Chapter 46: Oral Health

Although the nation’s oral health is believed to be the best it has ever been, oral diseases remain common in the United States. In May 2000, the first report on oral health from the US Surgeon General, Oral Health in America: A Report of the Surgeon General, called attention to a largely overlooked epidemic of oral diseases that is disproportionately shared by Americans: This epidemic strikes in particular the poor, young, and elderly. The report stated that although there are safe and effective measures for preventing oral diseases, these measures are underused. The report called for improved education about oral health, for a renewed understanding of the relationship between oral health and overall health, and for an interdisciplinary approach to oral health that would involve primary care providers.

In utero, the 20 primary teeth evolve from the expansion and development of ectodermal and mesodermal tissue at approximately 6 weeks of gestation. The ectoderm forms the dental enamel, and the mesoderm forms the pulp and dentin. As the tooth bud evolves, each unit develops a dental lamina that is responsible for the development of the future permanent tooth. The adult dentition is composed of 32 permanent teeth. Figure 46-1 shows the anatomy of the tooth and supporting structures. Table 46-1 outlines the eruption pattern of the teeth.

General Considerations

Dental caries (tooth decay) is the single most common chronic childhood disease, 5 times more common than asthma and 7 times more common than hayfever among children aged 5–7 years. Minority and low-income children are disproportionately affected. According to the Centers for Disease Control and Prevention (CDC), among children aged 2–4 years and 6–8 years, tooth decay is more prevalent in Mexican American, and African American, non-Hispanic communities. Among adults aged 35–44 years in those same communities, untreated tooth decay is 2 times more prevalent than among white non-Hispanics. In addition, one-third of persons of all ages have untreated tooth decay, 8% of adults aged >20 years have lost at least one permanent tooth to dental caries, and many older adults suffer from root caries.

Pathogenesis

Dental caries is a multifactorial, infectious, communicable disease caused by the demineralization of tooth enamel in the presence of a sugar substrate and of acid-forming cariogenic bacteria that are found in the soft gelatinous biofilm plaque (Figure 46-2). Thus, the development of caries requires a susceptible host, an appropriate substrate (sucrose), and the cariogenic bacteria found in plaque. Streptococcus mutans [also known as mutans streptococci (MS)] is considered to be the primary strain causing decay. Additionally, when plaque is not regularly removed, it may calcify to form calculus (tartar) and cause destructive gum disease.

Finally, the development of caries is a dynamic process that involves an imbalance between demineralization and remineralization of enamel. When such an imbalance is caused by environmental factors such as low pH or inadequate formation of saliva, dissolution of enamel occurs and caries result.

Clinical Findings

A. Symptoms and Signs

When enamel is repeatedly exposed to the acid formed by the fermentation of sugars in plaque, demineralized areas develop on the tooth surfaces, between teeth, and on pits and fissures. These areas are painless and appear clinically as opaque or brown spots (Figures 46-3,46-4, and 46-5). If infection is allowed to progress, a cavity forms that can spread to and through the dentin (the component of the tooth located below the enamel) and to the pulp (composed of nerves and blood vessels; an infection of the pulp is called pulpitis), causing pain, necrosis, and, perhaps, an abscess.

B. Diagnosis

Carious lesions progress at various rates and occur at many different locations on the tooth, including the sites of previous restorations. Demineralized lesions (white or brown spots) generally occur at the margins of the gingiva and can be detected visually; they may not be seen on radiographs. Advanced carious lesions such as those spread through dentin can be detected clinically or, if they occur between the teeth, by radiographs. Root caries, commonly seen in older adults, occur in areas from which the gingiva has receded.

Dental professionals use a dental explorer to detect early caries in the grooves and fissures of posterior teeth. To diagnose secondary caries (caries formed at the site of restorations), dental professionals use digitally acquired and postprocessed images.

