• Diabetes mellitus
• Autoimmune disorders (Sjogren syndrome, lupus erythematosus, rheumatoid arthritis, pemphigus vulgaris, cicatricial pemphigoid)
• Cardiovascular disorders (risk for infective endocarditis, atherosclerotic cardiovascular disease and screen for periodontitis and periapical infections)
• Coagulation disorders
• Eating disorders (anorexia nervosa, bulimia)
• Malnutrition and obesity
• End stage renal disease
• Greater than 10% unexplained weight changes in the past 6 months
• Inflammatory bowel diseases
• Neurodegenerative disorders affecting physical ability
• Systemic immunosuppressive therapy (organ transplant, primary immunologic disorders)
• Osteoporosis
• Pathologic immunosuppression (HIV, AIDS, malignancy)
• Pregnancy (for periodontal disease assessment and care)
• In vitro fertilization
• Likely to undergo mechanic ventilation (aspiration pneumonia)
• Tobacco use
• Dysphagia
• Orofacial pain
• Oral or pharyngeal cancer (pre-, intra-, and post-therapy)
• Chronic or recurrent oral mucosal lesions
• Poor oral hygiene (plaque and calculus)
• Gingivitis and periodontitis (inflamed gingival tissues)
• High caries risk (three or more carious lesions in the past 12 months)
• Xerostomia
• Taste alterations
• Halitosis

Periodontal Disease

Gingivitis and periodontitis (“periodontal disease”) are complex multifactorial inflammatory diseases caused by microorganisms in the biofilm (dental plaque) and the host response that effect the supporting tissues surrounding the teeth. In gingivitis, inflammation is limited to the gingiva, and the condition is characterized by the absence of attachment loss and is reversible by practicing good oral hygiene. Clinical signs of gingivitis include erythema, edema of the gingiva, changes in contour, consistency, texture, and bleeding on provocation. In periodontitis, the inflammation extends into the tissues affecting the attachment apparatus of the tooth and is a major cause of tooth loss in adults. Gingivitis and moderate periodontitis are rather common, and prevalence increases with age. Moderate periodontitis is estimated to affect 40–50% of adults and approximately 10% of the adult population of western countries suffers from severe forms of periodontitis [8]. Similar figures for the prevalence of severe periodontitis were reported in a Swedish study, although recently more individuals have a healthy periodontium as compared to reports in the early 1970s [9].
Although microorganisms, particularly Gram negative facultative or strictly anaerobe bacteria are needed for initiation, maintenance, and progression of periodontal diseases, the immune/inflammatory response of the host to the microbiological challenge is a critical element in determining the expression of periodontal disease. The genetic make-up of the host has a major influence on this response. An important corollary is that any systemic condition that is able to modulate the fine balance between the microbial composition of the dental plaque and the host response to this challenge can constitute a risk factor for periodontal diseases. Responses include vascular changes and involvement of various inflammatory and immune cells, which are coordinated by proinflammatory mediators including interleukin IL-1, IL-6, and tumor necrosis factor (TNF)-α, and anti-inflammatory mediators including IL-10. Eventually, the effectors of periodontal inflammation and destruction such as proteinases and osteoclasts are activated. Additionally, environmental factors including lifestyle factors such as nutrition and diet contribute to the development and progression of periodontal diseases. Some of the most frequent conditions and environment factors identified as modifying the expression of periodontal diseases are diabetes mellitus, immunosuppression, hormonal changes, smoking, stress, and dietary factors. Discussion of systemic diseases and conditions in relation to periodontal disease in this chapter is limited to cardiovascular disease; Chapter 11 addresses diabetes and periodontal disease in greater depth; Chapter 8 on nutrition and inflammation also addresses periodontal disease.

