Humans are surrounded and inhabited by an enormous number of microorganisms. The ability of these organisms to cause disease depends on both the microorganism and the state of the body’s defenses. The organism must be capable of causing disease, and the individual must be susceptible to the disease. Microorganisms are traditionally divided into those that produce disease (pathogenic microorganisms) and those that do not (nonpathogenic microorganisms). To cause disease the organism must gain access to the body, accommodate to growth in the human environment, and avoid multiple host defenses. These defense mechanisms include intact skin and mucosal surfaces, antimicrobial secretory and excretory products on the skin and mucosa, the competition among the components of the normal microflora, the inflammatory response, and the immune response.
Numerous infectious diseases can affect the tissues of the oral cavity. Bacterial, fungal, and viral infections are the most common; but even protozoan and helminthic infections, although extremely rare, have been reported.
The oral cavity can be the primary site of involvement of an infectious disease, or a systemic infection can have oral manifestations. These infections are transmitted from one individual to another by several different routes. Organisms can be transferred through the air on dust particles or water droplets. Some organisms require intimate and direct contact to be transferred. Some can be transferred on hands and objects, and others such as hepatitis B must be transferred from one person to another in blood or other body fluids. Microorganisms that initially invade the oral tissues can cause a local infection, systemic infection, or both. Microorganisms circulating in the bloodstream can cause lesions in the oral cavity, and microorganisms causing infection in the lungs can be transferred to oral tissues when they are present in sputum. The oral cavity contains numerous microorganisms that make up the normal oral microflora. Changes such as a decrease in salivary flow, antibiotic administration, and immune system alterations affect the oral microflora so that organisms that are usually nonpathogenic are able to cause disease. This type of infection is called an opportunistic infection.
Microorganisms penetrating epithelial surfaces act as foreign material and stimulate the inflammatory and immune responses. The inflammatory response is nonspecific, resulting in edema and the accumulation of a large number of white blood cells at the site. The responses of the immune system, both humoral and cell mediated, are highly specific; microorganisms are antigens, and specific antibodies are formed in response to specific antigens.
Humoral immunity (immunity that is mediated by antibodies) is an effective defense against some microorganisms, and cell-mediated immunity (immunity in which T lymphocytes are responsible for the response) is the primary defense against others, such as intracellular bacteria (tuberculosis), viruses, and fungi. Microbial infections are responsible for many more diseases than those included in this chapter. The diseases discussed here are common, cause specific oral lesions, and help to illustrate principles of infectious disease. Dental caries and periodontal disease clearly are infectious diseases that are important to dental hygienists. However, they are not included in this text because they are usually studied in courses other than oral pathology. The dental hygienist frequently encounters oral infectious diseases and must be able to recognize their clinical features and significance.
Impetigo is a bacterial skin infection caused primarily by Staphylococcus aureus and occasionally by Streptococcus pyogenes. Impetigo most commonly involves the skin of the face or extremities and is usually seen in young children. The organisms are present on skin. Nonintact skin is necessary for infection; areas of trauma such as cuts and abrasions and areas of dermatitis are likely sites of this infection. The lesions of impetigo are infectious. Direct contact is required for transmission. Impetigo presents as either vesicles that rupture, resulting in thick, amber-colored crusts, or as longer lasting bullae. Lesions may itch (pruritus), and regional lymphadenopathy may be present. Systemic manifestations such as fever and malaise generally do not occur with this infection. When impetigo affects the perioral skin, the lesions may resemble recurrent herpes simplex infection (herpes simplex infection is discussed later in this chapter). However, recurrent herpes simplex infection is much less common than impetigo in small children. The diagnosis of impetigo is made on the basis of the clinical presentation or by identification of the bacteria from cultures of the lesions. Topical or systemic antibiotics are used for treatment.
Tonsillitis and pharyngitis are inflammatory conditions of the tonsils and pharyngeal mucosa. Many different organisms cause them, including streptococci, adenoviruses, influenza viruses, and Epstein-Barr virus. The clinical features include sore throat, fever, tonsillar hyperplasia, and erythema of the oropharyngeal mucosa and tonsils.
Streptococcal tonsillitis and pharyngitis are common bacterial infections that are spread by contact with infectious nasal or oral secretions. The appearance of streptococcal tonsillitis and pharyngitis (i.e., “strep throat”) closely resembles tonsillitis and pharyngitis caused by other infections such as viral infections. Specific laboratory tests, including a rapid antigen detection test, are available for diagnostic confirmation of streptococcal infection. Antibiotics are used to treat streptococcal infection.
