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Periodontal disease is a bacterial infection mediated by many factors, including smoking, diabetes, age, race, medications, genetics, socioeconomic status, and personal oral hygiene habits. Its prevalence is widespread in the United States, affecting 47% of the population ≥ 30 years of age, distributed as 8.7% for mild periodontitis, 30% for moderate periodontitis, and 8.5% for severe periodontitis.1 Greater age is related to intensity levels, with higher numbers of adults ≥ 65 years old exhibiting moderate-to-severe disease. This significant health issue has caught the attention of the public through the media and social networks regarding the association of “gum disease and systemic disease.”
The paradigms for understanding the pathogenesis of periodontal diseases have changed throughout the decades, from the non-specific plaque hypothesis (plaque removal) to the specific plaque hypothesis (identified key microbial pathogens), to today’s current understanding that the progression and treatment of periodontal disease is multifactorial. This change in thinking has significantly impacted the way dental professionals assess, plan, and treat periodontal infections.
Periodontal Risk Assessment
Preventing, eliminating, or managing periodontal disease depends on the comprehensive documentation of clinical and historical data, coupled with the patient’s values and behaviors. Risk assessment is the evaluation of the qualitative and quantitative information gained from the medical, dental, and personal histories, dental and periodontal data collection, and screening process.2,3 Risk assessment is the cornerstone of the patient-centered care plan and helps enable patients to make informed decisions based on full disclosure of risks and expected outcomes.
Periodontal disease risk factors are either modifiable, ie, those behaviors that can be changed, or non-modifiable, ie, those behaviors that cannot be changed (Table 1), and are further categorized based on their etiologies: systemic, genetic, environmental, or behavioral.
Systemic Risk Factors Type 2 Diabetes
Type 2 diabetes is an epidemic in the United States, affecting 25.8 million people, which represents 8.3% of the population. Approximately 7 million with the condition are unaware they have it, ie, undiagnosed.4 Type 2 diabetes is more prevalent in people ≥ 65 years of age; however, the incidence in younger people is increasing due to rising rates of obesity.5
Diabetes is a significant risk factor for periodontal disease. It is well-established that diabetes and periodontal disease have a bidirectional relationship; diabetes increases the risk for periodontitis, and the systemic inflammatory burden associated with periodontitis negatively impacts glucose control.6
People with diabetes are twice as likely to develop periodontal disease, and the risk increases to 2.9 times higher for those with poor glycemic control. Add smoking to this mix and the risk for severe periodontal disease increases to 4.6 times.7 Each disease produces increased levels of systemic inflammation, which contributes to insulin resistance, poor glycemic control, and more aggressive periodontal disease.8
The presence of severe periodontal disease has also been associated with more serious diabetes-related complications and an increased risk for mortality from these complications. It has been reported that severe periodontal disease with type 2 diabetes is a strong predictor for mortality from ischemic heart disease, diabetic nephropathy, and end-stage renal disease.9,10 Children with diabetes are also at risk, with evidence suggesting twice as much inflammation with similar biofilm levels as children without diabetes, and attachment loss at 6 to 11 years of age that increased among adolescents (12 to 18 years of age).6,11
When the impact of periodontal therapy on improving glycemic control was studied, A1c levels were shown to statistically improve by 0.4% to 0.7%.12 Although these results are promising, longer-term studies are needed. For now, it is important to reduce the periodontal infection and systemic inflammation.
