The Role of Sugar-Free Chewing Gum in Dental Caries Prevention

*Marut Phuphaniat*

#### **Abstract**

The key to avoiding dental caries is managing the microorganisms on the tooth responsible for demineralization. Chewing gum has physical adhesive capabilities. It also promotes saliva flow, assisting in eliminating food particles and reducing the formation of bacterial biofilms in the oral cavity. Saliva flow also helps to balance the pH balance in the oral cavity, thereby reducing the risk of dental caries. In addition, sugar-free gum contains various antibacterial and remineralization substances, such as xylitol and casein phosphopeptide-amorphous calcium phosphate (CPP-ACP). In conclusion, sugar-free gum can remove food particles and tartar, stimulate saliva, increase oral pH, inhibit demineralization, and increase remineralization. These qualities aid in preventing dental caries.

**Keywords:** chewing gum, sugar-free, dental caries prevention, xylitol, casein phosphopeptide-amorphous calcium phosphate (CPP-ACP)

#### **1. Introduction**

Oral health is an important problem for public health, especially dental caries, which have a relatively high incidence rate. Dental caries is not a severe disease but causes economic loss, pain, and suffering. In addition, the inability to chew food, bad breath, and lesions in the tooth are breeding grounds for bacteria that weaken the body and lead to other diseases. Despite the campaign to disseminate dental health knowledge to people of all ages to realize the problem and pay attention to oral health, dental caries is still a problem for people of all ages. Especially among children, the leading cause of dental health problems is improper dietary habits and improper oral health care [1]. In addition, parents have incorrect oral health care attitudes and a lack of knowledge about dental caries prevention, resulting in children not receiving proper treatment. Dental caries is caused by four factors: the tooth, food, bacteria, and the time of tooth surface acid exposure (**Figure 1**).

Food particles adhered proximally and in the groove of the tooth produce dental caries. It provides energy to the bacteria in the oral. The process by which bacteria break down food debris produces acid, leading to the demineralization of tooth. Therefore, when food remains in the oral for a long time or is frequently eaten, it often causes the demineralization of tooth, thus causing dental caries (**Figure 2**). School-age children are a group at high risk of developing dental caries. Many factors involve biological, social, behavioral, and psychological factors. Therefore, dental

caries is still a problem among school-age children. Especially during the age of 9 years, when the premolar and molar tooth are coming. Therefore, there is a chance of quickly accumulating food particles in the tooth' grooves [2].

There are many ways to prevent caries by controlling the causative factors of dental caries, including the tooth, food, bacteria, and time. The most commonly used methods are physical methods such as brushing tooth and chemical treatments such as fluoride. Brushing tooth with fluoride toothpaste is a common practice these days, but cavities still occur due to many factors, such as the frequency of overeating; as a result, brushing tooth three times a day is insufficient to stop dental caries progression. Therefore, it is necessary to control the risk of caries during the day. Sugar-free gum is a good choice because the adhesive gum's physical nature helps eliminate food residues after eating food by attaching the direct contact of the gum to the food scraps. In addition, chewing gum increases saliva flow reduces bacterial biofilm on

the tooth surface, and maintains oral acid-base balance (pH > 5.5) [3, 4]. In addition, sugar-free gum contains a variety of substances that have antibacterial and remineralizing properties, such as xylitol and casein phosphopeptide-amorphous calcium phosphate (CPP-ACP), so sugar-free gum is more responsive to oral health care.

## **2. Sugar-free chewing gum and oral health**

Sugar-free gum is chewing gum that uses a sweetener instead of sugar. Popular sweeteners such as xylitol, sorbitol, and mannitol [5]. The general composition of chewing gum includes sweetener (50–65%), gum base (18–30%), corn syrup (12–20%), color and flavor (1–2%), and softeners (0.3–3%). More than half of the composition is sweetener, which is responsible for enhancing the flavor and texture of the gum [6]. Sugar-free gum has significantly impacted oral health because of its ability to stimulate saliva and accelerate the removal of carbohydrates that accumulate from food intake. These actions may lead to healing, reduction of tooth decay, and other oral health benefits [7]. The benefits of chewing gum on oral health are as follows: (**Figure 3**)


Nowadays, sugar-free gum has been produced for consumers to choose from in various styles. Chewing gum is another good way to clean tooth. Chewing gum may be used as auxiliary to dental brushing or when such method is impossible to be

performed, such as when you are outside, and it is not convenient to brush your tooth, you can chew gum to clean your tooth. Chewing sugar-free gum for 5–20 minutes after meals two to three times a day can help prevent tooth decay because gum helps to remove plaque and reduce gum inflammation. In addition, sugar-free gum stimulates saliva, which reduces acidity on the tooth surface and helps to self-cleansing can clean tooth [3, 8]. Several studies have concluded that sugar-free gum can inhibit the effects of oral bacteria [3, 4, 8]. This process is due to two main reasons: (1) the stimulation of saliva from chewing and (2) the use of sweeteners instead of sugar [9]. In addition, some substances promote healthy tooth, such as xylitol, andCPP-ACP, also known as Recaldent, which has been reported to enhance remineralization of the tooth surface [10–12]. A study on sugar-free gum chewing found that children who chewed sugarfree gum had fewer cavities than children in the control group who didn't chew gum [4, 13]. In addition, sugar-free gum was tested to prevent tooth decay in students. The students chewed 1 tablet of gum for 10 minutes after eating breakfast-afternoon every day. It was found that after 4 months of the experiment, the students had no more tooth decay [3, 8].

#### **2.1 Compounds that affect oral health**

#### *2.1.1 Xylitol*

Xylitol is a type of sweetener which is alcohol sugar. Xylitol was discovered in 1890 by German chemists Professors Emil Hermann Fischer and Rudolf Stahel by extracting the compound from beech [14] and later widely known in many countries such as the United States, Canada, Japan, etc. Xylitol has a molecular structure of 5 carbon atoms (**Figure 4**), chemical formula C5H12O5, and a molecular mass of 152.15 g/mol. Xylitol is a common sugar substitute. It is as sweet as sucrose. It can be used instead of sucrose in a ratio of 1:1, providing 2.43 cal/g of energy. In addition, it has the property of giving a cooling sensation while eating. Xylitol is a non-fermentable sugar that bacteria cannot use to synthesize for energy. Therefore, Xylitol is used as a glycemic control agent in Type 2 diabetes and as a product to prevent tooth decay [15].

Xylitol has been approved by the U.S. Food and Drug Administration (FDA) since 1960 as safe for children [16] and can be consumed in 30 g without causing harm. If consumed more than 30 g at a time can cause diarrhea. This may be because intestinal bacteria cannot metabolize large amounts of xylitol. In nature, it can be found in many natural plants, vegetables, and fruits, such as strawberries, carrots,

**Figure 4.** *Structure of xylitol.*

#### *The Role of Sugar-Free Chewing Gum in Dental Caries Prevention DOI: http://dx.doi.org/10.5772/intechopen.109067*

corn cobs, nuts, etc. Marketing xylitol is available in liquid and solid form. Its applications are mainly made into chewing gum, followed by confectionery, medicine, and beauty products [17]. In addition, Xylitol is recognized by the American Academy of Pediatric Dentistry (AAPD) and serves as a guideline for tooth decay prevention [18]. Xylitol has anti-cavities properties for two reasons: promoting remineralization and inhibiting caries-causing bacteria (**Figure 5**).

