13 minute read
Practicing Dentistry in the Age of Periodontal Risk Management
Practicing Dentistry in the Age of Periodontal Risk Management
Roger N. Warren, D.D.S.; Liana Umbrio, D.D.S.; Leena Palomo, D.D.S., M.S.D.
ABSTRACT
Purpose of review. To provide clinicians with knowledge of periodontal risk assessment that can be applied chairside effortlessly.
Recent findings. Detecting periodontal risk factors early may reduce the morbidity of oral and systemic diseases, as oral and systemic health can have a bidirectional relationship.
Summary. Dental professionals are equipped with evidence-based risk factors to predict and prevent the progression of periodontal disease. Implementing chairside risk assessment allows for prevention and early intervention, potentially reducing healthcare costs and promoting simpler solutions in an unpredictable economy.
The cultural, economic and historic backdrop of current times leaves the dentist to navigate and balance prevention with diagnosis and treatment. This mandates that the dentist behave as an actuary, responsible for predicting disease and intervening strategically as patients demand better, faster, cheaper care. The stakes have never been higher. Be it periodontitis, tooth loss or peri-implantitis, we live in the age of periodontal risk management. Luckily, there are simple tools to approach the challenge.
Periodontal risk assessment is defined by the American Academy of Periodontology as the process by which qualitative or quantitative assessments are made of the likelihood for adverse events to occur as a result of exposure to specified health hazards or by the absence of beneficial influences.[3]
Almost every disease that has been identified has certain “risk factors” that contribute to or modify the course of a disease process. Newman and Carranza’s text states that risk factors are “environmental, behavioral, or biologic factors that, when present, increase the likelihood that an individual will develop the disease. Risk factors are identified through longitudinal studies of patients with the disease of interest.”[4]
Thus, risk factors do not cause the disease, since causality is any factor without which the disease would not have occurred. Rather, risk factors are conditions that the disease experience would not have been the same without.
After Loe[5] demonstrated that the etiology of gingival inflammation was essentially bacteriologic, most of the other observations, both systemically and locally, regarding periodontal disease have been influencers or modifiers of periodontal disease or risk factors. Some are systemic; many are local factors. Some are modifiable; and many are not.
We will attempt to list the many risk factors observed to be related to periodontal disease and briefly comment on what the literature has found to be their effect on periodontal disease. The primary goal of this article is to present a review of evidence to provide clinicians with assessment and management options that translate from the research realm to chairside application seamlessly. The secondary goal is to create teamwork between the medical and dental community to provide clinicians with a pathway to improve overall quality of life.
Modifiable Factors
Differentiating modifiable from non-modifiable factors empowers the clinician to strategically affect patients’ periodontal health. Ideal care and attention to detail can enable the patient to experience optimal dental health and fulfill the challenge of dentistry expressed by Prichard that nature intended the teeth to last a lifetime. With proper home and professional care from early childhood, there are few people who cannot realize this expectation.[2]
Smoking Tobacco
Although tobacco smoking has been declining in the United States, a considerable number of smokers, about 30 million Americans, still exist. Tobacco smokers have more periodontal disease than nonsmokers, and they have a more rapid progression of periodontal disease. Smokers have a diminished response to periodontal therapy. Many surgical procedures are affected, as tobacco smoking alters the healing process. Implant failures are twice those of nonsmokers.[6] Smoking impairs vascular factors and inflammatory mediator production, antibody production, fibroblast activity and neutrophil function. However, the good news is that those who have quit smoking have a response similar to nonsmokers to both periodontal and implant procedures.[7]
