Chapter 8 PHYSICAL AND CHEMICAL INJURIES
accidental biting during mastication, overzealous
Fig. 8-4 Morsicatio buccarum. Oral mucosa exhibiting
greatly thickened layer of parakeratin with ragged surface
colonized by bacteria.
DIAGNOSIS
In most cases the clinical presentation of morsicatio
buccarum is sufficient for a strong presumptive diag-
nosis, and clinicians familiar with these alterations
rarely perform biopsy. Some cases of morsicatio may
not be diagnostic from the clinical presentation, and
biopsy may be necessary. In patients at high risk for
HIV infection with isolated involvement of the lateral
border of the tongue, further investigation is desirable
to rule out HIV-associated OHL.
TREATMENT AND PROGNOSIS
No treatment of the oral lesions is required, and no
long-term difficulties arise from the presence of the
mucosal changes. For patients who desire treatment,
an oral acrylic shield that covers the facial surfaces of
the teeth may be constructed to eliminate the lesions
by restricting access to the buccal and labial mucosa.
For patients desiring either confirmation of the cause
or preventive therapy, construction and use of two
lateral acrylic shields connected by a labial stainless
steel wire can provide quick resolution of the lesions
while being acceptable aesthetically and not interfer-
ing with speech. Several authors also have suggested
psychotherapy as the treatment of choice, but no exten-
sive well-controlled studies have indicated benefits
from this approach.
TRAUMATIC ULCERATIONS
Acute and chronic injuries of the oral mucosa are fre-
quently observed. Injury can result from mechanical
damage, such as contact with sharp foodstuffs or
287
toothbrushing, talking, or even sleeping. Some are self-
induced and clinically obvious, whereas others are
subtle and difficult to diagnose. Damage also may
result from thermal, electrical, or chemical burns. (Oral
mucosal manifestations of such burns are discussed
later in the chapter.)
Acute or chronic trauma to the oral mucosa may
result in surface ulcerations. The ulcerations may
remain for extended periods of time, but most usually
heal within days. A histopathologically unique type of
chronic traumatic ulceration of the oral mucosa is the
eosinophilic ulceration (traumatic granuloma,
traumatic ulcerative granuloma with stromal
eosinophilia [TUGSE], eosinophilic granuloma
of the tongue), which exhibits a deep pseudoinva-
sive inflammatory reaction and is typically slow to
resolve. Interestingly, many of these traumatic granu-
lomas undergo resolution after incisional biopsy.
Lesions microscopically similar to eosinophilic ulcer-
ation have been reproduced in rat tongues after
repeated crushing trauma and in traumatic lesions
noted in patients with familial dysautonomia, a
disorder characterized by indifference to pain. In addi-
tion, similar sublingual ulcerations may occur in
infants as a result of chronic mucosal trauma from
adjacent anterior primary teeth, often associated with
nursing. These distinctive ulcerations of infancy have
been termed Riga-Fede disease and should be con-
sidered a variation of the traumatic eosinophilic
ulceration.
In rare subsets of TUGSE, the lesion does not
appear to be associated with trauma, and sheets of
large, atypical cells are seen histopathologically. The
nature of these atypical cells remains in dispute,
although it has been suggested that they may represent
reactive myofibroblasts, histiocytes (atypical histio-
cytic granuloma), or T lymphocytes. Whether
these atypical eosinophilic ulcerations represent a
single pathosis or a variety of disorders that share
stromal eosinophilia is an area for future research. Of
these theories, several current investigations have
shown the atypical cells to be T lymphocytes with
strong immunoperoxidase reactivity for CD30. In
these cases, it is thought that this subset of TUGSE may
represent the oral counterpart of the primary cutane-
ous CD30+ lymphoproliferative disorder, which
also exhibits sequential ulceration, necrosis, and
self-regression.
In most cases of traumatic ulceration, there is an
adjacent source of irritation, although this is not present
invariably. The clinical presentation often suggests the
cause, but many cases resemble early ulcerative squa-
mous cell carcinoma; biopsy is performed to rule out
that possibility.
288 ORAL AND MAXILLOFACIAL PATHOLOGY
Fig. 8-5 Traumatic ulceration. Well-circumscribed
ulceration of the posterior buccal mucosa on the left side.
Fig. 8-6 Traumatic ulceration. Mucosal ulceration with a
hyperkeratotic collar located on the ventral surface of the
tongue.
