Reactive lesions

Dr. Rakefet Czerninski

The Department of Oral Medicine
 Reactive lesions
• Mechanical-
Mechanical Dental ,Iatrogenic, factitional
• Thermal-
Thermal Food, Electrical
• Chemical-
Chemical Medication, Mouth rinses,
Tobacco , Smoking

• Radiation-
Radiation U.V., Radiotherapy
 Ulcer

• Ulcer =loss of epithelium

• Ulcers-the most common

oral soft tissue lesions
 Traumatic ulcerations
USA-Incidence -unknown, considered the most
common oral ulcerations.

• Traumatic injuries -
formation of
surface ulcerations
acute /chronic.

• Causes:
Mechanical ,chemical,
electrical, thermal
 Mechanical -Traumatic ulcers
• Teeth: fractured, carious,
malposed, malformed teeth,
• Seen at the labial mucosa, lateral
border of the tongue.
• Dental appliances: Poorly
maintained and ill-fitting dental
prosthetic & orthodontic appliances,

• Iatrogenic- removal of adherent

cotton roll, negative pressure of
saliva ejector, overzealous tissue
manipulation
• Seen at the mucobuccal folds,
gingiva, and palatal mucosa.
 Newborns and infants
Sublingual ulcerations
(as in Riga-Fede disease=traumatic
eosinophilic granulation)

may occur as a result of too

adjacent anterior primary
teeth.

The trauma is often

associated with breast
feeding.
Traumatic ulcer-Clinical Features
Areas of erythema that
surround a removable,
central, yellow,
fibrinopurulent membrane.

Acute ulcer: clinical

sign & symptoms ‫טבלה‬
of acute
inflammation:
pain ,redness &
swelling
Involuntary
movements of the
tongue and
mandiblebuccal
mucosa

Orobuccal dyskinesia
(secondary parkinsonism)
 Histology
• surface ulceration -acute inflammatory cells
intermixed with fibrin (fibrinopurulent membrane ).

• The adjacent epithelial surface -hyperplastic &

areas of reactive squamous atypia.

• The ulcer bed is composed of a proliferation of

granulation tissue with areas of edema and an
infiltrate of acute and chronic inflammatory cells.
 Mechanical -Traumatic ulcers
• In most cases, the source of the injury
is identified.

• The patient's usual complaint is pain

or a painful ulceration.

• Traumatic ulcers are usually sensitive

to hot, spicy, or salty foods.
 Medical care
• With ulcerations induced by mechanical trauma or
thermal burns from food, remove the obvious cause.
 Medical care
Apply films to relief the pain
temporarily

Corticosteroids-controversial:
Success in healing vs. Delay

Consider CHX

These lesions typically

resolve within 10-14 days
 Treatment
• Antibiotics, usually penicillin, for prevention of
secondary infection
especially if the lesions are severe and deep seated.

• Most traumatic ulcers resolve without the

need for antibiotic treatment.
Some ulcers caused by trauma may resemble
• Squamous cell carcinoma
• Granulomatous ulcers:
Deep fungal infections
Tuberculosis.
Tuberculosis
If:
the cause of the ulceration is not obvious
at clinical examination
or
no response to local therapy is noted within 2
weeks,
biopsy may be indicated to exclude
these conditions.
‫גורם טראומה נוסף‬
 Chemical injuries
Cause of ulcer:
• Acidic /basic nature
• Allergens

Patient induced
• Attempt to resolve oral pain
Phenol ( cavity sterilizing agent and
cauterizing material). extremely caustic
OTC agent with low concentration of
phenol and high concentration of alcohol.
Eugenol
 Chemical injuries
• Aspirin- Aceylsalycilic acid against mucosa to
relieve toothache-mucosal burn/coagulative necrosis
• Hydrogen peroxide- popular intraoral
medication 1970’s,periodontitis-epithelial necrosis in
low concentration as well (1%)
• Silvernitrate- destroys nerve endings for pain -
aphthosis-mucosal damage is increased by its use
• Alcohol containing mouth washes

Holding a drug instead of swallowing

(Children, Psychiatric):
Chloropromazine,Promazine

.
 Chemical injuries
Iatrogenic:
• Oxidating agents
Hydrogen Peroxide 30%
(Vital bleaching)

• Endodontic materials-
Formocresol,
• Sodium Hypochloride,
• Acid etch materials
 Chemical injuries
Short exposure-
Superficial white wrinkled
appearance
Increased concentration/
longer time- Pain-
Desqumation of epithelium.
Mild erythema,.
Necrosis-removal-red bleeding
c.t. that subsequently will be Histology-necrosis
begins on the surface
covered by a yellowish membrane.
and moves basally
 Treatment

Prevention:
• Children-swallowing medication
and mouth rinse
• Rubber dum
Temporary protection:
protective emollient paste, pain relief agents

