Oral Health

14
Chapter

Samuel Zwetchkenbaum, DDS, MPH, and L. Susan Taichman, RDH, MPH, PhD

Key Points
 Many systemic medications have been

shown to have important oral health implications and have been associated with oral tissue complications (strength of recommendation: B).  The recognition and treatment of periodontal disease may be important due to the possible association with systemic conditions such as diabetes, cardiovascular diseases, and stroke (strength of recommendation: B).  The effects on oral health and the economic impact of altering the recall interval between dental checkups (i.e., the time period between one dental checkup and the next) are unclear; dental examinations are recommended annually if there is no significant disease and more frequently if the patient is prone to dental disease (strength of recommendation: C).  Currently, no acceptable studies exist to provide evidence to support the efficacy of early oral cancer detection programs, yet routine evaluation is recommended in high-risk patients (strength of recommendation: C).

Introduction
Abnormalities in oral health can significantly affect the general health of the male patient because many systemic diseases exhibit their
The authors thank Russell Taichman, DMD, DMSc, for his assistance in preparation of this chapter.

clinical signs in the tissues and dentition of the oral cavity. Epidemiologic research has delineated associations between oral infections and systemic conditions including diabetes mellitus, respiratory infections, and cardiovascular, autoimmune, and gastrointestinal diseases. Adult males are more likely than women to develop oral cancer and use alcohol and tobacco products, yet they are less likely to seek preventive dental care services.1 Furthermore, with the dramatic increase in the use of medications that can potentially affect the oral environment, and the knowledge that many of the effects of oral disease are cumulative, additional burden has been placed on healthcare providers for early identification of oral diseases. Standard medical school education includes only minimal discussion of the oral cavity and dentition, often limited to basic information such as the various types and numbers of infant and adult teeth. Often overlooked are the normal physiologic variations of dentition, both developmental and acquired, and how to distinguish normal from pathologic conditions. Including an oral and dental examination as part of the officeor hospital-based history and physical examination can provide insight into the overall health of an individual patient and can occasionally help to solve mysteries. Hospital-based dental programs receive consultations daily to assess the dentition as a potential source of infection, but it is a small percentage of medical centers that have dentistry programs or even dentists on staff. Requesting a consultation from a dentist outside the hospital may be challenging, but when recognized as part of the overall care, should be pursued. 243

The Adult Male For the primary care clinician, the recognition of salient signs and symptoms of oral diseases, as well as the identification of systemic disorders and conditions, may assist in the early diagnosis and prompt referral for appropriate specialist treatment. Since many of the most common oral diseases including periodontal disease and caries are largely preventable, disease detection and prevention needs to be established as a high priority by the medical community. The effects on oral health and their economic impact are unclear; nonetheless, dental examinations are recommended annually if there is no significant disease and more frequently if the patient is prone to dental disease.2 The goal of this chapter is to provide clinicians with an increased knowledge of the signs and symptoms of common oral conditions and the possible links between oral and systemic health for their male patients. from those used 50 years ago, so the restored dentition of an older patient may appear significantly different than that of a younger person. Use of gold with acrylic resin facings, silicates, and silver amalgam typically look less tooth-like and discolor easilyto the unfamiliar eye, these may appear more like a disease process than treatment of disease. Current practice produces restorations that would challenge even the most trained eye in detection. Stain and discoloration take away from the youthful appearance of the teeth, yet they are not pathologic and are commonly the result of cigarette smoke, coffee, wine, and other foods that contain darkly pigmented staining chemicals. Staining can increase the roughness of the teeth, making plaque more retentive and accelerating periodontal disease.

Dental Caries
Although still considered the infection of mankind with the highest prevalence, dental caries is significantly less likely to occur in a young man coming of age in the 21st century than in his father. Smooth surface caries, those occurring on the cheek side or between the teeth, have reduced significantly in number due to the widespread use of systemic fluoride. Pit and fissure caries, or those occurring in the grooves of the teeth, have experienced reduction thanks to the use of occlusal sealants, which are composed of an unfilled composite resin that dentists or hygienists can place on an eruption of the tooth. Thus, the norm for adolescent and adult men should be little to no tooth decay. Where there is significant decay, one must take a close look at the underlying cause. A number of conditions lead to xerostomia, or decreased salivation, and it is common to see rampant caries on the teeth of patients who are undergoing radiation therapy, who are taking psychiatric medications, or who have Sjogrens syndrome. Significant consumption of sugar-containing carbonated beverages can also result in a large number of teeth experiencing decay (Figure 14-1). A more recently described pattern of decay has been reported on the teeth of users of methamphetamine, commonly referred to as meth mouth. This decay is noted on the buccal surfaces of the teeth near the gum line and can wrap around the tooth, resulting in amputation of the crown. The rampant caries associated with methamphetamine use is attributed to the acidic nature of the drug, the drugs xerostomic effect, its propensity to cause cravings for high-calorie carbonated beverages, tooth grinding and

Overview of Dentition
The Normal Dentition
The enamel is the hard outer substance of the tooth and should not demonstrate significant breaks of its integrity. Exposure of underlying dentin can occur for a number of reasons, some physiologic, and some pathologic. Physiologic exposure of dentin may occur through tooth wear against another tooth or substance or erosion typically from a chemical (e.g., stomach acid in the case of gastroesophageal reflux disease). This process usually takes long enough that the odontoblasts of the tooth have built up reparative dentin and sensitivity rarely occurs. Notching in the cervical portion or neck of the tooth can result in great sensitivity. The cause of these lesions can either be via abfraction (i.e., the chipping of tooth structure) or abrasion, caused by mechanical contact such as aggressive toothbrushing. Although the nature of these lesions is still not fully understood, in clinical practice they seem to occur in males more frequently.

