Douglas K. MacLeod
David E. Kern
The purpose of this chapter is to provide guidelines for recognizing, treating, and referring patients with acute dental and oral problems and to increase awareness of chronic dental and oral problems that may require referral and treatment. These types of problems are often neglected by the patient because of fear or ignorance about possible corrective treatment, anticipated pain from the procedure, or the anticipated cost of treatment.
Oral Examination
The systematic examination of the oral cavity should include lips, cheeks (buccal mucosa), hard and soft palate, salivary ducts (parotid duct orifice in the buccal mucosa opposite the upper second molars and submandibular duct orifice beside the lingual frenulum), tonsillar area, tongue, floor of the mouth, gingiva, and teeth, noting the normal structures and any deviations from normal. A dental examination includes an evaluation of the number (20 in the primary dentition and 32 in the permanent dentition; Fig. 112.1), position, and arrangement of the teeth and a check for caries (see Dental Caries), erosions, abrasions, and fractures. It is important to examine the gingiva completely. The normal healthy gingiva is firm, pink, and nontender and does not bleed on palpation or probing. Figure 112.2 shows the parts of a tooth and its adjacent structures.
Acute Dental and Oral Problems
Toothaches (Pulpitis)
Presentation
Patients with toothache have a large carious lesion (see Dental Caries, below), a large restoration (filling), or a combination of both. In the early stages, there is inflammation involving a portion of the pulp tissue (the central portion of the tooth, containing vital soft tissue; Fig. 112.2A).
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FIGURE 112.1. Permanent dentition. |
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There is severe pain in response to thermal stimuli, particularly cold, and this pain persists for longer than 15 seconds after the stimulus is removed. As the area of inflammation increases, the pain becomes more severe; it may radiate to the suborbital area, the side of the face, or the ear. When total necrosis of the pulp occurs, sensitivity to thermal stimuli is lost. If, at this point, the inflammatory exudate cannot escape into the oral cavity, the pressure is released via the root apex, and there is exquisite sensitivity to percussion of the crown of the tooth. The signs and symptoms of pulpitis may be confused with pericoronitis (wisdom teeth pain, see below, Wisdom Tooth Pain) or periodontitis (see Periodontal Disease), and without further diagnostic aids (i.e., dental x-rays) it may be difficult to differentiate between these conditions.
If pulpitis is not treated, complications may occur, ranging from a localized alveolar abscess (an abscess of the bony supporting structure of the teeth) to facial cellulitis. The rate and type of complication depends on the location of the affected tooth, host resistance, and virulence of the bacteria present.
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FIGURE 112.2. Structure of normal teeth and gingiva. A: A tooth and its parts. B: Teeth and gingiva. |
Treatment
Depending on the situation when the patient is seen, one has three options. For patients who are afebrile and have no extraoral swelling (swelling that produces facial asymmetry) or intraoral swelling (swelling that disrupts the supporting alveolar bone and soft tissue), analgesics (acetaminophen 650 mg and/or codeine 30 mg or immediate-release oxycodone 5 mg every 4 hours) and referral within 24 hours are indicated. In this situation the value of antibiotics is unproven (1). When slight extraoral or intraoral swelling or a low-grade temperature elevation is present, antibiotics (penicillin V 250 mg or, for patients allergic to penicillin, clindamycin 300 mg every 6 hours) are recommended, and the patient should be seen by a dentist within 12 to 24 hours. Patients with temperatures greater than 101°F (38.5°C) with intraoral or extraoral swelling causing facial asymmetry need immediate consultation and treatment by a dentist. Treatment of these types of problems varies from extraction of the affected tooth, root canal therapy (endodontics), or incision and drainage to hospital admission for intravenous antibiotics for facial cellulitis.
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Pericoronitis (Third Molar or Wisdom Tooth Pain)
Presentation
Pericoronitis is acute inflammation of the tissue around the crown of a partially erupted tooth. Patients with pericoronitis are usually between the ages of 15 and 25, although rarely the condition can be seen in older patients if they still have their third molars. The patient may give a history of subacute episodes of pain of the gingiva that partially covers the crown of an incompletely erupted tooth. The tooth most often affected is the mandibular third molar (wisdom tooth). The space between the crown of the tooth and the overlying gingival flap is an ideal area for the accumulation of food and bacteria; this leads to inflammation. The flap is traumatized by contact with the tooth in the opposing jaw, usually the maxillary third molar, and the inflammation is aggravated.
The patient describes pain that radiates to the ear, throat, and floor of the mouth. He or she complains of a foul taste, and there is swelling of the affected area so that he cannot close the jaw properly. In severe cases, pain spreading to the oropharynx and base of the tongue makes it difficult to swallow. The gingival tissue is markedly red, swollen, and tender (Fig. 112.3A). Occasionally, tender lymphadenopathy and systemic manifestations (fever, leukocytosis, and malaise) are present. Peritonsillar abscess, cellulitis, and Ludwig angina (cellulitis of the floor of the mouth) are possible complications.
Treatment
In afebrile patients, one needs only to make a dental referral and prescribe analgesics. Febrile patients should be treated with antibiotics (penicillin V 500 mg or, for patients allergic to penicillin, clindamycin 300 mg every 6 hours), moderate analgesics (acetaminophen 650 mg and/or codeine 30 mg or immediate-release oxycodone 5 mg every 4 to 6 hours), and chlorhexidine gluconate 0.12% oral rinse and brush with a soft toothbrush twice a day (Peridex or Periogard, by prescription); the rinse should be expectorated after use. All patients should be seen by a dentist within 24 hours. Depending on many factors, the dentist either excises or debrides the flap or removes the partially erupted lower tooth. The preferred treatment for third molars that are erupting in a position that produces poor occlusion is to remove the traumatizing maxillary third molar tooth and allow the infected flap to heal. The mandibular tooth is then removed 7 to 10 days later, after the acute infection has resolved. When pericoronitis involves eruption of third molars that are in good position for occlusion, the inflamed gingival flap is removed and the teeth are left in place.
