White Lesions - College of Dentistry

self-study
course
2014
course
four
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Page 1
2014
course
four
WHITE LESIONS OF THE ORAL
CAVITY
This course will help dental professionals familiarize themselves with
common white lesions of the oral cavity and derive a differential diagnosis
for various white lesions.
INTRODUCTION
White lesions of the oral cavity are
one of the leading reasons for which
patients
seek
professional
treatment. These lesions can have a
wide spectrum of diagnoses
including
infectious,
reactive,
immune-mediated, premalignant,
and malignant conditions. Patient
history, clinical presentation, and
location can be very helpful in
narrowing down the differential
diagnosis of these various white
lesions.
INFECTIOUS WHITE
LESIONS
CANDIDIASIS
written by
neetha santosh, dds
edited by
rachel a. flad, bs
karen k. daw, mba, cecm
evan miller
Candidiasis is the most prevalent
oral fungal infection in humans.
Candida Albicans, part of the normal
oral micro flora, is the causative
organism. A complex interaction of
immune status and mucosal
environment of the host and strain
of C. Albicans controls the presence
of candidal infection.
Various
predisposing factors for oral
candidiasis include use of dentures,
xerostomia, recent broad-spectrum
antibiotic therapy, corticosteroid use
(aerosolized inhalants or topical
creams/gel), and immunodeficiency
(HIV infection or leukemia).
Clinical Features:
The clinical features of candidiasis
can vary from superficial
involvement of oral mucosa in
Pseudomembranous
Candidiasis
Dr. Carl Allen, The Ohio State
University College of Dentistry
immunocompetent individuals to
disseminated
infection
in
immunosuppressed patients. A
variety of clinical forms of oral
candidiasis exist, including:




Pseudomembranous
Erythematous
Hyperplastic
Mucocutaneous
Among these, the two clinical
forms which appear white are
pseudomembranous
and
hyperplastic candidiasis.
Pseudomembranous candidiasis
appears clinically as creamy, white
plaque (similar to cottage cheese
or curdled milk) and is usually
present on the buccal mucosa,
tongue, and palate. This plaque
can be removed by scraping or
wiping, which leaves an intact
normal or reddened underlying
mucosa. Diagnosis of alternative
white lesions such as lichen planus
should be considered if the
mucosa bleeds while scraping the
p l aqu e . T he pa t i e nt s w i t h
pseudomembranous candidiasis
usually complain of mild burning
sensation or bad taste. The
diagnosis is usually established by
Page 2
the relevant history of predisposing factors and
typical clinical appearance.
Isolation and identification of candidal hyphae or
yeasts by exfoliative cytology (smear), or, culture
on Sabouraud’s agar slant (swab) can confirm the
diagnosis.
Hyperplastic candidiasis presents as a white plaque
that cannot be removed by scraping or wiping. It
is most often present on the anterior buccal
mucosa near the commissures, as well as on the
tongue and lips. Hyperplastic candidiasis cannot
be clinically distinguished from routine
leukoplakia. The diagnosis is established by the
identification of candida by a cytologic smear or
culture and by total disappearance of plaque
following antifungal treatment. A biopsy of the
area will be prudent if any white plaque has
remained in order to rule out the presence of true
leukoplakia.
Care should be taken to avoid confusing
coated/hairy tongue with candidiasis. Coated
tongue is due to accumulation of keratin and
bacteria on the dorsal surface of the tongue,
resulting in a white and thickened appearance.
Hairy tongue has a typical hair-like appearance
due to elongation of and the keratin accumulation
on the filiform papillae of the dorsal tongue. The
diagnosis of coated/hairy tongue is distinguished
by its characteristic clinical appearance. Scraping
the tongue and improving oral hygiene is the
recommended treatment.
treatment regimen of patients with dentures. If
there is no improvement post-treatment, biopsy
of the area is recommended to exclude other
possible conditions. A referral to the physician is
also prudent to rule out underlying systemic
disorders.