CLINICAL FEATURES
Most injuries are unintentional and arise from a variety
of causes. As would be expected, simple chronic trau-
matic ulcerations occur most often on the tongue, lips,
and buccal mucosa—sites that may be injured by the
dentition (Fig. 8-5). Lesions of the gingiva, palate, and
mucobuccal fold may occur from other sources of
irritation. Overzealous toothbrushing can create linear
erosions along the free gingival margins. Although
these areas may superficially resemble a number of the
chronic vesiculoerosive processes, thorough question-
ing of the patient often leads to the appropriate diag-
nosis. The individual lesions appear as areas of erythema
surrounding a central removable, yellow fibrinopuru-
lent membrane. In many instances, the lesion develops
a rolled white border of hyperkeratosis immediately
adjacent to the area of ulceration (Fig. 8-6).
Eosinophilic ulcerations are not uncommon but fre-
quently are not reported. The lesions occur in people
Fig. 8-7 Traumatic granuloma. Exophytic ulcerated mass
on the ventrolateral tongue associated with multiple jagged
teeth.
Fig. 8-8 Riga-Fede disease. Newborn with traumatic
ulceration of anterior ventral surface of the tongue. Mucosal
damage occurred from contact of tongue with adjacent tooth
during breastfeeding.
of all ages, with a significant male predominance. Most
have been reported on the tongue, although cases have
been seen on the gingiva, buccal mucosa, floor of
mouth, palate, and lip. The lesion may last from 1 week
to 8 months. The ulcerations appear very similar to the
simple traumatic ulcerations; however, on occasion,
underlying proliferative granulation tissue can result in
a raised lesion similar to a pyogenic granuloma (see
page 517) (Fig. 8-7).
Riga-Fede disease typically appears between 1 week
and 1 year of age. The condition often develops in
association with natal or neonatal teeth (see page 81).
The anterior ventral surface of the tongue is the most
common site of involvement, although the dorsal
surface also may be affected (Fig. 8-8). Ventral lesions
contact the adjacent mandibular anterior incisors;
lesions on the dorsal surface are associated with the
maxillary incisors. A presentation similar to Riga-Fede
disease can be the initial finding in a variety of neuro-
Chapter 8 PHYSICAL AND CHEMICAL INJURIES
Fig. 8-9 Atypical histiocytic granuloma. Large ulceration
of the anterior dorsal surface of the tongue.
logic conditions related to self-mutilation, such as
familial dysautonomia (Riley-Day syndrome), con-
genital indifference to pain, Lesch-Nyhan syn-
drome, Gaucher disease, cerebral palsy, or Tourette
syndrome.
The atypical eosinophilic ulceration occurs in older
adults, with most cases developing in patients older
than age 40. Surface ulceration is present, and an
underlying tumefaction also is seen. The tongue is
the most common site, although the gingiva, alveolar
mucosa, mucobuccal fold, buccal mucosa, and lip may
be affected (Fig. 8-9).
HISTOPATHOLOGIC FEATURES
Simple traumatic ulcerations are covered by a fibrino-
purulent membrane that consists of fibrin intermixed
with neutrophils. The membrane is of variable thick-
ness, and the adjacent surface epithelium may be
normal or may demonstrate slight hyperplasia with or
without hyperkeratosis. The ulcer bed consists of gran-
ulation tissue that supports a mixed inflammatory
infiltrate of lymphocytes, histiocytes, neutrophils, and,
occasionally, plasma cells. In patients with eosinophilic
ulcerations, the pattern is very similar; however, the
inflammatory infiltrate extends into the deeper tissues
and exhibits sheets of lymphocytes and histiocytes
intermixed with eosinophils. In addition, the vascular
connective tissue deep to the ulceration may become
hyperplastic and cause surface elevation.
Atypical eosinophilic ulcerations exhibit numerous
features of the traumatic eosinophilic ulceration, but
the deeper tissues are replaced by a highly cellular
proliferation of large lymphoreticular cells. The infil-
trate is pleomorphic, and mitotic features are some-
what common. Intermixed with the large atypical cells
are mature lymphocytes and numerous eosinophils.
289
Although an associated immunohistochemical profile
rarely has been reported, several investigators have
shown the large cells to be T lymphocytes, the majority
of which react with CD30 (Ki-1). In many instances,
molecular studies for T-cell clonality by polymerase
chain reaction (PCR) have been performed on the
CD30+ cells and demonstrated monoclonal rearrange-
ment. Whether this monoclonal infiltrate represents a
true low-grade lymphoma or an unusual reactive lym-
phoproliferative process has not been determined.