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FIGURE 112.3. A: Pericoronitis of the mandibular third molar. B: Acute necrotizing ulcerative gingivitis. |
Acute Necrotizing Ulcerative Gingivitis (Vincent Infection, Trench Mouth)
Acute necrotizing ulcerative gingivitis (ANUG) may occur at any age, but it is more common among young to middle-aged adults.
Presentation
ANUG has a sudden onset and is usually associated with a debilitating illness or acute respiratory infection. Often there is a history of a change in the patient's life, such as protracted work without rest or recent psychologic stress. There is a fetid mouth odor, and the patient describes a foul metallic taste, increased salivation, spontaneous gingival hemorrhage, and pronounced bleeding with the slightest stimulation. The lesions are extremely sensitive to touch; pain is constant and gnawing and is intensified by hot or spicy foods. The oral findings are punched-out crater-like depressions at the crest of the interdental papillae or marginal gingiva. The surface of the gingiva is covered by gray pseudomembranous slough that is demarcated from the gingiva by a pronounced linear erythema (Fig. 112.3B). Patients usually have submandibular
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lymphadenopathy and slight elevation in temperature; in severe cases, high fever, tachycardia, leukocytosis, loss of appetite, and malaise are seen.
Most investigators believe that ANUG is caused by two agents, which are normal oral flora: a fusiform bacillus and Borrelia vincentii, a spirochete. Histologically, the stratified squamous epithelium of the gingiva is ulcerated and replaced by a thick fibrinous exudate containing many polymorphonuclear leukocytes and microorganisms.
Complications include destruction of the gingiva and underlying supporting tissues, which after repeated episodes of ANUG can result in the loss of teeth. In rare cases, severe sequelae, such as noma (rapidly spreading gangrene of oral and facial tissue, which occurs in the debilitated and nutritionally deficient patient), fusospirochetal meningitis, peritonitis, pneumonia, bacteremia, and brain abscess, have been reported.
Treatment
Patients with severe ANUG need immediate hospital admission, intravenous antibiotics, and supportive care (analgesics, hydrogen peroxide mouthwashes) until systemic symptoms subside. Patients with less severe ANUG need immediate attention by a dentist. At this visit, after treatment with a topical anesthetic, a cotton pellet and carbamide peroxide solution (an oxygenating and foaming agent, such as Gly Oxide) are used to remove the pseudomembrane and surface debris. Antimicrobials are usually prescribed for a few days by the dentist. After irrigation with warm water, the superficial calculus is removed. Patients are instructed to avoid tobacco and alcohol, to rinse with warm water and chlorhexidine gluconate 0.12% twice daily, and to confine toothbrushing to the removal of surface debris. When these instructions are followed after effective removal of all irritants by the dentist, a patient usually improves markedly within 5 days. If after the acute phase the patient does not continue periodic dental care, ANUG may recur and lead to eventual tooth loss.
Recurrent Aphthous Stomatitis
Aphthous ulcers, also called canker sores, occur at some time in 20% to 50% of the adult population, are slightly more common in females, have familial tendencies, and occur most often during the winter and spring (2). Recurrent aphthous stomatitis (RAS) was once thought to be a recurrent infection by the herpes simplex virus (HSV), but that is not the case; the cause of the condition is still unknown.
Presentation
Aphthous stomatitis is characterized by superficial ulcerations on the mucous membranes of the lips, cheek, tongue, floor of the mouth, palate, and gingiva. This condition begins with a prodromal burning 1 to 48 hours before the appearance of discrete vesicles, which are approximately 2 to 5 mm in diameter and are painful. After 2 days, they rupture and form saucer-like ulcers that consist of a red or grayish red central portion and an elevated rim-like periphery. There may be a single lesion or multiple ulcers.
The lesions heal spontaneously within 7 to 10 days. As a rule, the lesions are larger than those seen in acute herpetic gingivostomatitis (seenext section) and do not exhibit the diffuse gingival involvement or systemic symptoms seen in that condition.
RAS occurs in the following forms:
Treatment
Treatment of aphthae is symptomatic. There is some evidence that chlorhexidine gluconate mouth rinses or gels can reduce the severity of episodes (3). A mouthwash containing equal parts of Benadryl suspension and Kaopectate (Benadryl 5 mg/mL mixed with an equal amount of Kaopectate, prepared by a pharmacist) is helpful in reducing the pain, as is viscous Xylocaine applied by cotton-tip applicator to painful lesions. Topical corticosteroids (e.g., triamcinolone in Orabase) may decrease the duration of ulceration and symptoms (3). The Orabase aspect of this product is a paste specially designed to adhere to the surface of oral lesions.
In more severe cases, tetracycline has been successful in decreasing pain and duration of the ulcers; the patient should be instructed to empty a 250-mg capsule in 50 mL of water and to use this as a rinse, which is then swallowed, three or four times a day for 5 to 7 days. The patient should be encouraged to take sufficient amounts of nonirritating liquids or soft food to maintain hydration and nutrition. Intake may be facilitated by using a straw to prevent contact with the painful ulcers. Based on empiric experience, the amino acid L-lysine may also help reduce symptoms. The patient should be instructed to take orally 1,000 to 1,500 mg with each meal during prodromal symptoms and on the days lesions are present and then as a preventive measure, 500 mg with each meal indefinitely.