ORAL HAIRY LEUKOPLAKIA
Oral hairy leukoplakia is a lesion that occurs
mainly in immunocompromised individuals,
especially in AIDS patients. This lesion has also
been described in patients experiencing
extended corticosteroid therapy after organ
transplantation or other systemic conditions.
Epstein-Barr virus is the main causative organism
of oral hairy leukoplakia.
Clinical Features:
Oral hairy leukoplakia typically presents as white
vertical streaks or corrugated plaques on the
lateral border of the tongue. This lesion is usually
bilateral and can extend to the dorsal and lateral
surfaces of the tongue, and can also rarely involve
the buccal mucosa, soft palate, pharynx, and
esophagus. Oral hairy leukoplakia does not rub
off; differential diagnoses include hyperplastic
candidiasis,
true leukoplakia, proliferative
verrucous leukoplakia, morsicatio linguarum
(tongue chewing), and lichen planus. A definite
diagnosis can be established by identification of
Epstein-Barr virus within the lesion using in situ
hybridization or by histopathological examination
of the biopsied area.
Treatment:
Treatment:
A variety of topical and systemic antifungal agents
are available to treat oral candidiasis. Most of the
patients respond well to the topical treatment
which include Nystatin and Clotrimazole. The
systemic drugs available are Ketoconazole,
Fluconazole, and Itraconazole and are used usually
for chronic or disseminated candidiasis. The
recommended dosage of Clotrimazole is to
dissolve 1 troche (10 mg) slowly in the mouth 5
times per day for 10 days. Nystatin oral
suspension can be used by swishing 2-5 mL for
tw o minu tes and sw allow ing the reafter .
Disinfection of dentures by soaking them in 10%
household bleach (complete dentures) or in
Nystatin oral suspension (removable dentures
with metal parts) should be included in the
Usually, it is not necessary to treat oral hairy
leukoplakia. There can be resolution of the lesion
if the patient is on Highly Active Antiretroviral
Therapy (HAART) for HIV infection. HIV patients
diagnosed with oral hairy leukoplakia have higher
chances of disease progression to AIDS. Since
oral hairy leukoplakia is mostly seen in
immunocompromised individuals, its occurrence
in the absence of a known reason of
immunosuppression warrants referral to a
physician for a complete physical evaluation.
Page 3
REACTIVE WHITE LESIONS
LINEA ALBA
appearance. Isolated lesions on the lateral border
of the tongue without history of tongue chewing
should be thoroughly evaluated to rule out HIVassociated oral hairy leukoplakia.
Linea alba means “white line” in Latin and is one
of the most common variations of the buccal
mucosa. Pressure, frictional irritation, or sucking
trauma from adjacent facial surfaces of the teeth
are usually linked to this alteration.
No treatment is usually required for morsicatio
lesions. An oral acrylic shield may be fabricated to
protect buccal and labial mucosa from chewing
habits.
Clinical Features:
CHEMICAL INJURIES OF THE ORAL MUCOSA
Linea alba typically presents as a bilateral white
line on the buccal mucosa at the level of the
occlusal plane. It can have a scalloped appearance
and extend from the commissure to the posterior
teeth.
Prolonged periods of contact between various
drugs and chemicals and the oral mucosa can
cause temporary white lesions. Aspirin, hydrogen
peroxide, silver nitrate, phenol, eugenol,
formacresol, sodium hypochlorite, dental cavity
varnishes, and acid etch materials are some of the
most common drugs and chemicals that cause
oral mucosa. These white lesions are due to
epithelial necrosis and fibrinopurulent exudate
from the chemical injury.
Treatment:
Diagnosis of linea alba is made by the
characteristic clinical location and appearance,
with biopsy not usually being necessary. Linea
alba requires no treatment and it may disappear
on its own in some individuals.