Risk Assessment

Caries can develop at any time after tooth eruption. Early teeth are principally susceptible to caries caused by the transmission of MS from the mouth of the caregiver to the mouth of the infant or toddler. This type of caries is called early childhood caries (ECC) or baby bottle tooth decay (BBTD). According to the American Academy of Pediatric Dentistry, ECC “is defined as ‘the presence of one or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces’ in any primary tooth in a child 71 months of age or younger.” In children aged <3 years, any sign of smooth-surface caries is called severe early childhood caries (S-ECC). Children with a history of ECC or S-ECC are at a much higher risk of subsequent caries in primary and permanent teeth. (Guidelines on caries risk assessment and management may be found on the American Academy of Pedicatric Denistry website: http://www.aapd.org/media/Policies_Guidelines/G_CariesRiskAssessment.pdf).

Early childhood caries contribute to other health problems, including chronic pain, poor nutritional practices, and low self-esteem, which may lead to lack of self-esteem among older children and a great reduction in their ability to succeed in life.

The risk factors for adult caries are similar to those for childhood caries.

Differential Diagnosis

Developmental defects or pits in the tooth surface or visible groove is the differential diagnosis.

Prevention & Treatment

Fluoride, the ionic form of the element fluorine, is widely accepted as a safe and effective practice for the primary prevention of dental caries. Fluoride slows or reverses the progression of existing tooth decay by (1) being incorporated into the enamel before tooth eruption, (2) inhibiting demineralization, (3) enhancing remineralization, and (4) inhibiting bacterial activity in plaque. Unfortunately, only 73.9% of the US population has access to community water fluoridation, according to the CDC census in 2010. Systemic fluoride supplements (tablets, drops, lozenges) are recommended for children aged <6 months who are at high risk of the development of caries; for infants with ECC; for children aged 6 months to 16 years who live in nonfluoridated water areas; and for adults whose water is not fluoridated or who have diseases that produce a decrease in salivary flow, receding gums, or mental or physical disabilities. A supplemental fluoride dosage schedule is shown in Table 46-2. Topical fluoride supplements such as gels and varnishes are highly concentrated fluoride products that are professionally applied by a dental health provider or a parent (for gels). Varnishes, which are less toxic than gels and more effective than mouth rinses, are applied 3 times a week, once a year by disposable brushes, cotton-tipped applicators, or cotton pellets. (To learn more about fluoride varnish application visit the Smiles for Life website, www.smilesforlifeoralhealth.org).

Before prescribing supplemental fluoride, the primary care provider must determine the fluoride concentration in the child’s primary source of drinking water. Other sources of fluoride include well water exposed to fluorite minerals, certain fruits and vegetables grown in soil irrigated with fluoridated water, beverages, and foods such as meats or poultry that may contain 6–7% of total dietary fluoride. Although fluoride supplementation is not recommended for persons who live in communities whose water is optimally fluoridated (0.7–1.2 ppm or >0.6 mg/L), the bottled water used by many families may contain low levels of fluoride. Parents and caregivers should be educated about the benefits of fluoride and the possible side effects of too much fluoride, a condition called fluorosis. Fluorosis results when too much fluoride is obtained from any source when the permanent tooth is forming (Figure 46-6). Overall, 22% of children and adolescents aged 6–19 years have very mild or greater fluorosis. The benefits and side effects of fluoride use should be weighed against the risk of tooth decay among children at high risk of caries.

A second method of preventing dental caries is proper oral hygiene. Before the teeth erupt, a parent may use a washcloth or cotton gauze to clean an infant’s mouth and to transition the child to toothbrushing. Parents should supervise brushing and should discourage children aged <6 years from using fluoridated dentifrices because of the risk that toothpaste may be swallowed during brushing. A pea-sized amount of toothpaste is recommended for brushing. Generally speaking, children aged <2 years should avoid fluoride toothpaste.

Dental sealants, first introduced in the 1960s, are plastic films that coat the chewing surfaces of primary or permanent teeth. Sealants prevent decay from developing in the pits and fissures of teeth. Dental professionals often use sealants in combination with topical fluorides (Figure 46-7).

