Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
1
White & Red Lesions of The Oral Mucosa
soriasis
P
Psoriasis is a common chronic inflammatory disease of the skin, it affects
about 2% of the population.
Causes, multifactorial:
1. Strong genetic influences, 1/3 relatives & HLA
2. Psychological stress
3. Infection
4. Alcohol abuse
5. Certain drugs such as Lithium & β blockers
6. Possible association with AIDS
Clinical features:
1. Onset: during 2nd & 3rd decades of life
2. It’s characterized by development of erythematous papules & plaques
that are covered by a silvery scale
3. If the scales are scraped off, they will leave tiny pin point areas of
bleeding (Auspitz sign)
4. Lesions are often bilaterally symmetrical & most commonly affect
scalp, elbows, knees & site of local trauma (Koebner phenomenon)
Koebner phenomenon: It describes the formation of psoriatic skin
lesions on parts of the body that aren’t typically where a person with
psoriasis experiences lesions. This is also known as an isomorphic
response.
5. Sever form shows generalized pustular lesion
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
2
6. Low percentage (approximately 10%) may develop psoriatic arthritis
of TMJ
Oral lesions of psoriasis are rare, but there may be an association
between erythema migrans of the tongue (geographic tongue) or other
mucosal lesions with cutaneous psoriasis.
erythematous
,
erythema migrans
,
white plaques
Oral lesions appear as
. Sometimes oral lesions may be asymptomatic.
patches or ulceration
Increased prevalence of erythema migrans has been reported especially
in patients with generalized pustular psoriasis. Increased frequency of
fissured tongue has also been reported.
Treatment of Psoriasis:
1. No treatment for mild form of psoriasis
2. For moderate cases, topical corticosteroids may be used
3. For severe cases, UV light or systemic therapy such as Methotrexate,
Retinoid, or Cyclosporine
4. Symptomatic oral lesion, treated with topical anesthesia or
antihistamine and/or corticosteroids
Leukoplakia
Leukoplakia (Leuko=white & Plakia= patch): It’s defined as a white patch
which cannot be wiped off the oral mucosa or ascribed to any specific
disease process. This definition can be used for any white patch;
however, it should be reserved for idiopathic leukoplakia. The estimated
worldwide prevalence of oral leukoplakia is 2%. If investigations failed to
prove the real cause of the white patch, then the term leukoplakia is
applied.
Recent studies suggest that LK possesses high risk of malignant
transformation. The malignant transformation (dysplasia) of LK varies
from 1-20% over 1-30 years, this variation may be related to the clinical
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
3
subtype or due to various predisposing factors such as smoking or
alcohol consumption which may increase the risk; however, some
lesions may show no dysplasia even in smokers.
Clinical features:
LK is a tough adherent plaque which surface is usually irregular & slightly
raised above the surrounding surface.
LK mostly seen in middle-aged and older adults, with the vast majority
of cases occurring in persons over the age of 40 years.
Sites of Leukoplakia: The most common sites of oral leukoplakia OLK:
1. The buccal mucosa (especially posterior sites) and the tongue account
for almost half of OLK
2. The floor of the mouth and retro-molar region
3. The palate, maxillary ridge, and lower lip less frequently involved
* However, any site in the oral cavity can be involved occasionally
Etiology of Leukoplakia:
Despite the fact that there is no known etiology for LK, there are some
suggested or predisposing factors for LK:
I. Local factors:
1. Tobacco (OLK occurs up to 6 times more among smokers than
nonsmokers) including:
Smokeless tobacco (Chewable & Snuff)
Smoking tobacco (Cigar, Cigarette & Pipe)
2. Alcohol
3. Chewing betel (areca) nut & khat
4. Chronic irritation
5. Candidiasis (Candidal leukoplakia)
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
4
6. Galvanism or Electromagnetic reaction (as happens with dental
restorations)
7. Xerostomia
II. Systemic factors:
1. Syphilis (Syphilitic leukoplakia)
2. Vitamins deficiency especially vitamin A
3. Nutritional deficiency & anemias such as Sideropenic anemia
4. Drugs such as anti-cholinergic, anti-metabolic & others
5. Viruses such as Herpes virus, Epstein-Barr virus, and Human papilloma
virus
6. Endocrine disturbances
Subtypes of Leukoplakia:
Varieties of OLK have been identified:
1. Homogeneous leukoplakia or thick leukoplakia (LK, or HLK)
2. Nodular (speckled) leukoplakia (NLK, or SLK)
3. Verrucous leukoplakia or verruciform leukoplakia (VL)
4. Proliferative verrucous leukoplakia (PVL)
5. Other types such as candidal leukoplakia & syphilitic leukoplakia (both
discussed previously)
Homogeneous leukoplakia or thick leukoplakia: Refers to a usually
well-defined white patch, localized or extensive, which is slightly
elevated and may have a fissured, wrinkled, or corrugated surface.