TREATMENT AND PROGNOSIS
For traumatic ulcerations that have an obvious source
of injury, the irritating cause should be removed. Dyclo-
nine HCl or hydroxypropyl cellulose films can be
applied for temporary pain relief. If the cause is not
obvious, or if a patient does not respond to therapy,
then biopsy is indicated. Rapid healing after a biopsy
is typical even with large eosinophilic ulcerations
(Fig. 8-10). Recurrence is not expected.
The use of corticosteroids in the management of
traumatic ulcerations is controversial. Some clinicians
have suggested that use of such medications may delay
healing. In spite of this, other investigators have
reported success using corticosteroids to treat chronic
traumatic ulcerations.
Although extraction of the anterior primary teeth is
not recommended, this procedure has resolved the
ulcerations in Riga-Fede disease. The teeth should be
retained if they are stable. Grinding the incisal mame-
lons, coverage of the teeth with a light-cured composite
or cellulose film, construction of a protective shield,
or discontinuation of nursing have been tried with
variable success.
In patients demonstrating histopathologic similari-
ties to the cutaneous CD30+ lymphoproliferative dis-
order, a thorough evaluation for systemic lymphoma is
mandatory, along with lifelong follow-up. Although
recurrence frequently is seen, the ulcerations typically
heal spontaneously, and the vast majority of patients do
not demonstrate dissemination of the process. Further
documentation is critical to define more fully this
poorly understood process.
ELECTRICAL AND THERMAL BURNS
Electrical burns to the oral cavity are fairly common,
constituting approximately 5% of all burn admissions
to hospitals. Two types of electrical burns can be seen:
(1) contact and (2) arc.
Contact burns require a good ground and involve
electrical current passing through the body from the
point of contact to the ground site. The electric current
can cause cardiopulmonary arrest and may be fatal.
290 ORAL AND MAXILLOFACIAL PATHOLOGY
B
C affected area becomes necrotic and begins to slough.
Fig. 8-10 Eosinophilic ulceration. A, Initial presentation
of a large ulceration of the dorsal surface of the tongue.
B, Significant resolution noted 2 weeks after incisional
biopsy. C, Subsequent healing noted 4 weeks after biopsy.
Most electrical burns affecting the oral cavity are the
arc type, in which the saliva acts as a conducting
medium and an electrical arc flows between the elec-
trical source and the mouth. Extreme heat, up to
3000º C, is possible with resultant significant tissue
destruction. Most cases result from chewing on the
female end of an extension cord or from biting through
a live wire.
Most thermal burns of the oral cavity arise from
ingestion of hot foods or beverages. Microwave ovens
have been associated with an increased frequency of
thermal burns because of their ability to cook food that
is cool on the exterior but extremely hot in the
interior.
Fig. 8-11 Electrical burn. Yellow charred area of necrosis
along the left oral commissure. (Courtesy of Dr. Patricia Hagen.)
CLINICAL FEATURES
Most electrical burns occur in children younger than
4 years of age. The lips are affected most frequently,
and the commissure commonly is involved. Initially,
the burn appears as a painless, charred, yellow area
that exhibits little to no bleeding (Fig. 8-11). Significant
edema often develops within a few hours and may
persist up to 12 days. Beginning on the fourth day, the
Bleeding may develop during this period from expo-
sure of the underlying vital vasculature, and the pres-
ence of this complication should be monitored closely.
The adjacent mucobuccal fold, the tongue, or both also
may be involved. On occasion, adjacent teeth may
become nonvital, with or without necrosis of the sur-
rounding alveolar bone. Malformation of developing
teeth also has been documented. In patients receiving
high-voltage electrical injury, resultant facial nerve
paralysis is infrequently reported and typically resolves
over several weeks to months.
The injuries related to thermal food burns usually
appear on the palate or posterior buccal mucosa (Fig.
8-12). The lesions appear as zones of erythema and
ulceration that often exhibit remnants of necrotic epi-
thelium at the periphery. If hot beverages are swal-
lowed, swelling of the upper airway can occur and lead
to dyspnea, which may develop several hours after the
injury.
TREATMENT AND PROGNOSIS
For patients with electrical burns of the oral cavity,
tetanus immunization, if not current, is required. Most
clinicians prescribe a prophylactic antibiotic, usually
penicillin, to prevent secondary infection in severe
cases. The primary problem with oral burns is contrac-
ture of the mouth opening during healing. Without
Chapter 8 PHYSICAL AND CHEMICAL INJURIES
Fig. 8-12 Thermal food burn. Area of yellow-white
epithelial necrosis of the left posterior hard palate. Damage
was the result of attempted ingestion of a hot pizza roll.
intervention, significant microstomia can develop and
may produce such restricted access to the mouth that
hygiene and eating become impossible in severe cases.