Older children and adults should avoid frequent consumption of drinks and snack foods containing sugars. Chewing sugar-free gum or cheese after meals has a saliva buffer effect that may counter plaque acids. Xylitol has been proposed as preventing caries, however, its recommendation lacks consistent evidence.

General Considerations

Periodontal disease is the most common oral disease in adults affecting one of every two adults aged >30 years, according to the CDC. Three forms exist: gingivitis, chronic periodontitis, and aggressive periodontitis. It is uncommon among young children, affecting <1%; however in some studies, ≤25% of Hispanic children aged 12–17 years were affected. Like dental caries, periodontal diseases are caused by bacteria in dental plaque that create an inflammatory response in gingival tissues (gingivitis) or in the soft tissue and bone supporting the teeth (periodontitis). Risk factors that contribute to the development of periodontal disease include poor oral hygiene, environmental factors such as crowded teeth and mouth breathing, steroid hormones, smoking, comorbid conditions such as weakened immune status or diabetes, and low income.

Severe gum disease is defined as a 6-mm loss of attachment of the tooth to the adjacent gum tissue. Severe gum disease affects approximately 14% of adults aged 45–54 years and 23% of those aged 65–74 years. Approximately 25% of adults aged ≥65 years no longer have any natural teeth. The severity of periodontal disease does not increase with age. Rather, the disease is believed to occur in random bursts after periods of quiescence.

Pathogenesis

A. Gingivitis

Gingivitis is caused by a reversible inflammatory process that occurs as the result of prolonged exposure of the gingival tissues to plaque. Gingivitis may develop as a result of steroid hormones, which encourage the growth of certain bacteria in plaque during puberty and pregnancy and in women taking oral contraceptive pills.

No special tests are needed to diagnose gingivitis; rather, the disease is diagnosed by clinical assessment. Simple or marginal gingivitis may be painless and is treated by good oral hygiene practices such as toothbrushing and flossing. This type of gingivitis occurs in 50% of the population aged ≥4 years. The inflammation worsens as mineralized plaque forms calculus (tartar) at and below the gum surface (sulcus). Gingivitis may persist for months or years without progressing to periodontitis; this fact suggests that host susceptibility plays an important role in the development of periodontitis. Additionally, gingivitis (Figure 46-8) can be either acute or chronic. A severe form, acute necrotizing ulcerative gingivitis (ANUG), also known as Vincent disease or “trench mouth,” is associated with anaerobic fusiform bacteria and spirochetes. ANUG (Figure 46-9) is painful, ulcerative, and edematous and produces halitosis and bleeding gingival tissue. Predisposing factors include conditions that contribute to a weakened immune status, such as HIV infection, smoking, malnutrition, viral infections, and, possibly, stress. Chronic gingivitis affects >90% of the population and results in gingival enlargement or hyperplasia that resolves when adequate plaque control is instituted. Generalized gingival enlargement or swelling (gingiva hyperplasia) may be caused by drugs such as calcium channel blockers, phenytoin, and cyclosporin (Figure 46-10); by pregnancy; or by systemic diseases such as leukemia, sarcoidosis, and Crohn’s disease.

B. Periodontitis

Chronic periodontitis (CP) is caused by chronic inflammation of gingival soft tissue and supporting structures by plaque microorganisms, specifically gram-negative bacteria that affect gingival soft tissues and supporting structures, with resultant loss of periodontal attachment and bony destruction. CP is common in adults, affecting >50% of the population. Adult-onset periodontitis begins in adolescence and is reversible if treated in its early stages, when minimal pockets (gaps) have formed between the tooth and the periodontal attachment. Severe periodontitis is characterized by a 6-mm loss of tooth attachment as detected by the dental health professional by means of dental probes.

