A guide to common oral lesions

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Snuff lesion (smokeless tobacco lesion)

DESCRIPTION: The lesion develops on the mucosa where smokeless tobacco is held. The usual appearance is white, wrinkled or corrugated mucosa. Gingival recession is a common manifestation with cervical erosion of teeth a less frequent finding. Symptoms are uncommon.

ETIOLOGY: Prolonged use of smokeless tobacco produces such as chewing tobacco or snuff.

TREATMENT: Biopsy should be done to rule out dysplasia, otherwise no treatment is necessary.

PROGNOSIS: Verrucous and squamous carcinomas arise in smokeless tobacco lesions more than chance alone can explain. One article noted almost a 50-fold increased risk of cancers of the gingival and buccal mucosa in females who were chronic users. The duration necessary to induce dysplastic or malignant change is unknown but appears to be at least 20 years.

DIFFERENTIAL DIAGNOSIS: The clinical appearance of the lesion plus a history of using smokeless tobacco establishes the diagnosis. 

        

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Leukoplakia

DESCRIPTION: We use the term leukoplakia to mean a white lesion of mucous membrane that cannot be identified as any other “white” disease such as candidiasis or lichen planus. It carries no histologic connotation. Using this definition, biopsy is required for accurate diagnosis. Biopsy of oral leukoplakia will most often show hyperkeratosis, a purely reactive and harmless lesion. About 20%, however, will show dysplasia, a premalignant lesion or cancer. Leukoplakia is more common in males and favors older age groups. There are usually no symptoms.

ETIOLOGY: The exact cause is unknown although physical trauma, smoking, excessive alcohol intake and vitamin A deficiency are suspected.

TREATMENT: The treatment depends on the histologic findings and the extent of the lesion. For simple hyperkeratosis, removal of any apparent cause is indicated. Those showing dysplasia, or carcinoma, should be treated with the usual methods used in treatment of cancers.

PROGNOSIS: As stated above, the prognosis depends to a great extent on the precise histologic findings. One study indicates approximately 20% of oral leukoplakia lesions are dysplastic or malignant on the day of biopsy. Leukoplakia in the floor of the mouth and lateral/ventral tongue mucosa are more likely to be precancerous.

DIFFERENTIAL DIAGNOSIS: Lichen planus, candidiasis, and hairy leukoplakia. 

        

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Squamous cell carcinoma (epidermoid carcinoma)

DESCRIPTION: In excess of 90% of all oral cancers are of the squamous cell type. As stated in other sections in this monograph, early carcinoma may clinically appear as leukoplakia or erythroplasia. It may also appear as a mixture of erythroplasia and leukoplakia. Another common clinical appearance is an area of chronic ulceration.

Squamous carcinoma is about three times as common in men as in women. Risk of acquiring the disease increases with each passing decade but is seldom seen in those under forty. According to the American Cancer Society, there are about 21,000 new cases of oral cancer in the United States each year, an incidence rate of approximately 8 cases per 100,000 persons. Although no area of oral mucosa is immune, certain areas are more vulnerable. Soft palate, lateral and ventral tongue mucosa, and floor of the mouth are especially prone to develop squamous carcinoma. The tongue and floor of the mouth are the most common areas.

ETIOLOGY: The cause is unknown. Smoking and alcohol are risk factors, and the human papilloma virus is suspect. Time will show that mutations in genes that control the cell cycle, protooncogenes and tumor suppressor genes, are at the heart of many forms of cancer including oral cancer.

TREATMENT: Usual treatment consists of surgical excision and possible irradiation. Chemotherapy is adjunctive at this time.

PROGNOSIS: The overall five year survival rate is about 50%. Early diagnosis increases the chance of survival.

DIFFERENTIAL DIAGNOSIS: All ulcerations present for more than 2-3 weeks in which there is no apparent cause should be biopsied to rule out carcinoma, especially in adults whose lesions are in high risk areas. 

        

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Acquired immune deficiency syndrome (AIDS)

DESCRIPTION: Acquired immune deficiency syndrome is characterized by relentless destruction of CD4 T lymphocytes, key cells of the immune system. The eventual collapse of both the cellular and humoral arms of immunity leaves the host vulnerable to a wide variety of pathogenic organisms including bacteria, viruses, fungi and protozoa. It is important for health care workers to recognize that it is difficult to transmit the AIDS virus in the health care setting, from patient to worker or the reverse. However, opportunistic infectious diseases that AIDS patients are apt to have including tuberculosis, herpes-virus infections, hepatitis B and hepatitis C are readily transmissible.