Extensive scarring and disfigurement are typical in
untreated patients.
To prevent the disfigurement, a variety of microsto-
mia prevention appliances can be used to eliminate or
reduce the need for subsequent surgical reconstruc-
tion. Compliance is the most important consideration
when choosing the most appropriate device. Tissue-
supported appliances appear most effective for infants
and young children; older, more cooperative patients
usually benefit from tooth-supported devices. In most
cases, splinting is maintained for 6 to 8 months to
ensure proper scar maturation. Evaluation for possible
surgical reconstruction is usually performed after a
1-year follow-up.
Most thermal burns are of little clinical consequence
and resolve without treatment. When the upper airway
is involved and associated with breathing difficulties,
antibiotics and corticosteroids often are administered.
In rare cases, swelling of the airway mandates intuba-
tion or tracheotomy to resolve the associated dyspnea.
In these severe cases, oral intake of food often is dis-
continued temporarily with nutrition provided by a
nasogastric tube.
CHEMICAL INJURIES OF THE
ORAL MUCOSA
A large number of chemicals and drugs come into
contact with the oral tissues. A percentage of these
agents are caustic and can cause clinically significant
damage.
Patients often can be their own worst enemies. The
array of chemicals that have been placed within the
291
Fig. 8-13 Mucosal burn from tooth-whitening strips.
Sharply demarcated zone of epithelial necrosis on the
maxillary facial gingiva, which developed from the use of
tooth-whitening strips. Less severe involvement also is
present on the mandibular gingiva.
mouth in an attempt to resolve oral problems is
amazing. Aspirin, sodium perborate, hydrogen perox-
ide, gasoline, turpentine, rubbing alcohol, and battery
acid are just a few of the more interesting examples.
Certain patients, typically children or those under
psychiatric care, may hold medications within their
mouths rather than swallow them. A surprising number
of medications are potentially caustic when held in the
mouth long enough. Aspirin, bisphosphonates, and two
psychoactive drugs, chlorpromazine and promazine,
are well-documented examples.
Topical medications for mouth pain can compound
the problem. Mucosal damage has been documented
from many of the topical medicaments sold as treat-
ments for toothache or mouth sores. Products contain-
ing isopropyl alcohol, phenol, hydrogen peroxide, or
eugenol have produced adverse reactions in patients.
Over-the-counter tooth-whitening products also
contain hydrogen peroxide or one of its precursors,
carbamide peroxidase, which has been shown to create
mucosal necrosis (Fig. 8-13).
Health care practitioners are responsible for the use
of many caustic materials. Silver nitrate, formocresol,
sodium hypochlorite, paraformaldehyde, chromic acid,
trichloroacetic acid, dental cavity varnishes, and acid-
etch materials all can cause patient injury. Education
and use of the rubber dam have reduced the frequency
of such injuries.
The improper use of aspirin, hydrogen peroxide,
silver nitrate, phenol, and certain endodontic materials
deserves further discussion because of their frequency
of misuse, the severity of related damage, and the lack
of adequate documentation of these materials as
harmful agents.
292 ORAL AND MAXILLOFACIAL PATHOLOGY
Fig. 8-14 Aspirin burn. Extensive area of white epithelial
necrosis of the left buccal mucosa caused by aspirin
placement in an attempt to alleviate dental pain.
Fig. 8-15 Hydrogen peroxide burn. Extensive epithelial
necrosis of the anterior maxillary gingiva secondary to
interproximal placement of hydrogen peroxide with cotton
swabs.
ASPIRIN
Mucosal necrosis from aspirin being held in the mouth
is not rare (Fig. 8-14). Aspirin is available not only in
the well-known tablets but also as powder.
HYDROGEN PEROXIDE
Hydrogen peroxide became a popular intraoral medi-
cation for prevention of periodontitis in the late 1970s.
Since that time, mucosal damage has been seen more
frequently as a result of this application. Concentrations
at 3% or greater are associated most often with adverse
reactions. Epithelial necrosis has been noted with dilu-
tions as low as 1%, and many over-the-counter oral
medications exceed this concentration (Fig. 8-15).