#### *2.1.2 Casein phosphopeptide-amorphous calcium phosphate*

CPP-ACP, also known as "Recaldent", was discovered by Professor Eric Reynolds, School of Dental Science, University of Melbourne, Australia. CPP-ACP is divided into casein phosphopeptide (CPP) and amorphous calcium phosphate (ACP). CPP is a peptide derived from cow's milk by tryptic digestion of casein in cow's milk to produce a peptide containing phosphoseryl residue (Ser(P) – Ser(P) – Ser(P) – Glu – Glu –) a large amount of which binds calcium and phosphate in the ionized form to form a complex called ACP, which can cause calcium and phosphate ions. It is in a saturated state called metastable solution, i.e. it is saturated but does not form nucleation and does not precipitate calcium salts and phosphates, thus forming a nanocomplex between CPP and ACP known as CPP-ACP [19].

CPP-ACP has been proven to prevent tooth decay in laboratories, in vivo, and in humans; its efficacy is due to casein's ability to adapt to acidic environments. When the pH is acidic, the ACP is separated from the CPP, resulting in an increase in the levels of calcium and phosphate in the saliva, stabilizing the oral ACP [10] and increasing the calcium and phosphate content in the plaque. Furthermore, as an ion reserve, it inhibits demineralization [20] and stimulates the remineralization of tooth enamel by preventing the constant precipitation of calcium and phosphate in saliva [21]. It was also found that CPP directly affects bacterial apoptosis and impairs agglutination [22]. CPP-ACP can work with fluoride to form casein phosphopeptide-amorphous calcium fluoride phosphate (CPP-ACFP), readily strengthening enamel [20].

**Figure 5.** *The anti-cavity mechanism of xylitol.*

The continued use of dental products containing CPP-ACP produces ion saturation in saliva and biofilm, making it available for subsequent precipitation in the form of ACP, favoring the dental remineralization process. The process of dental demineralization/remineralization: (1) oral pH < 5.5 causes demineralization of hydroxyapatite (HA), chemical formula Ca10(PO4)6(OH)2 (2) upon saturation of the oral environment and biofilm with Ca2+ and PO43− ions, promoting the process of remineralization (**Figure 6**) [23].

In 1999, CPP-ACP was approved by the FDA that it is safe. CPP-ACP can be used in people with lactose intolerance because CPP-ACP does not contain lactose. However, CPP-ACP is not recommended for people with milk protein allergies [24]. CPP-ACP is used in various applications in food ingredients such as sugarfree candies or gum and in dental products such as toothpaste, mouthwash, dental implants, and glass ionomers. It is also available as a topical cream (paste) for ease of use [8].

#### **3. Chewing gum and removing food particles on the tooth surface**

Food debris is a factor in dental caries due to the accumulation of food particles in the mouth or on the tooth, especially starchy foods, which are the main energy source for bacteria. When the digestive bacteria are energized, they make acidic wastes that cause tooth demineralization. Therefore, removing food particles stuck in the tooth is necessary to prevent tooth decay. It is known that the gold standard for removing supragingival plaque is daily tooth brushing, flossing, and/or use of antimicrobial mouthwash. Still, in some cases, chewing gum may be used as auxiliary to dental brushing, or when such method is impossible to be performed. This led to the development of antimicrobial gum that would provide daily oral care and reduce plaque in the mouth [25]; due to the physical nature of gum as a binder, it

**Figure 6.** *Remineralization mechanism of CPP-ACP.*

helps to eliminate food residues left after food consumption. Due to the physical nature of gum as a binding agent, it helps to eliminate food residue after consuming food. Disposal is partly due to the direct attachment of the gum to the food debris, along with the increased occlusion and saliva, which washes away the food particles [8]. In case we are outside, and it is not convenient to brush our tooth, it is possible to chew sugar-free gum to clean the tooth. In addition, a research report concludes that chewing gum may be used as an aid to flossing when brushing is impossible [26]. In addition to removing food particles, chewing sugar-free gum reduces plaque on the tooth caused by the accumulation of food particles on the tooth surface [27].

Phoophaniat and Joankrajang [8] examined the effectiveness of chewing gum containing CPP-ACP and xylitol in preventing dental caries in school-aged children. The sample group consisted of 90 students, divided into 3 groups by simple random sampling. A group of 30 students received one of the following interventions: experimental group 1 used chewing gums containing CPP-ACP, experimental group 2 used chewing gums containing xylitol, and control group. The experimental groups chew gums for 10 minutes, times times a day for 16 weeks. The dental plaque was assessed five times: before the trial, week 4th, week 8th, week 12th, and week 16th. Dental caries was assessed twice, before and after the trial. The data were analyzed by the friedman test, wilcoxon signed ranks test, kruskal-wallis test, and mann whitney U test. The result showed that there was a statistically significant decrease in dental plaque level in experimental groups, experimental group 1 had mean dental plaque of 1.10, 0.83, 0.40, 0.16, and 0.13 ( χ<sup>2</sup> = 75.835, *P*-value < 0.001), and experimental group 2 had mean dental plaque of 1.00, 0.93, 0.51, 0.16, and 0.14 ( χ<sup>2</sup> = 66.905, *P*-value < 0.001), and less dental plaque than the control group. Experimental group 1 (*Z* = −1.000, *P*-value = 0.500) and experimental group 2 (*Z* = −1.414, *P*-value = 0.250) dental caries did not increase compared to before the trial, and less tooth decay than control group ( χ<sup>2</sup> = 7.164, *P*-value = 0.030). Suggestions that chewing gum containing CPP-ACP or xylitol, 1 tablet for 10 minutes, can reduce dental plaque. Consistent a study on chewing sugar-free gum in students found that students chewing one tablet of gum for 10 minutes after breakfast and afternoon daily was found to reduce the formation of dental plaque within 4 weeks and decreased dramatically at week 8 and then started to stabilize at week 12 because the amount of plaque on the tooth was already very low [3], consistent with research that found that most gum containing sugar substitutes, antimicrobial agents, and other minerals have an effect on reducing plaque [28]. The reduction of food particles and plaque on the tooth is one of the causative factors of tooth decay due to the physical nature of the gum and its beneficial compounds.

#### **4. Chewing gum and oral bacteria reduction**

Oral bacteria are endemic to everyone and are a common cause of oral health problems. The bacteria known as Streptococcus mutans are the main culprits that cause tooth decay. Controlling Streptococcus mutans can help reduce tooth decay. Dental plaque begins with a biofilm that binds the tooth surface between the saliva covering the tooth surface and bacteria. The physical nature of chewing gum helps to eliminate food debris, which is the energy source of bacteria, preventing them from growing [8]. In addition, sugar-free gum has other properties that eliminate bacteria, such as:

Xylitol is a sweetener instead of sugar. Xylitol molecules similar in shape to fructose are absorbed through the bacterial cell wall by the same mechanism that bacteria absorb sugar into cells. When xylitol gets into cells, bacterial enzymes cannot synthesize xylitol for energy, so bacteria cannot survive. Xylitol is a substance that helps reduce bacteria in the oral [8]. When compared to other oral bacteria, xylitol is more effective in inhibiting Streptococcus mutans [29]. Consistent with research findings, the samples had reduced plaque after 21 days of chewing gum containing xylitol [30]. Similarly, the research found that after chewing gum containing xylitol for 30 days, the samples had reduced plaque content. Thus confirming that chewing gum containing xylitol can reduce plaque [31].