Acute Herpetic Gingivostomatitis
Acute herpetic gingivostomatitis (AHGS) occurs most often in infants and children younger than the age of 6 years, and it is equally common in males and females. It is caused by herpes simplex virus (HSV) and most oral
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infections are caused by HSV type 1. However, it also occurs in older patients, including (rarely) the elderly (4). Most adults have developed immunity to HSV as a result of childhood infection, usually inapparent. Although recurrent acute herpetic gingivostomatitis has been reported, it does not usually recur unless immunity has been altered by a debilitating systemic disease.
Presentation
AHGS appears as a diffuse, erythematous, shiny involvement of the gingiva and the adjacent oral mucosa, with varying degrees of edema and gingival bleeding. In the initial stage it is characterized by the presence of discrete spherical gray vesicles that may occur in the gingiva, labial and buccal mucosa, soft palate, pharynx, sublingual mucosa, and tongue. Within 24 hours the vesicles rupture and form small painful ulcers with a red, elevated, halo-like margin and a depressed yellowish or grayish white central portion. Regional lymphadenopathy, fever as high as 105°F (40.5°C), and generalized malaise are common. The course is limited to 7 to 10 days, and the ulcers heal without scarring. This condition is differentiated by the presence of diffuse gingival involvement and systemic symptoms, which are not present in RAS. Tzanck testing was positive in 77% in a series of 13 patients (4). Viral culture is considered the gold standard and most sensitive of diagnostic techniques, but is seldom required.
Treatment
AHGS usually runs a benign, self-limiting course in immunocompetent patients. In the immunocompromized patient, prompt recognition and treatment is important, because these patients are at risk for dissemination. Symptomatic treatment includes a systemic analgesic and antipyretic, such as acetominophen, and a palliative mouth rinse, such as a diphenhdramine/Kaopectate mix (see RAS, above). Antibacterial agents are not helpful, and corticosteroids are contraindicated. The use of systemic or topical antiviral therapy (acyclovir, valacyclovir, famciclovir) is uncertain. Its use is probably warranted in the management of severely infected and immunocompromized patients, although this should be done in consultation with an infectious disease specialist or a dentist (see Chapter 102 for a discussion of antiviral therapy).
Herpes Simplex Labialis
Recurrent herpes simplex infections of the lips or perioral area occur in 20% to 40% of the adult population. Evidence suggests that recurrent herpes is not a reinfection but a reactivation of virus that remains latent in the nerve tissue.
Presentation
The natural history of this problem has been well delineated. Most affected subjects have several episodes during an average year. In approximately 60% of episodes, there is prodromal tingling for a number of hours before the appearance of the first vesicles. Pain is moderate to severe during the first 24 hours after appearance of vesicles and then rapidly diminishes. After 48 hours, vesicles are usually replaced by ulcer crusts. The process usually resolves after 7 to 9 days, but lesions may persist as long as 2 weeks. Chapter 117 discusses the therapy of this condition.
Sialadenitis
Presentation
Sialadenitis is an inflammation of the salivary gland. Patients with sialadenitis experience pain and enlargement of the affected gland. In bacterial sialadenitis, the pain and swelling are not related to eating. The overlying skin may be red and tense, and the affected gland yields a purulent discharge at the duct orifice. Bacterial sialadenitis is more common in children than in adults. Obstructive sialadenitis is more common than bacterial infection of the salivary glands and is associated with salivary stones or a mucous plug. It occurs most often in middle-aged men. The involved gland is enlarged and painful, and the symptoms are more prominent before, during, and soon after eating. The submandibular gland is most often affected (75% of cases), whereas the parotid (20% of cases) and major sublingual glands (5% of cases) are less often involved. Mumps is more common in children but does occur in adults, when it often is more severe. The parotid gland is swollen and tender, and there is usually no redness, heat, or discharge. Most often both parotids are involved and, often, other salivary glands. Systemic symptoms are common.
Treatment
Treatment of bacterial sialadenitis consists of heat application (external moist heat packs to the affected gland for 15 to 20 minutes and intraoral warm rinses), analgesics (acetaminophen 650 mg and/or immediate-release oxycodone 5 to 10 mg or codeine 30 mg every 4 to 6 hours), antibiotics (penicillin V 500 mg or, for patients allergic to penicillin, clindamycin 300 mg every 6 hours for 7 days), and a liquid diet for the first 2 to 3 days.
The management of obstructive sialadenitis is more complex. When this diagnosis is suspected, the patient should be referred to a dentist or otolaryngologist. In cases in which the stone is lodged in the duct, the acute phase is managed in the same manner as is bacterial sialadenitis, and after resolution has begun a sialogram is obtained to determine the extent of the problem. Surgical removal of the stone from the duct is eventually performed to prevent recurrence. In chronic obstructive sialadenitis, surgical
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excision of the gland is often necessary. The likelihood of recurrence after the first episode is unknown.
Temporomandibular Joint Pain
Several studies of healthy populations have shown that symptoms of temporomandibular joint (TMJ) disorders are present at some time in 25% to 50% of people but are not considered a serious problem by most patients (5). Most (70% to 90%) patients who have these symptoms are women between the ages of 24 and 40. Multiple factors may lead to TMJ pain; there may be a history of stress, bruxism (grinding of teeth), external blows to the jaws, or whiplash injury. TMJ pain may be present at some point in 20% of patients with rheumatoid arthritis. Patients with osteoarthritis of other joints may complain of TMJ clicking and snapping, but pain is usually absent.
Presentation
TMJ disorders are characterized by pain and tenderness in the muscles of mastication and in the TMJ, by crepitus when the joint is moved, and by a decrease in range of motion. In some severe cases there is a noticeable incoordination on the opening and closing of the jaw. This appears as a unilateral shift of the chin upon opening or closing the mouth. Examination may show malocclusion caused by teeth that interfere with the normal movement of the mandible or tenderness of the muscles of mastication.
