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. 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

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

Conclusion

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.

References

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