CPP-ACP can increase calcium and phosphate in plaque. When there are many calcium ions in the extracellular fluid, the bacterial cell wall becomes porous, and the cell breaks down. This results in killing bacteria or inhibiting bacteria [12]. In addition, chewing gum can help stimulate the flow of saliva to produce more secretions than usual [3]. The secretion of saliva and the physical nature of the gum as a binding agent facilitates the removal of food residues left after ingestion. The elimination is partly due to the direct attachment of the gum to food particles. This, together with increased occlusion and saliva, thus prevented bacterial formation and reduced the appearance of oral bacterial biofilms, consistent with the results of a study by Phoophaniat et al. [4, 8] that after chewing CPP- ACP for 12 weeks, subjects had a statistically significant reduction in dental plaque content.

#### **5. Chewing gum and oral pH balance**

It is well known that oral pH is an integral part of the caries process. It comprises acidogenic and aciduric bacteria that are responsible for lowering the pH and subsequent destruction of HA matrix in enamel and dentine. Therefore, preventing tooth decay requires maintaining a pH balance that is not too low (<5.5). Chewing gum has a physical mechanism in which chewing stimulates saliva flow. It is commonly known that saliva is the pH balance system in the oral. Therefore, when there is a lot of saliva flowing, it helps to balance the pH of the oral cavity. In addition, the properties of compounds that have a positive effect on oral health also help to improve the pH balance in the oral cavity [8], as follows:

Xylitol has been reported to increase saliva flow and adjust oral pH [14, 32]. This may be due to its cooling effect on xylitol, which stimulates salivary flow. Together with the properties that help eliminate bacteria in the mouth, thus making the pH value not lower because bacteria cannot synthesize xylitol. It is not acidic, like digesting sugars in general [15]. Tests of various brands of xylitol gum were found to increase pH within 15 minutes. There was a statistically significant difference with the control group [33]. Consistent with the test in children 8−10 years, it was found that after chewing gum with xylitol, saliva pH immediately increased and increased dramatically in 15 minutes [34].

CPP-ACP has the property to increase the pH of saliva by casein modulating an acidic environment [10]. ACP refining cleaves from CPP, resulting in increased calcium and phosphate levels in saliva. Therefore, conditions within the oral cavity become basal according to the properties of calcium and phosphate. This is consistent with research findings that CPP-ACP can increase the pH of saliva [35]. Consistent with the results of tests in children 8–10 years of age, it was found that after chewing the CPP-ACP chewing gum, the saliva pH immediately increased and increased dramatically in 15 minutes [34].

#### **6. Chewing gum and tooth strengthening**

In this regard, the physical appearance of chewing gum has no effect, but with the properties of compounds that are beneficial to oral health, such as xylitol and CPP-ACP, chewing gum containing such compounds has outstanding features in promoting oral health, as follows:

Although xylitol is not very prominent in its remineralization, it does so as xylitol prevents enamel resorption by inhibiting the migration of calcium ions and phosphate ions from the lesions. Xylitol acts as a carrier of calcium ions to the tooth, especially in areas of demineralization. It accelerates the remineralization of the tooth. This mechanism increases the strength of the tooth [11].

CPP-ACP is the most outstanding tooth remineralization agent. CPPs consist of a multiphosphoseryl sequence, which can stabilize calcium phosphate in ACP solution within a nano complex solution. CPP-APP nanoscale complex molecules bind to the tooth surface. It prevents demineralization and can induce remineralization in enamel subsurface lesions. The hardness of the tooth will be more CPP-ACP binds with fluoride ions (F− ) to form amorphous calcium fluoride phosphate (ACFP) and stabilizes with CPP at the tooth surface, where these substances can diffuse into the lesion area. Calcium phosphate and fluoride solutions can help speed up the remineralization process with fluorapatite (Ca5(PO4)3F2), which resists acidic conditions and can penetrate deep into the lesion of the tooth (**Figure 7**). The advantage of being able to penetrate into the lesion is the ability to restore opaque enamel or white spot lesion [36]. It was also reported that CPP-ACP promoted the efficiency of fluoride use. This is caused by combining fluoride ions with ACP to make ACFP at the enamel surface. Based on these findings, CPP-ACP helps fluoride adhere to the tooth surface and enhances anti-demineralization efficiency [37], which has been shown to increase the effectiveness of fluoride in preventing tooth decay [38].

**Figure 7.** *Remineralization mechanism of CPP-ACP with fluoride.*

## **7. Conclusion**

Dental caries is generally caused by four factors: the tooth, diet, bacteria, and acid exposure time. Therefore, methods for preventing tooth decay must properly control those four factors. Sugar-free chewing gum has both physical and chemical properties to prevent tooth decay. The physical property of chewing gum is the direct attachment of the gum to food particles in conjunction with increased chewing and saliva. Increasing saliva can help wash away food particles and chemical properties from betel nut constituents such as xylitol and CPP-ACP. These compounds reduce oral bacteria, improve oral hygiene, and strengthen tooth enamel. The properties mentioned earlier of sugar-free chewing gum were able to control the four causative factors of caries incidence. Therefore, it was concluded that sugar-free chewing gum had caries-prevention properties. Additionally, sugar-free chewing gums are easily accessible, can be chewed in any situation, whether on-site or off-site, and are popular with school-age children, teens, and adults. Therefore, chewing gum, although not as effective as brushing or flossing, is another way to clean your mouth and control cavities.

## **Conflict of interest**

The authors declare no conflict of interest.

## **Author details**

Marut Phuphaniat Faculty of Public Health and Allied Health Sciences, Sirindhorn College of Public Health Suphanburi, Praboromarajchanok Institute, Ministry of Public Health, Thailand

\*Address all correspondence to: marut@phcsuphan.ac.th

© 2023 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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#### **Chapter 8**

## Periodontitis, Its Associations, and Prevention

*Yasmine N. Alawaji*

#### **Abstract**

The ultimate goal of studying associations with diseases is to plan, implement, and evaluate preventive strategies. Today, after reviewing the body of evidence, one needs to ask: What has not been learned yet regarding periodontitis associations and its prevention? Current recommendations to prevent periodontitis are mostly limited to individual patient care while population-based approaches are nearly absent. Current strategies are not only time-consuming and costly but can be also ineffective to combat disease burden in populations. To initiate and sustain successful outcomes, prevention needs to be applied at multiple levels. Interventions need to target unhealthy behaviors along with their associated social and physical environmental constraints. The chapter presents highlights from current research on associations with periodontitis, its limitations, and the need to understand pathways linking periodontitis with its exposures over the life course. Finally, a suggested multilevel strategy for periodontitis prevention was outlined.

