ORAL PATHOLOGY

Oral ulcerative lesions

Dr. Rafil Rasheed Hameed

Injury to the oral mucosa, from whetever cause,
may result in a localised defect of the surface in
which the covering epithelium is destroyed,
leaving an inflamed area of exposed connective
tissue. Such defects are called ulcers or
erosions, the later term some times being used
to describe a superficial ulcer. Ulceration is the
most common lesion of the oral mucosa and is
a manifestation of many local and general
diorders.
 Causes of oral ulcerations
Infective
Bacterial
Viral
Fungal

Traumatic
• Mechanical Chemical Thermal Factitious injury Radiation
• Eosinophilic ulcer (traumatic ulcer)
• Idiopathic
• Recurrent aphthous stomatitis Minor aphthous ulcers
Major aphthous ulcers Herpetiform ulcers
• Associated with systemic disease
• Hematological disease
Gastroentestinal tract disease
Behcets diease (syndrome)
HTV infection

Associated with dermatological disease

Lichen planus
Chronic discoid lupus erythematous
Vesiculobullous disease

Neoplasms
Squamous cell carcinoma
Other malignant neoplasms
Traumatic Ulcerations
Ulcers are the most common oral soft tissue lesions. Most are
caused by simple mechanical trauma, and a cause-and-effect
relationship is usually obvious. Many are a result of accidental
trauma and generally appear in regions that are readily trapped
or abraded between the teeth, such as the lower lip, tongue, and
buccal mucosa. Prostheses, most commonly dentures, are
frequently associated with traumatic ulcers, which may be acute
or chronic.
Traumatic ulcers may be iatrogenic, induced by a health
practitioner. Overzealous tissue manipulation may result in
accidental soft tissue injury Ulcers also may be induced by the
removal of adherent cotton rolls, by the negative pressure of a
saliva ejector, or by accidental striking of mucosa with rotary
instruments is uncommon but entirely preventable.
In unusual circumstances, lesions may be self-induced
because of an abnormal habit, and in these
circumstances there is some psychological problem.
These so-called factitial injuries are often as difficult
to diagnose as they are to treat. Striking of mucosa with
rotary instruments is uncommon but entirely
preventable.
Chemicals may also cause oral ulcers because of their
acidity or alkalinity, or because of their ability to act as
local irritants or contact allergens. These may be
patient induced or iatrogenic. Aspirin burns are still
seen, although they are much less common than in the
past.
When acetylsalicylic acid is placed inappropriately against
mucosa in an attempt by the patient to relieve toothache, a
mucosal bum or coagulative necrosis occurs. The extent of injury
is dependent on the duration and number of aspirin applications.
Many over-the-counter medications for toothache, aphthous
ulcers, and denture-related injuries have the ability to damage
oral mucosa if used injudiciously.