Restored Dentition
Dental caries is the most ubiquitous infectious process in man, so it is not surprising that most people have had their teeth restored to some degree. The molars are the most commonly restored teeth; however, a Cochrane review3 found that preventive measures including fluoride supplementation via toothpaste and mouthwash rinses as well as occlusal sealants have significantly reduced the rate of decay. Materials that are used today differ 244

Oral Health

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Figure 14-1. Advanced dental caries in a patient who reports daily consumption of a 2-liter bottle of Mountain Dew. (Photograph courtesy of Kathryn Thornton, DDS.)

clenching, and its long duration of action leading to extended periods of poor oral hygiene.46 Although advanced caries are easy to diagnose, detection of early caries and knowing when to restore them is a matter of great controversy and lacks acceptable standards of evidence. The emergence of expensive high-technology equipment including laser-assisted tooth preparation and computer-aided design/computer-aided manufacturing milling of restorations may contribute to supplier-induced demand for these procedures. The presence of dental insurance often hides the cost of such procedures from patients.

review examining the use of mouthguards in contact sports found insufficient evidence to support their widespread use.7 Although early attention is important in tooth fractures to assist in pain control and to prevent microbial invasion of the pulp, it is the luxation or avulsion injury for which immediate attention can affect the long-term prognosis of the tooth. The avulsed tooth can be stored in milk, saliva, or in a Hanks balanced solution (e.g., Save-aTooth Emergency Kit [Phoenix-Lazerus, Inc., Pottstown, PA]). Early access to a dentist within 1 hour of injury should be expedited to ensure proper reimplantation and splinting. In some cases, root canal therapy within 1 week is necessary to maintain viability of the damaged tooth. Luxation injuries are treated in a similar fashion. Fractures in the enamel or dentin are typically not urgent and can be followed up in the coming days by a dentist. Fractures into the pulp require early access to a dentist for coverage, or possible root canal or extraction.8

Oral Cancer
Approximately 30,000 new cases of oral cancer are diagnosed in the United States every year, and prognosis is closely related to the stage of disease at the time of detection. In 2006, it was estimated that oral cancers accounted for 3% of total cancers in men and 2% in women, with African American men having almost double the cancer death risk (7.1 compared with 3.9).9 A males lifetime probability of developing a cancer of the oral cavity is estimated to be 1 in 73.9 Aggressive treatment is needed for advanced disease, including surgery, chemotherapy, and radiation therapy, and these can greatly affect quality of life. The high-risk patient population includes users of tobacco as well as heavy alcohol, a population that is less likely to seek regular dental visits. Currently, only 13% of adult men older than 40 years report having had an oral and pharyngeal examination to detect cancer within the past year.7 This places increasing importance on physicians to include an oral examination as a part of their routine annual health maintenance examination, which should include visual inspection of the buccal mucosa, the floor of mouth, the tongue, and palate, and palpation of submandibular glands and cervical lymph nodes. Patients with suspicious lesions should be promptly referred to either an oral surgeon for further evaluation including possible toluidine blue staining or biopsy of any suspicious lesions. The brush-biopsy technique is showing 245

Dental Trauma
Contact sporting activities (e.g., hockey, basketball, football, baseball) and non-sporting activities (e.g., falls, accidents, altercations) can result in dental trauma. Trauma may result in the displacement of teeth, defined as luxation (i.e., tooth displacement) and avulsion (i.e., completely displaced or knocked out of the dental socket), as well as fractures. Tooth fractures are categorized by the layer of tooth exposed (e.g., enamel, dentin or pulp) and the level (e.g., coronal or root). Ellis class I fractures consist of an enamel-only fracture and can be treated by either smoothing the tooth or simple restoration with a composite resin restoration. Ellis Class II fractures indicate exposure of underlying dentin, likely result in sensitivity to air, and may be simply covered. An Ellis class III fracture results in exposure of the pulp, and often root canal therapy is required. The use of protective mouthguards is encouraged by both professional and amateur sporting organizations to reduce the risk of trauma to the teeth during contact sports, yet a systematic

The Adult Male increasing acceptability among dentists for early cytologic evaluation of potential malignant disease. keratinized epithelium covering the cheeks, floor of the mouth and posterior pharynx and are termed alveolar mucosa. The gingival crevice (a cuff-like space between the gingiva and the teeth) is a blinded cul-de-sac. This area is bounded laterally on the tooth side by a specialized epithelium called the sulcular epithelium. The sulcular epithelium transitions into a tissue termed junctional epithelium that is positioned at the base of the crevice. In health, it is thought that through an active desquamation process of epithelial cells the underlying tissues are protected from bacterial invasion. The root surface is called the cementum. Connective tissue attachments are present between the alveolar bone and cementum. Alveolar bone is attached to the teeth through the periodontal ligament fibers, which form the tooth socket. The crest of the alveolar supporting bone, often viewed on typical dental radiographs, is approximately 2 mm below the point where the enamel of the crown of the tooth meets the root cementum (the cementoenamel junction).10

Periodontal Diseases
The Periodontium
The periodontium is defined as the tissues that surround and support the teeth (Figure 14-2) and comprises the following:  The gingival tissues (or gingiva, frequently called gums in laypersons terms) are the soft tissues that cover the alveolar bone of the jaws and the teeth up to the exposed crown of the teeth. In good health, the gingiva are generally pale pink and firm with a stippled surface texture, although considerable heterogeneity exists among individuals based on skin pigmentation and ethnicity. The interdental gingival lays between the teeth and typically fills the embrasures between the teeth, functioning to deflect food away from these areas. Between the anterior teeth, the gingiva are typically wedge-shaped, and in the posterior teeth they assume a saddle-shaped configuration. Further away from the crowns, the gingival epithelium is heavily keratinized and attached to the underlying structures including the hard palate termed attached or keratinized gingival tissue. These tissues transition sharply into a non-

  

Periodontal Disease
The generic term periodontal disease refers to a variety of clinical manifestations characterized by the inflammatory process of the tooths

Enamel Crown Dentine Pulp cavity Gingival sulcus Gingiva

Periodontal ligament Root Alveolar bone Cementum Root canal Attachment apparatus

Figure 14-2. Cross-section of the periodontium in health. (Marx J, Hockberger R, Walls R: Rosens Emergency Medicine: Concepts and Clinical Practice, ed 6, St. Louis, MO, 2006, Mosby.)

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Oral Health supporting structures. Periodontal diseases are generally divided into two groups:  Gingivitis, or inflammation affecting the gums.  Periodontitis, or inflammation and damage of the bone and connective tissue that supports the teeth.

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Epidemiology
More than 70% of adults have some form of periodontal disease,11 most typically composed of gingivitis. Research has demonstrated that nearly one in three US adults aged 3054 years and 50% of adults aged 5590 years have some form of periodontitis. In males, the incidence ranges from 34% to 56% in these age categories and from 23% to 44% in women, highlighting that periodontitis is more prevalent in males than females.12 Research has also shown that, among adults, males are at a higher risk of developing chronic periodontitis with advanced periodontal destruction than females.1315 Present knowledge regarding the pathogenesis of periodontal disease indicates that there are no inherent differences between men and women in their genetic susceptibility to periodontitis. Most existing data suggest the differences between genders may be related to poorer oral hygiene practices, less positive attitudes toward oral health, and decreased use of professional dental services. Typically, women perform better oral hygiene measures and use professional dental services more frequently.13

with reports of gingival bleeding on tissue manipulation, such as during a dental examination or routine tooth brushing. The primary risk factor for gingivitis is bacterial plaque resulting from poor oral hygiene. Supraand subgingival removal of plaque eliminates the inflammatory response and, in most cases, the gingival lesions will heal with a full restoration of tissue form and function. Although gingivitis does not always progress to periodontitis, periodontitis is always preceded by gingivitis.16,17