ETIOLOGY: The causes of AIDS is an RNA retrovirus of the lentivirus group. It is designated the human immunodeficiency virus (HIV) and there are several variants: HIV- 1 is the most common cases of AIDS. The virus attaches to the surface of cells that bear the CD4 receptor including helper T lymphocytes, B lymphocytes and macrophages. Although they lack a CD4 receptor, microglia, skin fibroblasts, and bowel epithelium become infected. The virus destroys the infected cells. With gradual depletion of the cells of immunity, especially T-helper lymphocytes and macrophages, the host becomes increasingly vulnerable to pathogenic organisms.

ORAL MANIFESTATIONS:

Candidiasis – Colonization and infection of the oral mucosa by Candida species is among the earliest and most common findings in HIV-infected patients. In one study, 88% had oral candidiasis. Lesions range from white to red or red/white combinations. The lesions may be asymptomatic or there may be mild discomfort. For stubborn infection, fluconazole is recommended.

Kaposi’s sarcoma – AIDS patients are vulnerable to a variety of oral malignancies including Kaposi’s sarcoma, malignant lymphoma and squamous carcinoma. Kaposi’s sarcoma is the most common. In one study, 20% of AIDS patients had Kaposi’s sarcoma and of these, the tumor was in the oral cavity in 1 of every 5 patients; the palate is the most common site. In the early stage, the tumor appears as a red to purple bruise. The tumor grows and eventually appears as a hemorrhagic mass. The cell of origin is endothelium; thus Kaposi’s sarcoma is a variety of angiosarcoma. They are locally invasive, cause pain and bleeding and interfere with normal function. Low-dose radiation therapy and intralesional or systemic chemotherapy are the treatments of choice. Herpes virus type VIII is thought to play a role in the pathogenesis of this tumor.

Hairy leukoplakia – This variety of leukoplakia was first recognized in HIV-infected patients but has been encountered in other immune deficiency states such as organ transplant patients who are intentionally immune suppressed. The lateral tongue is the most common location. Lesions are of rough texture, adherent and asymptomatic. The diagnosis of hairy leukoplakia can be suspected on routine biopsy specimens, but confirmation requires demonstration of the presence of the causative virus, the Epstein-Barr herpesvirus. This is ordinarily achieved by DNA in situ hybridization. A word of caution: hairy leukoplakia may be confused with candidiasis. A patient who presents with a white lesion should be treated with antifungal therapy first. If it fails to heal, it most likely is hairy leukoplakia.

Gingival and periodontal lesions – HIV-infected patients are vulnerable to necrotizing gingivitis and periodontitis (Fig. 5). The organisms recovered from these lesions are the same as those in non-HIV-positive patients. Lesions are treated by dental prophylaxis, debridement, and metronidazole. Good oral hygiene and daily rinses with chlorhexidine are beneficial.

Others – HIV patients also develop major aphthous-like lesions that respond to tetracycline and topical steroid therapy.

Thalidomide has been used successfully in their management. The human papillomavirus has also been found in both condylomas and focal epithelial hyperplasia. Cytomegalovirus infections and several fungal infections such as histoplasmosis and coccidiodomycosis are also common. Lastly, xerostomia secondary to salivary gland destructions has been reported. 

        

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Dental caries

DESCRIPTION: Caries ranks with gingivitis and periodontitis as one of the most common oral diseases. Treatment of these diseases and their sequelae constitutes the bulk of the practice of dentistry. Caries is the only disease that attacks that portion of the tooth exposed to the oral environment. Typical caries are most commonly located in the occlusal pits and fissures of molars and premolars, as well as beneath the contact points on the interproximal surfaces. Special consideration should be given to two types of caries, namely radiation type caries and early childhood caries (nursing bottle caries). Radiation type caries characteristically occur as multiple lesions in the cervical region of the teeth immediately adjacent to the gingival. These may completely encircle the tooth causing amputation at the gingival. Early childhood caries are multiple and rampant occurring in deciduous teeth of nursing infants and small children.

ETIOLOGY: Caries is caused by the decalcification of tooth enamel and destruction of the protein matrix. Acid produced by bacteria, mainly Streptococcus mutans, in dental plaque is the precipitating factor. After the enamel is destroyed bacteria enter the dentin and may extend to the pulp of the tooth. Radiation or cervical caries are usually related to xerostomia and/or chemical changes in saliva. Radiation therapy exceeding 4000 cGy to salivary glands is the most common cause. However, many common medications and systemic chemotherapy may also cause dry mouth and radiation type caries. Sjogren’s syndrome is a cause of xerostomia and a cause of radiation-type caries. Early childhood caries is due to frequent nursing with solutions containing high concentrations of sugar such as milk, soft drinks, and juices.