Tonsillitis and pharyngitis caused by group A β-hemolytic streptococci are significant because of their relationship to scarlet fever and rheumatic fever. Scarlet fever usually occurs in children. In addition to fever, patients with scarlet fever develop a generalized red skin rash that is caused by a toxin released by the bacteria. In addition to streptococcal tonsillitis and pharyngitis, oral manifestations of scarlet fever include petechiae on the soft palate and an appearance of the tongue that has been called strawberry tongue. The fungiform papillae are red and prominent, with the dorsal surface of the tongue exhibiting either a white coating or erythema. Throat culture is helpful in confirming the diagnosis of streptococcal pharyngitis in a patient with scarlet fever.
Rheumatic fever is a childhood disease that follows a group A β-hemolytic streptococcal infection, usually tonsillitis and pharyngitis. Rheumatic fever is characterized by an inflammatory reaction involving the heart, joints, and central nervous system. Rheumatic fever may result in permanent damage to heart valves.
Tuberculosis is an infectious chronic granulomatous disease usually caused by the organism Mycobacterium tuberculosis. The chief form of the disease is a primary infection of the lung. Inhaled droplets containing bacteria lodge in the alveoli of the lungs. After undergoing phagocytosis by macrophages, the organisms are resistant to destruction and multiply in the macrophages. They then disseminate in the bloodstream. After a few weeks dissemination ceases. The signs and symptoms of this lung infection include fever, chills, fatigue and malaise, weight loss, and persistent cough. The bacteria can be carried to widespread areas of the body and cause involvement of organs such as the kidneys and liver. This is called miliary tuberculosis. Involvement of the submandibular and cervical lymph nodes (usually as a result of ingesting the organism in nonpasteurized milk) causes enlargement of those nodes and is called scrofula or tuberculous lymphadenitis. The lung infection can occur at any age. Most commonly, foci of infection in the lungs become completely walled off and heal by fibrosis and calcification. A reactivation of the primary lesion can occur years after the initial infection. This reactivation is usually the result of a compromised immune response.
Oral lesions associated with tuberculosis occur but are rare. They most likely appear when organisms are carried from the lungs in sputum and transmitted to the oral mucosa (Figure 4-1). The tongue and palate are the most common sites for oral lesions of tuberculosis, but they may occur anywhere in the oral cavity, even in bone as in osteomyelitis. Oral lesions appear as painful, nonhealing, slowly enlarging ulcers that can be either superficial or deep.
Oral lesions of tuberculosis are identified by biopsy and microscopic examination of the tissue. The characteristic histopathologic lesions of tuberculosis are granulomas. The granulomas are composed of areas of necrosis surrounded by macrophages, multinucleated giant cells, and lymphocytes. Similar lesions occur in deep fungal infections and foreign-body reactions. Staining the tissue to be examined microscopically with a special stain may reveal the organisms. Tissue culture to diagnose tuberculosis requires a specialized laboratory.
A skin test is used to determine whether an individual has been exposed and infected with M. tuberculosis. An antigen called purified protein derivative is injected into the skin. If the individual’s immune system has previously encountered the antigen, a positive inflammatory skin reaction occurs (a type IV delayed-hypersensitivity reaction). This skin reaction indicates previous infection with the bacteria but not necessarily active disease. When a skin test result is positive, chest radiographs are taken to determine whether active tuberculosis disease is present. Once the skin test result is positive, it will always test positive.
Effective drug treatment for tuberculosis became available in the 1940s. In the United States most tuberculosis treatment centers had closed by the mid-1970s. State health departments reported a dramatic increase in new cases in the mid-1980s, particularly in densely populated urban areas. This increase was suggested to be related to human immunodeficiency virus infection and to noncompliance of patients with therapy. Recent public health efforts have focused on ensuring compliance with antituberculosis drug treatment; as a result the number of new cases reported has decreased.
Tuberculosis is an infectious disease that can be transmitted occupationally to dental health care personnel. Routine use of universal precautions, including eye protection, mask, or facial shield, is important in preventing the transmission of airborne droplet infections such as tuberculosis. However, for patients with active tuberculosis, routine dental treatment is deferred. When emergency dental treatment is needed, the use of a special mask is recommended to ensure prevention of transmission of the tuberculosis organism.
Oral lesions resolve with treatment of the patient’s primary (usually pulmonary) disease. Combinations of several different medications, including isoniazid and rifampin, are used to treat tuberculosis. Treatment continues for many months and may continue for as long as 2 years. Patients usually become noninfectious shortly after treatment begins. Consultation with the patient’s physician should confirm that treatment is ongoing and that the patient is no longer infectious.