Periodontitis
Periodontitis is the destruction of the supporting structures housing the tooth. If a sufficiently large amount of supporting bone and ligamentous attachment is lost, then the patient may present with a chief symptom of tooth migration or movement, loose teeth, and even tooth loss. The transition from gingivitis to periodontal disease with the associated loss of the connective tissue attachment usually goes undetected. Since periodontitis is generally not painful, it may display few, if any, outward signs initially. Chronic periodontitis, formerly referred to as adult periodontitis, is the most commonly occurring form of periodontitis in men older than 3544 years.18 The term chronic indicates that the disease progresses slowly and results in the progressive destruction of the supporting tissues of the tooth (i.e., periodontal ligament and alveolar bone) from the margins of the gingiva toward the apices of the roots of the teeth (Figure 14-4). Although the cumulative effects of the disease make it appear chronic in nature, the disease may occur as a series of acute episodes separated by quiescent periods of indeterminate duration. Periodontitis is not a natural consequence of the

Gingivitis
Gingivitis is an inflammatory response of the gingival tissues to the metabolic products and pathogenic toxins of bacteria found in oral plaque. Plaque-associated gingivitis most commonly presents as erythematous, edematous tissue that halos the teeth (Figure 14-3). Patients may present

Figure 14-3. Gingivitis. (Photograph courtesy of Keith Kirkwood, DDS, PhD.)

Figure 14-4. Severe periodontitis. (Photograph courtesy of Russell Taichman, DMD, DMSc.)

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The Adult Male aging process19; however, as repeated bouts with the disease results in cumulative damage and loss of tooth support, it is most frequently detected in middle-aged to older persons. Research indicates that chronic periodontitis in elderly persons is characterized by slow progression and usually does not lead to tooth loss. In cases in which periodontitis is reported as a leading cause of tooth loss in the elderly, it is most likely that the majority of teeth extracted have been seriously diseased for many years, rather than becoming diseased during old age.20 A smaller percentage of the population, estimated at 515%, are afflicted with generalized aggressive periodontitis that rapidly results in the loss of connective tissue support for the teeth.11,18 Such aggressive forms of periodontal disease are generally found in circumpubertal adolescents and young adults, yet it is important to note that older persons are not immune from these forms of disease. Most typically, aggressive periodontitis is localized to one or several teeth but may also be more widespread to be characterized as generalized. As with the chronic, or the most typical form of periodontal disease, the etiology is due to plaque-derived organisms but are also more frequently found in persons with an altered host resistance to the infections.21 periodontal disease. Suppurative material may exude from the periodontal pocket, which is often considered a sign that the infection has undergone a transition to a more active stage. Gingival and periodontal abscesses are frequently caused by infections within the tooth pulp and occur in some patients with long-standing periodontal conditions, usually occurring when the entrance to the gingival crevice becomes occluded, limiting the outward flow of the fluids from the gingiva into the oral cavity. These acute and exacerbated conditions are often best treated by obtaining an accurate differential diagnosis and by instituting broad-spectrum antibiotics and immediate tissue debridement.22

Etiologies
Bacterial Plaque. Both gingivitis and periodonti-

Clinical Presentation and Diagnosis

Typical symptoms of periodontal disease include swelling, erythema, bleeding, and recession of gingival tissue (see Figure 14-3). The gums may bleed during brushing, but the teeth are usually not mobile22; tooth mobility and pain are often seen in the later stages.23 Many patients have periodontal inflammation without being aware of any changes in their teeth or gums. By the time these symptoms are present, treatment alternatives are often limited. Therefore, it is imperative for the clinician to look for signs of and symptoms of periodontal disease in asymptomatic patients during the examination of the oral cavity and refer them appropriately and expeditiously for evaluation and treatment. In cases of severe periodontal disease, more than 30% of the attachment apparatus is lost, and the gingiva is receded, exposing the roots of the teeth (see Figure 14-4). The interdental papillae are often absent, and the gingivae are swollen, red, and boggy in character. Large amounts of calculus and food debris are present along the gum line. The teeth are mobile and the gums bleed easily when the teeth are brushed; the patient may report having sensitive teeth. Halitosis is a common presentation associated with 248

tis are the result of a complex interaction between pathogenic bacteria, host response, and systemic and local risk factors. Typically there are 300 500 specific species of microorganisms inhabiting the oral cavity at any one time.24 Both gingivitis and chronic periodontitis are believed to be caused by gram-negative bacteria in the dental plaque that lie in close proximity to the necks of the teeth and marginal gingival tissues, namely Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, and Campylobacter rectus.25 Thus, subgingival plaque found within the gingival crevice or the sulcus around the necks of the teeth is thought to house the etiologic agent(s).26 There is some evidence that the causative agents in the more aggressive forms of periodontitis may differ from those associated with gingivitis or chronic periodontitis. In the condition known as localized aggressive periodontitis, the small capnophilic (carbon dioxiderequiring) gram-negative rod Actinobacillus actinomycetemcomitans has been implicated.27,28
Tobacco Use. Epidemiologic and clinical studies have shown that smokers have a two- to six-fold greater risk of developing periodontal disease than nonsmokers, depending on the criteria used to define periodontal disease.29 The risk of periodontal disease appears to increase with the number of cigarettes smoked per day as well as duration of pack-years.3032 Although a clear relationship exists between smokeless tobacco and oral carcinoma,33,34 a definitive relationship between smokeless tobacco and generalized periodontitis has not been demonstrated. The exact mechanism that places smokers at greater risk for periodontal diseases remains unclear.35 Most evidence points to local and

Oral Health possibly systemic alterations in granulocyte function. Studies have demonstrated that smoking and nicotine increase the inflammation possibly by reducing oxygen in the gingival tissue and by triggering an overproduction of cytokines, which lead to destruction of the cells and tissues. Periodontal therapy, both surgical and nonsurgical, is less likely to be effective in smokers as well as increased risk of dental implant failure. In addition, periodontal disease is more likely to recur than in nonsmokers.
Genetics. Current evidence suggests that severe

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periodontal diseases are typically treated by a general dentist; patients with severe forms of the disease are often best referred to a periodontist. Treatment of periodontal disease includes a wide range of modalities including patient education and care instructions, scaling, root planing, surgery, local and systemic antibiotic therapies, and occlusal adjustment.