Recommendation: Smoking cessation has a positive effect on the occurrence and healing of periodontal disease.[8] The U.S. Department of Health and Human Services provides strategies for smoking cessation.[9] Two European workshops on the prevention and cessation of tobacco use reported the importance of tobacco smoking cessation by dental professionals.[10,11]
Cannabis
Now that recreational marijuana smoking is becoming more commonplace, accepted and legal, the prevalence of periodontal disease has increased, and altered healing is a factor in treatment planning. Besides greater attachment loss among frequent cannabis users, there are more complications following intraoral surgeries.[12] Cannabis has a profound influence on the oral microbiome and may compromise the immune response to plaque, resulting in greater attachment loss from periodontal disease.[13]
Recommendation: Smoking cessation, as regular, long-term use of cannabis is a risk factor manifesting as clinical attachment loss, deep pockets, gingival recession and enlargement.[14]
E-cigarettes
A combination of a carrier (propylene glycol or glycerin), nicotine and flavorings can increase the risks for cardiovascular and lung health and may affect the oral microbiome, making e-cigarettes a poor alternative to tobacco smoking. [12] There is an increase in Fusobacterium and Bacteroides subgingivally in people using e-cigarettes[15] and a higher amount of inflammation.[16]
Recommendation: Smoking cessation, as it is suggested that e-cigarettes increase destruction of the periodontium by the development of periodontitis.[17]
Systemic Factors
Diabetes
Epidemiologic data demonstrates that the prevalence and severity of periodontal disease is more significant in patients with Type 1 and Type 2 diabetes than those without diabetes, and that the level of diabetic control is a crucial variable in this link. There are more than 30 million diabetics in the United States, and many have yet to be diagnosed. It is estimated that one in four adults over the age of 65 is affected by diabetes. The dentist should keep apprised of the HbA1c level of their patient and communicate with the physician regarding the patient’s glycemic control. It may be necessary to modify therapy, depending on the patient’s assumed ability to heal satisfactorily. The dental profession must prevent and treat periodontal disease not only to preserve the dentition, but also to reduce the effect of periodontitis on diabetes and its complications.[18]
Recommendation: Diabetes-control interventions, such as dietary changes, exercise and oral health education.[19,20]
Cardiovascular Disease (CVD)
Periodontal disease contributes to the total infectious and inflammation burden and may contribute to cardiovascular events, such as stroke, in high-risk patients. The lipopolysaccharide and monocyte-related responses suggest a link between these two diseases.[21] There are risks and complications in patients undergoing periodontal therapy who are on anti-thrombotic therapy.[22]
Recommendation: Patient education on increased risk of CVD complications, and on how to control CVD risk factors.[23] Dental professionals should monitor patient blood pressure at appointments, use local hemostatic measures and consult the patient’s physician prior to invasive procedures.[22]
Obesity
Obesity increases the risk for periodontal disease, and there is an increase in periodontal disease prevalence in obese and overweight individuals. Over 35% of Americans suffer from obesity. There is an altered immune response, microbial dysbiosis, genetic polymorphisms and increased stress
in these individuals. Adipose tissue can be considered an inflammatory organ. The oral microbiome is altered in obese individuals—for example, Tannerella forsythia are present in greater proportions. Periodontal treatment can improve this situation.[24]
Recommendation: Dietary changes[19] and physical activity as potential tools for reducing the occurrence of periodontal disease.[20]
Stress
Stress makes it more difficult for the body to fight against infections, including periodontal disease. Stress markers have been found in the blood of people experiencing psychological stress. The composition of the biofilm is changed. Also, changes in lifestyle, such as ignoring oral hygiene, smoking, consuming more fat and sugars, plus an increase in IL-6, all play a role in increased susceptibility to periodontal disease. The hope is to develop a saliva test to identify people experiencing stress and then devise appropriate treatment.[25]
Recommendation: Stress decreases saliva flow and increases plaque formation. Also, cortisol is increased in the gingival crevicular fluid so that stressed individuals need a careful watch for periodontal disease.[26] Poor healing is also associated with stress,[27] suggesting close monitoring as well.[28]