If periodontitis is found in children or young adults or if it progresses rapidly, the primary care provider should be alert to the possibility of a systemic cause such as diabetes mellitus, Down syndrome, hypophosphatasia, neutropenia, leukemia, leukocyte adhesion deficiency, or histiocytosis. A less common, rapidly progressing form of adult periodontitis begins in the third or fourth decade of life and is associated with severe gingivitis and rapid bone loss. Several systemic diseases, including diabetes, HIV infection, Down syndrome, and Papillon-Lefèvre syndrome, have been associated with this rare form of periodontitis. Localized juvenile periodontitis (LJP) and localized prepubertal periodontitis (LPP) are forms of early onset periodontitis seen in young children and teenagers, respectively, without the evidence of systemic disease. LJP is more common among African American children. It affects the first molars and incisors, with rapid destruction of bone. Although there is some evidence for autosomal transmission, it is likely heterogenous. Both LJP and LPP are believed to be the result of a bacterial infection (specifically implicated is Actinobacillus actinomycetemcomitans) and, possibly, host immunologic deficits.

Clinical Findings

A. Symptoms and Signs

Clinical signs of gingivitis and periodontitis include interdental papillae edema, erythema, and bleeding on contact during tooth brushing or dental probing (Figure 46-11). The amount of gingival inflammation and bleeding and the probing depth of gingival pockets determine the severity of periodontal disease. Tartar, gum recession, and loose teeth are characteristics of severe periodontal disease. For children aged <4 years, loss of primary teeth may be the first clinical sign of periodontal disease and the systemic manifestation of hypophosphatasia. Dental probing by the dental health professional will detect sulcus depth.

B. Imaging Studies

Bone loss can be detected by radiographs and bone density scans.

Periodontal Health & Systemic Disease

Emerging evidence, particularly from the dental literature, suggests that periodontal disease may be a risk factor for systemic conditions such as cardiovascular disease, diabetes mellitus, and adverse pregnancy outcomes of preterm labor and low birth weight. Current evidence supports a bidirectional relationship between diabetes and periodontal disease. Periodontal disease is a risk factor for poor glycemic control among diabetic patients, and diabetes is associated with increased severity of periodontal disease. Studies showing the relationship between periodontal disease and cardiovascular disease have proposed that patients with chronic bacterial infection or periodontitis may have (1) a bacteria-induced platelet aggregation defect that contributes to acute thrombolic events, (2) injury to vascular tissue by bacterial toxins, or (3) vascular injury resulting from a host inflammatory response that predisposes the patient to a systemic disorder such as atherosclerosis. Additionally, the link between periodontal disease and preterm labor has several proposed biological mechanisms, one of which is the infection that is mediated by prostaglandins and cytokines among patients with severe periodontitis. This infection causes decreased fetal growth and premature labor.

Differential Diagnosis

Other causes of gingivitis include hormonal changes associated with pregnancy, and systemic disease such as diabetes, Addison disease, HIV, and mechanical injury such as popcorn kernels that might become wedged under the gums.

Gingiva hyperplasia caused by medications such as calcium channel blockers, phenytoin, and cyclosporine cause overgrowth of the gingiva that may occur with or without gingivitis.

Prevention & Treatment

Good oral hygiene is essential for the prevention and control of periodontal diseases. Gingivitis, the mildest form of periodontal disease, is reversible with regular toothbrushing and flossing. Nonsurgical and surgical treatments are available for periodontitis. An added benefit is provided by over-the-counter (OTC) and prescription antimicrobial mouth rinses, such as a 0.1–0.2% chlorhexidine gluconate aqueous mouthwash used twice a day. Caution is advised when chlorhexidine is used because it causes superficial staining of the teeth of patient who drink tea, coffee, or red wine. The treatment of periodontitis includes professional care to remove tartar and may require periodontal surgery.

Because tobacco use is an important risk factor for the development and progression of periodontal disease, patients should be counseled about tobacco cessation. Systemic diseases such as diabetes that may contribute to periodontal disease should be well controlled.

General Considerations

In the United States, cancers of the oral cavity and oropharynx constitute approximately 3% of all cancers among men (the ninth most common cancer among men) and 2% of all cancers among women. The prevalence of these cancers increases with age. Since the 1970s, the incidence of these cancers and the death rates associated with them have been slowly decreasing, except among African American men, for whom the incidence and 5-year mortality estimates are nearly twice as high as for white men.