Periodontal Disease and Alterations in Sex Hormones

Hormonal shifts occurring during puberty, the menstrual cycle, and pregnancy are proposed as one of the mechanisms responsible for increased expression of gingivitis during these physiological states [10]. Studies suggest that the prevalence, severity, and extent of gingivitis increase in adolescents reach a peak around the age of 12–14 years and decrease thereafter, with significantly lower values by the age of 16–17 years [11]. The increase in the severity and extent of gingivitis appear to parallel sexual maturation rather than plaque index, suggests an enhanced response of gingival tissues to the presence of dental plaque and supporting the role of puberty in the pathogenesis of gingivitis [12]. During puberty, the hormonal changes vary between girls and boys. In girls, there is a significant increase in estrogen and progesterone; in boys, testosterone reaches significantly higher values. The main mechanisms by which sex hormones affect periodontal tissues include host-related alterations such as angiogenesis and increased vasodilation, decreased epithelial keratinization, reduction in neutrophil chemotaxis, and changes in T cells and signal transduction molecules [13].
Changes in gingival appearance may also occur throughout the menstrual cycle. The menstrual cycle is associated with surges in progesterone and estrogen, although less dramatic than those seen in pregnancy. Gingival changes may manifest as increases in gingival crevicular fluid [14]. It appears that this increase occurs particularly during ovulation and pre-menstruation. A 2012 study concluded that while ovarian hormones have a negligible effect on a clinically healthy periodontium, these hormones may exaggerate pre-existing inflammation in gingival tissues [15].
More pronounced gingival inflammation has also been observed with the use of oral contraceptives. However, most studies on birth control pills were performed when the medication contained much higher levels of hormones compared to the medications in use today. A literature review concluded that current oral contraceptives no longer place users at increased risk for gingivitis or periodontitis [16].
In vitro fertilization in which women are treated with high levels of female sex hormones may increase the severity of gingivitis and pre-existent periodontitis [17]. In addition, it has been speculated that sex hormones administered for gender transformation may affect the periodontium.
During pregnancy, there is a significant increase in gonadotropins in the first trimester and in progesterone and estrogens in the second and third trimesters. It is well documented that pregnancy is associated with an increase in the prevalence and the severity of gingivitis which is reported in between 30 and 100% [18, 19]. During pregnancy, gingivitis increases in severity as early as the second month of pregnancy, increases further as the pregnancy advances, reaches a maximum around months 7 and 8, decreases in month 9, and returns to pre-pregnancy values in the postpartum period. The clinical signs of pregnancy gingivitis include increased gingival redness, bleeding, and swelling [18, 20]. These changes are independent of the amount of plaque present [21], but studies suggest that the bacterial composition of dental plaque shifts during pregnancy. A significant increase in the proportion of anaerobic bacteria has been reported, particularly of Prevotella intermedia which may be associated with the ability of these bacteria to use progesterone as a growth factor [22, 23]. In addition to direct effects of sex hormones on the gingival vascularization, shifts in immunological responses may be involved in the pathobiology of pregnancy gingivitis [24, 25]. Periodontitis may exacerbate during pregnancy, particularly in multiparous women [26]. Occasionally, pregnant women develop a “pregnancy epulis” or tumor of granulation tissue. This benign tumor often bleeds easily and can appear red and inflamed. In general, a pregnancy epulis is not painful and does not have the potential to become malignant. Usually it will become smaller and resolve after childbirth, but in some cases surgical excision is required.
Maternal periodontitis has a potential to influence the health of the fetalmaternal unit and has been associated with adverse pregnancy outcomes, including low birth weight, pre-term birth, growth restriction, pre-eclampsia, miscarriage, and stillbirth [27]. However, the strength of the observed associations is modest and seems to vary according to the population studied and with the definitions of periodontal disease. Maternal periodontitis represents a potential source of microorganisms that are known to routinely enter the circulation, and directly or indirectly may influence the health of the fetalmaternal unit [28]. Periodontal pathogens or their byproducts may reach the placenta and spread to the fetal circulation and amniotic fluid. Their presence can stimulate fetal immune and inflammatory responses characterized by the production of antibodies against the pathogens and the secretion of elevated levels of inflammatory mediators, which may cause miscarriage or premature birth [29]. Moreover, systemic infection and inflammation may cause structural placental changes leading to pre-eclampsia and impaired nutrient transport causing low birth weight. Finally, the systemic inflammatory induced response due to periodontitis may exacerbate local inflammatory responses at the fetoplacental unit and further increase the risk for adverse pregnancy outcomes.
Periodontal therapy has been shown to be safe and leads to improved periodontal conditions in pregnant women. However, periodontal therapy, with or without systemic antibiotics, does not reduce overall rates of pre-term birth and low birth weight [30, 31]. Future research should focus on various treatment strategies as well as timing and intensity of treatment. Nevertheless, as an important component of prenatal care, oral health and periodontal health, should be maintained or re-established in pregnant women, with specific attention to reduction of the periodontal microbial infection and related inflammatory responses.