Actinomycosis is an infection caused by a filamentous bacterium called Actinomyces israelii. These organisms were at one time thought to be fungi; therefore the name ends in the suffix “mycosis,” which usually indicates a fungal infection.
The most characteristic form of the disease is the formation of abscesses that tend to drain by the formation of sinus tracts (Figure 4-2). The colonies or organisms appear in the pus as tiny, bright yellow grains and are called sulfur granules because of their yellow color. The organisms can also be identified by microscopic examination. These organisms are common inhabitants of the oral cavity. It is not clear why they only occasionally cause disease. Predisposing factors have not been identified. The infection is often preceded by tooth extraction or an abrasion of the mucosa.
Syphilis is a disease caused by the spirochete Treponema pallidum. The organism is transmitted from one person to another by direct contact. The spirochete, a corkscrew-like bacterium, can penetrate mucous membranes but requires a break in the continuity of the skin surface to invade through the skin. The organisms die quickly when exposed to air and changes in temperature. Syphilis is usually transmitted through sexual contact with a partner who has active lesions. It can also be transmitted by transfusion of infected blood or by transplacental inoculation of a fetus from an infected mother.
The disease occurs in three stages: (1) primary, (2) secondary, and (3) tertiary (Table 4-1). The lesion of the primary stage, called the chancre, is highly infectious and forms at the site at which the spirochete enters the body (Figure 4-3). Regional lymphadenopathy accompanies the chancre. The lesion heals spontaneously after several weeks without treatment, and the disease enters a latent period.
The secondary stage occurs about 6 weeks after the primary lesion appears. In the secondary stage diffuse eruptions of the skin and mucous membranes occur. The skin lesions have many forms. The oral lesions are called mucous patches and appear as multiple, painless, grayish-white plaques covering ulcerated mucosa. The lesions of secondary syphilis are the most infectious. They undergo spontaneous remission but can recur for months or years. After remission the disease may remain latent for many years.
The tertiary lesions occur years after the initial infection if the infection has not been treated. They chiefly involve the cardiovascular system and the central nervous system. The localized tertiary lesion is called a gumma and is noninfectious. A gumma can occur in the oral cavity; the most common sites are the tongue and palate. The lesion appears as a firm mass that eventually becomes an ulcer. The gumma is a destructive lesion and can lead to perforation of the palatal bone.
Syphilis can be transmitted from an infected mother to the fetus because the organism can cross the placenta and enter the fetal circulation. Congenital syphilis often causes serious and irreversible damage to the child, including facial and dental abnormalities. The developmental disorders that result from fetal and neonatal syphilis are described in Chapter 5.
The diagnosis of syphilitic lesions occurring on skin can be made by a special microscopic technique called a dark-field examination to identify the spirochetes. However, other spirochetes are present in the oral cavity; therefore this examination is not reliable for oral lesions. Two of the serologic (blood) tests that are commonly used to confirm the diagnosis of syphilis include (1) the Venereal Disease Research Laboratory (VDRL) test, and (2) the fluorescent treponemal antibody absorption (FTA-ABS) test. These tests may produce negative results in primary syphilis because sufficient antibodies may not have formed for the test result to be positive. If syphilis continues to be suspected, retesting is done.
Syphilis is generally treated with penicillin. The VDRL test is used again to evaluate the success of treatment. The antibody titer decreases if treatment has been successful. The FTA test remains positive after treatment.
Necrotizing ulcerative gingivitis (NUG) was formerly called acute necrotizing ulcerative gingivitis (ANUG). This condition is more chronic than acute and therefore, is most appropriately called NUG. It is a painful erythematous gingivitis with necrosis of the interdental papillae (Figure 4-4). NUG is usually caused by a combination of a fusiform bacillus and a spirochete (Borrelia vincentii) and is associated with decreased resistance to infection.
The gingiva is painful and erythematous, with necrosis of the interdental papillae generally accompanied by a foul odor and metallic taste. The necrosis results in cratering of the interdental papillae area. Sloughing of the necrotic tissue presents as a pseudomembrane over the tissues. Systemic manifestations of infection such as fever and cervical lymphadenopathy may be present. Clinical features distinguish NUG from acute marginal gingivitis and the gingival component of acute primary herpes simplex infection (see Figure 4-20, B).
Pericoronitis is an inflammation of the mucosa around the crown of a partially erupted, impacted tooth (Figure 4-5). The soft tissue around the mandibular third molar is the most common location for pericoronitis. The inflammation is usually the result of infection by bacteria that are part of the normal oral microflora, which proliferate in the pocket between the soft tissue and the crown of the tooth. Compromised host defenses, ranging from minor illnesses to immunodeficiency, are associated with an increased risk of pericoronitis. Trauma from an opposing molar and impaction of food under the soft tissue flap (operculum) covering the distal portion of the third molar may also precipitate pericoronitis.
