Effects of Iatrogenic Agents on Oral Mucosa
Traumatic ulcers occur from acute or chronic injury to the lips, tongue, or cheek from biting the tongue or cheek or lacerating the mucosa with sharp objects or broken dentition. The ulcers are often painful and characterized by mild erythema surrounded by a central ulcer covered by a yellow fibrinopurulent membrane.
Injury from caustic chemicals varies with the degree of concentration of the agent and the duration of contact time with the mucosa, from no injury to severe ulceration.
An aspirin burn can result from residual acetylsalicylic acid from chewing an aspirin or from topically applied solutions. This can produce a surface necrosis with blebs, which later sloughs, leaving superficial erosion. The onset is rapid, as is healing. Use of hydrogen peroxide to treat oral conditions can result in epithelial necrosis when left in contact with the oral mucosa for too long or with concentrations that exceed 1% to 3%. Similarly, phenol or silver nitrate, both of which are used to treat aphthous ulcerations, can damage the mucosa and associated nerve endings.
Nicotine stomatitis presents as slightly raised, white papular lesions on the posterior aspect of the hard and soft palates, primarily in association with pipe or cigar smoking. The central portions of the papules have a reddish component resulting from inflammation of the minor salivary gland duct orifices.
Intensive chemotherapy and radiation therapy to the head and neck region frequently causes painful stomatitis, which can limit the dosage and frequency of the therapeutic regimens and interfere with oral intake. Inhibition of cell growth and maturation by these agents disrupts the mucosal barrier, allowing for opportunistic infections by otherwise normal oral microflora. Salivary glands can be affected as well, resulting in xerostomia, which further increases the vulnerability of the oral mucosa.
Stomatitis can be seen with less noxious ingestions than the neoplastic agents.
Wide-spectrum antibiotic use results in an imbalance of the endogenous flora, causing a secondary infection from Candida albicans. Pseudomembranous candidiasis or oral thrush is the most common presentation; it is characterized by multiple white creamy curdlike plaques located anywhere in the oral cavity.
The pale bluish-to-heavy-black lead line (Burton line or halo saturninus), along the gingival margin, is a symptom of lead absorption but not necessarily of lead intoxication. The primary cause of toxicity is the binding of lead with sulfhydryl groups competing with enzymes that use the binding site. Additionally it mimics metals such as calcium, iron, and zinc, which are needed cofactors in many enzymatic reactions. The lead line consists of lead sulfide that has precipitated in the capillaries or surrounding tissue, when the lead compounds circulating in the blood react with hydrogen sulfide. The latter is liberated by bacterial action from organic matter deposited around the teeth as a consequence of poor oral hygiene. Secondary invasion of fusiform and spirochetal organisms often occurs, producing a marked gingivitis.
Gingival hyperplasia is a complication of the anticonvulsive drug phenytoin. Edentulous mouths do not reveal the disturbance, emphasizing the role of local irritants and oral hygiene. All gradations of hyperplasia are observed, beginning with tumescence of the interdental papillae. The consistency is fibrotic, without edema, inflammation, or color change. The swellings may further proliferate to cover the crowns of the teeth with sessile, lobulated growths that are light pink in color and sharply defined from the surrounding gum.