Treatment
Patients with acute TMJ pain should be managed with moderate analgesics (acetaminophen 650 mg and/or immediate-release oxycodone 5 to 10 mg or codeine 30 mg every 4 to 6 hours) and referral to a dentist within 24 to 48 hours to begin therapy. The dentist's goal is to make the patient aware of the cause of the problem through education. Depending on the severity of symptoms and the state of the patient's dentition, the dentist will prescribe one or a combination of the following: avoidance of excessive jaw motion, moist heat to affected muscles, soft diet, disengagement of upper and lower jaws with a night guard to separate the upper and lower teeth (a hard appliance constructed to fit the individual patient, which is quite costly), therapeutic exercises, and vapocoolant spray (ethyl chloride to decrease muscle pain). In atypical cases, trigger point injections of xylocaine may be used to distinguish TMJ symptoms from trigeminal neuralgia (see Chapter 87). Once the acute episode has subsided (in about 7 to 14 days) the dentist can detect and eliminate any occlusal interferences and rule out any degenerative joint disease that may have predisposed the patient to TMJ symptoms. In the past, injections of sclerosing agents into the TMJ and condylectomy were tried, but with poor success. In a 10-year study, 97 of 100 patients treated conservatively improved. Of these, 83 had permanent improvement. Of the three patients who had intractable severe symptoms, two required prolonged psychotherapy and one developed systemic arteritis (6).
Local Alveolar Osteitis (Dry Socket)
Local alveolar osteitis (dry socket) is the most common complication of tooth extraction. It occurs in approximately 5% of all tooth extractions, but it is more common after the removal of an impacted third molar. This problem results from the loss of the blood clot located at the site of the extraction. Most often this occurs when the extraction has been difficult and has resulted in considerable trauma to the socket and gum.
Patients with this problem describe intense localized pain 2 or 3 days after an extraction. This pain is caused by irritation of the sensory nerves in the dry exposed bony socket. There is often a foul odor emanating from the socket, but no suppuration is present.
One should control the pain the patient is experiencing with immediate-release oxycodone, 5 to 10 mg or codeine 30 mg every 3 to 4 hours, and acetaminophen, 650 mg three to four times per day. The patient should be referred promptly to a dentist for irrigation and the placement of a dressing. The dentist needs to see the patient every day or two for approximately 10 days until the socket becomes reepithelialized. There are no long-term sequelae.
Chronic Dental and Oral Problems
Periodontal Disease (Pyorrhea)
Periodontal disease is a general term used to describe diseases that destroy the gingival and bony structures that support the teeth (Figs. 112.4 and 112.5).
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Periodontal disease is usually subdivided into gingivitis and periodontitis. The major difference between the two is that in periodontitis there is loss of the supporting bony apparatus of the teeth. Two thirds of young adults, 80% of middle-aged adults, and 90% of people in the United States older than 65 years suffer from periodontal disease (7).
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FIGURE 112.4. Dentogingival junction in health. A: Plaque free. B: Gingivitis resulting from plaque accumulation with inflammation of soft tissue. C: Periodontitis resulting from long-standing inflammation that has caused bone loss and tooth mobility. |
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FIGURE 112.5. Normal gingiva (A) and chronic periodontal inflammation (B) showing swelling, blunting of interdental papillae, erythema, and bleeding. |
Risk Factors
Poor oral hygiene, which permits plaque to accumulate on the teeth, is the major etiologic factor. Most periodontal dis-ease, and therefore most loss of teeth, is preventable. Pre-vention consists of routine plaque control (see Treatment).
Medical problems (8) that are risk factors for periodontal disease include smoking, oral tobacco use, and diabetes. Osteoporosis increases the risk of periodontal attachement loss (9). The presence of periodontal disease is associated with an increase risk for cardiovascular disease and stroke (10,11), although it is unclear whether the relationship is causal (12).
Medications that commonly cause gingival overgrowth include phenytoin, cyclosporine, and calcium channel blockers. Calcium channel blocking drugs are widely used for management of cardiovascular conditions. Nifedipine is one of the most often prescribed drugs in this group and the first to be associated with gingival overgrowth.
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Most other calcium channel blocking agents have been associated with gingival enlargement, although not to the same degree as nifedipine. The onset of gingival enlargement usually appears within 2 months after initiation of nifedipine therapy and is most pronounced in the anterior facial gingiva. The tendency for overgrowth occurs in approximately 15% to 20% of patients, and although it does not appear to be dose related, occasionally a decrease in enlargement after dosage reduction has been reported. The histologic, histochemical, and electron microscopic examinations of nifedipine-induced gingival enlargement closely resembles phenytoin- or cyclosporine-induced gingival overgrowth, suggesting a similar pathogenic mechanism. Chronic inflammation is always present, and an association between plaque accumulation and drug-induced overgrowth has been documented. Meticulous plaque control does not usually cause remission or consistently stop recurrence after surgical removal. Whenever gingival overgrowth develops, an alternative to nifedipine should be considered. If a calcium channel blocking agent is essential for the patient, an agent other than a dihydropyridine should be used. Examples of such agents that could be used in this situation include diltiazem and verapamil.
Patients who have had organ transplants may be taking cyclosporine, an immunosuppressant drug used extensively to suppress organ and bone marrow transplant rejection. The combination of cyclosporine and calcium channel blocking agents appears to have a synergistic effect on the gingiva. The hyperplasia produced is extreme and often recurs after surgical excision.
Gingivitis
Presentation
Gingivitis is usually seen in one of four forms: acute, a painful condition that has a rapid onset and is of short duration; subacute, which is less severe than the acute condition; recurrent, which reappears after being eliminated by treatment or after disappearing spontaneously; and chronic, the most common form, which has a slow onset, is of a long duration, and is usually painless unless complicated by acute exacerbations (Fig. 112.5).