**Keywords:** periodontitis, prevention, associations, pathways, life course, social determinants of health

#### **1. Introduction**

A common approach in our clinical care is to advice patients to adopt healthy behaviors including smoking cessation, oral self-care (e.g., tooth brushing and use of interdental aids), healthy dietary habits, and physical activity [1]. While plenty of theories have been suggested trying to explain or change health behaviors, such approach can be limited without considering social and physical environmental exposures [2, 3]. For example, using different strategies with patients to quit smoking including referral to smoking cessation clinics could have limited benefits [4–6]. In contrast, implementing sin tax and age restrictions on tobacco products by policymakers can make these products less affordable and accessible. Consequently, more cost-effective and radical change may occur at population level; people may quit smoking or refrain from smoking in first place. The social and environmental exposures can be collectively called social determinants of health, which include socioeconomic status, housing, residential neighborhood, environmental safety, social support network, social norms, structural racism, and discrimination [4, 5, 7–9]. Although targeting the social determinants of health can be effective in prevention of

diseases along with their related behaviors, they could be more effective when applied as multilevel strategies including clinical care.

In Geoffrey Rose's seminal paper "*sick individuals and sick populations*", key concepts of studying disease etiology and its prevention were discussed [10]. Rose highlighted the importance of considering different ecological levels when studying the disease etiology. When an exposure is uniformly distributed within a population, it could hamper its detection, which necessitates studying its variations among populations. Besides Rose's remarks, lack of variations in distribution could be also indicative of methodological limitations in measuring, summarizing, or analyzing the disease and its exposures [11]. During periodontal indices' era, it was believed that gingivitis leads to periodontitis and consequently results in tooth loss in virtually everyone [12, 13]. These notions of lack of variations in susceptibility to periodontitis were attributed to several methodological limitations. Periodontal disease was measured using indices including Russell's Periodontal Index [14] which was based on the presence or absence of pockets without precise measurements. Thus, it did not properly differentiate between gingivitis and periodontitis [12]. The gingivitis and periodontitis were measured as continuous process using gradually increasing scores, summarized for as individual's mean index score, then summarized for a population as mean score based on individual's mean scores. Consequently, variations within and between individuals were lost [12, 13]. The periodontal indices, which measure and summarize periodontal disease as mean score, were abandoned by the end of 1980s and replaced by site-specific measurements [15, 16]. The improvement of periodontal measurement methods allowed detection of variations at multilevels (site-level, tooth-level, individual level, and between populations) [17–22]; consequently, it motivated research on host susceptibility and associations with periodontitis [23–25].

Since the periodontal indices were abandoned, periodontitis is summarized in population-based studies using prevalence, extent, and severity [12, 26]. Prevalence can be defined as the proportion of individuals with periodontitis, extent can be defined as mean proportion of sites or teeth with periodontitis, and severity can be defined as mean clinical attachment loss (CAL) or mean periodontal probing depth (PPD). Among these summaries, periodontitis severity is calculated as a mean score for population; such summary does not properly account for the multilevel nature of the measurements and its variations at site level, tooth level, and individual level before it is summarized for the population [11, 27]. The summary also averages diseased and nondiseased sites in individuals with or without periodontitis. Similar issues are encountered when periodontitis progression is calculated as mean annual score in longitudinal studies [28]. This summary does not provide proper insights regarding the variations at different periods of observation in addition to the limitations abovementioned for periodontitis severity. Therefore, it appears that methodological limitations of the twentieth century still apply to some current research approaches. Other limitations of studying associations with periodontitis were discussed in the following sections.

#### **2. Associations with periodontitis**

Among dominant notions in the twentieth century was dental plaque considered the cause of periodontal diseases; it was thought that unless plaque is prevented, gingivitis invariably leads to periodontitis and subsequently tooth loss [13, 29]. Russell, who was considered the father of periodontal disease epidemiology, analyzed two population-based data and concluded that plaque and age alone explain around

#### *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

90.3% of variations in periodontal disease regardless of which population being studied [30]. Similarly, an experimental gingivitis study was used to support the evidence that plaque is the cause of periodontal disease [31]. Consequently, clinical practice of that era almost solely focused on plaque control [32–34]. Though, these findings reflect the abovementioned methodological limitations of periodontal and plaque indices. By 1980s, studies on untreated populations used site-specific measurements, unveiled variations in susceptibility to periodontitis despite accumulations of uniformly high levels of plaque and calculus [19, 22, 35–39]. Variations in susceptibility to periodontitis were observed among individuals, population groups, and teeth sites. Thus, it was no longer accepted that plaque is the only cause of periodontal disease. Several theories evolved trying to explain the role of dental plaque including nonspecific and specific plaque theories [40]. Currently, there is a general agreement that dysbiosis of oral biofilm may induce an inflammatory response in susceptible hosts to cause periodontitis [41]. Dysbiosis is a shift in the species within the oral microbiome that results in loss of homeostasis and may impact the human health; it can result due to an expansion of pathogenic microorganisms, altered metabolic capacity, decreased beneficial microorganisms, or reduced species diversity. Thus, the etiology of periodontitis can be attributed to "*sufficient cause*" where a set of components (exposures) can be sufficient for causing the disease that requires dysbiotic biofilm as a necessary component [42–44]. However, the biofilm alone is not sufficient cause of periodontitis. Hypothetical sets of sufficient causes for periodontitis are depicted in **Figure 1**.

#### **Figure 1.**

*Hypothetical sets of sufficient causes for periodontitis using sufficient cause component model (Rothman's pies) [45]. Dysbiotic biofilm is a necessary component but insufficient for causation [42, 44].*

Periodontitis and other chronic diseases including atherosclerotic cardiovascular disease, obesity, and diabetes mellitus are associated with increased low-grade systemic inflammation and oxidative stress [46–49]. Evidence suggests that aggregation of chronic diseases within individuals is associated with higher level of inflammation and oxidative stress compared to having a single condition [46, 48, 49]. Chronic diseases also have common risk factors with periodontitis including underlying exposures and health behaviors [50, 51]. Underlying exposures can be either non-modifiable including age, sex, ethnicity, and genetics or modifiable such as the social determinants of health. Underlying exposures are mostly associated

#### **Figure 2.**

*Behavioral and biological pathways that could link the underlying exposures with the adverse health outcomes including periodontitis.*

with periodontitis or other chronic diseases mainly through behavioral or biological pathways (**Figure 2**).

Several models were proposed to conceptualize disease causation including sufficient component cause model (**Figure 1**), web of causation, and structural equation models [44, 45, 52]. Nancy Krieger criticized the use of sufficient component cause model and web of causation for lacking accountability for unjust disparity in disease distribution when proposed her ecosocial theory [53, 54]. Krieger's theory is not a method of disease causation since it is concerned with individuals and their communities between the past and present. "*Shared observations of disparities in health do not necessarily translate to common understandings of cause; it is for this reason theory is key*" [53]. The term "*embodiment*" was introduced to refer to interactions between society and biology. The theory also focused on pathways of these interactions at multiple ecological levels over the life course while considering the accountability for injustice. Ecological levels can be conceptualized at multiple levels and domains including home, school, and work. In contrast to causal models that can be used for testing specific hypotheses, Krieger's theory can be useful for identifying knowledge gaps, generating research questions, articulating increments of evidence from separate studies to understand disease etiology, and taking the theory into action [54].

