Optimizing the Oral Health of Patients Through Risk Assessment and Prevention

Dental plaque biofilm accumulation is the initiating factor for many common oral diseases, including caries, gingivitis, periodontitis, and peri-implantitis. These conditions are widely prevalent, affecting a large portion of the population and having a significant impact on individuals and society. Active dental caries affects more than one-quarter of US adults and one in five (20%) children aged 5 to 11 years.¹ Furthermore, nearly half (42.5%) of US adults aged over 30 years have periodontitis, with 9% of adults demonstrating severe periodontitis.²

The economic impact of these oral diseases is also considerable with more than $45 billion in lost productivity in the United States due to untreated oral disease and approximately 2.1 million emergency room visits for dental emergencies.^3,4 In fact, astonishingly, every 15 seconds a patient visits an emergency room to receive care for a dental condition.⁴ Given the overwhelming clinical and economic impact of biofilm-related dental diseases, a focus on prevention and oral wellness in clinical dental practice is critically important and may have a broad impact on patients and populations.

Risk factors are attributes, characteristics, and/or exposure of an individual that increases the likelihood of developing disease or injury.⁵ These risk factors may be local, genetic, systemic/acquired, and/or environmental.⁶ For periodontal disease, these factors may influence the microbiota and/or the host response to that biofilm.⁶ Established risk factors for periodontitis include: (1) environmental risk factors: nicotine consumption, alcohol consumption, poor nutrition, stress, certain medications, and illicit drugs; (2) systemic risk factors: diabetes mellitus, pre-diabetes, obesity/weight gain, and rheumatoid arthritis; (3) local risk factors: oral hygiene levels, bleeding on probing, deep pocket depths, clinical attachment loss, furcation involvement, subgingival calculus, tooth anatomical factors, and restorative factors; (4) genetic risk factors: genetic polymorphisms (eg, IL-1 polymorphisms) and epigenetic changes (changes in gene expression through chemical alteration to DNA and proteins).^7-17 Caries risk factors include high levels of cariogenic bacteria (eg, Streptococcus mutans), high frequency of consumption of simple carbohydrates, low intraoral pH, decreased salivary flow, low frequency of exposure to ingestible and/or applied fluoride, tooth pit-and-fissure anatomy, and poor oral hygiene practices.^18,19 Given the varied risk factors that individual patients may present with, risk stratification and more aggressive interventions in high-risk individuals are critical to reduce rates of periodontal disease and dental caries.

A recent revision of the classification system for the diagnosis of periodontal and peri-implant diseases was conducted by the American Academy of Periodontology and the European Federation of Periodontology.²⁰ This classification utilizes the patient's current clinical presentation to develop a periodontitis stage and direct or indirect evidence of past disease progression as well as systemic grade modifiers to develop a grade.^20,21 The classification also captures extent and distribution of disease.^20,21 In essence, the periodontitis stage is a snapshot of the severity of disease progression at initial presentation, and the periodontitis grade is a predictor of future disease progression and likely response to therapy based on risk factors.²¹ The incorporation of risk assessment into the diagnostic system allows practitioners to identify individuals who may require more intense treatment and more rigorous maintenance protocols to prevent disease recurrence.^21-24

The American Dental Association has developed a caries risk assessment form for individuals aged 0 to 6 years and >6 years.^25,26 Characteristics that place a patient at high caries risk include:

Sugary foods or drinks: bottle or sippy cup with anything other than water at bedtime (ages 0 to 6 years), or frequent or prolonged between-meal exposures per day (ages >6 years)

Eligible for government programs: Women, Infants and Children (WIC) programs, Head Start, Medicaid, or State Children's Health Insurance Program (SCHIP) (ages 0 to 6 years)

Caries experience of mother, caregiver, and/or other siblings: carious lesions in the past 6 months (ages 0 to 14 years)

Special healthcare needs: developmental, physical, medical, or mental disabilities that prevent or limit performance of adequate oral healthcare by themselves or caregivers (ages 0 to 14 years)

Chemo/radiation therapy (ages >6 years)

Visual or radiographically evident restorations/cavitated carious lesions: carious lesions or restorations in the past 24 months (ages 0 to 6 years)

Noncavitated (incipient) carious lesions: new lesions in the past 24 months (ages 0 to 6 years)

Cavitated or noncavitated (incipient) carious lesions or restorations (visually or radiographically evident): three or more carious lesions or restorations in the past 36 months (ages >6 years)

Teeth missing due to caries: any (ages 0 to 6 years) or in the past 36 months (ages >6 years)