Acute osteomyelitis involves acute inflammation of the bone and bone marrow (Figure 4-6, A). Acute osteomyelitis of the jaws is most commonly a result of the extension of a periapical abscess. It may follow fracture of the bone or surgery, and may also result from bacteremia.
The diagnosis of the specific organism causing acute osteomyelitis is based on culture results, and treatment is based on antibiotic sensitivity testing. Microscopic examination shows nonviable bone, necrotic debris, acute inflammation, and bacterial colonies in the marrow spaces. No change is seen on the radiograph unless the disease has been present for more than 1 week.
Chronic osteomyelitis is a long-standing inflammation of bone. It may occur in inadequately treated acute osteomyelitis, long-term inflammation of bone with no recognized acute phase, Paget disease, sickle cell disease, or bone irradiation that results in decreased vascularity. The involved bone is painful and swollen, and radiographic examination reveals a diffuse and irregular radiolucency that can eventually become radiopaque as bone forms within the chronically inflamed tissue (Figure 4-6 B). When radiopacity develops, the condition is called chronic sclerosing osteomyelitis. Recently, cases of osteonecrosis of the mandible and maxilla have been reported in patients taking bisphosphonate medication. This may appear clinically similar to chronic osteomyelitis. Bisphosphonate-associated osteonecrosis is described in Chapter 9.
Candidiasis, also called candidosis, moniliasis, and thrush, occurs as a result of an overgrowth of the yeastlike fungus Candida albicans. It is the most common oral fungal infection. This fungus is part of the normal oral microflora in many individuals, particularly those individuals with diabetes mellitus and those who wear dentures. Overgrowth of Candida albicans is associated with many different conditions (Box 4-1).
Newborn infants are particularly susceptible to an overgrowth of this fungus because they do not have either an established oral microflora or a fully developed immune system. Pregnant women often have Candida vaginitis because they are somewhat immunosuppressed in order to maintain the fetus. The organism is transmitted to the infant while it passes through the birth canal. Antibiotics can alter the bacteria of the oral microflora, which can allow the overgrowth of Candida albicans. Systemic and topical corticosteroids, diabetes, and cell-mediated immune system deficiency are other factors that allow the overgrowth of this fungus. Candidiasis is one of the most common oral lesions that occur in association with immunodeficiency. Candidiasis generally affects the superficial layers of the epithelium; therefore, when it is present, the proliferating organisms are easily identified in a sample obtained by scraping the surface (mucosal smear) of the lesion.
Several forms of oral candidiasis exist; recognition of their clinical features is important so that candidiasis is appropriately included in the differential diagnosis of a variety of clinical presentations. The types of oral candidiasis are as follows:
An erythematous, often painful, mucosa is the presenting complaint in erythematous candidiasis (Figure 4-8). This type of candidiasis may be localized to one area of the oral mucosa or be more generalized. Irregular, patchy depapillation of the tongue is often seen in this type of candidiasis.
Denture stomatitis is the most common type of candidiasis affecting the oral mucosa. It is also called chronic atrophic candidiasis (Figure 4-9). This type of candidiasis also presents as erythematous mucosa, but the erythematous change is limited to the mucosa covered by a full or partial denture. The lesions may vary from petechiae-like to more generalized and granular. It is most common on the palate and maxillary alveolar ridge. Denture stomatitis is asymptomatic and is usually discovered by the dentist or dental hygienist during a routine oral examination.
Chronic hyperplastic candidiasis (Figure 4-10) appears as a white lesion that does not wipe off the mucosa. Candidal leukoplakia and hypertrophic candidiasis are other names for this type of oral candidiasis. An important diagnostic feature of this type of candidiasis is its response to antifungal medication: when leukoplakia is caused by candidiasis, it disappears when treated with antifungal medication (therapeutic diagnosis). If the lesion does not respond to antifungal therapy, biopsy should be considered to establish the diagnosis of the lesion.
Candida organisms are often the cause of angular cheilitis (Figure 4-11), especially if saliva collects at the corners of the mouth. It appears as erythema or fissuring at the labial commissures. Angular cheilitis may be caused by other factors such as nutritional deficiency or a combination of candidiasis and bacterial infection; however, it most commonly results from Candida infection. Angular cheilitis frequently accompanies intraoral candidiasis.
A severe form of candidiasis that usually occurs in patients who are severely immunocompromised is called chronic mucocutaneous candidiasis. The patient has skin lesions as well as chronic oral and genital mucosal candidiasis. Oral involvement may appear as pseudomembranous, erythematous, or hyperplastic candidiasis; and angular cheilitis is common. The skin lesions usually involve the nails and skinfolds.