Obesity and Metabolic Syndrome
According to the Centers for Disease Control and Prevention, more than one-third (34.9%) of adults were obese in 2011-2012. The rate is slightly higher among middle-aged adults (39.5%) compared with younger people (30.3%) and older people (35.4%). The prevalence of obesity is higher in non-Hispanic blacks (47.8%) and Hispanics (42.5%) compared with non-Hispanic whites (32.6%). Childhood obesity has more than doubled and adolescent obesity has tripled in the past 30 years, rising from 7% to 18% for 6- to 11-year-olds and 5% to 18% for 12- to 19-year-olds. In 2010, more than one-third of children and adolescents were overweight or obese.13
Obesity is recognized as an inflammatory condition, a significant risk factor for type 2 diabetes, and is associated with several chronic diseases. Obesity increases the risk for cardiovascular events, orthopedic complications, and cancer, and creates social and psychological problems.13 Obesity is a significant predictor of periodontal disease, and insulin resistance appears to mediate the relationship.14 Researchers believe adipocytes in fat tissue impact the levels of pro-inflammatory mediators, producing a hyperinflammatory state that may increase the risk for periodontal disease and insulin resistance.14
Metabolic syndrome is a cluster of risk factors that can occur in some individuals (Table 2). The risk for metabolic syndrome is closely related to obesity and a lack of physical activity. This cluster of risks should be taken into consideration during the screening and assessment of dental patients who are overweight or obese.15
Osteoporosis and Osteopenia
The World Health Organization (WHO) defines osteoporosis as bone mineral density (BMD) of -2.5 (T-score) or more below the mean value for young healthy women. Osteopenia is a T-score between -1.0 and -2.5 below the mean for young healthy women.16 National Health and Nutrition Examination Survey (NHANES) III data estimate that 4 million to 6 million women have osteoporosis and 13 million to 17 million have osteopenia compared to men, who range from 1 million to 2 million and 8 million to 13 million, respectively. The main risk for osteoporosis in women is menopause leading to increased bone-resorption from changes in estrogen levels.17
Data show that osteoporosis is a risk factor for tooth loss and osteoporosis of the mandible.18,19 One study reported that for each 1% decrease in whole-body BMD per year, the risk for tooth loss quadrupled in postmenopausal women.18 Some studies have shown a correlation between a decrease in BMD and an increase in clinical attachment loss and alveolar bone loss, but the strongest link is for tooth loss.18,19
Treatment for osteopenia and osteoporosis varies from calcium supplements and vitamin D to use of hormone replacement therapy, antiresorptive agents, and agents that stimulate bone formation. The implications for these agents in periodontal therapy are beyond the scope of this article.
Genetics
Mapping of the genome has identified genetic risk factors for coronary heart disease, type 2 diabetes, and many other diseases. It has recently been used to assess the genetics of periodontal disease. In one study that included 1,020 adults with a range of periodontal conditions from healthy to severe, the researchers found 13 loci that suggested evidence of an association with periodontal pathogen colonization but failed to show statistical significance with periodontal disease status.20 The sample size was small, and it was noted that risk factors such as smoking and obesity may play a more significant role than a genetic factor.
The genetic marker responsible for the increased risk for severe periodontitis includes polymorphisms in the interleukin-1β gene (IL-1 genotype) and is responsible for up to threefold increase in IL-1 production. This cannot be attributed to the general population, as it was found mainly in white, non-Hispanic participants, and the evidence is lacking for other races and ethnic groups.21
The IL-1 genotype does not cause periodontal disease, but like other risk factors, it plays a role in the onset and severity of the periodontal infection and response to treatment. This is due to the impact on the host response with the over-production of pro-inflammatory mediator response to the bacterial challenge.21,22 Since many people with severe periodontal disease are smokers it was important to separate the impact of smoking on disease progression and severity versus the impact of IL-1 genotype. Kornman et al found severe disease in non-smokers who were genotype positive. In smokers severe disease did not correlate with genotype. In this study 86% of subjects with severe periodontitis were accounted for by either smoking or the IL-1 genotype. This discovery provides an explanation for those patients who seem to lack obvious risk factors yet have an exaggerated response to biofilm and unexplained periodontal breakdown.21
Environmental Risk Factors
Smoking is a well-established risk factor for oral disease and oral cancer. All patients, including children and adolescents, should be screened for tobacco use. Each day, almost 4,000 children and adolescents under 18 years of age try their first cigarettes and more than 950 will become regular smokers.23 Adolescents who smoke have more visible plaque, increased pocket depths (≥ 4 mm), and subgingival calculus. They also have a higher prevalence and severity of disease compared with their peers who do not smoke.24,25 Adolescents who have smoked at least 100 cigarettes in their lifetimes report that they would like to quit but find it difficult.23
Smokers are as much as 20 times at greater risk for periodontal disease compared with former smokers and never-smokers.26 Smokers tend to have greater alveolar bone loss and recession, deeper pockets, increased furcation involvement, and tooth loss.25,27,28 Nicotine interferes with the inflammatory process, resulting in a less favorable response to therapy and appears to be dose related, with heavy smokers exhibiting more attachment losses and worse prognoses.29 Smokers should be informed about smoking’s impact on their oral cavities and the less favorable outcomes of periodontal treatment.26,27 They should also be informed that patients who quit smoking have better responses to periodontal therapy.30
Smoking cessation is important for the preservation of the oral cavity and the patient’s overall health and well being. Most health history forms include a smoking-related question. The first step is to gather the data, including frequency and dose. It is the author’s opinion that this is only useful if it is incorporated into the patient’s treatment plan and risks for complications and therapy outcomes are shared and smoking cessation discussed. Dental professionals can choose to provide counseling in the office or refer patients for smoking-cessation treatment (Table 3).