Osteoporosis
Osteoporosis is usually asymptomatic until a fracture occurs. It is present in both men and women; however, onethird of women aged 60 to 70 have osteoporosis, defined as 2.5 standard deviations below the norm. Both osteoporosis and periodontal disease are bone-resorptive diseases; and they appear to be correlated. Osteoporotic individuals have increased severity of periodontal disease and experience greater tooth loss. Altered trabeculation on dental radiographs can be an indicator of skeletal bone mineral density. Therefore, some reports of reduced bone mass make one more susceptible to periodontal disease.[29]
Recommendation: Hormone replacement therapy with estrogen as treatment for postmenopausal osteoporosis suggests some evidence of reduction in bleeding on probing (BOP) and pocket depth, but has a minimal effect on radiographic bone loss and tooth loss.[30]
Pregnancy
Hormonal changes during pregnancy can result in gingival hyperplasia and an exaggerated response to plaque bacteria. Both the innate and adaptive immunity are affected, resulting in possible magnified degree of periodontal disease. Pregnant women have increased BOP, deeper pocket depths and greater inflammation. It is hypothesized that hormonal changes lead to a reduced resistance to bacterial inflammation and the ability to repair.[31] Low birth weight babies and premature births were also cited due to a direct pathway through dental bacteremia.[32]
Recommendation: Treatment of gingivitis and periodontitis during pregnancy is associated with decreased risk of adverse pregnancy outcomes.[33]
Hormonal Influence
Circulating corticosteroids, androgens, estrogens and progesterone cause increased bone resorption, stimulate fibroblast synthesis, immune suppression and increased fluid exudation. Also, oral contraceptives and the second trimester of pregnancy cause an increase in Porphyromonas [Bacteroides] intermedius. The result is increased probing depths, which leads to a change in attachment levels and bone loss.[34]
Recommendation: Strict oral hygiene measures for patients using oral contraceptives to prevent or decrease severity of periodontitis.[35]
Respiratory Diseases
According to several researchers, periodontal disease can have an influence on chronic obstructive pulmonary disease (COPD), asthma, pneumonia, obstructive sleep apnea and COVID-19. This may be due to the aspiration of oral pathogens and/or the systemic effect of pro-inflammatory mediators produced in the periodontal tissues. The effect may be bidirectional. Porphyromonas gingivalis and Treponema denticola appear to be the main etiologic agents. Asthma and pneumonia present the weakest connection to periodontal disease.[36]
Recommendation: For COPD, smoking cessation is critical because smoking is a risk factor for periodontitis and COPD. Reinforcing oral hygiene is imperative because insufficient oral hygiene has been shown to be associated with exacerbations of COPD.[23]
Kidney Disease
Periodontitis has been established as an independent risk factor for chronic kidney disease (CKD).[37] The hypothesis that an increased inflammatory response in kidney disease destroys endothelial vasculature may be related to periodontal inflammation and the development and progression of kidney disease is suggested. Screening for periodontal disease may help prevent the progression of kidney disease.[38]
Recommendation: There is a bidirectional relationship between CKD and periodontal disease; therefore, managing periodontal disease is important in treating CKD.[39] Periodontal treatment can have a positive effect on the estimated glomerular filtration rate, a measure of kidney disease.[40]
Alzheimer’s Disease
Alzheimer’s disease is considered a neuroinflammatory disease and because periodontitis results in increased proinflammatory mediators, it may exacerbate this condition.[41]
Recommendation: Multidisciplinary treatment plan with physician, caregiver, family and patient. Establish oral hygiene routine and manage dietary habits. Encourage autonomy of patient for as long as possible.[42]
Age
Older people have higher rates of periodontal disease. Severity and prevalence increase with age. About two-thirds of patients over the age of 65 have periodontal disease, whereas, overall, there is about a 47% prevalence of periodontal disease. Advanced age may modify periodontal disease by increased exposure to plaque, a different composition of plaque, greater susceptibility to periodontal disease and/or slower wound healing.[43]