Superficial areas of necrosis resolve

completely without scarring in 10-14 days
‫• נתניה‪ :‬בת ‪ 12‬נכוותה מקצף שהותז לפיה במהלך‬
‫חגיגות העצמאות‬
‫בת ‪ 12‬מנתניה אושפזה אתמול בבית חולים לניאדו‬
‫בעיר לאחר שקצף מתרסיס הותז לתוך פיה במהלך‬
‫חגיגות יום העצמאות‪ .‬מבית החולים נמסר כי לילדה‬
‫נגרמה כווייה בתוך הפה‪ .‬מצבה מוגדר קל ‪.‬‬
 Thermal injuries
• Ingestion of hot food /beverages-
Uncommon
• Microwave oven; Pizza burn Hot
sticky food- hard palate
• Hot liquids- burn the tongue & soft
palate
• Tooth impression materials:
Palate, posterior buccal mucosa
Zone of erythema and ulceration with
remnants of necrotic epithelium at the
periphery.
 Electrical burns
Uncommon-5%of all oral burns

Arc type: Chewing end of extension cord or

biting a live wire. Saliva=conducting medium
and electrical arc flows to the mouth-extreme
heat & tissue destruction.
Usually children<4

Lips, Commissures.
Painless charred yellow area, no bleeding
Significant edema within few hours to 12days
4th day- necrosis & slough ,adjacent teeth –non vital
 Electrical burns
Treatment:
• Tetanus immunization
• Prophylactic antibiotics (Penecillin)
Problem-Contracture of mouth opening during
healing
Untreated patient- extensive scarring and
microstomia
Treatment- splinting up to 8 months
Chronic ulcerations as a result of
trauma
have not been associated
with premalignant / malignant
transformation
in the oral mucosa
 Frictional Hyperkeratosis
White patches: First step:
use a 2 X 2 piece of gauze to
wipe off the lesion or lesions.

If the patch is not easily

wiped off, this suggests
the presence of
hyperkeratinization
 Focal (frictional) Hyperkeratosis
Constant irritation:
Production of excessive keratin with
a subsequent change in the
thickness and the color of the
involved mucosa.
Commonly traumatized areas:
lips, tongue-lateral, buccal
mucoocclusal line, edentulous ridge

At first pale ,translucent later

dense white & rough surface
felt by the tongue
 Pathophysiology

Constant
irritation
Focal (frictional) Hyperkeratosis
 Focal (frictional) Hyperkeratosis
Histopathology: thick hyperkeratosis, few chronic
inflammatory cells, epithelium -hyperplastic no
dysplastic
Diagnosis: careful history taking & examination

Discontinue habit/remove origin

of trauma resolution
Treatment:
• Observation
• Control of habit
• Questionable etiology-biopsy
 Linea alba
Horizontal thickening of
the buccal mucosa
along the occlusal
line.
It is thought to result
from chronic cheek
biting

FK has no propensity for malignant transformation

 Habits, Chronic Cheek Bite,
Morsiccatio Buccarum
• Conscious or unconscious
chronic cheek chewing,

• Higher prevalence in people

who are under stress or
have a variety of psychologic
conditions.

• Most patients are aware of

their habit, many deny the
self inflicted injury
1/800 adults has active lesions.
F2:1M ; 3 times more >35
Bilateral,( might be unilateral ).
Buccal mucosa,
Labial mucosa (Morsiccatio Labiorum),
Lat.borders tongue(Morsiccatio linguarum)
Mid portion along
the occlusal plane,
large lesions when
habit involves
pushing the tissue
with a finger
‫"אבל מה עם התענוג"‪...‬‬
(Ulcers) may be the result of voluntary, self-induced, and
deliberate acts by patients with physical or psychological
symptoms who are seeking medical attention
 Differential Diagnosis
• White patches associated
with smoking can be
clinically indistinguishable
from FK.
• Clinical information
regarding tobacco is
essential

Differentiating between lesions from

smoking and FHK is important because their
prognosis is different from that associated
with FHK, which is excellent.
 Cigarette smoking
• About 25% of all American adults, 46.3 million
people, smoke.
• USA :M 28.1% F 23.5%
• Other tobacco products :pipes, cigars, snuff -
less than 10% of use of all tobacco products
• In Israel 2002- 27% of all Israelis 2003-24.3%
• adults: Jewish 2002:F 24% M 30%
• 2003: 21% 29%
• Arab 7.4% 43%

http://www.health.gov.il/units/spoke/index.htm
 Cigarette smoking
• Remains the leading cause of death and illness
among Americans.
• 430,000/y Americans die from illnesses caused
by tobacco use,
• 1/5 of all deaths.
• Tobacco use costs about $100 billion each year
in direct medical expense and lost productivity
 The risk of smoking
• Cigarette smoking has been linked strongly to the following illnesses:
• Heart disease
• Stroke
• Other diseases of blood vessels (poor circulation in the legs)
• Respiratory illness, including the following:
– Lung cancer
– Emphysema
– Bronchitis
– Pneumonia Increased risk of dying from:
• Cancers, including:
– Lip or mouth •Lung, throat or mouth cancer: x14
– Pharynx or larynx voice box
– Esophagus •Cancer of esophagus: x4
– Pancreas
– Kidney •Heart attack: x2
– Urinary bladder
– Cervix
• Peptic ulcer disease
• Burns
 Smoking & Oral Cancer
The relative risk is dose & time dependant for cigarette
smokers
• Heavy smokers- increased risk of OSCC x5- 25
• Onset- below 18 years
• Duration- over 35 years high risk factors.