Two epidemiological concepts relevant to disease prevention that need to be distinguished are the life course approach and the natural course of disease. The life course epidemiology is concerned with understanding psychosocial and physical environmental exposures and when they can impact health behaviors or become biologically embedded over the life course (intrauterine life, childhood, adolescence, early adulthood, late adulthood, or across generations) [55–57]. While earlier approaches for life course focused on diseases as its end points, recent approaches shifted to study multiple aspects of physiological functions [55]. The exposures are studied for their impact independently, cumulatively, or for their interactions. In contrast, the natural course of disease is a disease specific concept and based on different stages of disease development (susceptibility, asymptomatic, symptomatic, and terminal stages) in the absence of treatment [11, 58, 59]. Recruitment of study population that is either never treated or all treated similarly for periodontal conditions can control for treatment status. However, disregarding impacts of treatment can lead to erroneous interpretations of study findings [11, 13]. This can be especially true when considering that periodontal treatment (non-surgical or surgical) has non-negligible impacts on the periodontitis severity, extent, and progression [11]. Unfortunately, studying the periodontitis associations while disregarding the treatment impacts is a common approach in periodontal research.

#### **2.1 Impact of age on periodontitis: What has not been learned yet?**

Based on cross-sectional surveys, periodontitis increased in severity, extent, and prevalence with age [11, 60–63]. When periodontitis defined using CAL, its association with age was more consistent, whereas PPD had less clear pattern [11, 15, 60, 64, 65]. When periodontitis included non-severe thresholds (CAL ≤4 mm, PPD ≤6 mm, or ≤ 1/3 bone loss), the prevalence steeply increased after 20 years through 30s until it reaches its peak between 35 and 45 years [11, 38, 60, 66, 67]. The prevalence before 20 years, although less frequent, widely varied within and among populations; estimates from different populations were between 1.0% and 69.2% [11, 60, 62, 66, 68–70]. Similar patterns were observed when periodontitis incidence was studied in longitudinal surveys [67, 71, 72]. In contrast, when periodontitis was defined at severe thresholds, majority of its variations, within populations, were mostly confined to adults [38, 64, 66, 73, 74]. Despite that clinical classifications consider molar-incisor pattern suggestive of localized aggressive periodontitis in young age groups [75–78], evidence from epidemiological surveys indicates that such pattern is common in all age groups [17, 18, 22, 29, 79]. Similar pattern was observed in a study on untreated population; most impacted teeth were upper molars and lower incisors of different age cohorts (**Figure 3**) [11].

There is general agreement that age association with periodontitis is due to accumulative effect of exposures and disease experience over time rather than having an increased susceptibility to periodontitis at specific age [15, 80]. However, it worth noting that such association remains robust after adjustment for different exposures including sex, social, behavioral, and medical exposures in cross-sectional or longitudinal studies [11, 60–62, 81, 82]. In a study in untreated Sri Lankan tea workers, periodontitis progression had an independent association with both age and follow-up time [83]. These age-related findings may suggest that effect of age on periodontitis cannot be completely explained as function of accumulation of exposures and disease experience over time. Among the difficulties of fully understanding the effect of age, in periodontal literature, is that majority of studies either focus on younger or older age groups excluding direct age-related comparisons [11]. Such approach could hide age-related patterns of periodontitis distribution and its associated exposures. Another limitation is that periodontitis progression is often studied as mean annual CAL or PPD for comparisons among age groups [28]. As previously stated, such summary does not properly account for variations in the rate of progression within or between individuals, subgroups, and at different periods.

An ideal study design to better understand the role of age on susceptibility to periodontitis would be a life course approach. Such approach can identify if there are sensitive periods in development, which can have behavioral or biological impacts [55]. Sensitive periods can be psychologically, socially, or physiologically defined [84]. Behaviors including smoking, unhealthy dietary habits, and inadequate coping with social adversity are often acquired during adolescence. This makes interventions

**Figure 3.**

*Periodontitis severity for maxillary and mandibular teeth in an untreated population [11, 60]. The most impacted teeth were the lower incisors and upper molars across different age cohorts.*

to combat certain behaviors such as smoking most effective at that stage [84]. At older age, compromised manual dexterity and physical disability could limit oral self-care and utilization of dental care. The life course study design is mostly limited due to its feasibility especially when considering the lengthy latency periods between exposures and periodontitis incidence.

#### **2.2 Sex**

Males almost consistently had higher periodontitis prevalence, extent, and progression compared with females in epidemiological studies [60, 61, 81, 85–87]. In contrast to suggestions that sex-related differences can be attributed to better oral health behaviors in females [80, 88], studies on populations with uniformly high levels of plaque and minimal access to dental care also found an increased periodontitis prevalence, extent, and progression in males [11, 60, 86, 87]. National surveys from Brazil, France, and the United States reported higher periodontitis prevalence in males despite the adjustment for behaviors including patterns of dental visits, smoking, and alcohol consumption [61, 81, 89, 90]. In contrast, a recent systematic review found almost no sex-related differences in terms of periodontitis progression rates [28]. This finding was based on a subgroup meta-analysis of two studies only. However, subgroup meta-analysis can be only conducted when there are minimally 10 available studies [91]. In addition, the sex-related differences were compared based on mean annual progression, which does not properly account for multilevel variations. In a study Brazilian population, males had an unadjusted risk ratio (RR) of 1.24 (95% confidence interval [CI]: 1.09, 1.42). After adjustment for smoking, males had an adjusted RR of 1.22 (95% CI: 1.08, 1.39). This may be interpreted as having small effect of smoking on sex. However, the study found an interaction between smoked packs per year and sex; females who smoked 30+ packs had higher RR of periodontitis progression after adjustments for age and level of education.

Sex dimorphism in immunological responses was suggested as plausible biological mechanism that may explain the differences in susceptibility to diseases [85]. Circulating levels of sex steroids could alter as a function of age mainly during puberty and menopause. However, such findings were mostly based on responses to acute infections. Although the use of life course approach would have been ideal to understand the sex dimorphism in susceptibility to periodontitis, cross-sectional surveys with wide age ranges may provide indirect evidence to identify these differences as function of age. This approach may narrow down the required observation time before conducting longitudinal studies. For example, in a study on untreated population, the sex-related differences in periodontitis prevalence and extent (**Figures 4** and **5**) were mainly observed after 20 years [26, 60]. Similarly, periodontitis had no association with sex in 15–19-year adolescents from several Latin American nations [70]. These findings may suggest the need to study the sex-related differences in exposures prior to 20 years.

#### **2.3 Race/ethnicity**

Studies from the United States almost consistently presented an association between race/ethnicity and adverse health outcomes including periodontitis [61, 94–96]. In the first National Health and Nutrition Examination Survey (NHANES), higher periodontitis prevalence was found in black Americans compared with whites with an adjusted odds ratio (OR) of 1.31 (95% CI: 0.78, 2.19) [94]. In NHANES III, the adjusted OR in Blacks increased to 2.09 (95% CI: 1.68, 2.60); the adjustments in both surveys were done for age, socioeconomic indicators, smoking, diabetes, and time elapsed since last dental visits. In NHNANES (2009–2012), both Hispanics and non-Hispanic blacks had higher periodontitis prevalence than

#### **Figure 4.**

*Periodontitis prevalence per age and sex groups in an untreated population [11, 60]. Periodontitis defined based on criteria by the Centers for Disease Control and Prevention and American Academy of Periodontology (CDC/ AAP) [92, 93].*

whites [61]. Ethnicity-related associations were not confirmed in Brazilian population [81, 82]. Disparities in health outcomes based on race/ethnicity could not be explained by genetic differences but could rather reflect differences in social, cultural, and behavioral factors between the past and the present [53, 94, 96]. Thus, ethnicity is mainly considered as a social construct, and more information needs to be provided to explain its role within a broader context.

