetic susceptibility have been identified as prominent factors substantially affecting the disease process. With the combination of targeted questions and the use of a new genetic test, dentists can now better predict a patient's response to bacteria, improve their ability to assign a prognosis, and intervene more confidently on an individual patient basis. Using combinations of new and previously tested methods, the dental professional can now come closer to the goal of maintaining his or her patients' oral health in comfort and function throughout their lives. As increasing links between periodontal disease and other chronic inflammatory medical diseases are confirmed, the dentist's role may serve an even greater purpose in supporting the overall health of patients.

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To request a printed copy of this article, please contact/Thomas G. Wilson, Jr., DDS, 5465 Blair, Suite 200, Dallas, TX 75231.