Behavioral Stress
The effects of stress, distress, and depression on oral health have been studied and shown to increase the risk for periodontal disease. Recent studies have looked at the association with chronic periodontal disease and found that patients with significant chronic stress were associated with more severe periodontitis. However, those with better coping skills had less-severe disease than those with poor coping skills.31
Two reasons account for the link: behavioral and physiologic. Individuals under stress tend to pay less attention to diet and oral hygiene, and may increase smoking and alcohol use. People who have constantly high levels of stress secrete higher amounts of the hormone cortisol, which impacts the body’s ability to regulate inflammation.31
Poor Oral Hygiene
Poor oral hygiene is one of the most easily modified risk factors for periodontal disease. Yet data show that many patients are not proficient at this task.32 Most individuals do not clean interdentally, and brushing habits tend to follow ineffective patterns, often missing the same area each time.32
The patient’s challenge is daily control of biofilm. Patients with implants, diabetes, orthodontics, and crowns and bridges and those in periodontal maintenance programs typically have difficulty accomplishing effective biofilm control. Traditionally, recommendations have been limited to brushing and flossing. The evidence does not support this practice.
One systematic review33 evaluated clinical trials that compared brushing and flossing with brushing alone. Comparing data up to December 2007, the researchers determined only 11 studies met their inclusion criteria and most showed no difference between brushing alone and brushing and flossing for either plaque removal or the reduction of bleeding or gingivitis. After the meta-analysis was performed, the authors could find no differences between the groups for baseline scores and final scores for plaque and gingival index reported. The authors concluded no scientific evidence existed for the regular recommendation of string floss for interdental cleaning. They believed it should be reserved for patients who could demonstrate a high level of technique.
A more recent systematic review34 compared data up to October 2011. The objective of this study was to assess the effects of flossing in addition to brushing as compared with brushing alone in the management of periodontal diseases and dental caries in adults. Twelve trials were included. These authors reported weak and unreliable evidence that adding flossing to brushing may be associated with a small reduction in plaque over a short period. No evidence showed a reduction in dental caries attributed to flossing plus brushing. This supports an earlier review35 that found no data showed interproximal caries are reduced by flossing plus brushing.
Recently, water flossing has gained attention based on comparison studies to string floss demonstrating superior plaque removal36 and reduction of gingivitis37 and gingival bleeding.38 These data have provided dental practitioners with a more effective alternative to string floss that addresses the issues of compliance, adherence, and poor oral health. Water flossing has also been shown to be more effective than traditional oral hygiene for patients with implants,39 diabetes,40 and orthodontics,41 and those in periodontal maintenance programs.42 In addition to the ability to prevent oral infections and promote oral health, water flossing has been shown to reduce pro-inflammatory mediators in gingival crevicular fluid and blood serum.40,43 These studies extend beyond the measure of typical indices to demonstrate a host modulation effect and a reduction in inflammation.
Conclusion
Prevention and health promotion are the foundations to dental and dental hygiene practice. A thorough and comprehensive evaluation of the patient’s medical and dental histories provides information that is critical to comprehensive treatment planning.
Developing a comprehensive treatment plan requires collaboration and communication between several parties. It may be necessary to discuss aspects of treatment with the patient’s primary medical healthcare provider or specialists such as an endocrinologist or cardiologist. Treatment may be postponed to allow the patient to begin a smoking cessation program. If successful, certain procedures might be avoided or the prognosis of restorative treatment improved. This is a team effort where recommendations are reinforced and discussed by each member of the dental team. It is also a fluid process and should be taken in steps. First and foremost is establishing periodontal health that can be easily maintained. Starting elective restorative treatment before stabilization of periodontal disease is a disservice to the patient and unethical. It may be necessary to revisit a complicated plan and make changes based on evaluation of the process of care.
Reducing the impact of periodontal disease requires more than a mere “cleaning.” Without understanding risk factors, it may be simply managed neglect.
ABOUT THE AUTHOR
Deborah M. Lyle, RDH, BS, MS
Director of Professional and Clinical Affairs
Water Pik, Inc.,
Fort Collins, Colorado
Queries to the author regarding this course may be submitted to authorqueries@aegiscomm.com.
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