MORSICATIO BUCCARUM (CHRONIC CHEEK
CHEWING)
White lesions can appear on the oral mucosa due
to chronic cheek biting or sucking. These are
most common on bilateral buccal mucosa
(morsicatio buccarum) and are also present on the
tongue (morsicatio linguarum) and lips
(morsicatio labiorum).
Clinical Features:
Morsicatio lesions are often seen in people who
have psychologic conditions or in those who are
under stress. Women are twice as likely to be
affected by these lesions.
The lesions are
frequently seen bilaterally on the anterior buccal
mucosa along the occlusal plane and have a
distinctive irregular and ragged appearance due
to constant nibbling. Similar lesions can be
present on the labial mucosa or lateral borders of
the tongue.
Treatment:
Morsicatio lesions are diagnosed by the history of
chewing habits and the typical ragged clinical
Clinical Features:
A brief exposure with chemicals causes the oral
mucosa to appear white and wrinkled; prolonged
exposure leads to epithelial necrosis and
desquamation.
Necrotic epithelium can be
removed,
which
exposes
erythematous
underlying connective tissue and is later covered
by a yellowish-white fibrinopurulent membrane.
The injury to the mucosa can be very extensive
depending upon the duration of exposure and
concentration of the chemical. The attached
mucosa is more resilient to the chemical injury
compared to the unattached mucosa.
Treatment:
The ideal treatment of chemical injuries is carried
out by preventing exposure of oral mucosa to
potential caustic medications. If such medications
have to be used, care should be taken to swallow
the drug immediately to avoid any prolonged
contact with oral mucosa. Children should be
monitored as well. Healing occurs in superficial
lesions within 1-2 weeks. Deep and extensive
lesions may require surgical debridement and
antibiotic therapy to quicken healing and prevent
infection.
Page 4
CONTACT STOMATITIS
Treatment:
A wide variety of agents including food, food
additives, chewing gum, candy, oral hygiene
products such as toothpaste and mouth washes,
and dental treatment materials such as gloves and
rubber dam materials, topical anesthetics,
restorative materials, acrylic denture materials,
dental impression materials, and denture adhesive
preparations can cause allergic reactions in the
oral cavity.
If the patient stops the use of cinnamon flavored
product or tartar-control toothpaste, lesions
should resolve within a week. The lesions will
reoccur within 24 hours if the patient reuses the
product. A topical corticosteroid can provide
faster recovery in some patients. Biopsy of the
area will be prudent to rule out other conditions if
contact stomatitis still persists after two weeks of
discontinuation of the offending products.
Clinical Features:
FRICTIONAL KERATOSIS
Contact stomatitis occurs more frequently in
females and can be acute or chronic. Two
commonly occurring contact stomatitis in oral
mucosa are oral cinnamon reaction and
toothpaste related sloughing.
Frictional keratosis refers to a white patch on the
oral mucosa due to constant mechanical irritation.
Sources of mechanical irritation can be numerous
including broken tooth cusps, sharp restorations,
orthodontic brackets, and rough or ill-fitting
dentures. Alveolar ridge keratosis is a form of
frictional keratosis occurring on the crest of an
edentulous ridge or retromolar pad area and
results from chronic friction from dentures or
mastication. Linea alba and morsicatio lesions can
also be grouped under frictional keratotic
conditions.
Oral cinnamon reaction occurs due to the artificial
cinnamon oil used as a flavoring agent in gum,
candy, toothpaste, mouth washes, breath
fresheners, soft drinks, processed meat, etc.
Patients usually complain of pain and a burning
sensation. Clinical presentation of oral cinnamon
reaction varies depending upon the medium of
delivery. While a diffuse reaction is seen with
toothpaste
containing
artificial
cinnamon
flavoring, a more localized pattern occurs with
chewing gum and candy. The buccal mucosa and
the tongue are the frequent locations affected
from chewing gum and candy. Oblong patches of
reddened areas with overlying white, shaggy
hyperkeratosis are observed on buccal mucosa
along the occlusal plane. The tongue can also
have a similar appearance involving the lateral
border and dorsal surface. Diagnosis is often
made by the clinical appearance and history of
artificial cinnamon use. Differential diagnosis
includes morsicatio lesions and oral hairy
leukoplakia.