Prevention of Periodontal Diseases

Prevention is the cornerstone of treatment of periodontal disease and it begins with patient education. Patients should be informed about the causes, treatment and methods used to prevent periodontal disease (Table 14-1). The American Dental Association and the American Dental Hygienists Association have a variety of patient education materials that are readily accessible, and many local and state organizations are suitable providers for high-quality educational materials, as well.41,42 Periodic examinations to screen for periodontal diseases and oral health conditions should be a high priority among healthcare professionals. The timing of these visits depends on whether disease is present and whether the patient complies with care instructions. Physicians can aid in primary prevention by reviewing with their patients the need for good oral hygiene and periodic dental examinations. Physicians may also play an important role in prevention by looking for signs of periodontal disease when they examine the oral cavity because early diagnosis and treatment can significantly reduce the morbidity associated with periodontal disease. Although the common recommendation for dental recall visits is every 6 months, the systematic review by Beirne and others2 found no evidence to support this traditional recall schedule. As noted previously, adult males have a higher prevalence of periodontal disease, most likely the result of poor oral home care and lower dental care utilization. At the present time, there is no literature to support an increased routine dental recall for adolescent or adult males.

forms of periodontal disease (i.e., aggressive periodontitis) have a strong genetic component. Rare syndromes that affect neutrophil function, leukocyte adhesion deficiencies, as well as other inherited phagocyte disorders including collagen and enzyme defects, can produce periodontal manifestations. In chronic periodontitis, evidence for a genetic component has been demonstrated in data on concordant twins suggesting that half of population variance for periodontitis may be due to genetic factors.36,37 Increasing evidence indicates that a combination of two polymorphisms in the interleukin-1 gene is associated with susceptibility to chronic periodontitis.38,39 Although there is little doubt that periodontitis has a genetic component, insufficient evidence exists to warrant the widespread use of genetic testing to assess for risk of development of periodontal disease.
Compromised Host Defense. Almost any alter-

ation of the adaptive or innate immune responses, or any condition that impedes normal tissue turnover, is thought to place persons at a greater risk for periodontal disease. Recent attention has focused on human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS)-associated periodontal conditions, but nearly any process that alters tissue metabolism including stress, trauma, endocrine alterations, and hematologic dyscrasias may result in periodontal diseases that can be exacerbated by the systemic conditions. Particular attention by primary care physicians should be directed in consideration that any limitation of the ability to fight infection or during the repair process might result in more severe forms of periodontal disease. Dental care is indicated for these patients to prevent and treat intra-oral infections, restore dental function, and improve quality of life.40
Treatment. The role of the primary care physi-

Gingival Recession
Gingival recession is the apical migration of the marginal tissue from the crown of the tooth resulting from destructive periodontal disease, periodontal surgery, or trauma from forceful tooth brushing exposing the underlying root surface.10 It may also be the result of periodontal treatment in which regenerative therapies were 249

cian in treating periodontal disease consists chiefly of diagnosis and referral of the symptomatic or asymptomatic patient for treatment. Mild

The Adult Male

Table 14-1. Preventive Strategies Against Periodontal Disease

Preventive Action Toothbrushing123126 Mechanism Prevents the accumulation of plaque and disrupts the bacterial colonies on teeth and in the gingival crevice Prevents the accumulation of plaque and disrupts the bacterial colonies on teeth and in the gingival crevice Effectiveness Toothbrushing is effective in preventing gingivitis. Brushing may prevent periodontitis. Flossing is effective in preventing gingivitis. Flossing may prevent periodontitis. Recommendation Brush 23 times a day. Use a soft-bristle toothbrush. Floss daily using waxed or unwaxed floss. Floss aids may help persons who have difficulty with the mechanics of flossing.

Flossing124,127

Use of oral rinses as adjunct to toothbrushing (e.g., over-the-counter Listerine oral rinse130,131 prescription CHX [Peridex])128,129

These mouthrinse contain a mixture of phenolic compounds with bactericidal properties and anti-inflammatory effects. Peridex is a 0.12% solution of CHX, a bis-biguanide antiseptic Various anticalculous agents containing crystal growth inhibitors which prevent the development of mineralized plaque

More effective on gingivitis than dental plaque reduction Effective in reducing gingivitis

Toothbrushing with anticalculus toothpaste132

Effective in reducing supragingival calculus

No evidence to recommend to general population; may benefit patients who are at high risk of calculus development

OTC, Over the counter; CHX, chlorhexidine.

not effective. The exposed root surfaces are often of concern due to enhanced risk of carious lesions and reduced esthetics. Gingival recession is associated with age, yet this association does not reflect a physiologic effect but rather a cumulative effect of toothbrush trauma for longer periods of time.43

Presentation
Patients may report gingival recession accompanied by dentinal hypersensitivity consisting of a transient sharp pain with varying levels of intensity. It has been estimated that approximately 50% of the general population complains of acute or chronic dentinal hypersensitivity, with the highest incidence between the ages of 3040 years.44

In addition, over-the-counter toothpastes containing 5% potassium nitrate have been suggested as a conservative treatment (Table 14-2).4648 Antihypersensitivity toothpastes act by depolarizing the nerves located at the dentin-pulpal interface. Potassium ions in the toothpaste prevent the repolarization of the sensory nerve endings, interrupting the transmission of paincausing nerve impulses associated with dentin hypersensitivity.49 To date, systematic reviews have not supported the efficacy of potassium nitrate toothpaste for the treatment of dentine hypersensitivity.50

Pericoronitis
Pericoronitis is defined as an oral abscess of the soft tissues typically surrounding the crown of a tooth, commonly a mandibular third molar that has partially erupted into the oral cavity.10 Patients with pericoronitis often present with acute pain ranging from mild to intense that may radiate to the external neck, throat, ear, or the oral floor and swelling in the tissues around the partially erupted third molar (Figure 14-5) resulting in limited jaw opening (trismus). Cervical lymphadenopathy, fever, leukocytosis, and malaise may also be present, as well as concurrentipsilateral tonsillitis or upper respiratory tract infections. Patients presenting with chronic pericoronitis

Treatment
Referral to a dentist for instruction of proper tooth-brushing technique and for plaque control can reduce both the sensitivity and risk for root caries. Professional treatments for dentinal hypersensitivity include reduce flow into the dentin tubules by occluding or sclerosing the tubules with dentin sealers (i.e., resins), stannous fluoride, strontium chloride hexahydrate, sodium citrate, and sodium monofluorophosphate, as well as others.45 Invasive procedures may include gingival surgery, application of resins, pulpectomy, or laser treatment. 250

Oral Health
Table 14-2. Over-the-Counter Toothpastes Designed to Treat Dentinal Hypersensitivity
Product Name Aquafresh Sensitive Colgate Sensitive Plus Crest Sensitivity Protection Natural Toothpaste for Sensitive Teeth Oral-B Rembrandt Extra Whitening Toothpaste Sensitive Teeth Sensodyne Manufacturer GlaxoSmithKline Colgate-Palmolive Procter and Gamble Toms of Maine Oral-B GlaxoSmithKline Active Ingredient 5% potassium nitrate 5% potassium nitrate 5% potassium nitrate 5% potassium nitrate 5% potassium nitrate 5% potassium nitrate

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Figure 14-5. Pericoronitis. (Photograph courtesy of Russell Taichman, DMD, DMSc.)