Borrell *et al*., suggested that disparity in periodontitis prevalence between African Americans and Caucasians in the United States can be attributed to discrimination, racism, and residential segregation [94]. Residential segregation for example may impact health outcomes by potentially impacting exposures to environmental hazards, quality of education, employment opportunities, and influencing certain behaviors such as increased tobacco consumption is some neighborhoods. In a study that analyzed the association between ethnicity and periodontitis based on different socioeconomic status (SES), black Americans with high income had the highest periodontitis prevalence compared to both high-income whites and low-income blacks. This finding illustrates how increased income may not directly improve health outcomes. Possible explanations include increased income may occurred short term after development of periodontitis or was not accompanied by skills in managing resources. Social epidemiologists suggested that income increase in short term (e.g., winning lottery) can be associated with unhealthy behaviors such as increased smoking [84]. Another possible explanation is that high-income blacks may experience

#### *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

#### **Figure 5.**

*Periodontitis extent per age and sex groups in an untreated population [11, 60]. PPD: Periodontal probing depth, CAL: Clinical attachment loss.*

stressful conditions and increased social isolation, which adversely impact their health. Therefore, information about structural racism and residential segregation within a historical context provides better insights about the social and physical environmental constrains rather than "*blaming the victim*" for their behaviors and health conditions [53, 54, 97].

#### **2.4 Socioeconomic status, its pathways, and embedment over the life course**

SES is a term describes the social standing and power in society, and it is often measured using indicators such as level of education, income, and occupation. Social status may also be determined by the level of power "*In the context of workplace, there are those who occupy positions of supervisory authority over subordinates versus those who take orders from above*" [84]. Lower education was associated with periodontitis with a pooled OR of 1.86 (95% CI: 1.66, 2.10) from 18 studies [98]. The association between periodontitis and SES is almost consistently positive in the literature when using level of education and income as indicators [60, 61, 88, 95, 99]. However, such approach can be limited without studying this association within a broader context that could explain the link between the SES indicators and periodontitis. It has been suggested in the literature that income mainly acts as a mediator for the association between education and disparities in health outcomes; thus, some researcher would elect to report

only one of these two indicators. Though, both education and income demonstrated independent association with periodontitis after adjustments in multivariate models [99]. The neighborhood SES also had an independent association with periodontitis after the adjustment for individual level SES, age, sex, marital status, ethnicity, smoking, and diabetes [100]. Low and medium neighborhood SES had an adjusted OR of 1.73 (95% CI: 1.29, 2.32) and 1.63 (95% CI: 1.23, 2.17), respectively, compared to high SES.

SES can be linked to disparities in health outcomes through interrelated pathways (**Figure 6**) where the association can be mediated by psychosocial exposures, material factors (resources), and health behaviors [9, 95, 99, 101]. In neo-material pathway, effect of education can be mediated by income, occupation's working conditions, related resources such as health insurance; consequently, it can improve housing, residential neighborhood, affordability of hygiene products, and access to health/ dental care. In psychosocial pathway, higher educational attainment can be associated with having broader social network, which can provide social support, enhancement of control beliefs, problem-solving, and coping skills; consequently, improve response to stressors. In behavioral pathway, education can increase the chance of being surrounded by well-educated people, change the social norms, and increase health literacy, which can improve health behaviors.

SES needs to be conceptualized as a dynamic approach over the life course; income and occupation could fluctuate (increase or decrease) over time while education either remains stable or increases. A dynamic approach for SES also implies reciprocities where increased SES could improve health and vice versa. Some relevant questions to be asked regarding life course approach include when is the sensitive period in development where SES could impact behaviors or can be biologically embedded?

#### **Figure 6.**

*Suggested pathways that could link socioeconomic status (SES) to periodontitis or other chronic systemic diseases over the life course.*

#### *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

What is the latency period between exposure to SES and having behavioral or biological impacts? Does the SES have accumulative impacts throughout life? Is the individual SES during adulthood or the parents' SES during childhood more relevant to periodontal health? Are childhood SES and adulthood SES correlated or independent? What is the impact of social mobility (transition to higher or lower SES)? It worth mentioning that in populations with rapid changes, social mobility needs to be assessed at smaller intervals over the life course rather than limiting the comparisons between childhood and adulthood.

Suggested models for dynamic approach for studying SES include [84]:


The importance of understanding the impact of SES on health and its related behaviors is to know when to intervene to achieve the best health outcomes. Based on a recent systematic review on seven longitudinal studies, early life SES had positive association with periodontitis [102]. However, the included studies had heterogeneous study designs and definitions of both SES and periodontitis; thus, made it difficult to arrive at a more specific conclusion. In one study, the parents' SES had no significant association with periodontal status in 15–16 years individuals; though, the parents' SES (income) was predictive for utilization of dental care [103]. In another study, early SES measured as parents' occupational status was associated with periodontitis in 26 years individuals, whereas the individual's SES in adulthood was not significant [104]. In contrast, the adult SES was more relevant to smoking and depression. The role of social mobility was also evaluated; highest periodontitis proportion was found in those with persistent low SES, followed by upward mobility group, then downward mobility group [104]. The lowest periodontitis proportion was found in those with persistent high SES. In another study that assessed the periodontal health at 15 years (baseline) up to 31 years, childhood SES was associated with periodontitis in adults, which was not mediated by adulthood SES or behaviors; RR was 1.85 (95% CI: 1.06, 3.24) [105]. So, studies that used the life course approach suggested that early SES during childhood can be more predictive of periodontitis rather than adulthood SES. These findings support the critical period model for impact of SES on periodontal health. However, the longest follow-up was up to 38 years, and the possible accumulative effect of SES cannot be excluded.

#### **2.5 Psychosocial exposures, their pathways, and interactions**

When negative life events occur, they undergo an appraisal process, if the stressors exceed the individual's coping ability, they can be perceived (appraised) as stressful [106, 107]. The physiological responses to stressors can be mediated by negative emotions including anxiety, depression, anger, or mixed emotions [107]. The "*allostatic load*" was a term introduced by McEwen to refer to wear and tear from chronic

over- or underactivity of protective body systems against stressors including the autonomic nervous system, hypothalamic–pituitary–adrenal (HPA) axis, metabolic, immune, and cardiovascular systems [108]. The perceived stress can be associated with health conditions (including periodontitis) through interrelated behavioral and pathophysiological pathways (**Figure 7**) [109, 110].

Different psychological exposures had an association with periodontitis [112–114]. In one study, psychosocial stress was not associated with periodontitis but had positive association with oral health behaviors (smoking and oral self-care) in 65–74 years women [115]. Among different daily strains, only financial strain was associated with higher CAL and bone loss after adjustment for age, sex, and smoking [113]. Intrinsic mechanisms that could regulate and the stresses include coping [116]. Inadequate coping (high emotion-focused and low problem-focused coping) was associated with higher CAL and bone loss regardless of the level of financial strain [113]. Problemfocused coping includes reappraisal of stressful events as challenging events and applying strategies that focus on solving the problems [116]. In contrast, emotionfocused coping includes applying strategies that deals with the emotions rather than the problem; it can include positive strategies such as regulations of emotions, meditation, spirituality, distracting oneself, and seeking support from social network. However, it can be also negative when denying the event, avoiding dealing with it, or adopting negative health behaviors such as unhealthy dietary habits, smoking, consuming alcohol, and drugs. Thus, emotion focused coping can be an inadequate coping strategy with stresses. Other behaviors related to inadequate coping include negligence of oral self-care and lack of sleep [111, 117, 118]. In contrast to coping, social network support and positive life events could buffer the impact of stressors through external pathways [106, 119]. Social support can be received (actual support) or perceived, which refers to the subjective beliefs about the availability of support; the perceived social support can be more effective in buffering the impact of stressors (**Figure 7**) [106].