SILVER NITRATE
Silver nitrate remains a popular treatment for aphthous
ulcerations, because the chemical cautery brings about
rapid pain relief by destroying nerve endings. In spite
Fig. 8-16 Phenol burn. Extensive epithelial necrosis of
the mandibular alveolar mucosa on the left side. Damage
resulted from placement of an over-the-counter, phenol-
containing, antiseptic and anesthetic gel under a denture.
(Courtesy of Dr. Dean K. White.)
of this, its use should be strongly discouraged. In all
cases the extent of mucosal damage is increased by its
use. In some patients an abnormal reaction is seen,
with resultant significant damage and enhanced pain.
In one report, an application of a silver nitrate stick to
a small aphthous ulceration led to a necrotic defect that
exceeded 2 × 2 cm and had to be débrided surgically.
In addition, rare reports have documented irreversible
systemic argyria secondary to habitual intraoral use of
topical silver nitrate after recommendation by a dentist
(see page 315).
PHENOL
Phenol has occasionally been used in dentistry as a
cavity-sterilizing agent and cauterizing material. It is
extremely caustic, and judicious use is required. Over-
the-counter agents advertised as “canker sore”
treatments may contain low concentrations of phenol,
often combined with high levels of alcohol. Extensive
mucosal necrosis and (rarely) underlying bone loss
have been seen in patients who placed this material
(phenol concentration 0.5%) in attempts to resolve
minor mucosal sore spots (Fig. 8-16).
A prescription therapy containing 50% sulfuric acid,
4% sulfonated phenol, and 24% sulfonated phenolic
agents is being marketed heavily to dentists for treat-
ment of aphthous ulcerations. Because extensive necro-
sis has been seen from use of medicaments containing
0.5% phenol, this product must be closely monitored
and used with great care.
ENDODONTIC MATERIALS
Some endodontic materials are dangerous because of
the possibility of soft tissue damage (Fig. 8-17) or their
injection into hard tissue with resultant deep spread
Chapter 8 PHYSICAL AND CHEMICAL INJURIES
Fig. 8-17 Formocresol burn. Tissue necrosis secondary to
leakage of endodontic material between a rubber dam clamp
and the tooth.
and necrosis. Because of the past difficulty of obtaining
profound anesthesia in some patients undergoing root
canal therapy, some clinicians have used arsenical
paste or paraformaldehyde formulations to devitalize
the inflamed pulp. Gingival and bone necrosis have
been documented as a consequence of leakage of this
material from the pulp chamber into the surrounding
tissues. In addition, extrusion of filling material con-
taining paraformaldehyde into the periapical tissues
has led to significant difficulties, and its use should be
discouraged. Sodium hypochlorite produces similar
results when it leaks into the surrounding supporting
tissues or is injected past the apex, leading some to
suggest chlorhexidine as a safer irrigant. The following
can reduce the chances of tissue damage:
● Using a rubber dam
● Avoiding excessive pressure during application
● Keeping the syringe needle away from the apex
CLINICAL FEATURES
The previously discussed caustic agents produce similar
damage. With short exposure, the affected mucosa
exhibits a superficial white, wrinkled appearance. As
the duration of exposure increases, the necrosis pro-
ceeds and the affected epithelium becomes separated
from the underlying tissue and can be desquamated
easily. Removal of the necrotic epithelium reveals red,
bleeding connective tissue that subsequently will be
covered by a yellowish, fibrinopurulent membrane.
Mucosa bound to bone is keratinized and more resis-
tant to damage, whereas the nonkeratinized movable
mucosa is destroyed more quickly. In addition to
mucosal necrosis, significant tooth erosion has been
seen in patients who chronically chew aspirin or hold
the medication in their teeth as it dissolves.
293
Fig. 8-18 Cotton roll burn. Zone of white epithelial
necrosis and erythema of the maxillary alveolar mucosa.
The use of the rubber dam can dramatically reduce
iatrogenic mucosal burns. When cotton rolls are used
for moisture control during dental procedures, two
problems may occur. On occasion, caustic materials
can leak into the cotton roll and be held in place against
the mucosa for an extended period, with mucosal injury
resulting from the chemical absorbed by the cotton. In
addition, oral mucosa can adhere to dry cotton rolls,
and rapid removal of the rolls from the mouth often can
cause stripping of the epithelium in the area. The latter
pattern of mucosal injury has been termed cotton roll
burn (cotton roll stomatitis) (Fig. 8-18).
