Periodontal Disease Prevention: Identifying Risk Factors
Periodontal diseases have long been defined as bacterial infections involving dental plaque made of polymicrobial communities. Current knowledge, however, suggests they are complex, multifactorial diseases whose signs and symptoms are attributable to bacterial biofilm, host’s immune system, and inflammatory response.
Periodontal diseases have long been defined as bacterial infections involving dental plaque made of polymicrobial communities. Current knowledge, however, suggests they are complex, multifactorial diseases whose signs and symptoms are attributable to bacterial biofilm, host’s immune system, and inflammatory response. These responses are influenced by local, systemic, genetic and environmental risk factors.1 The risk factors for periodontal diseases can be broadly classified as individual and local. Table 1 provides a simple classification system for these factors.1,2
Individual Modifiable Risk Factors
Cigarette smoking is associated with periodontal diseases and tooth loss.3 In a cross-sectional observational study, Grossi et al4 showed that the relative risk of light smokers developing periodontal diseases was 2.05; the risk increased to 4.75 among heavy smokers. This environmental risk factor is also associated with a higher prevalence of severe forms of disease, tooth loss and edentulism. The noxious effect of smoking is dose dependent and attributable to its effect on periodontal pathogens, host microcirculation, dysfunction of neutrophils, production of pro-inflammatory cytokines, and increased levels of pathogenic T cells.1,5 Due to these significant risks, the consensus report by the 11th European Workshop on Effective Prevention of Periodontal Disease suggests identification of smokers and implementation of the AAR (ask, advise, refer) approach as the minimum standard in dental settings for all tobacco users.6 Smoking status is key to assessing periodontal disease risk and to make evidence-based clinical decisions.
Diabetes mellitus is a global epidemic and its prevalence continues to grow.7 Studies show that individuals with diabetes experience a higher prevalence and severity of periodontal disease.8 The current American Academy of Periodontology (AAP) classification recognizes that patients with HbA1C of ≥ 7.0% are at risk of rapidly progressing periodontal disease compared with those who are normoglycemic.9
The detrimental effects of hyperglycemia in multiple organs of the body—including the periodontium—are mainly due to microangiopathy, macroangiopathy, and a hyperinflammatory response to bacterial challenge. Neutrophil defects, hyper-responsive monocytes, increased proinflammatory cytokines, oxidative stress reactions and impaired healing processes are all part of this inflammatory response. A major factor that may drive these responses is the accumulation of advanced glycation end products and their interaction with their cognate receptors.7,10–13
Research has demonstrated a bidirectional relationship between periodontitis and diabetes. Periodontal treatment can result in mean reduction in HbA1C of 0.36% at 3 months. This is because infection and inflammation can result in insulin resistance.14–16 The effective management of patients with diabetes in the dental setting includes educating patients; providing comprehensive exams, treatment planning, and preventive care regimens; promptly addressing dental and periodontal issues; and close monitoring of periodontal changes.15
Obesity is an emerging public health concern. Obesity induces a chronic systemic inflammatory state resulting in its association with several chronic diseases, including periodontal diseases. Impairment of systemic immune response, increased production by adipose tissue of humoral factors (adipokines) and attenuation of macrophage infiltration and activation may contribute to the pathogensis of periodontal diseases in patients with obesity.17-19 The overall odds ratio of developing periodontal diseases in obese or overweight individuals is 2.13, and the risk of periodontitis grows with increase in body mass index.1 Patients with obesity should also be managed by the dental and medical team to reduce complications related to obesity along with stabilizing their periodontal conditions.
Other modifiable factors that are of low to moderate significance in the development and progression of periodontal diseases include osteoporosis, psychological stress, dietary vitamin D and calcium deficiency, alcohol consumption, socioeconomic status, metabolic syndrome, and inflammatory diseases, such as rheumatoid arthritis.1,2,7
Individual Nonmodifiable Periodontal Risk Factors
Nonmodifiable risk factors—such as age, genetics, gender, and ethnicity—should also be considered. While these cannot be modified, recognizing them can help oral health professionals determine the most appropriate interventions.1
Age is weakly related to the prevalence of periodontal diseases. However, this relationship may be due more to age-related cumulative periodontal breakdown, nutritional deficiencies, concurrent medical diseases and complications, and inability to perform self-care than age alone.2,20-22
It has been hypothesized that some genes may modify the course of periodontal diseases and are involved in disease development by gene-gene interactions and gene-environmental interactions (epigenetics). The genetic influence in young individuals with aggressive disease is better established than the chronic form of periodontal diseases.1,23,24
Men of all ages, ethnicity and geographic location have a higher prevalence, extent and severity of periodontal diseases. A systematic review by Shiau et al25 showed that gender exhibited a significant association with prevalence, reflecting 9% difference between males and females. This difference is attributable to lifestyle, hormonal disparity leading to dimorphism in immune response, and host susceptibility.21,25,26
Eke et al27 showed that periodontitis prevalence was highest among Hispanics (63.5%) and non-Hispanic blacks (59.1%), followed by non-Hispanic Asian Americans (50.0%) and lowest in non-Hispanic whites (40.8%). Differences in socioeconomic status, access to care, education levels and also genetics could account for this disparity among ethnicities.21
Local factors—such as enamel pearls and cementoenamel projections—have been implicated in molar furcation involvement. This may be due to inability of connective tissue to attach on enamel projections, making the site susceptible to further breakdown.2,28,29 Tooth malposition, or crowding, can make it difficult for patients to maintain oral hygiene via routine self-care measures. Periodontal breakdown in these sites could also be accelerated due to root proximity and thin or absent cortical bone.2,30,31 Palatoradicular grooves are commonly found on maxillary lateral incisors and tend to be associated with poor periodontal health, more plaque accumulation; hence, they are vulnerable to rapid breakdown.32
Prevention of periodontal diseases and their progression is an essential component of comprehensive dental management, as the periodontium forms the foundation of oral health. A number of risk factors and models have been identified that can help clinicians develop a personalized periodontal treatment plan for every patient.