Figure 14-6. Orthopantomogram demonstrating impacted third molars (arrows). (Photograph courtesy of Darnell Kaigler, Jr, DDS, Ph.D.)

Treatment
may have acute episodes or may present with moderate discomfort around the region of the third molar or complain of a bad taste. Occasionally, pericoronitis may progress to a fascial space abscess or cellulitis. An impacted third molar may lead to caries or resorption of adjacent teeth, or cyst development. Pericoronitis is often obvious from intraoral examination, but an orthopantomogram may be helpful to further delineate an etiology that cannot be readily identified (Figure 14-6). Chronic pericoronitis may be alleviated by the use of chlorhexidine mouthwashes, warm salt water rinses, or by measures taken to improve oral hygiene. Referral to a dentist should occur as quickly as possible for evaluation to determine if symptomatic treatment can suffice until eruption is complete or if surgical therapy to remove the gum flap or the underlying tooth is necessary. Treatment considerations for acute pericoronitis include debridement, saline irrigation of the undersurface of the peri-coronal flap, and when indicated, systemic antibiotics. A 1980 NIH (National Institutes of Health) consensus51 and extensive literature reviews52,53 support the removal of wisdom teeth when associated with symptoms of pain or pathologic conditions. However, the routine removal of asymptomatic third molars in adults has recently been challenged because the benefits may not outweigh the potential complications of removal.54,55

Etiology
Eruption of the mandibular second or third molars, which generally occurs between the ages of 17 and 25 years, may occur partially or not at all. Infection can occur in the soft tissues partly covering the crown and may spread into the oropharyngeal area, or to the tongue or may progress to an abscess or cellulitis. Risk factors associated with pericoronitis include poor oral hygiene, trauma from the opposing tooth on the soft tissues, smoking, and concurrent upper respiratory tract infections.

Necrotizing Periodontal Diseases

Etiology
The clinical presentation and clinical course of necrotizing ulcerative gingivitis (NUG) is completely 251

The Adult Male Necrotizing ulcerative periodontitis (NUP) occurs when NUG extends to involve the surrounding and underlying bone and connective tissues supporting the teeth.62 This form of the disease may cause severe and rapid destruction along with a distinctive fetid odor, loss of the tips of the interdental papilla (seen clinically as a punched out papilla), and spontaneous gum tissue bleeding (Figure 14-8). NUP is associated with systemic immune suppression as seen during HIV infection. NUP may indicate deterioration of the immune system and in some cases may be useful in the diagnosis of AIDS and in patients with severe nutritional deficiencies.63,64

different from gingivitis. NUG, previously known as acute necrotizing ulcerative gingivitis, is related to a diminished systemic resistance to bacterial infection in the periodontal tissues. It is chiefly characterized by clinical appearance of necrotic gingival tissues resulting in a white pseudomembranous surface, significant pain, bleeding, loss of the tips of the interdental papilla (described as punched out), halitosis, and occasionally fever and malaise (Figure 14-7). NUG is a relatively uncommon condition (0.110% of the population) and is commonly a disease of young adults aged 1830 years; however, in developing countries, it can also affect young children. Patients with NUG generally seek treatment due to the significant intraoral pain associated with the condition.56 As with gingivitis and periodontitis, the etiology of NUG is a mixed floral infection via Streptococcus intermedia (alpha-hemolytic streptococci), Actinomyces species, and a number of different oral spirochetes.57 In fact, several studies have shown that the spirochetes may actually infiltrate into the surrounding tissues.52,55,5860 At-risk persons include those who have recently undergone stressful events including new military recruits, students during examinations, and persons experiencing major life-transition events. Other factors include poor oral hygiene and diet, and tobacco and alcohol use. During World War I, NUG was described as Vincents infection or trench mouth. For immediate relief of symptoms, NUG can be treated with systemic antibiotics such as metronidazole and topical antimicrobials such as chlorhexidine; however, resolution is dependent on the patient receiving a professional cleaning of the teeth and implementation of good home dental care.61,62 NUG generally responds well to treatment if the host defenses remain intact but may require more aggressive therapy in persons with persistent immune deficiencies.

Treatment
Patients with acute NUG and NUP often require systemic and topical analgesic therapy for pain management and to maintain adequate nutrition. The standard of care is gradual, gentle local debridement of the inflamed areas during the initial visit, supplemented with subgingival povidone-iodine irrigation, if possible. Chlorhexidine gluconate 0.120.2% mouthrinse twice daily or saline rinses can help to speed resolution. Oral rinses with a 3% hydrogen peroxide solution also may also be of benefit. For the treatment of ulcers, metronidazole administered in a 500-mg loading dose and followed by 250 mg four times daily until ulcers are healed can be used; penicillin or tetracycline can be used alternatively or in patients who cannot tolerate metronidazole. Topical antifungal medications such as clotrimazole troches can be given for patients with a history of oral candidiasis. Use of nystatin rinse is not encouraged in dentate patients due to the high sugar content. Recommendations to reduce current physical or mental stressors should be used, as well

Figure 14-7. Necrotizing ulcerative gingivitis. (Photograph Courtesy of Russell Taichman, DMD, DMSc.)

Figure 14-8. Necrotizing ulcerative periodontitis. (Photograph courtesy of Russell Taichman, DMD, DMSc.)

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Oral Health as proper oral hygiene instructions. Most patients are reevaluated within 3 days to ensure improvement. Deep scaling and root planing after cessation of spontaneous bleeding and pain from periodontal lesions is recommended.65,66

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Herpes-related Gingivitis
Primary herpetic gingivostomatitis occurs primarily in children, although the condition may occur at any age. The onset is often very painful and debilitating. The lesions appear as small punctuate vesicular lesions that may coalesce with indurated and slightly raised borders. Secondary herpetic gingivostomatitis occurs primarily on the tongue, buccal mucosa, and keratinized gingiva. Occurrence of these lesions is commonly of a rapid onset, usually in response to trauma or stress; the condition is generally selflimited and resolves within 710 days. Treatment of either primary or secondary herpetic gingivostomatitis is primarily palliative because the intense oral pain can make maintaining adequate nutrition difficult. Oral rinses with 2% viscous Xylocaine (lidocaine hydrochloride) before eating may prove to be palliative. Several local anesthetic-based compounds that can be obtained as over-the-counter preparations may provide some transient relief but have not been shown to decrease time to resolution. Along with antiviral medications such as acyclovir, analgesics and antipyretics are often recommended to reduce fever (if present) and pain.