Severe dry mouth (xerostomia, ages >6 years) or visually inadequate salivary flow (ages 0 to 6 years)

Risk stratification of caries risk can inform patient interventions, including behavior modification, nutritional counseling, and restorative and preventative treatments.²⁷

It is well-established that a large minority of patients with periodontitis do not respond as anticipated to therapy.²⁴ These patients demonstrate a failure to resolve inflammation and arrest periodontal attachment loss and/or experience recurrent disease progression.^21,24 Dental caries is prevalent throughout the population,²⁸ but the distribution of severe caries has become increasingly skewed, with severe disease clustering in a small group of high-risk individuals.^29,30 Given the variations in disease progression and development, utilization of advanced techniques, including biomarker and plaque sampling to screen for high-risk patients, may allow for optimal prevention, early detection, and/or intervention.

Various tests to analyze plaque samples have been developed and are in current use, including microscopy, bacterial culture, enzymatic assays, immunoassays, nucleic acid probes, and polymerase chain reaction assays. Commercially available tests that identify individual bacteria are generally focused on classifying a variety of periodontal pathogens and yeasts.³¹ Quantification of overall levels of these bacteria and the overall ratios of them in dental plaque has been associated with disease recurrence, and elimination of periodontal pathogens within periodontal pockets has been associated with an increased likelihood of establishing periodontal health.^32,33 Furthermore, counts of S. mutanshave been correlated with an increased risk of developing dental caries and can inform interventions.²⁷

It should be noted that many clinical studies evaluating the utility of microbiological diagnostic tests in guiding treatment planning decisions determined that these tests were mainly of benefit for patients who did not respond favorably to initial therapies.^31,34,35 In such patients, adjunctive antimicrobial therapy guided by the microbial sampling has resulted in improved clinical outcomes.^35-40 Conversely, the use of microbial sampling after active therapy and during maintenance has been efficacious in identifying individuals who demonstrate continued health and/or individuals who are at low risk for disease progression, and an increase above a critical threshold of one or more species of periodontal pathogens has been associated with a 2.5-fold increased risk for periodontal disease recurrence.⁴¹ Given these findings, microbial sampling can be a useful tool in identifying high-risk individuals for disease progression and to identify early disease recurrence in those patients who have successfully completed therapy.

Periodontitis:The primary prevention of periodontitis involves the treatment and reversal of gingivitis, either in an intact or reduced periodontium.^8,42 To prevent and treat gingivitis, removal of dysbiotic biofilm and establishment of a eubiotic biofilm is critical. Data supports the belief that professionally administered plaque control significantly improves gingival inflammation and lowers plaque scores, with some evidence that reinforcement of oral hygiene provides further benefit.⁸ Utilization of air polishing both supra- and subgingivally has been associated with decreased counts of periodontal pathogens and increased patient perceived comfort.⁴³ Additionally, the use of adjunctive laser therapy with nonsurgical therapy is associated with decreased gingival inflammation and probing depths for 3 to 6 months.^43,44

Dental caries: Oral hygiene optimization, dietary alterations, pit-and-fissure sealants, and fluoride application have been associated with decreased caries rates.^27,45-47 Other common recommendations for caries rate reduction include the use of xylitol, antimicrobial rinses, and education of caregivers.^27,45-47 Silver diamine fluoride (SDF) 38% has been cleared for marketing by the US Food and Drug Administration for treating dentin hypersensitivity in adults, and it also has been evaluated for arrest of carious lesions with biannual application.⁴⁸ A current dental technology (CDT) code adopted in 2016 (D1354-interim caries arresting medicament application) allows for coding the off-label use of SDF for caries arrest.^49,50

Due to the infectious nature of dental caries, vaccines against S. mutansin the form of proteins, recombinant or synthetic peptides, DNA/mRNA-based products, or protein-carbohydrate conjugates have been proposed. They have been tested and demonstrated the ability to elicit a response blocking S. mutansor inactivating glucosyl transferases.^51-53 While such vaccines are not currently available commercially, research is ongoing and the promise of a caries vaccine could be revolutionary for individual and public health.

While much of the work done in dentistry focuses on the treatment of oral diseases, the dental profession is, at its core, a preventative discipline. The push by dental healthcare providers for municipal fluoridation is an example of one of the greatest public health works in the history of the United States. Focusing on risk assessment and prevention is critical to optimizing the oral health of patients and is the responsibility of all dental healthcare providers.

Maria L. Geisinger, DDS, MS

Professor, Department of Periodontology, and Program Director, Advanced Education in Periodontology, University of Alabama at Birmingham School of Dentistry, Birmingham, Alabama; Diplomate, American Board of Periodontology