The overall survival rate for patients with oral and oropharyngeal cancers is only ∼51% and has not changed substantially since the early 1990s. However, the 5-year survival estimate for patients with lip carcinoma is >90%; this high survival rate is due in part to early detection. Most oral and oropharyngeal cancers are squamous cell carcinomas that arise from the lining of the oral mucosa. These cancers occur most commonly (in order of frequency) on the tongue, the lips, and the floor of the mouth. Approximately 60% of oral cancers are advanced by the time they are detected, and ∼15% of patients have another cancer in a nearby area such as the larynx, esophagus, or lungs. Early diagnosis, which has been shown to increase survival rates, depends on the discerning clinician who recognizes risk factors and suspicious symptoms and can identify a lesion at an early stage.

Table 46-3 shows the risk factors associated with oral and oropharyngeal cancers. Tobacco use and heavy alcohol consumption are the two principal risk factors responsible for 75% of oral cancers. The incidence of oral cancer is higher among persons who smoke or drink heavily than among those who do not.

Prevention

All forms of tobacco, including cigarette, pipe, chewing, and smokeless, have been shown to be carcinogenic in the susceptible host. Alcohol has been identified as another important risk factor for oral cancer, both independently and synergistically when heavy consumers of alcohol also smoke. Therefore, primary prevention in the form of reducing or eliminating the use of tobacco and alcohol has been strongly recommended. The US Preventive Services Task Force (USPSTF) has not endorsed annual screening (secondary prevention) for asymptomatic patients, stating that “there is insufficient evidence to recommend for or against routine screening” and “clinicians may wish to include an examination for cancerous and precancerous lesions of the oral cavity in the periodic health examination of persons who chew or smoke tobacco (or did so previously), older persons who drink regularly, and anyone with suspicious symptoms or lesions detected through self-examination.” However, the American Cancer Society and the National Cancer Institute’s Dental and Craniofacial Research Group support efforts that promote early detection of oral cancers. The American Cancer Society recommends annual oral cancer examinations for persons aged ≥40 years.

Because primary care providers are more likely than dentists to see patients at high risk of oral and oropharyngeal cancers, providers need to be able to counsel patients about their behaviors and be knowledgeable about performing oral cancer examinations. The primary screening test for oral cancer is the oral cancer examination, which includes inspection and palpation of extraoral and intraoral tissues (Table 46-4).

Clinical Findings

A. Symptoms and Signs

Early oral cancer and the more common precancerous lesions (leukoplakia) are subtle and asymptomatic. They begin as a white or red patch, progress to a superficial ulceration of the mucosal surface, and later become an endophytic or exophytic growth. Some lesions are solitary lumps. Larger, advanced cancers may be painful and may erode underlying tissue.

According to the definition of the World Health Organization, leukoplakia is “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease.” The lesions may be white, red, or a combination of red and white (called speckled leukoplakia or erythroleukoplakia). Multiple studies have shown that these lesions undergo malignant transformation. Biopsies have shown that erythroplakia and speckled leukoplakia are more likely than other types of leukoplakia to undergo malignant transformation with more severe epithelial dysplasia. Figures 46-12 and 46-13 show leukoplakia.

Oropharyngeal carcinomas can be found in the intraoral cavity, the oral cavity proper, and the oropharyngeal sites. The most common intraoral site is the tongue; lesions frequently develop on its posterior lateral border. Lesions also occur on the floor of the mouth and, less commonly, on the gingiva, buccal mucosa, labial mucosa, or hard palate.

A common cancer of the oral cavity proper is lower lip vermilion carcinoma. These lesions arise from a precancerous lesion called actinic cheilosis, which is similar to an actinic keratosis of the skin. Dry, scaly changes appear first and later progress to form a healing ulcer, which is sometimes mistaken for a cold sore or fever blister. Figure 46-14 shows actinic cheilosis.