Dental cavity medications, especially those containing phenol,

may cause iatrogenic oral ulcers. Tooth-etching agents have been
associated with chenrical bums of mucosa. Endodontic and vital
bleaching procedures, which use strong oxidizing agents such as
30% hydrogen peroxide, have also produced bums.
Thermal or heat bums may cause intraoral ulcers as‫؛‬
pizza bum caused by the hot cheese have been noted on
the palate. Iatrogenic heat bums may also be seen after
use of impression materials such as hydrocolloid, wax or
impression compound.
Oral ulcerations are also seen during the course of
therapeutic radiation and certain types of
chemotherapy for head and neck cancers. In those
malignancies—particularly squamous cell carcinoma—
that require large (60 to 70) doses of radiation, oral
ulcers are invariably seen in tissues within the path of
the beam.
CLINICAL FEATURES
Acute traumatic ulcers of oral mucous membranes exhibit the
clinical signs and symptoms of acute inflammation, including
variable degrees of pain, redness, and swelling. The ulcers are
covered by a yellow-white fibrinous exudate and are surrounded
by an erythematous halo.
Chronic traumatic ulcers occur most often on the tongue, lips,
and buccal mucosa—sites that may be injured by the dentition.
Lesions of the gingiva, palate, and mucobuccal fold may occur
from other sources of irritation. Overzealous tooth bmshing can
create linear erosions along the free gingival margins.
They may cause little or no pain. They are covered by a yellow
membrane and are surrounded by elevated margins that may
show hyperkeratosis .Induration, often associated with these
lesions, is due to scar formation and chronic inflammatory cell
infiltration. The lesions occur in people of all ages, with a
significant male predominance.
Traumatic granuloma, traumatic ulcerative
granuloma with stromal eosinophilia [TUGSE],
eosinophilic granuloma of the tongue
These lesions exhibit a deep pseudo invasive
inflammatory reaction and is typically slow to resolve.
Interestingly, many of these traumatic granulomas
undergo resolution after incisional biopsy.
A 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 considered a
variation of the traumatic eosinophilic ulceration. Riga-
Fede disease typically appears beftveen 1 week and 1 year
of age.
The condition often develops in association with
natal or neonatal teeth.
The anterioi. ventral surface of the tongue is the
most common site of involvement, although the
dorsal surface also jnay be affected. Ventral
lesions contact the adjacent mandibular anterior
incisors; lesions on the dorsal surface are
associated with the maxillary incisors.
Treatment
Most reactive ulcers of oral mucous membranes are
simply observed. If pain is considerable, topical
treatment may be beneficial, such as the forjn of a
topical corticosteroid. Healing of traumatic granuloma
is spontaneous, but topical and intralesional steroids
can accelerate healing and reduce symptoms.
Recurrent aphthous stomatitis
Of all the types ofnon-traumatic ulceration that affect oral
mucosa, aplrthous ulcers (canker sores) are probably the
most common. Incidence ranges from 20% to 60٥/..
Prevalence tends to be higher in professional persons, ‫ئ‬
those in upper socioeconomic groups, and in those who do
not smoke.
Etiology: Although the cause of aphthous ulcerations is
unknown, several possibilities have been posftrlated. There
is considerable evidence that aphthous ulcers are related to a
focal immune dysfimction in which T lymphocytes have a
signiflcant role. The causative agent could be endogenous
(autoimmune) antigen or exogenous antigen, or it could be a
nonspecific factor, such as trauma in which chemical
mediators may be involved.
THE POSSIBLE ETIOLOGICAL FACTORS Allergy:
food
Genetic predisposition: HLA family Nutritional
deficiency: B12, folic acid and iron
Hematological abnormalities Hormonal
influences: Female, menstrual period Infectious
agents: AIDS, HSV, VZV
Hypersensitivity to bacterial antigens of
Streptococcus sanguis Malabsorption conditions
such as celiac disease and Crohn’s disease
Trauma Stress
THE POSSIBLE ETIOLOGICAL FACTORS
Allergy: food
Genetic predisposition: HLA family
Nutritional deficiency: B12, folic acid and
iron Hematological abnormalities
Hormonal influences: Female, menstrual
period Infectious agents: AIDS, HSV, VZV
Hypersensitivity to bacterial antigens of
Streptococcus sanguis Malabsorption
conditions such as celiac disease and Crohn’s
disease Trauma Stress
Clinical Features.
Three forms of aphthous ulcers have been recognized:
Minor, major, and herpetiform aphthous ulcers. All are
believed to be part of the same disease spectrum, and
all are believed to have a common etiology. Differences
are essentially clinical and correspond to the degree of
severity. All forms present as painful recurrent ulcers.
Patients occasionally have prodromal symptoms of
tingling or burning before the appearance of lesions.
The ulcers are not preceded by vesicles and
characteristically appear on the vestibular and buccal
mucosa, tongue, soft palate, fauces, and floor of mouth.
Only rarely do these lesions occur on the attached gingiva
and hard palate, thus providing an important clinical sign
for the separation of aphthous ulcers from secondary
herpetic ulcers.
In patients with AIDS, however, aphthous-like ulcers may
occur at any mucosal site.
Minor Aphthous Ulcers
The most commonly encountered form
Usually appears as a single and painful
Ulcers are oval, less than 0.5 cm in diameter, covered by a yellow
fibrinous membrane and surrounded by an erythematous halo
Multiple oral aphthae may be seen.
Generally last 7 to 10 days and heal without scar formation.
Recurrences vary from one individual to another. Periods of
freedom from disease may range from a matter of weeks to as long
as years.
Major Aphthous Ulcers
Lesions are larger (>0.5 cm) and more painful
and persist longer than minor aphthae.
Ulcers appear craterform clinically and heal
with scar formation.
Lesions may take as long as 6 weeks to heal,
and as soon as one ulcer disappears, another
one starts.
systemic health may be compromised
because of difficulty in eating and
psychological stress.
Herpetiform Aphthous Ulcers.