TREATMENT: Prevention is the best treatment. Caries can be prevented by brushing and flossing to remove plaque. A well-balanced diet without excessive sugars is also beneficial. Topical and systemic fluoride are highly effective in reducing caries, especially if given during the formative years of the teeth. Fluorides have significantly reduced the incidence of caries in the United States in the last several decades. Radiation type caries can also be prevented by a daily regime of topical fluoride. Fluoride applications applied with a custom mouth guard should begin as soon as radiation is started. Patients who have received head and neck radiation should continue daily treatments for life to prevent caries that could lead to extractions and possible osteoradionecrosis. Once caries have developed, dental restorative procedures are the only treatment, although there is now evidence that very early lesions, under intact surface enamel (white spots), may be remineralized with topically applied agents.

PROGNOSIS: Prognosis is good if the disease is treated early. If ignored, caries is a major cause of tooth loss and suffering from infection of bone and soft tissues.

DIFFERENTIAL DIAGNOSIS: None 

        

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Periodontitis

DESCRIPTION: Extension of gingival inflammation into the underlying bone and periodontal ligament is referred to as periodontitis. Since bone resorption is the outstanding feature, it is best seen on radiographs. Periodontitis is a silent disease with an occasional acute exacerbation in the form of local, painful abscesses. The gingiva is usually inflamed. The chief indicators of this disease are increased gingival sulcus depth as determined by gingival probing, and loss of alveolar bone as seen on radiographs. The conventional form of this disease starts in the teens or early adult years and without treatment shows gradual progression throughout life. It is the major cause of tooth loss in adults.

Three subtypes have been identified: (1) rapidly progressive periodontitis (RRP) affecting young adults; it resembles the conventional disease except that bone destruction is accelerated and occurs over a period of weeks or months rather than years; (2) juvenile periodontitis (JP) formerly known as periodontosis and typically affecting teenagers and characterized by destruction of alveolar bone around only first permanent molar teeth and incisor teeth; and, (3) prepubertal periodontitis (PP) affecting the deciduous teeth.

ETIOLOGY: Bacterial plaque is thought to be responsible for periodontitis. In the rapidly progressive type, there is evidence for increased activity of Bacteroides, Actinobacillus, Porphyromonas, and Prevotella organisms coupled with defects of leukocyte chemotaxis. In the juvenile (periodontosis) type, research has implicated a similar array of gram negative anaerobic rods as pathogens but there is no plausible explanation for the selective involvement of first molar and incisor teeth other than the “first erupted-first involved” theory. In the prepubertal form of periodontitis, genetically determined leukocyte adhesion molecule deficiency has been implicated. Disabling mutations in the gene for Cathepsin C account for the Papillon-Lefevre syndrome. From the above, it is obvious that alterations in plaque flora and reduced immunity are encountered in the subtypes of periodontitis.

TREATMENT: In conventional periodontitis, prevention is achieved through good dental hygiene. Unless treated, continued loss of alveolar bone eventually necessitates extraction of teeth. In those patients who still have adequate bone support, periodontal surgery to reduce the sulcus depth may be of benefit.

PROGNOSIS: The prognosis depends on the stage of the disease at the time treatment is instituted.

DIFFERENTIAL DIAGNOSIS: Most forms of periodontitis are easily recognized with periodontal probing and dental radiographs. Langerhans granulomatosis and Burkitt’s lymphoma should be ruled out in prepubertal periodontitis. Children with prepubertal periodontitis combined with hyperkeratosis of the palms and soles are said to have the Papillon-Lefevre syndrome. Prepubertal periodontitis has also been described in children with Ehlers-Danlos syndrome. 

        

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 Pulpitis

DESCRIPTION: Inflammation of the pulp is one of the most common lesions seen in dental practice. No illustration is shown because pulpitis is not amenable to clinical photography. Pulpitis usually causes a toothache (pulpalgia) ranging from mild to excruciating, although in some cases, there are no symptoms.

ETIOLOGY: Pulpitis is usually brought about by pulp infection occurring as a consequence of caries, but may also be caused by physical trauma, dental instrumentation, and irritating restorative materials.

TREATMENT: Treatment consists of elimination of the responsible agent. Irreversible cases are treated by endodontic procedures or extraction.

PROGNOSIS: The prognosis depends on the extent and severity of the pulp involvement.

DIFFERENTIAL DIAGNOSIS: It is frequently stated that periodontal infections, sinusitis, and referred pain may masquerade as pulpitis. When patients complain of pain in vital teeth, the diagnosis of atypical odontalgia or phantom tooth pain should be considered.

        

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