Dentifrice sloughing is a reaction to certain
ingredients in toothpaste, such as sodium lauryl
sulfate, pyrophosphate (tartar-control agent), and
artificial flavoring like cinnamon and mint. Diffuse
erythema of the oral mucosa along with sloughing
of superficial layers of epithelium is seen. Typical
clinical appearance of string-like sloughed mucosa
along with history of tartar-control or flavored
tooth paste use is good enough to make a
diagnosis.
Clinical Features:
Clinically, frictional keratosis can mimic true
leukoplakia and is analogous to a callus on the
skin. It appears as a rough hyperkeratotic area
that usually blends into the adjacent normal
mucosa and is seen frequently on the buccal
mucosa, lateral borders of the tongue, and
retromolar pad area.
Treatment:
The diagnosis of frictional keratosis is usually made
by the clinical examination and evidence of a
source of chronic irritation.
Malignant
transformation has not been reported in this
condition. Frictional keratosis is usually treated by
removing the offending agent. Smoothing a
sharp tooth or restoration and correction of the illfitting denture can reduce the mechanical
irritation on the mucosa. Ideally, the condition
should disappear in two weeks after removing the
irritating factor. If the lesion still persists, biopsy of
the area is recommended to rule out true
leukoplakia.
Page 5
NICOTINE STOMATITIS
Clinical Features:
Nicotine stomatitis is a white lesion which is
typically seen on the palate of pipe or cigar
smokers. It is also known as smoker’s palate or
nicotine palatinus. This condition has not been
associated with malignant transformation and
most likely is due to mucosal response to high
heat associated with smoking.
Interestingly,
denture wearers who smoke do not have this
condition because the upper denture usually
protects the palatal mucosa from heat. People
who drink very hot beverages have also reported
similar lesions on the palate.
Smokeless
tobacco
keratosis
is
usually
asymptomatic and is identified during routine
examination. Duration of the smokeless tobacco
habit, brand and type of smokeless tobacco,
length of daily use, and amount of tobacco used
are some of the factors determining the
development of this lesion. The mandibular
vestibule is where the tobacco is most often in
contact with the mucosa. Gingival recession with
alveolar bone destruction in the area of tobacco
contact may also be present. The mucosa appears
grayish white and has a wrinkled appearance. The
absence of tobacco in the mouth during clinical
examination makes the stretched mucosa appear
fissured, and a “pouch” (where the tobacco was
kept) can be seen. People who chronically put
materials such as hard candy, beef jerky, sunflower
seeds, etc. in their vestibule can also develop
similar mucosal changes. Typically, smokeless
tobacco keratosis develops within 1 to 5 years of
smokeless tobacco use. With chronic use in some
individuals, the mucosa thickens to form a white
leathery or nodular appearance.
Clinical Features:
Nicotine stomatitis is reported in patients above
45 years of age and the palatal mucosa being the
characteristic location.
The palatal mucosa
appears white, while multiple raised papules with
red centers are seen. The papules are inflamed
salivary glands and the red centers represent
inflamed openings of salivary gland ducts. The
overall palatal mucosa has a dried mud
appearance due to hyperkeratosis. Teeth with
black tobacco stains are also evident, most of the
time.
Treatment:
The diagnosis of nicotine stomatitis is established
by the characteristic clinical presentation and
correlation with the use of pipes or cigars or hot
beverages. With smoking cessation, nicotine
stomatitis is completely resolvable within 2 weeks.
If the condition persists after 2 weeks of smoking
cessation, biopsy of the area is mandatory to rule
out true leukoplakia. Patients with nicotine
stomatitis should also be thoroughly examined for
tobacco-related changes such as true leukoplakia
in the entire oral mucosa.