The early signs of inflammation of the gingiva, which precede frank gingivitis, are increased gingival fluid secretion and bleeding from the gingival sulcus upon gentle probing. Healthy gingiva is usually coral pink, whereas in gingivitis the gingiva becomes bright red secondary to increased vascularity and a decrease in keratinization. These changes start in the interdental papillae and free gingiva and spread to the attached gingiva. Both acute and chronic forms produce changes in the normally firm resilient consistency of the gingiva. In acute gingivitis the gingiva has a diffuse edematous appearance, whereas in the chronic form the tissue has a fibrous appearance that pits on pressure.
The development of gingivitis is a consequence of supragingival and subgingival plaque formation (Fig. 112.4). Plaque is a transparent deposit composed primarily of bacteria and their byproducts. Gram-positive filamentous rods, mainly Actinomyces, appear to be of major significance. Small amounts of plaque are not visible unless they are stained. As plaque accumulates, it becomes visible as a mass that varies in color from gray to yellowish gray to yellow. Measurable amounts of plaque may form within 1 hour after a thorough cleaning of the teeth, with maximal accumulation in 30 days or less. Bacterial plaque, if left undisturbed, mineralizes and forms calculus (tartar), as shown in Fig. 112.4C. This process usually starts between the first and fourteenth day after plaque formation. Calculus is always covered by plaque. When calculus is present, the gingival tissues are unhealthy by definition. The major complication of untreated gingivitis is periodontitis, that is, the extension of the inflammation to the supporting bony structures of the teeth (see Periodontitis and Fig. 112.4C).
Treatment
Patients presenting with any one of the four forms of gingivitis usually require one to three dental visits (spread over about a 4-week period) for treatment. The mechanical removal of plaque and calculus from the affected areas of the teeth and gingiva (scaling) and smoothing of root surfaces (root planing) result in a decrease in probing depth and a decrease of attachment loss between the gingiva and tooth (13). After all the plaque and calculus have been removed by the dentist, the disease process is explained to the patient, who is then instructed in proper plaque control measures, including effective brushing and flossing. A soft-bristled toothbrush or a battery-powered rotating or oscillating toothbrush should be recommended. Effective brushing cleans both the teeth and gingiva and facilitates the removal of plaque. Powered toothbrushes have been shown to be more effecte than manual burshes in removing plaque and reducing gingivitis (14). Floss should be rubbed vertically up and down three to five times in each interdental space first against the one tooth and then against the adjacent one, once daily. Maintenance of the disease-free state is possible only by continued effective plaque control measures by the patient and by professional cleaning every 4 to 12 months (to remove plaque and calculus that may be missed by brushing and flossing). Topical antimicrobial mouthwashes provide modest benefit (15,16). Chlorhexidine gluconate, 0.12% oral rinse twice daily (Peridex or PerioGard, available by prescription), has been shown to be microbicidal. The rinse should be expectorated after use. Complications from its use are common and include a brown stain of the teeth, possible taste alterations, and increase in calculus formation. For these reasons a patient should not use the material without consulting a dentist. Factors that usually result in recurrence are incomplete removal of plaque and calculus, inadequate plaque control
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because of insufficient patient instruction, premature dismissal of the patient before competence is demonstrated, and lack of patient cooperation.
Periodontitis
Presentation
A patient with periodontitis has red and bleeding gums and an unpleasant taste in his or her mouth but is usually free of pain unless there is an acute infection superimposed on the underlying chronic process. The principal physical findings are the signs of inflammation of the gingiva described above and periodontal pockets around the teeth, from which pus may often be expressed upon gentle pressure. As periodontitis advances, the teeth loosen and spread apart, creating unattractive spaces and exposing the roots of the teeth as the bony support is lost. Mastication is impaired, and spontaneous pain and acute abscess may occur. The most important consequence of periodontitis is the destruction of the alveolar bone, which deprives the teeth of their support and is responsible for the loss of the teeth. The essential steps leading to destruction of bone are gingivitis, degeneration of collagen bundles of the periodontal ligament, and conversion of the shallow (3 mm or less) physiologic gingival sulcus to a deepened periodontal pocket (more than 3 mm). As this pocket deepens, more debris accumulates in it. Inflammation progresses further inward, and the gums recede permanently. The apically progressing inflammation eventually reaches the alveolar crest, and bone resorption begins. This process continues, resulting in continued destruction of the alveolar bone.
Treatment
Most patients with periodontitis can be treated effectively, provided the diagnosis is made before a significant amount of supporting alveolar bone is lost. The aims of treatment are to preserve the teeth by eliminating the disease, restore effective function, and prevent recurrence. When treated in the early stages, the major consequence of periodontitis (loss of bone support for the teeth) can be prevented. If proper treatment is postponed, there may be insufficient bone support once treatment is undertaken, and the natural teeth may eventually be lost. Although some patients do not seem concerned with this problem, many are subsequently disappointed when they find dentures do not function as efficiently as natural teeth.
Treatment of periodontitis is divided into two phases. Phase I is similar to the treatment of gingivitis described above; that is, removal of local irritant (plaque and calculus) and institution of effective plaque control (continual removal of the plaque). This treatment allows resolution of the inflammation. Although both topical (15,16) and systemic (17) antibiotics provide modest adjunctive benefit, their role in the treatment of periodontal disease is not well established. They are usually used in conjunction with mechanical débridement in patients with fever, lymphadenopathy, resistant or severe disease. Smoking cessation should always be counselled (see Chapter 27). The success of Phase I of therapy depends largely on the patient's ability to maintain plaque-free teeth (see Gingivitis, above). Phase II is the surgical phase, in which the goal is to improve the gingival architecture that remains despite the disease. Experience shows that patients have difficulty preventing inflammation in periodontal pockets greater than 5 mm. Surgical treatment is therefore designed to decrease the depths of the pockets.
