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May 2022
Volume 43, Issue 5

Optimizing the Oral Health of Patients Through Risk Assessment and Prevention

Maria L. Geisinger, DDS, MS

Dental caries, gingivitis, periodontitis, and peri-implant diseases are all initiated by dysbiotic dental plaque biofilm. For this reason, a critical component for the prevention and treatment of these common dental diseases is effective delivery of oral hygiene by practitioners and patients. To enhance biofilm disruption and adequately assess risk for oral disease development and progression, dental healthcare practitioners should educate patients and utilize tools that allow for stratification of patients based on their individual risk profiles for oral diseases. This article seeks to highlight emerging trends to enhance disease prevention and promote wellness for dental healthcare providers in clinical practice.

The Impact of Oral Diseases

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 Assessment for Caries and Periodontal Disease

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

Oral Microbial Sampling

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.

Innovative and Emergent Preventative Therapies

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.

About the Author

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


1. Dye BA, Li X, Beltrán-Aguilar ED. Selected oral health indicators in the United States, 2005-2008. NCHS Data Brief. No 96. Hyattsville, MD: National Center for Health Statistics; 2012.

2. Eke PI, Thornton-Evans GO, Wei L, et al. Periodontitis in US adults: National Health and Nutrition Examination Survey 2009-2014. J Am Dent Assoc. 2018;149(7):576-588.e6.

3. Righolt AJ, Jevdjevic M, Marcenes W, Listl S. Global-, regional-, and country-level economic impacts of dental diseases in 2015. J Dent Res. 2018;97(5):501-507.

4. Health Policy Institute. Emergency department visits for dental conditions - a snapshot. American Dental Association. April 2020. Accessed April 7, 2022.

5. World Health Organization. Risk factors. WHO website. Accessed February 21, 2022.

6. Kornman KS, Page RC, Tonetti MS. The host response to the microbial challenge in periodontitis: assembling the players. Periodontol 2000. 1997;14:33-53.

7. Bartold PM. Lifestyle and periodontitis. the emergence of personalized periodontics. Periodontol 2000. 2018;78(1):7-11.

8. Chapple ILC, Van der Weijden F, Doerfer C, et al. Primary prevention of periodontitis: managing gingivitis. J Clin Periodontol. 2015;42(spec iss 16):S71-S76.

9. Albandar JM, Streckfus CF, Adesanya MR, Winn DM. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol. 2000;71(12):1874-1881.

10. Shariff JA, Ahluwalia KP, Papapanou PN. Relationship between frequent recreational cannabis (marijuana and hashish) use and periodontitis in adults in the United States: National Health and Nutrition Examination Survey 2011 to 2012. J Periodontol. 2017;88(3):273-280.

11. Hach M, Holm-Pederson P, Adegboye AR, Avlund K. The effect of alcohol consumption on periodontitis in older Danes. Int J Dent Hyg. 2015;13(4):261-267.

12. Suvan JE, Finer N, D'Aiuto F. Periodontal complications with obesity. Periodontol 2000. 2018;78(1):98-128.

13. Scher JU, Ubeda C, Equinda M, et al. Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis. Arthritis Rheum. 2012;64(10):3083-3094.

14. Berthelot JM, Le Goff B. Rheumatoid arthritis and periodontal disease. Joint Bone Spine. 2010;77(6):537-541.

15. Kurushima Y, Tsai PC, Castillo-Fernandz J, et al. Epigenetic findings in periodontitis in UK twins: a cross-sectional study. Clin Epigenetics. 2019;11(1):27.

16. Liu X, Li H. A systematic review and meta-analysis on multiple cytokine gene polymorphisms in the pathogenesis of periodontitis. Front Immunol. 2022;12:713198.

17. Van Dyke TE, Sheilesh D. Risk factors for periodontitis. J Int Acad Periodontol. 2005;7(1):3-7.

18. Hunter PB. Risk factors in dental caries. Int Dent J. 1988;38(4):211-217.

19. Kirthiga M, Murugan M, Saikia A, Kirubakaran R. Risk factors for early childhood caries: a systematic review and meta-analysis of case control and cohort studies. Pediatr Dent. 2019;41(2):95-112.

20. Caton JG, Armitage G, Berglundh T, et al. A new classification scheme for periodontal and peri-implant diseases and conditions - introduction and key changes from the 1999 classification. J Periodontol. 2018;89(suppl 1):S1-S8.

21. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: framework and proposal of a new classification and case definition. J Periodontol. 2018;89(suppl 1):S159-S172.

22. Harrel SK, Cobb CM, Sottosanti JS, et al. Clinical decisions based on the 2018 classification of periodontal diseases. Compend Contin Educ Dent. 2022;43(1):52-56.

23. Ravida A, Galli M, Saleh MH, et al. Maintenance visit regularity has a different impact on periodontitis-related tooth loss depending on patient staging and grading. J Clin Periodontol. 2021;48(8):1008-1018.

24. Steigmann L, Sommer C, Kornman KS, Wang HL. Staging and grading discussion of borderline cases in gray zones. Clin Adv Periodontics. 2021;11(2):98-102.