Oral Manifestations of Systemic Disease

The oral manifestations of certain systemic diseases can mimic the signs and symptoms of periodontitis or gingivitis. Such diseases include immunologic, infectious, neoplastic, and metabolic disorders. In comparison to periodontitis and gingivitis, these disorders are considerably less common, yet since their diagnosis and management differ significantly, a high index of suspicion is required when evaluating a patient who presents with gingival or periodontal disease.

Diabetes Mellitus
Epidemiologic studies have reported consistent results of an association between periodontitis and both type I and type II diabetes mellitus.67 In general, persons with diabetes have a much greater likelihood of experiencing severe periodontitis than non-diabetics. The majority of studies investigating type I diabetes and periodontal disease have reported a greater prevalence, extent, and severity of periodontal disease among persons with type I diabetes mellitus compared with non-diabetics of the same age.6870 A epidemiologic cross-sectional study of the Pima Indians of Arizona showed that persons with type II diabetes had a 2.8- to 3.4-fold increase in odds of having periodontitis compared with non-diabetic subjects after adjusting for the effects of confounding variables such as age, gender, and oral hygiene measures.71,72 Studies suggest that the most critical issue in managing periodontitis a patient with diabetes is the degree of glycemic control achieved.73 Persons with well-controlled diabetes have the same periodontal risk as non-diabetics; however, those with poorly controlled diabetes have a two to three times greater risk of periodontitis and progressive bone loss.74 The mechanisms by which diabetes may mediate the increased severity of periodontal disease expression include vascular changes, impaired wound healing, impaired collagen metabolism and bone matrix component production, advanced glycosylation end products, and altered subgingival microflora.75

Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome

In early studies, the relationship of HIV-positive status and periodontal disease was unclear. Current evidence now suggests that HIV-related disease has a relatively minor effect on the progression of chronic periodontitis because patients who are HIV-positive and immunosuppressed can present with distinctive forms of the previously described necrotizing gingivitis and periodontitis.76 It has been suggested that the risk of chronic periodontitis among HIV-positive patients may vary due to factors such as oral hygiene measures, smoking habits, medications being taken, and preexisting periodontal disease. In addition, NUP in HIV-infected persons can present with a clinical appearance similar to Burkitts lymphoma, cytomegalovirus infection, or herpes zoster infection of the periodontal tissues.7779 These similarities can often make accurate diagnosis difficult. The wide variation in prevalence data from epidemiologic studies has brought about the call for standardized evaluation criteria to define periodontal diseases seen in HIV-positive persons. Furthermore, 253

The Adult Male with the introduction of highly active antiretroviral therapies, it has been suggested that the presence of necrotizing periodontal problems associated with HIV has been reduced in populations with access to this therapy.80,81 Various hematologic disorders such as leukemia, thrombocytopenia, and leukocyte disorders including agranulocytosis, cyclic neutropenia, and leukocyte adhesion deficiency can be associated with increased severity of periodontal disease. Persons with gastrointestinal diseases including hepatitis and Crohns disease, connective tissue and other autoimmune disorders including systemic lupus erythematosus and scleroderma, pulmonary disorders such as chronic obstructive pulmonary disease, and genetic disorders such as Down syndrome are at a higher risk for periodontal disease.
Table 14-3. Drugs That Can Cause Extrinsic Tooth Discoloration
Drug Chlorhexidine Oral iron salts Amoxicillin-clavulanate Essential oils Discoloration Caused Yellow/brown Black Yellow or grey-brown Yellow/brown

Adapted from: Tredwin CJ, Scully C, Bagan-Sebastian JV: Druginduced disorders of teeth, J Dental Res 84(7):596602, 2005.

Table 14-4. Drugs That Can Cause Intrinsic Tooth Discoloration

Drug Fluoride Tetracycline Minocycline Discoloration Caused White/brown discoloration Yellow to brown/grey Green-gray/blue-grey Greenish

Oral Side Effects of Systemic Disease Treatment

Medications may affect the dentition through several mechanisms, leading to either extrinsic (Table 14-3) or intrinsic (Table 14-4) discoloration, whereas others may result in damage to the tooth structure (Table 14-5). Several medications prescribed to treat systemic conditions have been shown to be associated with gingival hyperplasia and xerostomia. Educating patients about the potential for oral side effects of these medications is critical in reducing medication-related periodontal conditions.

Ciprofloxacin

Adapted from: Tredwin CJ, Scully C, Bagan-Sebastian JV: Druginduced disorders of teeth, J Dental Res 84(7):596602, 2005.

Gingival Hyperplasia
Gingival hyperplasia has been most frequently associated with the use of oral anticonvulsants

(e.g., phenytoin), calcium channel blockers (e.g., nifedipine), and immunosuppressants (e.g., cyclosporine). Although the molecular mechanisms of action are different for each drug class, most evidence suggests that the mechanism relates to inhibition of collagenolytic activity and buildup of fibrous tissue.82 Precise estimates of the prevalence of gingival enlargement associated with each class of drug are difficult to accurately obtain, given the different indices of gingival overgrowth, differing populations, and lack of control over comedication. However, reported prevalence of phenytoin-associated overgrowth was found to be

Table 14-5. Drugs That Can Cause Damage to Tooth Structure

Drug Sugar-containing oral (liquid) medication Drugs that result in decreased salivary secretion (i.e., xerostomia) Drugs with a pH low enough to cause tooth erosion Drugs that may increase susceptibility to gastroesophageal reflux disease Drugs used for internal tooth bleaching Drugs used for treatment of childhood cancer and leukemia Examples Various liquid medications (e.g., nystatin) See Table 14-7. Aspirin, anti-asthmatic drugs (e.g., terbutaline or fluticasone inhalers) Theophylline, anticholinergics, progesterone, calcium channel blockers Hydrogen peroxide and sodium perborate Cytotoxic agents Possible Damage to Tooth Structure Dental caries Dental caries Dental erosion Dental erosion Cervical root resorption Abnormal tooth development

Adapted from: Tredwin CJ, Scully C, Bagan-Sebastian JV: Drug-induced disorders of teeth, J Dental Res 84(7):596602, 2005.

