Epidemiology and Etiology of Caries and Periodontal Disease in a US Population
Dental caries result from the breakdown of the hard tissues of the tooth (enamel, dentin, and cementum). This disease is initiated by the acid by-products caused by the bacterial metabolism of simple carbohydrates on a susceptible tooth surface.21,22 Overall acidity within the mouth, the buffering capacity of the saliva, the hardness of tooth enamel, and available mineral content for remineralization of the hard tissues influence the rate and severity of the progression of carious lesions.12 A patient’s risk of developing caries is influenced by many factors, including conditions and medications that affect salivary flow, intraoral pH, poor oral hygiene, dietary carbohydrate and acid content, and fluoride availability.13
Tooth minerals exposed to the oral environment are constantly undergoing remodeling through a demineralization-remineralization process.23 As pH within the oral cavity or at a local intraoral site drops, demineralization occurs and as the pH increases, remineralization of those tissues occurs. The net resultant mineral exchange over relatively longer periods ultimately determines caries development and progression.23
Given these mechanisms for caries formation, oral healthcare professionals (OHCPs) seek multiple avenues to reduce caries formation and/or to remineralize incipient carious lesions. Fluoride availability within the oral cavity allows for remineralization to incorporate fluoride, forming fluorapatite. The presence of fluorapatite in tooth minerals results in an increase in acid-resistance in the resulting remineralized tooth tissues.24 Fluoride exposure is combined with recommendations to limit exposure to acids and sugar substrate, which can result in acid formation after metabolism. Acid from dietary, intrinsic, and extrinsic sources may decrease pH and facilitate the demineralization process..23,24
To accomplish these goals, current guidelines for optimal oral health and hygiene recommend limiting sugar intake and between-meal snacking to decrease the amount of time that intraoral pH drops below a demineralization threshold.14,15 Further, exposure to fluoride in dentifrice (toothpaste) and mouthrinses as well as public health efforts aimed at water fluoridation and fluoride varnish application in elementary school children have been deemed important to reduce caries rates.14,15 In fact, community water fluoridation has proven to be one of the most cost-effective methods for reducing overall caries rates in the population with every $1 spent on water fluoridation returning from $5-32 in decreased healthcare costs within the community!25
Dental caries is a highly prevalent disease in both children and adults, despite declining rates of both treated and untreated caries since the 1970s. Approximately 13% of US children ages 2-19 years had untreated caries in 2015-2016, and the total incidence of caries (treated and untreated) amongst this group was 48.5%.26 Untreated decay is also highly prevalent among US adults; nearly 32% of US adults ages 20-44 years have untreated caries27 and 92% of dentate adults have decay in a permanent tooth.28 The average adult has 3.28 decayed, missing, or filled teeth and tooth loss and decay are more prevalent in some groups of individuals, including: children and older adults, individuals with lower socioeconomic status, Hispanic ethnicity, and non-Hispanic blacks.28 Patients’ quality of life is negatively affected by poor oral health and high caries and edentulism rates with the impact being significant in both children and adults.29 It has been reported that dental caries result in 5 million restricted activity days, more than 1.6 million days in bed, and more than 1.7 million missed school days in children under 18 years old.30 Additionally, children with poor oral health demonstrated higher levels of dental pain and lower scholastic performance than children with higher levels of oral wellness.31 It is also well-established that disability due to dental caries is not limited to children. Sixty-seven point five percent of the population lost work/school hours in seeking unplanned (urgent/emergent) dental care,32 and employed adults lose 92.4 million work hours million work hours each year to dental disease.33 The impact of this lost time and its impact on decreased worker productivity, impacted scholastic achievement, and emotional well-being highlights the critical importance of professional dental care and adequately delivered oral hygiene and home care for the management and prevention of dental caries (Figure 1).
Periodontal diseases include inflammatory diseases of the supporting structures around the teeth, gingiva, periodontal ligament, alveolar bone, and cementum.34 Research shows all individuals are susceptible to gingivitis, a reversible form of gingival inflammation, and may be the precursor to more serious, irreversible forms of periodontal diseases.35 Gingivitis is caused by a dysbiotic dental biofilm and, in general, gingivitis severity is related to the amount and type of bacteria that have accumulated at and around the gingival margins throughout the mouth. Additionally, the oral modifying factors for gingivitis, including local (dental biofilm retentive factors and oral dryness) and systemic factors (smoking, metabolic factors, nutritional factors, pharmacologic agents, sex steroid hormone elevation, and hematologic conditions) are contributing factors.7,35,36 Removal of biofilm and local etiologic factors results in the reversal of gingivitis symptoms and reduces local and systemic levels of inflammatory markers in patients with gingivitis.7,11,35
Periodontitis is a chronic multifactorial inflammatory disease of the hard and soft tissues supporting the teeth associated with a dysbiotic dental plaque biofilm. This dysbiotic biofilm then initiates a host immuno-inflammatory response that, over time, may result in progressive destruction of the periodontal ligament and alveolar bone if not adequately resolved.34,37 Average progression of periodontal disease demonstrates a slow to moderate rate of disease progression with approximately 0.1mm of attachment loss and 0.2 teeth lost annually.38 Groups with fastest and slowest disease progression differed considerably with accelerated attachment loss associated with access to comprehensive dental care as well as local and/or systemic factors.38 In an updated classification system from the American Academy of Periodontitis (AAP) and European Federation of Periodontitis (EFP), individuals are classified with a Stage and Grade to characterize disease severity and risk of future disease progression.37,39 Periodontitis Stage is assigned as I-IV and is assessed by patients’ current disease presentation, including attachment, bone, and tooth loss, and the case complexity.37,39 Periodontitis Grade is defined as A-C and is based upon risk and evidence of the rapidity of disease progression over time.37,39 The prevalence of periodontitis has been estimated to be over 42% of U.S. adults over 30 years of age.40 Of those individuals, 7.8% had severe periodontitis and severe periodontitis was most prevalent among adults 65 years or older, Mexican Americans, non-Hispanic blacks, and smokers.40 These statistics suggest that the prevalence of periodontitis among US adults is nearly 4-fold greater than that of diabetes mellitus41 and over 6-fold greater than that of coronary artery disease.42 Periodontitis is extremely prevalent and after initiation by bacteria and bacterial virulence factors, disease progression and tissue destruction occurs through host-mediated inflammatory pathways,36 which may vary based upon genetic and other risk factors.43-46 The result is a chronic immune-inflammatory disease that may pose a significant systemic burden for individuals47 (Figure 2).
Because both gingivitis and periodontitis are associated with a dysbiosis of microbial biofilm, the removal of bacteria and their food sources from hard and soft tissues in the oral cavity is critical for the prevention, control, and management of periodontal disease.