Present clinically as recurrent crops of small ulcers.

Although movable mucosa is predominantly affected,

palatal and gingival

mucosa may also be involved.

Pain may be considerable, and healing generally occurs

in 1 to 2 weeks. Unlike herpes infection, herpetiform

Behcet’s Syndrome
BehCet’s syndrome is a rare multisystem inflammatory disease
(gastrointestinal, cardiovascular, ocular, CNS, articular,
pulmonary, dermal) in which recurrent oral aphthae are a
consistent feature. Although the oral manifestations are usually
relatively minor, involvement of other sites, especially the eyes
and CNS, can be serious.
Clinical Features. Lesions of Beh‫؟‬et’s syndrome typically affect
the oral cavity (100% incidence), the genitalia (62% of cases), and
the eyes. Other regions or systems are less commonly involved.
Recurrent arthritis of the wrists, ankles, and knees may be
associated. Cardiovascular manifestations are believed to result
from vasculitis and thrombosis.
Oral manifestations of this syndrome appear identical to the
ulcers of aphthous stomatitis. The ulcers are usually the minor
aphthous form and are found in the typical aphthous
distribution.
Diagnosis. The diagnosis of Behcet’s syndrome is based
on clinical signs and symptoms associated with the
various regions affected. No specific findings are noted in
biopsy tissue, and no supportive laboratory tests are
available.
Treatment. No standard therapy is known for Behqet’s
syndrome. Systemic steroids are often prescribed
Immunosuppressive drugs.
Erythema Multiforme
EM is usually an acute, self-limited process that affects
the skin or mucous membranes or both. It may on
occasion be chronic, or it may be a recurring acute
problem .Between 25% and 50% of patients with
cutaneous EM have oral manifestations of this disease.
The term erythema multiforme was coined to indicate
the multiple and varied clinical appearances that are
associated with cutaneous manifestations of this
disease. It has been divided into two subtypes: a minor
form, usually associated with an HSV trigger, and a
major severe form, triggered by certain systemic
drugs.
Etiology and Pathogenesis.
The basic cause of EM is unknown, although a
hypersensitivity reaction is suspected. Some evidence
suggests that the disease mechanism may be related to
antigen-antibody complexes that are targeted for
small vessels in the skin or mucosa.
Precipitating or triggering factors generally fall into the
two large categories of infections (frequently reported
include HSV infection (due to HSV types 1 and 2), TB,
and histoplasmosis) and drugs.
Malignancy, vaccination, autoimmune disease, and
radiotherapy, are occasionally possible triggers.
Clinical Features
Young adults are most commonly affected. Individuals
often develop EM in the spring.
In recurrent disease, prodromal symptoms may be
experienced before any eruption.
The classic skin lesion of EM is the target or iris
lesion. It consists of concentric erythematous rings
separated by rings of near-normal color. Typically, the
extremities are involved, usually in a symmetric
distribution. Other types of skin manifestations of EM
include macules, papules, vesicles, bullae, and
urticarial plaques.
Orally, presents as an ulcerative disease,
varying from a few aphthous-type lesions to
multiple superficial, widespread ulcers in EM
major. Short-lived vesicles or bullae are
infrequently seen at initial presentation. Any
area of the mouth may be involved, with the
lips, buccal mucosa, palate, and tongue being
most frequently affected. Symptoms range from
mild discomfort to severe pain.
Stevens-Johnson syndrome EM spectrum (EM
major)
At the severe end of the intense involvement of the
mouth, eyes, skin, genitalia, and occasionally the
esophagus and respiratory tract may be seen
concurrently. This form has a strong relationship to
medications, in particular analgesics, where oxicams