Israel-average age M 15.3 F 15.7

• Cigar & pipe smoking - greater risk for development of

oral cancer than cigarette

Blot, WJ, McLaughlin, JK, Winn, DM, et al. Smoking and drinking in relation to oral and pharyngeal cancer.
Cancer Res 1988; 48:3282.
Spitz, MR. Epidemiology and risk factors for head and neck cancer. Semin Oncol 1994; 21:281.
 Nicotine stomatitis
• Nicotinic stomatitis (smoker's palate), described since 1926.

• In 1941, Thoma named the lesion stomatitis nicotine because

it is almost exclusively observed in individuals who smoke
tobacco.

• Observed most often in pipe and reverse cigarette smokers

;less often in cigarette and cigar smokers.
• Incidence-USA-unknown
 Nicotine stomatitis
• Affects the oral mucosa of
the hard palate posterior
to the rugae and less
often to the adjacent soft
palate

• Severity in correlation
with intensity of smoking
 Nicotine stomatitis
• Nicotine stomatitis first: reddened
area .
• Slowly progresses: white, thickened,
and fissured appearance.
• Minor salivary glands -swollen, the
orifices become prominent- speckled
white and red appearance.
• Asymptomatic / mildly irritating.

• Patients -unaware of the lesion or

have had it for many years without
changes.
 Nicotine stomatitis
• Not associated with dysplastic/malignant changes.

• Reverse smoking- The concentrated heat and

chemicals increase the potential for malignant
change .
• Common in some parts of the Caribbean and
Southeast Asia.
Asia
 Nicotine stomatitis
Denture protected
Mechanism of action - areas- unaffected
heat irritation from a
tobacco product that
acts as a local irritant,
stimulating a reactive
process.
Dentures often protect
the palate from these
irritants
 Prognosis
• Nicotine stomatitis -reversible
(even if present for many years)
once the irritant is removed .
• The prognosis is excellent.
• Palate returns to normal within
1-2 w of cessation.

Any white lesion of the palate

which persist after 1
month of cessation
should be considered as
leukoplakia
• Nicotine stomatitis -not
premalignant condition,
monitor these patients
because of their risk factors.

• Investigate more thoroughly

the changes to the palate or
adjacent lesions that appear
different than the classic
pattern described.
 Smokeless Tobacco
Used in USA ,Scandinavia ,India ,South east Asia
• Tobacco –higher pH (8.2-9.3)-mixture with gradients
areaca (betel) nut, lime spices camphor
• Snuff-Ground
Snuff & finely cut Chewing-loose
Chewing leaf Tobacco

•Long term exposure (years)- (mainly snuff)- white

granular wrinkled patches, mucobucal fold of mandible.
•Inflammation ,keratosis, dysplastic changes
Asymptomatic.
Discontinuation of Tobacco use-some lesions will
disappear

Increase the risk for

cancer, lower than
smoking
 Smokers melanosis

Focal pigmentation multiple brown pigmented macules attached labial gingiva

Buccal mucosa and palate pigmentation –associated with pipe smoking
25-31% of Tobacco users, after 3rd decade

Melanin deposition within the basal cell layer & lamina propria
 Treatment
Many cigar and pipe smokers believe that
they are not at risk for cancer because
they do not inhale.
The only definitive treatment is smoking
cessation.
 Smoking cessation -a significant
decrease in relative risk with no excess
risk at 20 years
Smoking cessation before age 50 years
have half the risk of dying in the next 15
years compared with those who
continue to smoke
 Educate patients concerning the
dangers of tobacco use.

Once they understand the need to stop

using tobacco products,
make a referral to a comprehensive
tobacco-cessation program
 Solar (actinic) cheilitis
Tissue degeneration
due to prolonged
& regular exposure
to sunlight.
Whites; fair skin
Lower lip
Atrophic pale-gray
Areas of
hyperpigmantation
& keratosis
 Solar (actinic) cheilitis
Areas of
hyperpigmantation
& keratosis
Fissuring ,erosions, ulcerations
Craking, wrinkling, crusting
 Solar (actinic) cheilitis

Histology-epithelium-atrophic/focaliy & irregulary

hyperplastic+surface keratosis..
Dysplastic changes:slight atypia-Ca. in situ.
Submucosa: telangiectatic vessels, curled elastin
fibers(special stains)

Premalignant lesion by
WHO
 Solar (actinic) cheilitis

Treatment:Premalignant lesion.
In case of induration,
persistent ulceration:

• Biopsy;
• consider vermiliomectomy & mucosal
advancement
 Solar (actinic) cheilitis
In case of epithelial atypia; epithelial changes;
• Protection from sun:
life style, hat, sun protection lip agents
Topical application of 5-fluouracul, retinoic acid

• Periodic examination

Invasive cancer development

can happen after 20-30 years
SCC