Periodontal Disease and Atheriosclerotic Cardiovascular Diseases

Cardiovascular disease (CVD) encompasses several pathological conditions involving the heart and vascular system including coronary heart diseases, hypertension, cerebrovascular diseases, and peripheral vascular diseases. The most common pathologic basis for these diseases is atherosclerosis, which is a pathological condition affecting the mid- and large-sized arteries. Its lesions are characterized by accumulation of lipids and fibrous elements formed within the intimal layer of the vessels. Inflammation has emerged as an integrative factor for atherosclerosis and can operate in all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis [32]. The major risk factors for atheroscleroslerotic cardiovascular disease (ACVD) include dyslipidemia, hypertension, obesity, smoking, physical inactivity, poor diet, and diabetes. Obesity alone is associated with mortality as well as being a risk factor for diabetes, metabolic syndrome, ACVD, coronary heart disease, and stroke. Along with the growth in prevalence of obesity, the prevalence of diabetes, both diagnosed and undiagnosed, and prediabetes have also increased in adults and children. Similarly, the prevalence of metabolic syndrome has also increased. Combined, the prevalence of all these risk factors, in the end, increases risk for ACVD [33].
Both mechanistic and clinical studies have been published examining the possible role(s) of periodontal disease in the pathogenesis of CVDs and associations between the two diseases [34]. The first study that found positive epidemiological evidence for an association between periodontitis and ACVD was reported in 1989 [35]. Thereafter, remarkable pathological and epidemiological associations between these two diseases have been presented [36]. Bahekar and coworkers performed a systematic review on the association between periodontitis and ACVD revealing five prospective cohort studies, five case-control studies and five cross-sectional studies. Meta-analysis of the cohort studies (86,092 patients) indicated that individuals with periodontitis had a 1.14 times higher risk than the controls (relative risk 1.14, 95% CI 1.074–1.213, P < 0.001). The case-control studies (1,423 patients) showed an even greater risk (OR 2.22, 95% CI 1.59–3.117, P < 0.001). The prevalence of CVD in the cross-sectional studies (17,724 patients) was significantly greater among individuals with periodontitis than in those without periodontitis (OR 1.59, 95% CI 1.329–1.907, P < 0.001) [37]. The studies were adjusted for confounding factors shared by periodontitis and CVD which include increasing age, male sex, race and ethnicity, education and socioeconomic status, stress, smoking, alcohol abuse, diabetes mellitus, physical inactivity, and overweight [38, 39].
Although a causal relationship is debated and presently not demonstrated [34], the recent joint workshop of the European Federation of Periodontology (EFP) and the American Academy of Periodontology (AAP) reported that there is consistent epidemiologic evidence that periodontitis increases the risk for future ACVD [40]. However, epidemiological evidence does not address causality or the mechanistic nature of the associations.
Several pathophysiological pathways have been suggested to explain the association between periodontitis and atherosclerosis. Periodontitis is associated with increased systemic levels of IL-1, IL-6, IL-8, TNF-α, C-reactive protein (CRP), fibrinogen, and other acute phase reactants [41]. CRP and other inflammatory reactants promote systemic inflammation and are associated with atherosclerosis. Endothelial cells stimulated by these inflammatory reactants increase their expression of various leukocyte adhesion molecules. Once adherent to the activated endothelial layer, the monocyte penetrates into the inner layer of arteries and initiates an atherosclerotic lesion. Subsequently, monocytes become macrophages undergoing a series of changes that ultimately lead to foam cell formation. These foam cells contain large amounts of a fatty substance, usually cholesterol and characterize the early atherosclerotic lesion. Macrophages within atherosclerotic plaques also secrete a number of growth factors and cytokines involved in lesion progression [42]. In addition, recent evidence suggests that periodontitis is associated with increased platelet activation [43]. Periodontal bacteria may induce activation of endothelial cells and platelets, which contributes to a procoagulant state and constitutes a risk for atherothrombosis. In addition, bacteremia originating from the mouth is a common event that occurs not only with invasive dental treatment, but also from activities of daily living including chewing and tooth brushing, especially in patients suffering from gingivitis and periodontitis [44]. Periodontal pathogens (i.e., Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Treponema denticola, and Eikenella corrodens) enter the circulation via the gingival sulcus. These periodontal pathogens adhere to and invade the vascular endothelial cells. Infection of these endothelial cells by the periodontal pathogens induces a procoagulant response that might contribute to formation of an atherosclerotic plaque. Moreover, periodontal pathogens have been found in atherosclerotic plaques [45].
Mechanisms described above may act in concert to increase systemic inflammation associated with periodontal disease and to promote or exacerbate atherogenesis. However, proof that the increase in systemic inflammation attributable to periodontitis impacts inflammatory responses during atheroma development, thrombotic events, or myocardial infarction or stroke is presently lacking [46].
With respect to interventions, there is moderate evidence that periodontal treatment reduces systemic inflammation as evidenced by reduction of CRP and improvement of both clinical and surrogate measures of endothelial function. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure, and subclinical atherosclerosis after periodontal therapy. Nevertheless, there is no effect on serum lipid profiles [47].
Continued research is necessary to determine what factors in individuals with periodontal disease additionally predict risk for ACVD as well as alternate explanations for the observed epidemiological associations [48]. Future studies should explore common genetic susceptibility factors present in both diseases leading to increased inflammatory responses, as well as other shared risk factors for periodontal and cardiovascular diseases. Additional prospective, case-controlled studies are needed to clearly demonstrate that proposed associations are real and independent of common risk factors and intervention trials on the impact of periodontal treatment on prevention of ACVD are needed.
Although evidence for a causal relationship is lacking, practitioners should be aware of the emerging and strengthening evidence that there are strong associations between periodontitis and ACVD. In the light of these associations, patients with either disease should be screened for the other one. Based on the evidence presently available, individuals with periodontitis and other risk factors for atherosclerosis, such as hypertension, diabetes mellitus, overweight and obesity, smoking, etc., who have not seen a physician within the last year, should be referred to their primary care provider for evaluation of systemic health including ACVD. Early diagnosis of ACVD, coupled with secondary prevention strategies such as lifestyle changes, has been shown to have a favorable effect on the course of the disease. In addition, individuals with CVD and periodontitis should be referred to an oral healthcare professional for treatment of their periodontal disease [40].