When impact of social network was studied for association with periodontitis, marital status had no significant association with periodontitis prevalence or progression rate [61, 82, 114, 120]. However, having fewer friends and being

#### **Figure 7.**

*Illustration of psychosocial interactions. Stressors can have adverse health impacts after being perceived (appraised) as stressful [106]. Negative emotions could be mediators of perceived stress and their impact on health could occur through interrelated pathophysiological pathways and behavioral pathways [109–111]. The perceived social support may buffer the impact of psychological stresses either before or after perceiving the event as stressful [106].*

#### *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

widowed were associated with higher periodontitis extent [120]. In a prospective study on healthcare professional men, having at least one friend was associated with a lower risk of periodontitis; RR was 0.70 (95% CI: 0.51, 0.96) after adjustments for age, marital status, smoking, body mass index (BMI), alcohol consumption, and diabetes mellitus [114]. Furthermore, participation in religious meetings had a lower risk of periodontitis and the adjusted RR was 0.73 (95% CI: 0.64, 0.83). In a cross-sectional study by Zini *et al*., religiosity had protective association with periodontitis through spirituality (intrinsic pathway) and social support (extrinsic pathway) [121]. Other studies did not find an association between social support and periodontitis [60, 122].

Possible mechanisms of how social network positively impact health (**Figures 6** and **7**) is by buffering impact of stressors, shaping norms for health behaviors, sharing information can increase health literacy and awareness, helping in problem-solving, sharing funds and resources, and improving overall wellbeing [119, 123, 124]. In a recent systematic review, social support had positive association with oral health literacy, quality of life, and behaviors including utilization of dental care in immigrants and ethnic minorities [125]. It is important to keep in mind, however, that impact of psychosocial exposures can be either positive or negative [11]. For example, perceived stress manifested as anxiety can stimulate sympathetic nervous system and HPA axis; consequently, help people to meet certain deadlines and get the job done [107]. The allostatic load, up to a certain limit, can be within the body's reparative capabilities before it can be associated with pathological changes. Similarly, social network could have positive influence on behaviors (e.g., oral self-care), negative influence (e.g., smoking), enable certain behaviors (e.g., utilization of dental care), or constrain such behaviors [123]. Social network could also be a source of conflicts, stressors, or transmission of diseases. Thus, measurement of social network in terms of its size and range (structural indicators) alone can be deficient without considering specific functions [106, 119] or social norms [11]. Among different social support functions, emotional and informational support was the most responsive to buffer wide range of stressors [106, 119]. However, the overall research on mechanisms, pathways, and interactions of psychosocial exposures is still limited in periodontal literature.

#### **2.6 Oral health behaviors**

Health behaviors can be largely shaped by social environment including social adversity, social norms, social support, and socioeconomic status [3, 101, 113, 120, 123]. Health behaviors appear to cluster within individuals. For example, those who are physically active can also follow healthy dietary habits, regularly utilize dental/health care, regularly practice oral self-care, and vice versa. Unhealthy behaviors often aggregate in individuals with low SES [84]. In addition, behaviors such as smoking, negligence of oral self-care, and lack of utilization of dental care could be indicative of inadequate coping with social adversity [111, 117, 118].

Impacts of smoking on periodontium were well documented, and evidence was considered adequate to conclude that smoking is a cause of periodontitis by the office of surgeon general in 2004 [126]. The frequency and duration of smoking had a dose response association with periodontitis prevalence and progression [82, 127]. Smoking also had positive association with periodontitis in adolescents (15–19 years) with an adjusted OR of 1.6 (p-value: 0.017) after adjustments for demographics, plaque scores, and bleeding on probing [70]. Number of years since quitting of smoking also had a gradient reduction in susceptibility to periodontitis. Based on a systematic review on 14 prospective studies, periodontitis incidence in smokers had an RR of 1.85 (95% CI: 1.5, 2.2) [128]. Smokers also had poor periodontal treatment outcomes (non-surgical and surgical) compared to never smokers [129–131].

Despite that oral self-care had clear association with gingivitis [31, 80], its association with periodontitis was not consistent. Based on systematic review on 14 studies, tooth brushing had an OR of 1.44 (95% CI: 1.21, 1.71) [132]. Infrequent oral self-care and presence of calculus had positive association with periodontitis in young populations (14–29 years) [62, 69]. Good oral self-care had protective association with overall periodontal treatment need in Portuguese population [133]. Other studies did not confirm the association of oral self-care with periodontitis [82, 134]. It worth noting here that self-reported oral self-care can be subject to social desirability bias, that is, study participants could report daily brushing and use of interdental aids because they are socially desirable behaviors [11]. Therefore, measurements of full mouth plaque scores can be used to validate such self-reported measures.

Several models were proposed to conceptualize the utilization of health/dental services [135–140]. Access is a term refers to potential access to health service based on enabling resources while utilization is the actual use of service [136]. Barriers to utilize health services can be structural such as accessibility (transportation), availability of resources, and accommodation (availability of appointments); financial barriers include affordability; personal barriers include acceptability (including trust in dental care providers), psychosocial factors, and awareness [135, 138, 140]. Populations with no (or minimal) access to dental care had an overall higher periodontitis prevalence, extent, severity, and progression compared to estimates from general populations [11, 17, 18, 22, 35, 37, 38, 60, 65]. Frequency of dental visits had positive associations with periodontitis in adults [81, 82] and young population (15 to 21 years) [69].

#### **3. Periodontitis prevention: are we there yet?**

The ultimate goals of studying the etiology of diseases are to plan, implement, and evaluate interventions to combat disease burden [141]. Clinical interventions, mostly based on behavioral theories, had positive periodontal outcomes for smoking cessation, diabetes control, dietary habits modifications, weight control, and increased physical activity [142]. The study periods ranged from few weeks to 24 months. Despite the positive outcomes for changing behaviors by clinicians, such strategies can be potentially challenging, costly, time-consuming, and have temporary or limited effectiveness if not implemented as multilevel strategies [2, 3, 10]. Economic burden of periodontitis in 2018 was estimated to be ≥150 billion dollars in the United States and ≥ 150 billion euros in Europe [143]. However, up to most recent recommendations to prevent periodontitis were mostly confined to individual clinical care [142, 144–146]. A recent review also indicated that preventive strategies for periodontitis at population level are almost non-existent [51].