Recommendation: Early and individualized treatment of most pathologic conditions usually leads to a more favorable outcome.[44]
Socioeconomic Status
Decreased dental awareness or lack of regular care can increase the risk of periodontal disease, but low socioeconomic status alone will not cause periodontal disease. The prevalence of periodontal disease is lower with a healthy lifestyle compared to an unhealthy lifestyle.[45] Income inequity relates to oral health in that lower individual/household income is associated with increased occurrences of dental caries, periodontal disease, traumatic dental injuries and oral cancer.[46]
Recommendation: Implement outreach programs in areas of socioeconomic at-risk populations to increase access to care.[47,48]
Sex
Men have a greater risk for destructive periodontal disease, but studies have yet to show that they are at higher risk for more rapid periodontal destruction than women. Poorer oral hygiene and irregular care, in addition to a genetic difference, may account for this disparity. Sex steroids influence inflammatory cytokines, especially IL-1β and TNF-α, to magnify injury and infection in men.[49]
Recommendation: Since men are more likely to ignore their oral health, it is critical to develop education and treatment strategies to improve their oral health.[50]
Education
There seems to be a correlation between less education and income with periodontal disease prevalence and severity. [51]
Recommendation: Implement oral health education programs and endorse educational attainment.[47]
Genetics
Some people have a genetic predisposition to periodontal disease despite regular care and good oral hygiene. If detected early, aggressive intervention is indicated. IL-1α is a cytokine associated with a susceptibility to periodontal disease. Control of the inflammatory process and the proresolution process result in a degree of periodontal destruction. Currently, 65 genes have been associated with periodontal disease, so the problem is quite complex.[52]
Recommendation: Epigenetics is a reversible change to how the body reads a DNA sequence.[52] Epigenetics, altering gene expression resulting in a modification of the structure of DNA rather than changes in the genetic code as in mutations, is a possible route towards a perio-systemic health link.[28] DNA methylation or histone modifications can selectively activate or deactivate genes, resulting in the outcome of many inflammatory diseases, including periodontitis.[53]
Medications
Several medications, such as calcium channel blockers, phenytoin and cyclosporine, can cause gingival hyperplasia and promote periodontal disease. Unregulated fibroblasts produce increased amounts of collagen and/or extracellular connective tissue matrix. Anti-inflammatory drugs such as corticosteroids and NSAIDs affect the balance between pro-inflammatory cytokines and the anti-inflammatory cytokines (IL-4, IL-10) but have no effect on the severity of periodontal disease. Immunosuppressive medications for rheumatoid arthritis result in increased inflammation and periodontal disease. Oral contraceptives can exaggerate the body’s response to plaque bacteria. Bisphosphonates are anti-resorptive osteoclastic inhibitors that when taken intravenously can cause osteonecrosis of the jaw. Minimizing infection and improving plaque control prior to taking bisphosphonates is beneficial. Anti-platelet drugs are beneficial in minimizing inflammation in animal studies. Statins lower cholesterol and are anti-inflammatory. Anticancer treatments result in transient neutropenia, which can exacerbate periodontal disease.[54]
Recommendation: Discontinue or change the offending medication if appropriate and after consulting with the patient’s physician, in conjunction with surgical and nonsurgical treatments.[55]
Conclusion
Available evidence provides the clinician with a number of potential risk factors for the progression of infection and inflammatory diseases, such as periodontal and periimplant diseases. Risk assessment empowers dentists and hygienists to identify potential problems early on and provide focused, proactive interventions for cases that are susceptible to disease or disease progression[56] (Figure 1). Preliminary data show that this approach can reduce shortand long-term health-care costs. As the economy continues on its unpredictable path, we are optimistic that such strategic, early interventions will reduce the need for more costly, and often more traumatic, complex treatments and promote simpler, more highly predictable and, likely, more durable solutions to dental disease.
Queries about this article can be directed to Dr. Warren at rw845@nyu.edu.