Tobacco Pouch
Keratosis
Dr. Kristin McNamara, The Ohio State
University College of Dentistry
Treatment:
SMOKELESS TOBACCO KERATOSIS
Smokeless tobacco keratosis is a white fissured
plaque seen on the oral mucosa in the area of
direct contact with smokeless tobacco. It is also
known as snuff pouch, snuff dipper’s lesion,
tobacco pouch keratosis, and spit tobacco
keratosis. Chewing tobacco, moist snuff, and dry
snuff are the various types of smokeless tobacco
prevalent in the United States.
The history of placing smokeless tobacco in the
altered mucosal site and the characteristic clinical
presentation are all that is required to make the
diagnosis. Mucosal alteration associated with
chronic smokeless tobacco use should completely
disappear within two weeks of habit cessation or
alteration of the original site. Any lesions which
persist after 6 weeks without smokeless tobacco
Page 6
contact should be biopsied to rule out a true
leukoplakia. Biopsy is also indicated for more
severe lesions, which have leathery white plaques,
verrucous appearance, ulceration, or hemorrhage.
IMMUNE-MEDIATED WHITE
LESIONS
LICHEN PLANUS
Lichen planus is one of the very common
mucocutaneous disorders. Cutaneous lesions
usually involve skin, nailS, and scalp, while mucosal
lesions affect oral and genital mucosa. Cutaneous
lesions are seen in 25-30% of individuals with oral
lesions. The exact cause of this lesion is presently
unknown and is most likely due to an autoimmune
process.
Clinical Features:
Lichen planus is seen more commonly in middleaged women. Skin lesions are characterized by
purple, pruritic, polygonal papules on the flexor
surface of extremities. Fine, white interlacing lines
called Wickham’s Striae are seen on the skin
papules.
Orally, the lesions are seen on bilateral buccal
mucosa. Other sites such as the tongue, labial
mucosa, gingiva, and palate can also be affected.
The two forms of lichen planus seen in oral mucosa
are reticular and erosive.
Reticular lichen planus is more commonly
presented than the erosive type.
It is
asymptomatic and usually affects the posterior
buccal mucosa. It gets its name because of the
typical pattern of interlacing white lines. These
lesions may wax and wane very often. Lichen
planus on the dorsal surface of the tongue does
not have characteristic reticular white lines and
instead manifests itself as smooth, white plaque
with atrophy of papillae.
Erosive lichen planus is a painful condition
compared to the reticular type, causing patients to
seek medical care frequently. The lesions usually
present as reddened areas with ulceration on the
bilateral buccal mucosa. The margins of the
reddened area usually have white lace-like striae;
the tongue and gingiva also can be affected.
When only gingival mucosa is involved, the
presentation is known as desquamative gingivitis
and biopsy should be done to rule out mucous
membrane pemphigoid and pemphigus vulgaris,
since they have similar clinical features.
Treatment:
Diagnosis of reticular lichen planus is based on the
clinical presentation. The classic lace-like pattern
of reticular lichen planus can be obscured if there
is co-infection with candidiasis. Treatment with
antifungal therapy in such proven cases can reveal
the classic reticular pattern following therapy.
Once the diagnosis of reticular lichen planus is
established, there is no need for any treatment, as
it is asymptomatic. Reassuring the patient and
periodic follow-up to monitor any clinical changes
are all that is required.
Erosive lichen planus is usually biopsied to get a
histopathologic and immunofluorescent diagnosis
in order to rule out chronic ulcerative stomatitis
and
systemic
lupus
erythematosus.
Corticosteroids are used to provide relief to the
patients. One of the recommended corticosteroids
is Diprolene gel (betamethasone dipropionate gel
0.05%). The patient should apply a thin film to the
affected area 4-6 times a day until the issue is
resolved. It is important to exclude other lichenoid
mucositis conditions such as lichenoid drug
reaction, lichenoid amalgam reaction, and graftversus-host disease.