Oropharyngeal carcinomas commonly arise on the lateral soft palate and the base of the tongue. Presenting symptoms may include dysphagia, painful swallowing (odynophagia), and referred pain to the ear (otalgia). These tumors are often advanced at the time of diagnosis. Oral cancer metastasizes regionally to the contralateral or bilateral cervical and submental lymph nodes. Distant metastases are commonly found in the lungs, but oral cancer may metastasize to any other organ.

B. Diagnosis

All patients whose behaviors put them at risk of oral cancer should undergo a thorough oral examination that involves visual and tactile examination of the mouth; full protrusion of the tongue with the aid of a gauze wipe; and palpation of the tongue, the floor of the mouth, and the lymph nodes in the neck. Because oral cancer and precancerous lesions are asymptomatic, primary care providers need to carefully examine patients who are at risk of oral or oropharyngeal carcinomas. Using a scalpel or small biopsy forceps, the primary care physician should perform a biopsy of any nonhealing white or red lesion that persists for >2 weeks. Alternatively, the patient may be referred to a dentist, an oral surgeon, or a head and neck specialist, who can perform the biopsy. Patients with large lesions or advanced disease should undergo a complete head and neck examination, because 15% of these patients will have a second primary cancer at the time of diagnosis. Neck nodules with no identifiable primary tumor may be evaluated by fine-needle aspiration.

C. Imaging Studies

Imaging studies such as computed tomography with contrast and magnetic resonance imaging of the head and neck are used to determine the extent of disease and involvement of the cervical lymph nodes for the purposes of staging.

Differential Diagnosis

Precancerous white lesions may be confused with frictional keratosis: lesions that result from chronic chewing of the cheek and nicotine stomatitis, a condition with hyerkeratotic epithelial changes on the hard palate as a result of cigarette smoking.

Other white lesions include hairy leukoplakia, geographic tongue, and candidiasis, which should be included in the differential of precancerous lesions.

Treatment

Treatment for oral and lip cancers includes chemotherapy, surgery, radiation, or some combination of these therapies, depending on the extent of the disease. These treatments can cause severe stomatitis (inflammation of the mouth), xerostomia (dry mouth), disfigurement, altered speech and mastication, loss of appetite, and increased susceptibility to oral infection. The management of these complications requires a multidisciplinary team approach by the clinician, oral surgeon, oncologist, and speech therapist. Early diagnosis allows better treatment, cosmetic appearance, and functional outcome and increases the probability of survival. Patients should be encouraged to visit their dental health provider before beginning cancer therapy so that existing health problems can be treated and some complications can be prevented.

Oral Effects of Medications

Medications used to treat certain systemic conditions may have oral manifestations. Most commonly these include xerostomia (dry mouth), gingival hyperplasia, dental caries and erosions, and osteonecrosis of the jaw.

Xerostomia, commonly seen in the elderly, is caused by hypofunction of the salivary gland, but has also been caused by antihypertensives, antidepressants, protease inhibitors, antihistamines, and diuretics. Xerostomia increases the risk of denture sores and caries, since saliva is a lubricant with antimicrobial properties. Symptoms include a sensation of dry mouth. Treatment is avoidance of medications known to cause xerostomia and careogenic foods, good oral hygiene, and salivary substitutes or stimulants.

Gingiva hyperplasia has been associated with calcium channel blockers, methotrexate, cyclosporine, and phenytoin. Dental caries may be caused by syrups such as cough medicines, and dental erosions may follow use of β-blockers, calcium channel blockers, nitrates, and progesterone. Treatment is avoidance of medications associated with gingiva hyperplasia.

Avascular osteonecrosis of the mandible and maxilla have been associated with bisphosphonates. Symptoms include swelling and pain, difficulty eating, bleeding, lower lip paresthesia, and loose and mobile teeth. Since radiographs are nonspecific, lesions should be biopsied for definitive diagnosis. Risk factors include IV bisphosphonates, cancer, invasive dental procedures, smoking, steroid use, radiation therapy, and poor dental hygiene. Patients should be advised to avoid dental procedures while taking these medications.

Global References for Oral Health