Denture Problems
Twenty million American adults are missing all their teeth. Of these, many have obtained dentures. Additionally, many of the edentulous population have managed well without teeth, are content to remain as they are, and, regardless of the quality of dentures constructed, are unwilling or unable to adapt to using dentures.
Presentation
Often a patient who has had dentures for years, upon specific questioning, indicates the dentures are not satisfactory. The most common denture problems are looseness and discomfort. If the patient is followed at least yearly by his or her dentist, one can generally assume the present situation is the best that can be achieved. On the other hand, if the patient has tolerated the same set of loose or uncomfortable dentures without seeking help for a number of years, he or she should be encouraged to seek care promptly. Failure to remove dentures at night is the reason for denture problems in some patients. This practice can cause bony erosion with loss of conformity of the dentures to the supporting structures, mucosal ulceration, and oral candidiasis.
Treatment
Depending on the condition of the patient's oral cavity, the present dentures, and the edentulous ridges, a number of treatment modalities are available, including rebasing or relining the existing dentures (5 to 7 days), making a new set of dentures (2 to 5 weeks), and preprosthetic correction of soft and hard tissue (4 to 6 weeks of healing), followed by relining, rebasing, or remaking of dentures. In recent years, there have been marked improvements in dental implants for patients who have had trouble using dentures (especially lower dentures). The placement of implants is expensive (about $1,600 to $1,800 per implant, often with a reduction in price for multiple installations, and often five to six implants are used per arch) and time consuming (2 to 3 months) and requires that new dentures are made after placement of implants. The implants function as a replacement for the teeth roots the patient
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had previously lost through dental caries, periodontitis, or trauma. Most conservative dentists reserve implants for the patient missing at least all posterior teeth or all natural teeth.
Dental Caries
Dental caries is a disease of the calcified tissues of the teeth characterized by demineralization of the inorganic portion (enamel and dentin of the tooth; Fig. 112.2A). Dental caries is one of the most common diseases in humans. It affects all people regardless of race, location, or economic stratum, and it can occur at any age. Poor oral hygiene and a diet high in sugar promote caries, whereas routine oral hygiene and raw coarse foods tend to reduce caries. Ingestion of fluorides in drinking water reduces susceptibility to caries. The form of the tooth affects caries; that is, the deep pits and fissures on molars and premolars especially predispose these teeth to the disorder.
Presentation
Dental caries usually presents as a nonpainful, white, brown, or black spot on the enamel of a tooth. The most common location is the biting surface in conjunction with the pits and fissures of the tooth. Other locations include the smooth surfaces where the teeth come into contact with each other. Without the aid of special equipment (radiographs and hand instruments) and expertise of dental personnel, the best indicator of dental caries is the presence of brown or black spots in areas associated with lost portions of the tooth.
When a caries progresses rapidly to involve the pulp, as in children, the term acute caries is used. Slowly progressing caries seen in adults is called chronic caries. Occasionally, a carious lesion may cease to progress (arrested caries). This is caused by breakage of enamel walls, thereby exposing the lesion to the cleaning action of the toothbrush, saliva, fluoride, and mastication. The term recurrent caries is used for carious lesions that begin around the margins of defective restorations.
A carious lesion usually develops after bacterial plaque (see Gingivitis) forms on the tooth surface. The primary bacteria involved in this process are Streptococcus mutans and Lactobacillus acidophilus. These bacteria metabolize dietary fructose to produce lactic acid, which results in decalcification of the enamel. The rate of development of caries depends on the susceptibility of the enamel.
Prevention
The most cost-effective preventive approach to preventing dental caries is the fluoridation of public water supplies (18). Individual approaches that are effective in reducing tooth decay include good dental hygiene (see Gingivitis) and the use of topical flourides (toothpastes, mouthrinses, gels, or varnishes) (19).
Treatment
The treatment for most carious lesions is their removal, followed by a restoration (filling) that replaces the lost portions of the tooth. The goals are to remove the lesion, protect the pulp from irritants, and restore the tooth to function. With the advent of enamel and dentin bonding agents, a sealant (a thin plastic layer of resin) can be placed over a noncarious tooth in the deep fissures to prevent dental caries (20). In cases when caries involves a tooth already significantly affected by periodontal disease, the tooth must be removed.
The major complication that results from delaying treatment is acute pulpitis and its complications (see Toothaches). Additionally, delaying treatment may result in a more difficult restoration or possible loss of the involved tooth. In cases in which the existing decay process is very close to the pulp, the heat generated by the rotary instruments used to prepare the restoration may result in a transient pulpal inflammation. This inflammation results in a dull ache in the tooth for 2 to 3 days, which is usually relieved by aspirin or ibuprofen or other nonsteroidal anti-inflammatory drug (NSAID). When the restoration process leaves only a paper-thin layer of dentin covering the pulp tissue, the transient pulpitis may be converted to acute pulpitis (irreversible), which then requires tooth extraction or root canal therapy for relief of pain. Root canal therapy consists of three parts: Removal of the infected nerve tissue, débridement and preparation of the nerve canal space, and obturation (filling) of the canal space with a biologically inert material.
Angular Cheilosis
Presentation
Angular cheilosis is characterized by a feeling of dryness and a burning sensation at the corners of the mouth. The epithelium at the commissures appears wrinkled and macerated. In time, the wrinkles deepen to fissures that appear ulcerated but do not bleed, although a crust may form. These lesions stop at the junction of the mucous membranes. They show a tendency for spontaneous improvement; only rarely do the lesions completely disappear.