Caries is one of the most common chronic infectious diseases in the world [49, 50]. Dental caries is an infectious microbial disease that results in dissolution and destruction of calcified tooth structure. Host (bacteria, saliva) and environmental (intake of fermentable carbohydrates in foods and fluids, oral hygiene, other dietary factors) influence the demineralization and remineralization processes occurring on tooth surfaces [51, 52]. The current incidence and prevalence data for caries is limited; the most recent as of 2013 are data from 1999–2004 [50]. For 2–11-year-old children, the prevalence of caries in the permanent dentition for 1999–2004 was 21  and 42% in the primary dentition of this age group. For adults during this same time period, the incidence is approximately 90% for coronal caries and 14% for root caries [50]. Up to 80% of the caries observed in children are only in about 25% of the children; this cohort represents children with primarily socioeconomic risk factors for disease. In particular, there is increased risk for root caries in these older individuals who have experienced varying degrees of gingival recession because of periodontal disease [53, 54]. Although fluoridation has had the single largest impact on the incidence of caries followed by dental sealants, improved oral hygiene, diet, education, and overall health have also played major roles [50, 55].
While the most common risk factors for caries are poor oral hygiene, diet (frequency of carbohydrate intake), low income, low education, and lack of community fluoridation, any systemic or local disease or medical therapy that results in salivary hypofunction may dramatically increase the risk for and incidence and progression of dental caries [56, 57]. Impaired salivary gland neurosecretory action caused by pharmacologic blockade is a common side effect of many medication classes (particularly antihypertensive, antihistaminic, antianxiety, and antidepressant medications), and any person with three or more carious lesions in one area who is taking a new medication should be evaluated for possible drug side effects [58] (see Chapter 6 on Medications). Several autoimmune disorders (e.g., Sjogren syndrome) can result in salivary gland damage, hyposalivation, leading to increased caries incidence (see Chapter 14 on Autoimmune disorders). Radiation therapy for the treatment of malignancy in the head and neck, when the major salivary glands are included in the treatment field, can result in profound hyposalivation leading to rampant dental demineralization and dental breakdown [59] (see Chapter 13 on Management of Cancer Therapies). Chemotherapy for cancer may also result in hyposalivation, which may recover with time from treatment and is typically less profound than that of other etiologies listed above.
Apical periodontitis, subsequent to the presence or restoration of deep lesions or fractured teeth, may result in inflammatory processes in the periodontal tissues that are initiated and maintained by an endodontic source of irritants [60]. Acute apical periodontitis is characterized by vascular dilatation, an exudate of neutrophil leucocytes, and edema in the apical periodontal ligament. Clinically, symptoms such as pain, tenderness, and swelling may be present [61]. Although these lesions most often confined to the oral region, they may extend to both nearby and distant body compartments along the anatomical pathways. Hence, an acute periapical abscess may spread and reach the brain, the cavernous sinus, the eye, or the mediastinum. [62].
Chronic apical periodontitis is characterized by an inflammatory cell infiltrate rich in lymphocytes, plasma cells, macrophages, and granulation tissue. Most teeth with chronic apical periodontitis are asymptomatic. They are revealed most often by routine radiographic examination. It must be realized that the tissue reaction to irritation is a dynamic response, often fluctuating between acute and chronic inflammation. In root infections, bacteria are present not only in planktonic cells but also in biofilms, which are more resistant to host defense mechanisms and disinfectants.
It is well documented that bacteremia with oral bacteria, particularly streptococci, may lead to endocarditis [63]. In addition, in compromised hosts with cancer, unregulated diabetes, or immunodeficiency bacteria may multiply in the blood, resulting in potentially life-threatening bacteremia. In an epidemiologic study during a maximum follow-up of 32 years with 708 male adults, lesions of endodontic origin among those younger than 40 years old were statistically significantly associated with risk of ACVD after controlling for known risk factors [64], but as compared to periodontitis few studies are directed to a potential link between endodontic infection and inflammation and systemic diseases.
Guidelines for caries risk assessment (CRA) in both pediatrics and adults [51, 52, 65] are available. Risk assessment approaches look at the frequency of consumption of fermentable carbohydrates (including sucrose, glucose, fructose, and cooked starches) not the total volume [51]. Any patient with three or more carious lesions in the past 2 months is considered at high risk for future caries and should be evaluated for underlying causes (diet, hygiene, hyposalivation, and medications). Despite the continually high consumption of sugars and other sugar-based products, the widespread availability of fluoridated tap water and its use in other fluids has dampened the impact of dietary sugars consumption on the incidence of caries. The American Academy of Pediatric Dentistry [65] CRA addresses several factors relative to diet for children up until the age of 5 years and under including intake of more than three sugar-containing snacks or beverages between meals and going to bed with a bottle that contains sugared beverages. Featherstone’s CRA includes between meal food/beverage snacks containing fermentable carbohydrates more than three times a day. Caries prevention strategies include attention to dental mineralization (fluoride, calcium, and phosphate supply), assessing levels of cariogenic flora, and diet intervention addressing healthy eating patterns and what the patient/client consumes between meal and bedtime with regard to fermentable carbohydrates [51, 52, 65]. Xylitol containing gums and mints have been promoted as anti-cariogenic measures [51, 65, 66]. Xylitol is a five-carbon sugar alcohol seen in the USA as one of several sweeteners used in some gums and mints, however its use is limited due to cost. When consumed in solution, xylitol does not cause a drop in plaque pH since oral bacteria do not metabolize it to organic acids. Xylitol also has an antimicrobial effect and can reduce mutans streptococci counts in plaque [67]. The American Academy of Pediatric Dentistry Caries Management Protocol for children aged 6 years and older recommends postprandial xylitol as gum or mints for those at high risk of caries [65].