LICHENOID MUCOSITIS
Certain drugs, dental restorative materials such as
amalgam, and artificial food flavoring can present
similar histopathologic pattern as lichen planus.
These immune-mediated reactions are classified as
lichenoid drug reaction, lichenoid amalgam
reaction, or oral cinnamon reaction, depending on
the causative agent. These conditions should be
separated from lichen planus as they are linked to
a specific cause; they will be resolved if the
causative agent is eliminated, whereas in lichen
planus no specific causative factor has yet been
identified.
Page 7
Clinical Features:
Lichenoid drug reaction usually presents as
irregular erosions on the posterior buccal mucosa
and lateral borders of the tongue. Clinically, these
may resemble erosive lichen planus. There have
been numerous prescription and over-the-counter
drugs linked to lichenoid reaction. NSAIDs such as
Ibuprofen,
Naproxen
and
Fenclofenac,
antihypertensives such as ACE inhibitors,
Chlorothiazide and Propranolol, oral hypoglycemic
agents such as chloropropamide and tolbutamide,
antimicrobials such as amphotericin, ketoconazole,
chloroquine, pencillamine, streptomycin, and
tetracycline are few among the extensive list of
medications which can cause lichenoid drug
reaction.
Lichenoid amalgam reaction affects the oral
mucosa which comes in contact with amalgam
restoration. White patches with radiating borders
is the common clinical presentation. The altered
mucosa will always be in contact with amalgam
restoration of adjacent teeth. Buccal mucosa and
lateral borders of the tongue are typical sites of
occurrence.
PREMALIGNANT WHITE LESIONS
LEUKOPLAKIA
Leukoplakia means “white patch” and is described
by the World Health Organization (WHO) as “a
white patch or plaque that cannot be
characterized clinically or histopathologically as
any other disease”. It is the most common
precancerous lesion in the oral cavity. The term
leukoplakia is a clinical description, and
histopathologically it can include atypical oral
epithelium, mild epithelial dysplasia, moderate
epithelial dysplasia, severe epithelial dysplasia, and
carcinoma-in-situ. Clinical diagnosis of leukoplakia
should be rendered only after white lesions such
as lichen planus, morsicatio lesions, frictional
keratosis, tobacco pouch keratosis, nicotine
stomatitis, leukoedema, and white sponge nevus
are excluded by history, location, and clinical
appearance. If in doubt, biopsy of the area is
necessary to evaluate if there is any evidence of
precancerous changes.
Treatment:
The diagnosis of lichenoid drug reaction is usually
made by the history of offending drug usage and
clinical presentation. Elimination of the suspected
medication
should
result
in
complete
disappearance
of
the
lesion;
however,
reoccurrence can happen if the drug is consumed
again. Temporary relief can be provided by
application of corticosteroids on the affected area
until the medication is completely eliminated from
the body. Biopsy of the area is prudent if lesions
persist after cessation of the suspected medication.
Lichenoid amalgam reaction is diagnosed by the
presence of an amalgam restoration in contact
with altered mucosa. Removal of the adjacent
amalgam and replacement of the filling by
nonmetallic restorative materials can provide a
complete resolution in two weeks. If the condition
does not improve, biopsy of the area should be
performed to exclude other possible conditions,
such as true leukoplakia.
Leukoplakia
Dr. Kristin McNamara, The Ohio State
University College of Dentistry
Clinical Features:
Leukoplakia tends to affect people above 40 years
and has a stronger male predilection. Tobacco
usage is the most common cause of leukoplakia.
Alcohol use with tobacco and sanguinaria are
among the other causative factors. Although most
leukoplakic lesions are seen on buccal mucosa,
lips, and gingiva, the lesions on the tongue and
floor of the mouth often have precancerous or
cancerous changes. Clinical presentations can
Page 8
vary from person to person, along with time. The
white patches may appear translucent or thin,
homogenous or thick, granular or nodular, and
verrucous. One of the most important features to
look for is the sharply demarcated borders from the
normal mucosa.