- Genco RJ, Borgnakke WS. Risk factors for periodontal disease. Periodontol 2000. 2013;62:59–94.
- Nunn ME. Understanding the etiology of periodontitis: an overview of periodontal risk factors. Periodontol 2000. 2003;32:11–23.
- Bergström J, Preber H. Tobacco use as a risk factor. J Periodontol. 2012;65:545–550.
- Grossi SG, Zambon JJ, Ho AW, et al. Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol. 1994;65:260–267.
- Tonneti MS. Cigarette smoking and periodontal diseases: etiology and management of disease. Ann Periodontol. 1998;3:88–101.
- Tonetti MS, Eickholz P, Loos BG, et al. Principles in prevention of periodontal diseases: consensus report of group 1 of the 11th European Workshop on Periodontology on effective prevention of periodontal and peri-implant diseases. J Clin Periodontol. 2015;42:S5–S11.
- Albandar JM, Susin C, Hughes FJ. Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: case definitions and diagnostic considerations. J Clin Periodontol. 2018;45:S171–S189.
- Nelson RG, Shlossman M, Budding LM, et al. Periodontal disease and NIDDM in Pima Indians. Diabetes Care. 1990;13:836–840.
- 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:S159–S172.
- Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2013;40:S113–134.
- Lalla E, Papapanou PN. Diabetes mellitus and periodontitis: a tale of two common interrelated diseases. Nat Rev Endocrinol. 2011;7:738–748.
- Polak D, Shapira L. An update on the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2018;45:150–166.
- Sanz M, Ceriello A, Buysschaert M, et al. Scientific evidence on the links between periodontal diseases and diabetes: Consensus report and guidelines of the joint workshop on periodontal diseases and diabetes by the International diabetes Federation and the European Federation of Periodontology. Diabetes Res Clin Pract. 2018;137:231–241.
- Engebretson S, Kocher T. Evidence that periodontal treatment improves diabetes outcomes: a systematic review and meta-analysis. J Periodontol. 2013;84(4 Suppl):S153–S169.
- Chapple IL, Genco R. Diabetes and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol. 2013;40(Suppl 14):S106–S112.
- Katz J. Elevated blood glucose levels in patients with severe periodontal disease. J Clin Periodontol. 2001;28:710–712.
- Nishida N, Tanaka M, Hayashi N, et al. Determination of smoking and obesity as periodontitis risks using the classification and regression tree method. J Periodontol. 2005:76:923–928.
- Chaffee BW, Weston SJ. Association between chronic periodontal disease and obesity: a systematic review and meta-analysis. J Periodontol. 2010:81:1708–1724.
- Genco RJ, Borgnakke WS. Risk factors for periodontal disease. Periodontol 2000. 2013;62:59–94.
- Eke PI, Thornton-Evans GO, Wei L, Borgnakke WS, Dye BA, Genco RJ. Periodontitis in US adults: National Health and Nutrition Examination Survey 2009-2014. J Am Dent Assoc. 2018;149:576–588.
- Eke PI, Wei L, Thornton-Evans GO, et al. Risk indicators for periodontitis in US adults: NHANES 2009 to 2012. J Periodontol. 2016;87:1174–1185.
- Eke PI, Wei L, Borgnakke WS, et al. Periodontitis prevalence in adults ≥ 65 years of age, in the USA. Periodontol 2000. 2016;72:76–95.
- Michalowicz BS, Aeppli D, Virag JG, et al. Periodontal findings in adult twins. J Periodontol. 1991;62:293–299.
- Michalowicz BS, Diehl SR, Gunsolley JC, et al. Evidence of a Substantial Genetic Basis for Risk of Adult Periodontitis. J Periodontol. 200071:1699–1707.
- Shiau HJ, Reynolds MA. Sex differences in destructive periodontal disease: a systematic review. J Periodontol. 2010;81:1379–1389.
- Shiau HJ, Reynolds MA. Sex differences in destructive periodontal disease: exploring the biologic basis. J Periodontol. 2010;81:1505–1517.
- Eke PI, Dye BA, Wei L, et al. Update on prevalence of periodontitis in adults in the United States: NHANES 2009 to 2012. J Periodontol. 2015;86:611–622.
- Bissada NF, Abdelmalek RG. Incidence of cervical enamel projections and its relationship to furcation involvement in Egyptian skulls. J Periodontol. 1973;44:583–585.
- Hou GL, Tsai C-C. Relationship between periodontal furcation involvement and molar cervical enamel projections. J Periodontol. 1987;58:715–721.
- Ainamo J. Relationship between malalignment of the teeth and periodontal disease. Scand J Dent Res. 1972;80:104–110.
- el-Mangoury NH, Gaafar SM, Mostafa YA. Mandibular anterior crowding and periodontal disease. Angle Orthod. 1987;57:33–38.
- Withers JA, Brunsvold MA, Killoy WJ, Rahe AJ. The relationship of palato-gingival grooves to localized periodontal disease. J Periodontol. 1981;52:41–44.