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.