Proliferative verrucous leukoplakia (PVL) is a type of
leukoplakic lesion which is more aggressive than
leukoplakia and has multiple leukoplakic patches in
the oral cavity. PVL is more prevalent in women
compared to men and they usually do not have a
history of tobacco use. The mean age of
occurrence of PVL for men is 50 years of age, and
65 years for women. The buccal mucosa (in
women), the hard and soft palate, the alveolar
mucosa, the tongue (in men), and the floor of the
mouth are the common sites of occurrence. The
process starts as a hyperkeratotic area and, with
time, enlarges to form warty lesions and become
multifocal.
Treatment:
Biopsy of leukoplakia is mandatory to obtain a
histopathologic diagnosis because the treatment
depends on the diagnosis. Small lesions can be
removed completely by surgical excision and
should be sent for histopathological analysis.
Biopsy of multiple sites should be performed if the
lesion is large. If there is epithelial dysplasia
(especially moderate or severe) in a large lesion,
complete removal should be done by surgical
excision, cryosurgery, electrosurgery, or laser
excision. The patient should be followed up
periodically and should be biopsied if there is any
clinical change or recurrence, as 35% of completely
excised lesions can reoccur. PVL lesions should be
monitored more vigorously as they have higher
chances of having epithelial dysplasia and
transformation into verrucous or squamous cell
carcinoma.
ACTINIC CHEILITIS
Actinic cheilitis is a premalignant white lesion on
lips due to prolonged sun exposure. A similar type
of lesion that affects the sun exposed skin is called
actinic keratosis.
affected area of actinic cheilitis. It is seen usually in
fair-skinned individuals older than 40 years old
and who have a history of chronic skin exposure.
Actinic cheilitis is normally presented as white
patches on lips with loss of normal
dermatoglyphics. Presence of scales and fissures
are also common.
Treatment:
The main treatment for actinic cheilitis is surgical
excision and submitting the tissue for
histopathological diagnosis. The patient should
be followed up periodically and should be rebiopsied if there is any clinical change or
reoccurrence, as 35% of the lesions can undergo
malignant transformation to squamous cell
carcinoma.
MALIGNANT WHITE LESIONS
SQUAMOUS CELL CARCINOMA
Over 90% of oral malignancies are squamous cell
carcinoma. Tobacco smoking (with or without
alcohol usage) is the causative factor associated
with 75-80% of oral squamous cell carcinoma. The
other 20-25% typically occurs on the lateral
tongue of younger people and gingiva of older
women, and are not linked with any risk factor.
Clinical Features:
Squamous cell carcinoma usually occurs in older
adults and more commonly affects men. The
lateral border and ventral surface of the tongue
and floor of the mouth are the most frequently
affected sites. It can be seen clinically in several
forms such as exophytic fungating mass,
endophytic ulceration, or as mixed red and white
patches (early presentation). Surface ulceration,
induration on palpation, and rolled borders are
some of the common features of squamous cell
carcinoma. This condition is asymptomatic in the
beginning, which prolongs the time before
seeking medical treatment. Sometimes the tumor
can destroy the underlying bone and cause motheaten radiolucencies.
Clinical Features:
The lower vermilion zone of the lip is the most
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Treatment:
Biopsy is mandatory on all clinically suspicious
lesions including non-healing ulcers of the oral
cavity. After confirming the diagnosis of squamous
cell carcinoma, wide surgical excision and/or
radiation therapy are the first choices of treatment.
Since most patients are diagnosed at the late stage,
survival rates are very bad and metastasis to
regional lymph nodes are very common. After
treatment, patients should be followed-up
periodically and should be re-biopsied if there is
any clinical change or reoccurrence.
squamous cell carcinoma.
Post-treatment,
patients should be followed-up regularly and
should be re-biopsied if there is any clinical
change or reoccurrence.
CONCLUSION
White lesions can have various clinical
presentations, ranging from reactive to malignant
conditions. A correct diagnosis of white lesions is
very important as it can change previous
treatment plans.