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Oral Health 50% in one particular study of a noninstitutionalized population.83 Twenty to thirty percent of adults taking cyclosporine have reported gingival overgrowth,84 as have 615% of adults taking calcium channel blockers, including nifedipine.85,86 Risk factors known to contribute to gingival hyperplasia include the presence of established dental plaque, the depth of the periodontal pocket, male gender, and the dose and duration of drug therapy.8789 tion intake and oral hygiene resulting in increased caries, periodontal disease, and other oral infections.88 In general, gingival hyperplasia associated with phenytoin and other drugs is most common in children and young adults. Overgrowth usually begins within 36 months of initiation of therapy. Gingival enlargement is exacerbated by dental plaque decreasing a persons ability to maintain good oral hygiene; therefore, excellent oral hygiene is necessary.90

14

Presentation
Gingival hyperplasia usually begins in the interdental papilla and is located in the anterior segment of the mouth. Inflammatory enlargements are characterized by swelling or edema, redness, and a tendency to bleed during tissue manipulation (Figures 14-9 and 14-10). Long-standing gingival enlargements have a significant fibrotic component as well. Chronic enlargements are generally painless and slowly progressing, whereas acute enlargements are characterized by an acute, painful onset. Generalized enlargements may be disfiguring and may impair nutri-

Treatment
Meticulous patient self-care combined with frequent professional dental care can slow the development of gingival hyperplasia and the need for surgical recontouring of the gingiva. Patients scheduled to receive a medication associated with a potential for gingival overgrowth should be referred to a dentist for a baseline periodontal evaluation before the initiation of drug therapy and for future evaluations of periodontal tissues. The most effective treatment for gingival hyperplasia is medication substitution or withdrawal.88 Introductions of a new generation of anticonvulsants such as levetiracetam (Keppra) and topiramate (Topamax) have made phenytoin substitution more feasible.91 It has also been suggested that changing a patients antihypertensive treatment from nifedipine to another class of medications such as thiazide diuretics, beta blockers, or angiotensin-converting enzyme inhibitors may result in regression of gingival enlargement.92 Switching from cyclosporine to tacrolimus has been shown to cause significant resolution or complete regression of the gingival enlargement in renal transplant recipients.9294 If gingival overgrowth occurs and leads to subsequent increased dental plaque accumulation, then surgical treatment may be indicated.95

Figure 14-9. Phenytoin-induced gingival enlargement. (Photograph courtesy of Russell Taichman, DMD, DMSc.)

Figure 14-10. Cyclosporine-induced gingival hyperplasia. Presentation of a patient before (A) and 12 weeks after (B) corrective surgery to reshape the gingival tissues. (Photograph courtesy of Rodrigo Neiva, DDS, MS.)

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Bisphosphonate-Induced Osteonecrosis
Recent reports of osteonecrosis in the jaws of patients receiving intravenous bisphosphonate therapy for bone cancers, such as multiple myeloma and metastatic prostate cancer, have caused great concern (Figure 14-11). These drugs, including pamidronate and zoledronic acid, work by inhibiting osteoclast action and result in an impairment of the normal bone repair mechanism. The repetitive microtrauma of mastication routinely results in bone remodeling, but this is significantly impaired in these patients.96,97 Although painless, the exposed bone is alarming to the patient and his physician. Patients who have been treated with intravenous bisphosphonates are advised to avoid surgical procedures such as extractions to minimize the risk of osteonecrosis.

Xerostomia
The presence of saliva is typically taken for granted and is often not appreciated until it is either altered or reduced in quantity. Men who are taking medications that induce dry mouth, or those who have undergone head and neck radiation therapy, often report a reduced quality of life and constantly carry water to sip and lubricate their mouths. Adequate and appropriate saliva is important for oral homeostasis; any significant derangements can lead to pathologic conditions of the oral cavity.

The Functions of Saliva

Saliva is composed predominantly of water and mucins, making a good oral lubricant and buffer

for the many acidic foods that we consume. It carries a large number of enzymes and salivary amylases that break down proteins and carbohydrates as the first stage of digestion. The major salivary glands, the parotid, submandibular, and sublingual glands, produce saliva that differs in its mucous and serous nature due to different glandular components (Table 14-6). Minor salivary glands line the lips, palate, and buccal mucosa for additional lubrication. Saliva not only buffers the acids in the foods we eat, but it also buffers the acids produced by bacteria that metabolize the sugars on our gums and teeth. Patients with decreased salivary flow are therefore at a greater risk of tooth decay. The lubricating properties of saliva are important for speech, swallowing, food manipulation, and the use of dentures. As the fluid that lines the main portal of entry and the start of the digestive tract, saliva contains antimicrobial agents to maintain homeostasis of the normal oral flora, in addition to immunoglobulin A, lactoferrin, lysozyme, and peroxidases. Salivary flow and composition may differ based on stimulation or lack thereof. Stimulated saliva is brought on not just by the ingestion of food but also the sight, smell, or anticipation of it (i.e., pavlovian response). Salivary flow is controlled predominantly through the parasympathetic nervous system as a part of a series of activities geared toward maintaining homeostasis. Changes that inhibit the parasympathetic nervous system, such as the fight or flight response, or various anticholinergic medications will cause a reduction in salivary flow. Decreased

Table 14-6. Functions of Salivary Molecules

Functional Property Antibacterial Antiviral Antifungal Buffering Digestion Mineralization Lubrication Tissue coating Salivary Molecule Amylase, cystatins, histatins, mucins, peroxidases Cystatins, mucins Histatins Histatins, carbonic anhydrases Amylases, mucins Cystatins, histatins, proline-rich proteins, satherines Mucins, satherines Amylase, cystatin, mucins, proline-rich proteins, satherines

Figure 14-11. Bisphosphonate-induced osteonecrosis associated with the mandibular anterior alveolus. (Photograph courtesy of Brent Ward, DDS, MD.)

Adapted from: Humphrey SP, Williamson RT: A review of saliva: normal composition, flow, and function, J Prosthet Dent 85 (2):162169, 2001.