There are several causes for cheilosis. A number of microorganisms may cause it in otherwise healthy people: Candida albicans, staphylococci, and streptococci. Additionally, angular cheilosis caused by overclosure of the jaws may be seen in edentulous patients. Overclosure causes a fold to be produced at the corners of the mouth in which saliva tends to collect, inviting the growth of microorganisms. Angular cheilosis is also seen in riboflavin deficiency, which usually occurs in patients with multiple vitamin
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deficiencies. The lips show fissures, painful cracks, and scaling; these changes become severe at the corners of the mouth and are similar in appearance to angular cheilosis caused by overclosure of the mandible.
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FIGURE 112.6. Candidiasis (thrush) of the hard palate. |
Treatment
Edentulous patients troubled by angular cheilosis should be referred to a dentist, who will evaluate them for mandibular overclosure, because correction of this problem (making or remaking of dentures) may lead to remission. Treatment is otherwise symptomatic and consists of applying petrolatum-containing ointment (e.g., Vaseline, Chapstick) to the scaling area to minimize discomfort.
Thrush (Oral Candidiasis)
Presentation
The typical lesions of oral candidiasis are white curd-like plaques on an erythematous mucosa (Fig. 112.6). These plaques are loosely attached and may be scraped off the oral mucosa. They begin as pinpoint spots. Involvement may include the corners of the mouth, as noted in the previous section. The tongue is often reddened, and the patient describes a burning sensation.
Thrush may occur chronically in patients with poor oral hygiene and poor nutrition. It may also be brought on or exacerbated by debilitating systemic illness, antibiotic therapy, impaired immune system, corticosteroids, immunosuppressive agents, or dental extraction. Thrush does not appear to be more common in diabetic patients. It is common in patients with human immunodeficiency virus infection (see Chapter 39).
The white plaques of thrush may suggest hyperkeratosis or leukoplakia. In these instances, a potassium hydoxide preparation of scrapings reveals pseudo-hyphae and budding spores characterisitic of candidiasis.
Treatment
The patient should be advised to use good oral hygiene practices. Specific treatment consists of nystatin oral suspension, 4 to 6 mL held in the mouth for several minutes before swallowing, four times daily. Thrush usually resolves entirely after 1 to 2 weeks of treatment. Treatment should be continued for several days after visible lesions have disappeared. More intensive treatment is needed in patients with human immunodeficiency virus infection (see Chapter 39).
Halitosis
Presentation
Halitosis is a foul or offensive odor emanating from the oral cavity. Mouth odors originate from local or remote sites. The local causes can be retention of odoriferous food particles on or between the teeth, ANUG (see above), caries, chronic periodontal disease, dentures, tobacco smoking, medications and other causes of xerostomia (dry mouth), healing of surgical or extraction wounds, or debris accumulated between the small papilla of the tongue. Extraoral causes of halitosis include infection in adjacent structures (rhinitis, sinusitis, tonsillitis), pulmonary infections, alcoholic breath, the acetone odor of the diabetic, or the uremic breath associated with renal failure. Metabolites from certain foods that are excreted through the lungs (e.g. onions, garlic, pastrami, alcohol, meats) can also produce halitosis. Breath odor worsens with age, as regressive changes occur in the salivary gland that affect the quantity and quality of saliva.
Treatment
Local causes of this condition are treated by improvement in oral hygiene (brushing teeth and tongue) and by specific treatment of the underlying conditions by a dentist. If these measures are unsuccessful, mouthwashes (21) or breath fresheners used frequently (every 2 to 4 hours) may greatly reduce the problem. Halitosis caused by remote factors may be masked with mouthwashes and fresheners until the remote problem has been resolved. When foods or medication are a factor, dietary or medication changes may help.
Xerostomia (Dry Mouth)
Presentation
Xerostomia, or dry mouth, results from a partial or complete lack of saliva. This defect results in cracking of the
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lips, difficulty in swallowing, or changes in the tongue texture. The patient often increases liquid consumption to eliminate the dryness. Xerostomia may be a secondary complication of salivary gland disease (e.g., Sjögren syndrome) or radiation treatment, but medication is the most common cause. Anticholinergic, decongestant, and antihistamine drugs are the most common offenders.
The loss of saliva results in a loss of the protective coating of the mucous membranes of the oral cavity. Infections, severe dental caries, problems with dentures, and halitosis commonly result from the loss of saliva.
Treatment
Treatment of xerostomia is symptomatic. Patients should be referred to a dentist for an evaluation to identify a related problem such as caries, and for instruction in the use of daily topical fluoride to help prevent recurrence of caries. The dryness may be lessened if the patient regularly irrigates the mouth with topical methylcellulose or a saliva substitute (Glandosane, Oralube, MOI STIR, Salive Substitute [Roxane Laboratories] or Xerolube, all available without prescription). The saliva substitutes also decrease the risk of caries because they contain sodium fluoride.
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FIGURE 112.7. Common benign problems of the tongue. A: Geographic tongue. B: Hairy tongue. C: Median rhomboid glossitis. |
Common Tongue Conditions
Geographic Tongue
Benign migratory glossitis, or geographic tongue, is an asymptomatic inflammatory condition consisting of multiple areas of desquamation of the filiform papillae of the tongue in an irregular pattern (Fig. 112.7A). The central portion of an affected area is usually denuded, and the border may be outlined by a thin yellowish white line or band. The fungiform papillae persist in the desquamated area as small, elevated, red dots. The areas of desquamation remain for a short time in one location and then
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heal and reappear in other locations. The condition may persist for weeks or months and then regress, only to recur at a later date. Women are affected twice as often as men, and there is no racial difference. Because the cause is unknown and the condition is benign, management consists of reassurance. Large doses of vitamins are not effective.