25. American Dental Association. Caries Risk Assessment Form (Age 0-6). ADA website. Accessed April 7, 2022.

26. American Dental Association. Caries Risk Assessment Form (Age >6). ADA website. Accessed April 7, 2022.

27. Maheswari SU, Raja J, Kumar A, Seelan RG. Caries management by risk assessment: a review on current strategies for caries prevention and management. J Pharm Bioallied Sci. 2015;7(suppl 2):S320-S324.

28. National Institute of Dental and Craniofacial Research. Dental caries (tooth decay) in adults (age 20 to 64). NIDCR website. Accessed April 7, 2022.

29. Mosha HJ, Fejerskov O, Langebaek J, et al. Caries experience in urban Tanzanian children 1973-84. Scand J Dent Res. 1988;96(5):385-389.

30. Wei SH, Holm AK, Tong LS, Yuen SW. Dental caries prevalence and related factors in 5-year-old children in Hong Kong. Pediatr Dent. 1993;15(2):116-119.

31. Loomer PM. Microbiologial diagnostic testing in the treatment of periodontal diseases. Periodontol 2000. 2004;34:49-56.

32. Socransky SS, Haffajee AD: Periodontal microbial ecology. Periodontol 2000. 2005;38:135-187.

33. Paster BJ, Boches SK, Galvin JL, et al. Bacterial diversity in human subgingival plaque. J Bacteriol. 2001;183(12):3770-3783.

34. Rosenberg ES, Torosian JP, Hammond BF, Cutler SA. Routine anaerobic bacterial culture and systemic antibiotic usage in the treatment of adult periodontitis: a 6-year longitudinal study. Int J Periodontics Restorative Dent. 1993;13(3):213-243.

35. Ishikawa I, Kawashima Y, Odo S, et al. Three case reports of aggressive periodontitis associated with Porphryromonas gingivalis in younger patients. J Periodontal Res. 2002;37(5):324-332.

36. Kamma JJ, Lygidakis NA, Nakou M. Subgingival microflora and treatment in prepubertal periodontitis associated with chronic idiopathic neutropenia. J Clin Periodontol. 1998;25(9):759-765.

37. Pachceo JJ, Coelho C, Salazar F, et al. Treatment of Papillon-Lefevre syndrome periodontitis. J Clin Periodontol. 2002;29(4):370-374.

38. Renvert S, Dahlen G, Wikstrom M. Treatment of periodontal disease based on microbiological diagnosis. Relation between microbiological and clinical parameters during 5 years. J Periodontol. 1996;67(6):562-571.

39. Worch KP, Listgarten MA. Treatment considerations in rapidly progressive periodontitis: a case report. Compend Contin Educ Dent. 1998;19(12):1203-1216.

40. Worch KP, Listgarten MA, Korostoff JM. A multidisciplinary approach to the diagnosis and treatment of early-onset periodontitis: a case report. J Periodontol. 2001;72(1):96-106.

41. Chaves ES, Jeffcoat MK, Ryerson CC, Synder B. Persistent bacterial colonization of Pophryromonas gingivalis, Prevotella intermedia, and Actinobaccilus actinomycetemcomitansin periodontitis and its association with alveolar bone loss after 6 months of therapy. J Clin Periodontol. 2000;27(12):897-903.

42. Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(suppl 1):S74-S84.

43. Müller N, Moëne R, Cancela JA, Mombelli A. Subgingival air-polishing with erythritol during periodontal maintenance: randomized clinical trial of twelve months. J Clin Periodontol. 2014;41(9):883-889.

44. Everett JD, Rossmann JA, Kerns DG, Al-Hashimi I. Laser assisted non-surgical periodontal therapy: a double blind, randomized clinical trial. Open Dent J. 2017;11:79-90.

45. American Dental Association. Caries risk assessment and management. ADA website. Accessed April 7, 2022.

46. Sanders TA. Diet and general health: dietary counselling. Caries Res. 2004;38(suppl 1):3-8.

47. Fontana M, Gonzalez-Cabezas C. Are we ready for definitive clinical guidelines on xylitol/polyol use? Adv Dent Res. 2012;24(2):123-128.

48. Featherstone JDB, Horst JA. Fresh approach to caries arrest in adults. Decisions in Dentistry. October 5, 2015. Accessed April 7, 2022.

49. American Dental Association. CDT 2016: Dental Procedure Codes. Chicago, IL: American Dental Association; 2015.

50. Horst JA, Ellenikiotis H, Milgrom PL. UCSF protocol for caries arrest using silver diamine fluoride: rationale, indications and consent. J Calif Dent Assoc. 2016;44(1):16-28.

51. Lee Y. Diagnosis and prevention strategies for dental caries. J Lifestyle Med. 2013;3(2):107-109.

52. Smith DJ. Prospects in caries vaccine development. J Dent Res. 2012;91(3):225-226.

53. Kt S, Kmk M, N B, et al. Dental caries vaccine-a possible option? J Clin Diagn Res. 2013;7(6):1250-1253.


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