or propionic acid derivatives have been used.
Characteristically, the lips show crusting ulceration
at the vermilion border that may cause pain.
Superficial ulceration, often preceded by bullae, is
common to all sites affected. Ocular inflammation
(conjunctivitis and uveitis) may lead to scarring and
blindness.
Treatment
EM minor, symptomatic treatment,
including keeping the mouth clean with
bland mouth rinses, may be all that is
necessary.
EM major, topical corticosteroids with
antifungals may help control disease. The
use of systemic corticosteroids remains
controversial.
LUPUS ERYTHEMATOSUS (LE)
Lupus erythematosus is a classic example of an
immunologically mediated condition. It may exhibit
any one of several clinicopathologic forms. Systemic
lupus erythematosus (SLE).
Discoid Lupus erythematosus (DLE).
Systemic (Acute) lupus erythematosus (SLE) is a
serious multisystem disease with a variety of cutaneous
and oral manifestations. Although genetic factors
probably play a role in the pathogenesis of SLE, the
precise cause is unknown. An interplay between
genetic and environmental factors occurs. Chronic
cutaneous lupus erythematosus (CCLE) may represent
a different, but related, process. It primarily affects the
skin and oral mucosa,
and the prognosis is good. Subacute cutaneous lupus
erythematosus is a third form of the disease, which has
clinical features intermediate between those of SLE and
CCLE.
Clinical Features
Systemic lupus erythematosus.
Women are affected nearly 8 to 10 times more frequently
than men. The average age at diagnosis is 31 years.
Common findings include fever, weight loss, arthritis,
fatigue, and general malaise.
In 40% to 50% of affected patients, a characteristic rash,
having the pattern of a butterfly, develops over the
malar area and nose. Sunlight often makes the lesions
worse.
The kidneys are affected in approximately 40% to 50%
of SLE patients. This complication may ultimately lead
to kidney failure; thus it is typically the most significant
aspect of the disease.
Cardiac involvement is also common being the most
frequent complication.
Oral lesions of SLE develop in 5% to 25% of these
patients. The lesions usually affect the palate, buccal
mucosa, and gingivae. Varying degrees of ulceration,
pain, erythema, and hyperkeratosis may be present.
Other oral complaints such as xerostomia, candidiasis,
and periodontal disease have been described, but the
direct association of these problems with SLE remains
to be proven.
Diagnosis: Serological tests for antibodies show
positive results in patients with SLE. The ANA
(antinuclear antibody) test is regarded as a reliable and
specific test for SLE.
Treatment
Patients with SLE should avoid excessive exposure to
sunlight because ultraviolet light may precipitate
disease activity. Mild active disease may be effectively
managed using non- steroidal anti- inflammatory
agents combined with antimalarial drugs. For more
severe, acute episodes that involve arthritis, pericarditis,
thrombocytopenia or nephritis, systemic corticosteroids
are generally indicated; these may be combined with
other immunosuppressive agents.
Discoid Lupus Erythematosus (DLE)
Characteristically seen in middle age, especially in women.
Lesions commonly appear solely on the skin, most
commonly on the face and scalp.
On the skin, lesions appear as disc-shaped erythematous
plaques with hyperpigmented margins. As the lesion
expands peripherally, the center heals, and formation of scar
and loss of pigment are noted. Involvement of hair
follicles results in permanent hair loss (alopecia).
The buccal mucosa, gingiva, and vermilion are most
commonly affected. Lesions may be erythematous or
ulcerative with delicate white, keratotic striae radiating
from the periphery. The diagnosis of oral lesions may not
be evident on the basis of clinical appearance.