Hairy Tongue
Hairy tongue is a condition characterized by hypertrophy of the filiform papillae of the tongue caused by the lack of normal desquamation of the keratin layer (Fig. 112.7B). This results in a thick matted layer on the dorsum of the tongue. The color of the papillae varies from yellowish white to brown or even black depending on their staining by extrinsic factors (tobacco, foods, or medications). The hypertrophied tissue may touch the palate and produce gagging in some patients. Most patients with hairy tongue are heavy smokers, but the cause is unknown. Treatment of this benign condition consists of brushing the tongue with a tongue blade or toothbrush to promote desquamation and remove debris.
Median Rhomboid Glossitis
Median rhomboid glossitis is a congenital abnormality of the tongue that appears clinically as an ovoid-, diamond-, or rhomboid-shaped reddish patch on the dorsal surface of the tongue. On examination, there is a slightly raised or flat area that is distinctive because there are no filiform papillae (Fig. 112.7C). Despite its name, this abnormality is not inflammatory; it is caused by failure of the tuberculum impar to retract before fusion of the lateral halves of the tongue, so that a structure free of papillae is interposed. The prevalence of the abnormality is less than 1%, and there are no sex or racial differences. The only clinical significance of this innocuous condition is that it is occasionally mistaken for a carcinoma; differentiation from cancer is aided by the presence of the lesion since childhood and the fact that a carcinoma rarely develops on the dorsum of the tongue. If one is unsure of the diagnosis, the patient should be referred to a dentist.
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FIGURE 112.8. Leukoplakia showing early changes of epidermoid carcinoma. |
Leukoplakia and Erythroplakia
Presentation
Leukoplakia and erythroplakia are asymptomatic conditions of the oral mucosa that may become malignant. Leukoplakia varies in appearance from a grayish white, flattened, scaly lesion to a thick irregularly shaped plaque (Fig. 112.8). Histologically, there is hyperkeratosis, acanthosis, and some degree of dyskeratosis. It is commonly associated with underlying inflammation caused by a chronic irritant (tobacco, alcohol, poorly constructed dentures). Leukoplakia may be found anywhere in the oral cavity but most often is found in the buccal mucosa, followed, in descending order, by the alveolar mucosa, tongue, lip, hard and soft palates, floor of the mouth, and gingiva.Erythroplakia refers to a lesion that is velvety red in appearance, small (2 cm or less), and with or without a hyperkeratotic component. It is found in the floor of the mouth, soft palate, and ventrolateral border of the tongue.
The significance of these lesions has been delineated in a longitudinal study of mucosal lesions (22). Of 200 white lesions examined by biopsy, only four were malignant. In the same study, an erythroplastic component was present
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in 90% of the 158 asymptomatic squamous cell carcinomas found, suggesting, but not proving, that erythroplakia may be an important precursor of squamous cell cancer. Pathologically, erythroplakia usually is manifest as high-grade dysplasia.
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FIGURE 112.9. Squamous cell carcinoma of the floor of the mouth. |
Treatment
It is impossible to determine which lesion showing leukoplakia or erythroplakia will undergo malignant transformation, although erythroplakia is more likely to do so. Discontinuance of chronic irritants is recommended, followed by a 14-day observation period to allow inflammatory lesions to heal. If the lesion persists, referral to a dental surgeon for a biopsy and regular followup surveillance, even if the lesion is benign, are indicated. The biopsy procedure is as simple as having a restoration (filling) or a tooth extraction.
Other conditions that may resemble leukoplakia or erythroplakia are lichen planus, chemical burns, candidiasis (thrush), psoriasis, lupus erythematosus, and syphilitic mucous patches. Each of these has characteristic histologic features.
Squamous Cell Carcinoma
More than 90% of all malignant tumors of the oral cavity are squamous cell carcinomas. They are four times more common in men than women and are most common after the fourth decade. In the United States, oral cancer is the eighth most common form of cancer in men and the twelfth in women. Fifteen thousand new cases are found each year, and about 7500 patients die of this disease annually. Of lip carcinomas, 95% occur on the lower lip and appear as an ulcer, wart, sore, or scale (22). This lesion is more common in fair-skinned patients. Of the intraoral carcinomas, 50% occur on the tongue (usually the ventrolateral border; Fig. 112.9) and 16% on the floor of the mouth; the remaining 34% are equally distributed between the gingival mucosa, palate, and buccal mucosa. Sixty percent of intraoral carcinomas present as ulcers, 30% as growths, and the remaining 10% as white lesions or other abnormalities of the mucosa (23). Carcinoma of the tongue and floor of the mouth metastasizes early and carries a poor prognosis.
The cause of oral carcinoma is unknown. Tobacco use and alcohol abuse are the major risk factors. Certain viral infections (e.g., Epstein-Barr and human papilloma virus), radiation exposure, dietary, and genetic factors may also increase risk.
Presentation and Evaluation
Patients usually give a history of knowledge of the lesion for 6 to 18 months when they first present; for many reasons they have not sought evaluation. All patients with suspicious lesions should be referred promptly to a dental surgeon for biopsy. Biopsy is a simple procedure, not very different from having a restoration or tooth extraction. Usually it is done under local anesthesia.
Treatment
Definitive surgery is a team effort between the otolaryngologist and the dentist. The dentist's role is to evaluate, for long-term prognosis, any teeth not to be removed in the surgical field and to remove any of these teeth affected with untreatable periodontitis. This is done to avoid osteoradionecrosis, a condition seen in the postradiation patient in whom the socket of an extracted tooth fails to heal as the result of diminished blood supply. Lip tumors have the highest success rate (10-year cure rate between 80% and 92%), whereas only one-fifth of patients with tongue cancer live longer than 5 years.
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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