Caustic materials injected into bone during end-
odontic procedures can result in significant bone
necrosis, pain, and perforation into soft tissue. Necrotic
surface ulceration and edema with underlying areas of
soft tissue necrosis may occur adjacent to the site of
perforation.
HISTOPATHOLOGIC FEATURES
Microscopic examination of the white slough removed
from areas of mucosal chemical burns reveals coagula-
tive necrosis of the epithelium, with only the outline of
the individual epithelial cells and nuclei remaining
(Fig. 8-19). The necrosis begins on the surface and
moves basally. The amount of epithelium affected
depends on the duration of contact and the concentra-
tion of the offending agent. The underlying connective
tissue contains a mixture of acute and chronic inflam-
matory cells.
TREATMENT AND PROGNOSIS
The best treatment of chemical injuries is prevention
of exposure of the oral mucosa to caustic materials.
When using potentially caustic drugs (e.g., aspirin,
294 ORAL AND MAXILLOFACIAL PATHOLOGY
Fig. 8-19 Chemical-related epithelial necrosis. Oral
mucosa exhibiting superficial coagulative necrosis of the
epithelial cells.
chlorpromazine), the clinician must instruct the patient
to swallow the medication and not allow it to remain
in the oral cavity for any significant length of time.
Children should not use chewable aspirin immediately
before bedtime, and they should rinse after use.
Superficial areas of necrosis typically resolve com-
pletely without scarring within 10 to 14 days after dis-
continuation of the offending agent. For temporary
protection, some clinicians have recommended cover-
age with a protective emollient paste or a hydroxypro-
pyl cellulose film. Topical dyclonine HCl provides
excellent but temporary pain relief. When large areas
of necrosis are present, such as that related to the use
of silver nitrate or accidental intrabony injection of
offending materials, surgical débridement and antibi-
otic coverage often are required to promote healing
and prevent spread of the necrosis.
NONINFECTIOUS ORAL
COMPLICATIONS OF
ANTINEOPLASTIC THERAPY
No systemic anticancer therapy currently available is
able to destroy tumor cells without causing the death
of at least some normal cells, and tissues with rapid
turnover (e.g., oral epithelium) are especially suscepti-
ble. The mouth is a common site (and one of the most
visible areas) for complications related to cancer
therapy. Both radiation therapy and systemic chemo-
therapy may cause significant oral problems. The more
potent the treatment, the greater the risk of complica-
tions. Each year almost 400,000 patients in the United
States suffer acute or chronic oral side effects from
anticancer treatments. With the advancement of
medical practice, these complications are becoming
more common as more patients have longer survival
times and as intense therapies, such as bone marrow
transplantation, become more commonplace. Oral
complications are noted almost uniformly in patients
receiving head and neck radiation, and close to 75% of
bone marrow transplant patients are affected. The
prevalence of chemotherapy-associated oral complica-
tions varies from 10% to 75%, depending on the type
of associated cancer and the form of chemotherapy
used.
CLINICAL FEATURES
A variety of noninfectious oral complications are seen
regularly as a result of both radiation and chemother-
apy. Two acute changes, mucositis and hemorrhage,
are the predominant problems associated with chemo-
therapy, especially in cancers, such as leukemia, that
involve high treatment doses.
Painful acute mucositis and dermatitis are the most
frequently encountered side effects of radiation, but
several chronic alterations continue to plague patients
long after their courses of therapy are completed.
Depending on the fields of radiation, the radiation
dose, and the age of the patient, the following outcomes
are possible:
● Xerostomia
● Loss of taste (hypogeusia)
● Osteoradionecrosis
● Trismus
● Chronic dermatitis
● Developmental abnormalities
HEMORRHAGE
Intraoral hemorrhage is typically secondary to throm-
bocytopenia, which develops from bone marrow sup-
pression. Intestinal or hepatic damage, however, may
cause lower vitamin K–dependent clotting factors, with
resultant increased coagulation times. Conversely,
tissue damage related to therapy may cause release of
tissue thromboplastin at levels capable of producing
potentially devastating disseminated intravascular
coagulation (DIC). Oral petechiae and ecchymosis sec-
ondary to minor trauma are the most common presen-
tations. Any mucosal site may be affected, but the
labial mucosa, tongue, and gingiva are involved most
frequently.
MUCOSITIS
Recent research suggests that mucosal damage second-
ary to cancer therapy is much more complex than pre-
viously thought and appears to arise from an extended
series of molecular and cellular events that take place
not only in the epithelium but also in the underlying
stroma. Genetic differences in the rate of tissue apop-