Among several approaches of defining periodontitis cases that evolved over history, current classification system by the AAP and European Federation of Periodontology (EFP) seemingly has resolved several longstanding issues [75, 147]. Periodontitis is mainly defined under single category rather than relying on age. Such approach may help overcoming issues of discontinuity in reporting findings for younger and older individuals to better understand the effect of age on periodontitis [11]. Periodontitis staging follows the clinical stages of natural course of disease, and its practical implications were explicitly outlined [75]. Stage I and II were classified

#### *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

separately, though, their practical implications were similarly confined to nonsurgical periodontal treatment. Stage III and IV mainly require surgical periodontal treatment and the latest additionally requires functional rehabilitations. The grading aims were to identify the progression rate, responsiveness to therapy, and possible impact on systemic health. The grading is assigned based on rate of progression and clinical phenotype then modified based on two risk factors: glycemic control and cigarette smoking. In contrast to staging, the practical implications of periodontitis grading were not explicitly suggested. Staging can be readily applied in populationbased studies while grading's application can be limited due to relying on radiographic examinations, could fluctuate over time, and limited to two risk factors (diabetes mellitus and smoking) [11]. However, other exposures could also have direct impact on patient care including barriers to utilize dental care (e.g., anxiety, lack of trust, lack of awareness, lack of perceived need for care) which may impede patients from seeking clinical care or complying with supportive periodontal therapy. In addition, the staging/grading framework is limited to the latest stages of the natural course of disease; therefore, its implications are confined to individual patient care.

While most of the periodontitis exposures can have practical implications for different stakeholders, recommendations based on too many exposures related to periodontitis alone can be exhaustive and impractical [11]. The common risk factor approach to integrate prevention of several chronic diseases (e.g., cardiovascular disease, diabetes mellitus, and obesity) has been suggested [50, 51]. This approach simultaneously targets risk factors/indicators of several chronic diseases such as tobacco consumption, unhealthy diet, sedentary lifestyle, lack of glycemic control, and psychological stress when planning population-based strategies. The common risk factor approach might also be more manageable at the population level rather than suggesting disease specific preventive approaches. Also, duplication of efforts in combatting diseases can be avoided [50]. This can be especially important when considering that periodontitis is not a life-threatening disease and may not be perceived as a priority by policymakers compared with other chronic diseases (e.g., cardiovascular diseases). It is important to consider, however, that common risk factor approach can achieve its benefits the most when applied as a multilevel strategy. When considering common risk factor approach in clinical care, there is a possible need for integrated dental and medical care. Dentists may routinely refer their patients for medical care, but more help is required from medical care providers to refer their patients to dentists once they are diagnosed with chronic medical conditions such as diabetes mellitus [11]. Patients may prioritize medical over dental care either due to having more serious consequences, dental anxiety, or limited dental insurance coverage [11, 60].

#### **3.1 Periodontitis prevention as a multilevel strategy**

A framework suggested by the author for applying periodontitis prevention at multilevel was outlined in **Table 1** [11]. Periodontitis diagnoses integrated early stages (susceptibility stages) of the natural course of disease with the AAP/EFP staging criteria [75]. The diagnostic criteria follow the assumption that staging is irreversible; once a diagnosis is assigned, it can only be upgraded [75]. The common risk factor was a recommended approach for all levels of prevention along the natural course of disease. The framework may also enhance knowledge translation where evidence from clinical/epidemiological research can be applied in clinical, population, and public health practice and vice versa.



*Underlying exposures include non-modifiable exposures including age, sex, and genetics or modifiable exposures such as the social determinants of health. Periodontitis risk factors/exposures include medical and behavioral exposures that could have more direct association with periodontitis. CAL: Clinical Attachment Loss, PPD: Periodontal Probing Depth, SES: Socioeconomic status.*

## **Table 1.**

*A multilevel prevention strategy for periodontitis with integrated use for individual clinical care and population/public health [11].*

## *Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

#### *3.1.1 Susceptibility stages*

In *stage of underlying exposures*, primordial prevention is applied to the population, and it aims to reduce development of disease specific risk factors including adopting unhealthy behaviors [11]. This level of prevention mainly benefits the population at an early stage in development, that is, during childhood and teenage [148, 149]. The strategies can be mainly applied by governments and policy makers to target the social determinants of health and take into consideration the nonmodifiable exposures. Examples of preventive strategies include imposing sin tax on tobacco- and added sugar containing products, increase safe public places for indoor or outdoor physical activities, and reduce barriers to access dental and health care such as facilitating health and dental insurance for low profile jobs. The latest can be accompanied by conditional strategies that enforce regular attendance to dental/ medical care.

In *stage 0*, primary level of prevention can be applied to individuals or population subgroups who developed periodontitis specific risk factors/indicators [11]. It aims to reduce periodontitis incidence and strategies can be mainly applied by public health practitioners. Examples include health awareness campaigns and use of behavioral theories to apply public health interventions for smoking cessation, glycemic control, modification of dietary habits, and weight loss.

#### *3.1.2 Periodontitis stages*

Periodontitis stages have similar diagnostic criteria proposed for periodontitis staging by the AAP/EFP [75]. Exposures of susceptibility stage still apply to periodontitis stages based on the current understanding that periodontitis develops in a susceptible host. The grading criteria were removed since their application may not be suitable for population-based studies due to the abovementioned limitations [11]. Periodontitis stages are mainly managed by clinicians following the secondary and tertiary levels of prevention. An additional strategy is to apply the common risk factor approach in clinical stages including the need for integrated dental and medical care. Medical professionals need to refer their patients once diagnosed with chronic systemic disease. Stage I and II were combined since they are managed similarly by non-surgical periodontal treatment. Diagnosis of stage I can be challenging when assessments are conducted by non-periodontists due to the use of low disease threshold. Population-based surveys commonly consider CAL ≥3 mm as minimum threshold to avoid misclassifying cases [92, 93, 150]. However, diagnosing periodontitis cases at lower thresholds allows early interventions, which can be particularly important in younger population [11].

#### **3.2 Additional considerations for the multilevel prevention framework**

Despite that gingivitis precedes periodontitis, it was not included in the framework because pristine gingival health may not exist even under optimal oral self-care [151–154]. Also, gingivitis can be reversible or self-limited. However, periodontitis staging is assigned with a purpose of being irreversible. Similarly, plaque per se is a universal finding even in individuals following stringent plaque control strategies [34, 155–157]. Plaque needs to be controlled in all members of the population. In addition, plaque is a reversible exposure, which makes it unsuitable for periodontitis staging.

*Periodontitis, Its Associations, and Prevention DOI: http://dx.doi.org/10.5772/intechopen.109015*

When applying multilevel preventive strategies, it is recommended to consider outlining a specific plan for each exposure at a time [2]. For example, strategies for combatting tobacco consumption at population level could include imposing sin tax, age restrictions, and increase smoke-free spaces [6]; for smokers population subgroup, smoking cessation interventions and awareness campaigns can be implemented; for periodontitis patients, smoking cessation strategies including referral to smoking cessation clinics can be applied.

#### **4. Concluding remarks**

Key messages that need to be emphasized include:


*Human Teeth – From Function to Esthetics*

#### **Author details**

Yasmine N. Alawaji1,2,3

1 Preventive Dental Science Department, College of Dentistry, King Saud bin Abdul-Aziz University for Health Sciences, Riyadh, Saudi Arabia

2 King Abdullah International Medical Research Center, Riyadh, Saudi Arabia

3 University of British Columbia, Vancouver, Canada

\*Address all correspondence to: alawajiy@alumni.ubc.ca

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Section 3