Oral Mucosal Disease

Painful oral mucosal lesions can result in several local, systemic, and nutrition-related problems: impaired oral intake because of pain, damaged epithelial integrity as a portal for infection, altered taste, and a variety of complications related to treatment of the mucosal disorder may affect oral function). Representative oral mucosal disorders include local (oral cancer, aphthous stomatitis, reactive or traumatic lesions, recurrent [herpetic] viral lesions, candidiasis) and systemic disorders with oral manifestations (immune mediated, inflammatory conditions e.g., lichen planus, pemphigus vulgaris, mucous membrane pemphigoid, lupus erythematosus, Graft-versus-host disease). Oral mucositis due to cancer therapy has a significant impact on quality of life, is associated with significant pain, and affects oral function, including oral intake. This section addresses cancer therapy induced oral mucositis. Chapter 13 addresses diet and nutrition management strategies for individuals with head and neck cancers in-depth.

Cancer Therapy Induced Oral Mucositis

Oral mucositis is defined as inflammation of oral mucosa commonly resulting from cancer therapy typically manifesting as erythema, ulceration, and pain. The condition may be exacerbated by local factors, such as microbial colonization or trauma from teeth. Trauma to the oral mucosal tissues may also result from eating or drinking hard or abrasive foods or hot liquids. The term stomatitis refers to any inflammatory condition of oral tissue, including mucosa, dentition/periapices, and periodontium. Stomatitis thus defines a broader range of pathoses of oral tissues, including mucositis. A number of instruments to evaluate the observable, subjective, and functional dimensions of oral mucositis are available, which may be used to facilitate patient care and in clinical trial research [68]. In addition, patient-reported outcomes of mouth and throat soreness have been developed [69

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