Several studies have reported an association between median rhomboid glossitis (Figure 4-12) also called central papillary atrophy and candidiasis. It appears as an erythematous, often rhombus-shaped, flat-to-raised area on the midline of the posterior dorsal tongue. Candida organisms have been identified in some lesions, and some lesions disappear with antifungal treatment. However, the response to antifungal treatment is not consistent; therefore, although this lesion has been associated with candidiasis, the cause is not yet clear.
Because Candida is part of the oral microflora in many individuals, a culture is not useful for diagnosis. A positive culture result indicates that the organisms are present but not that they are causing infection. Clinical features and the use of the mucosal smear/cytologic preparation (Figure 4-13) are usually more helpful. The surface of the lesion is scraped vigorously with a tongue blade, wooden spatula, or specially designed brush; and the scrapings are spread on a glass slide and fixed with alcohol. The slide is then sent to an oral pathology laboratory for staining and examination. In addition to the smear, the response of the lesion to antifungal treatment is important in confirming the diagnosis of candidiasis. Lesions caused by Candida should resolve with antifungal treatment. Both topical and systemic medications are used for candidiasis. However, in some patients, particularly those who are immunocompromised, candidiasis is persistent and recurrent.
Although the final diagnosis and management of a patient with oral candidiasis is the responsibility of the dentist, dental hygienists are often the first to recognize the oral changes characteristic of this condition. Recurrent oral candidiasis may be an early sign of a severe underlying medical problem.
Oral lesions occur in some deep fungal infections (e.g., histoplasmosis, coccidioidomycosis, blastomycosis, and cryptococcosis). They are all characterized by primary involvement of the lungs. Oral lesions are caused by implantation of the organism carried by sputum from the lungs to the oral mucosa.
Infections caused by these organisms are more common in certain areas of the United States than in others. Histoplasmosis is widespread in the midwestern United States, and coccidioidomycosis is more prevalent in parts of the western United States, particularly the San Joaquin Valley of California. Blastomycosis is common in the Ohio and Mississippi River basin areas. Therefore oral lesions caused by these organisms are most likely seen in areas of the country in which the infection is most common.
Cryptococcosis is transmitted through inhalation of organisms contained in dust from bird droppings, particularly from pigeons. In addition to the regional distribution of these infections, reactivation, including the development of oral lesions, can also occur in patients who are immunocompromised.
The initial signs and symptoms of these deep fungal infections are usually related to the primary lung infection. Oral lesions are preceded by pulmonary involvement. These oral lesions are chronic, nonhealing ulcers that can resemble squamous cell carcinoma (Figure 4-14). Diagnosis is made by biopsy and microscopic examination. Special staining of the tissue reveals the organisms, which can be identified by their microscopic appearance. The tissue can also be cultured; this is useful in establishing the diagnosis.
Mucormycosis, also called phycomycosis, is a rare fungal infection. The organisms are a common inhabitant of soil and are usually nonpathogenic. However, infection with this organism occurs in diabetic and severely debilitated patients. The disease often involves the nasal cavity, maxillary sinus, and hard palate and can present as a proliferating or destructive mass in the maxilla. The diagnosis is made by biopsy and identification of the organisms in the tissue.
Human papillomavirus (HPV) selectively infects skin and oral mucosa. Infection occurs by direct contact. More than 150 different types of HPV have been identified; some of these types have been found to cause neoplasia and therefore are called high-risk types. Others that cause benign lesions or are not associated with lesions are called low-risk types. At least 40 different types of HPV have been identified in oral mucosa. A recent study that examined both high-risk and low-risk types of HPV in the oral cavity found the overall prevalence of HPV in the oral cavity to be 6.9%. This included both high-risk and low-risk types. HPV has been clearly associated with carcinoma of the vaginal cervix (cervical cancer). High-risk types have been identified and associated with squamous cell carcinomas that form in the oropharyngeal region (see Chapter 7). Evidence of their role in the pathogenesis of these cancers is emerging, but is not yet completely clear.
For HPV to infect skin and oral mucosa, it must infect the basal cells of the epithelium. This usually requires a break in the surface of these tissues. HPV matures in the spinous layer and then the virus is released on the surface of the tissue. Proliferation of the basal cells of the infected epithelium is a characteristic of benign lesions that are caused by HPV infection.
Like other viruses, HPV incorporates itself into the nuclear material of infected cells. HPV-infected cells, called koilocytes, are characterized microscopically by an irregular nucleus surrounded by clear cytoplasm (Figure 4-15).