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Oral Health salivary flow while sleeping is due in part to reduced oromotor functions but is also thought to be due to circadian rhythms.98 Xerostomia, the reduction in salivary flow, may be due to medications with anticholinergic side effects (Table 14-7). Patients who take medications for psychiatric illnesses including depression or schizophrenia are also less likely to demonstrate positive oral health habits, such as good oral hygiene, avoidance of a cariogenic diet, and routine dental care. Radiation therapy to the head and neck of doses greater than 2000 rads can produce permanent damage to salivary glands and result in chronic dry mouth. Rampant tooth decay can result within 12 months of completing treatment.99
Table 14-7. Drug Classes Associated with Xerostomia
Class Analgesic narcotics Anti-asthmatics/ bronchodilators Anticholinergics Antidepressants Antihistamines Antihypertensives Anxiolytics Anti-Parkinson agents Antipsychotics Decongestants Anti-acne medications Muscle relaxants Anticonvulsants Antiarrhythmics Anorexiants Antidiarrheals Antiemetics Examples Codeine, morphine Beclomethasone, tiotropium Scopolamine Fluoxetine, doxepin, MAOIs Cetirizine, hydroxyzine, clemastine Diuretics, atenolol Triazolam Benztropine Thioridazine, clozapine Ephedrine Isotretinoin Tizanidine Carbamazepine Disopyramide Phentermine Loperamide Droperidol, thiethylperazine, ondansetron Phenetidin, transretinoic acid

14

Prevention
Recognition of the importance of saliva has led to innovations intended to prevent xerostomia where it most often occurs. Radiation therapy regimens can now use computer technology to spare the parotid gland while delivering adequate treatment limited to cancerous tissue. Pharmacologic advances have resulted in antipsychotic and antidepressant medications with less negative effect on salivary flow. Communicating the availability and benefit of these advances to primary care practitioners is of paramount importance. Attention toward good oral health habits, including brushing, flossing, and avoidance of cariogenic foods, is necessary to prevent tooth decay in this high-risk population. Also recommended is the daily use of a highly concentrated fluoride product, either 1.0% sodium fluoride or 0.4% stannous fluoride in a gel form.100 Some oral lubricants and saliva substitutes are available, many of which are formulated to match the biochemical properties of saliva; however, most patients still rely on carrying a bottle of water for continued oral lubrication.

Chemopreventive agents

MAOIs, Monoamine oxidase inhibitors. Adapted from: USP DI Drug Information for the Healthcare Professional, ed 24, Englewood, CO, 2004, Micromedix Inc. Table based on Sreebny LM, Schwartz SS: A reference guide to drugs and dry mouth2nd edition. Gerodontology 14(1):3347, 1991; Wynn RL, Meiller TF, Crossley HL: Drug Information Handbook for Dentistry, 20022003, ed 8, Hudson, OH, 2002, Lexi-Comp.

Systemic Effects of Oral Disease

Periodontitis Associated with Systemic Conditions
Recent evidence suggests that there are two sides to the relationship between periodontal diseases and systemic health. For some time it has been known that systemic factors (e.g., smoking, diabetes, immunodeficiencies, blood dyscrasias) have a negative impact on periodontal health.101,102 More recently, an appreciation that chronic oral infections may have an adverse

effect on a persons systemic health has been recognized. This concept is not entirely new, yet greater appreciation for the health consequences of controlling dental and oral conditions by the healthcare community is most welcome. This is a rapidly expanding field in dental research and has received considerable attention in the lay and scientific press. For example, coronary occlusive diseases, diabetes, aspiration pneumonias, and cerebrovascular events including stroke have all been linked in cross-sectional studies to periodontal disease.73,103106 The critical component is that few of these conditions have been definitively proven as causative of periodontal disease. Nevertheless, it seems prudent to treat infections promptly and adequately independent of whether oral infections are causative for systemic conditions. 257

The Adult Male

Diabetes Mellitus
A substantial body of evidence suggests a bidirectional relationship between diabetes and periodontal disease. The scientific evidence is strongest for the association of type I diabetes mellitus being related to periodontal disease, yet patients with type II diabetes mellitus also appear to be at a greater risk for severe periodontal disease.107 Increasing evidence suggests that the treatment of periodontal infections through mechanical therapy combined with systemic antibiotics may improve glycemic control.108111 However, other studies in which scaling and root planing were performed without the use of systemic antibiotics showed no effect on glycemic control.112 Also, a recent meta-analysis attempting to quantify the effects of periodontal treatment on hemoglobin A1c (HbA1c) level among persons with diabetes found that periodontal therapy with antibiotics appeared to decrease HbA1c levels by a statistically nonsignificant 0.71% among patients with type 2 diabetes.113 Additional research is necessary to firmly establish that treating periodontal infections can contribute to glycemic control management and possibly to the reduction of type 2 diabetes complications.114 Regardless of causation, prompt diagnosis of periodontitis and aggressive therapy targeted at lowering glycosylated hemoglobin levels in a patient with diabetes is likely to be of benefit for persons at risk for periodontal disease.

atherosclerosis and its sequelae; rather, periodontitis and cardiovascular disease share risk factors including tobacco smoking, male gender, race/ ethnicity, stress, and aging.117,121 Longitudinal studies with large numbers of participants will be required if causality is to be established.

Respiratory Diseases
The role of oral pathogens in the development of respiratory diseases has been studied extensively but is not fully understood. Both decayed teeth and the periodontium can serve as a reservoir for bacteria, which can seed the lungs and result in aspiration pneumonia. This is a significant concern in alcoholics, bed-bound elderly persons, and others who are dependent on caregivers to provide oral hygiene.104,105

Bacterial Endocarditis
The workup for patients with bacterial endocarditis typically includes a dental evaluation and often extraction of diseased teeth as a prophylactic measure. This is performed to rule out the dentition as a potential source of infection and to address the finding of oral pathogens in the bloodstream and on heart valves. In a review of the literature on bacterial endocarditis and oral health, Lockhart122 finds little evidence that dental procedures can be conclusively linked as causative. Patients with endocarditis are often found to be intravenous drug users, and such behavior often goes hand in hand with poor dental habits such as a cariogenic diet and poor routine dental care.

Cardiovascular Disease
Several epidemiologic studies and systematic reviews have suggested an association between periodontal disease, coronary heart disease, and stroke.111,115,116 Other epidemiologic studies have found no relationship between periodontal disease and cardiovascular diseases.105,117 Chronic inflammation has been associated with atherosclerosis.118 Periodontal disease inflammation has been suggested to play a role in the initiation or progression of coronary artery disease and stroke.116 Current evidence links C-reactive protein as the common association between periodontal disease and cardiovascular diseases. Another suggested linking mechanism is the gram-negative bacteria itself, whereby antibodies to the bacteria are produced, resulting in arterial injury.119 The treatment of periodontitis to eliminate infection has not been shown to reduce cardiovascular disease.120 Several authors have suggested that the evidence does not support a causal relationship between periodontitis and 258

Conclusion
This chapter has attempted to expose readers to the topic of oral health and disease with the vision of increasing observation of the oral cavity during routine health examinations as an integral component of systemic health. Various medical conditions and therapies can cause oral pathology, and increasingly it is found that oral health can significantly affect systemic conditions. As our society divides further along socioeconomic strata into those who seek dental care and those who do not, primary care physicians may find it necessary to include an oral examination as part of their physical examination and to make appropriate referrals for dental care when they discover significant findings. As the field of dentistry has just begun to examine its data from an evidence-based practice standpoint, dental and medical professionals will be able to

Oral Health communicate well in seeking cost-effective and beneficial care for their patients. References
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