Biopsy of the lesion and
submission of the tissue for histopathological
examination is mandatory if clinical diagnosis is in
doubt. Patients with premalignant and malignant
conditions should be referred to an oral and
maxillofacial pathologist as they should be
monitored regularly for any clinical change or
reoccurrence.
REFERENCES
1. Neville B, Damm D, Allen C, Bouqot J. Oral &
Maxillofacial Pathology. 3rd ed. Philadelphia,
PA: Saunders Company; 2009.
Squamous Cell
Carcinoma
Dr. Neetha Santosh, The Ohio State
University College of Dentistry
2. Greenberg M, Glick M, Ship J. Burket’s Oral
Medicine. 11th ed. Hamilton, Ontario: BC
Decker Inc.; 2008.
VERRUCOUS CARCINOMA
Verrucous carcinoma is a less aggressive type of
squamous cell carcinoma. Smokeless tobacco use
has been linked to the development of this
carcinoma.
Clinical Features:
Verrucous carcinoma usually affects older men.
The alveolar mucosa, hard palate, and buccal
mucosa are the most frequently affected sites. It
presents clinically as thick-white or mixed red and
white plaques with wart-like surface proliferations.
It is usually asymptomatic which prolongs the time
before seeking medical treatment.
Treatment:
Wide surgical excision is the preferred choice of
treatment of verrucous carcinoma. One-fourth of
verrucous carcinoma can show areas of routine
ABOUT THE AUTHOR
NEETHA SANTOSH
NEETHA SANTOSH GRADUATED SUMMA CUM LAUDE FROM
CHRISTIAN DENTAL COLLEGE, INDIA; WHERE SHE FURTHER
COMPLETED HER GENERAL PRACTICE RESIDENCY. SHE THEN
PURSUED A POSTDOCTORAL FELLOWSHIP IN ORAL BIOLOGY AT
INDIANA UNIVERSITY SCHOOL OF DENTISTRY. CURRENTLY, SHE IS
DOING HER RESIDENCY IN ORAL AND MAXILLOFACIAL PATHOLOGY
AT THE OHIO STATE UNIVERSITY. HER RESEARCH AT OSU
PRIMARILY FOCUSES ON IDENTIFYING BIOMARKERS THAT CAN
PREDICT THE PROGRESSION OF ORAL PREMALIGNANT LESIONS TO
SQUAMOUS CELL CARCINOMA. HER FUTURE CAREER PLAN IS TO JOIN
ACADEMICS WHERE SHE CAN TEACH AND PRACTICE ORAL AND
MAXILLOFACIAL PATHOLOGY.
NEETHA SANTOSH CAN BE CONTACTED AT
SANTOSH.2@OSU.EDU.
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1
T
F
Erosive lichen planus is more painful than
reticular lichen planus and often requires
treatment.
2
T
F
The exact cause of lichenoid mucositis, like lichen
planus, is unknown.
F
Oral hairy leukoplakia can be removed by
scraping or wiping which leaves a normal or
reddened underlying mucosa.
SUBMIT
ONLINE
SUBMIT
ONLINE
3
T
4
T
F
Proliferative verrucous leukoplakia is a more
aggressive form of leukoplakia and needs to be
monitored closely for malignant transformation.
5
T
F
Frictional keratosis has been observed to exhibit
malignant transformation.
6
T
F
Actinic cheilitis is a premalignant lesion due to
excessive tobacco use.
F
Smokeless tobacco keratosis should completely
disappear within two weeks of habit cessation or
alteration of the original site.
F
The ventral surface and lateral border of the
tongue are the most common locations for oral
squamous cell carcinoma.
7
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T
T
director
john r. kalmar, dmd, phd
kalmar.7@osu.edu
assistant director
karen k. daw, mba, cecm
daw.37@osu.edu
channel coordinator
rachel a. flad, bs
flad.4@osu.edu
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