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
5
Nodular (speckled) leukoplakia:
Nodular (speckled) leukoplakia is a granular or nonhomogeneous
leukoplakia subtype. The name refers to a mixed red-and-white lesion in
which keratotic white nodules or patches are distributed over an
atrophic erythematous background.
This type of leukoplakia is associated with a higher malignant
transformation rate, with up to two/thirds of the cases in some series
showing epithelial dysplasia or carcinoma.
Verrucous leukoplakia or verruciform leukoplakia (VL):
This term is used to describe the presence of thick white lesions with
papillary surfaces and/or thick white lesions with sharp or blunt, wart-
like projections in the oral cavity. Some of these lesions may exhibit an
exophytic growth pattern
These lesions are usually heavily keratinized and are most often seen in
elder adults in the sixth to eighth decades of life. Common sites affected
are buccal mucosa, palate, gingivae and tongue.
Proliferative verrucous leukoplakia (PVL):
Represents a rare, poorly defined and potentially very aggressive form
of oral leukoplakia. The lesions of this special type of leukoplakia have
been described as extensive papillary or verrucoid white plaques
(keratotic plaques with rough surface projections) that tend to slowly
involve multiple mucosal sites in the oral cavity.
Common sites affected are gingivae, alveolar mucosa, buccal mucosa,
and tongue (same as VL). Patients affected are elderly with strong
predilection for females over males (1:4 male to female ratio).
Though they have been implicated, no definite causative role has been
established for tobacco, alcohol, human papillomavirus (HPV), or
Epstein-Barr virus.
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
6
PVL has a very high risk for malignant transformation. The lesions start
as flat leukoplakias, which over a prolonged period of time (decades),
develop a proliferative verrucous surface and eventually progress to
verrucous or squamous carcinoma.
Therefore, if the diagnosis was made late after a patient developed
multiple lesions over a course of many years, will eventually progress to
squamous cell carcinoma.
Diagnosis of leukoplakia:
1.History & Clinical examination
2.Biopsy
Treatment of leukoplakia:
1. Elimination of susceptible etiological factors
and B complex)
, E
A
Vitamins
2. Vitamin supplement & therapy (
3. Conventional surgery (Excision)
4. Cryosurgery
5. Laser therapy 6. Follow up
Sublingual keratosis
The term ‘sublingual keratosis’ is applied to white lesions on the floor of
mouth and ventral surface of the tongue. It’s unclear whether this lesion
is a different entity from other leukoplakias. The risk of malignant
transformation is about 10% of the cases.
Clinical features:
1. Sublingual keratosis is a white, soft plaque, usually with a finely
wrinkled surface, an irregular but well-defined outline and sometimes
bilateral with a butterfly shape.
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
7
2. The plaque typically extends from the anterior floor of the mouth to
the under (ventral) surface of the tongue.
3. There is usually no associated inflammation (asymptomatic)
Pathology:
Sublingual keratosis is not distinctive pathologically from leukoplakia,
and the histopathological appearance may be similar to leukoplakia.
Treatment: Same as leukoplakia
(Erythroplasia) Erythroplakia
It’s defined as a red lesion, patch or plaque that cannot be characterized
clinically or pathologically as any other condition.
The prevalence of oral erythroplakia ranges from 0.01% to 0.83% of
population. Though it’s uncommon in the oral cavity, but it possesses
high risk for malignant transformation and half of the lesions often show
malignancy on the first biopsy. Major risk factors include tobacco and
alcohol use.
Clinical features:
1. Erythroplakia is predominantly a disease of middle-aged to older
adults with no significant gender predilection.
2. The floor of mouth, tongue, and soft palate are the most common
sites of involvement, and multiple lesions may present.
3. Lesion may appear either as a well-demarcated, erythematous patch
or plaque with a soft, velvety texture, or mostly appear as flat eroded or
depressed red lesion with distinct demarcation against the surrounding
normal appearing mucosa.
4. Erythroplakia is usually asymptomatic, although some patients may
experience a burning sensation in conjunction with food intake.
Dr. Ahmed Salih Khudhur
BDS, M.Sc., PhD. Newcastle University/UK
8
5. In some cases, erythroplakia may present in a combination with an
adjacent leukoplakia to be known as (erythroleukoplakia).
6. Several clinical variants of erythroplakia have been described
however, there is no generally accepted classification) :
)
Homogenous Erythroplakia, Erythroleukoplakia & Granular or speckled
erythroplakia
Diagnosis of erythroplakia (erythroplasia):
1.History & Clinical examination
2.Toluidine blue test (stain the lesion with 1% to demonstrate areas with
possible premalignant or malignant changes)
3.Laboratory diagnosis (Especially Biopsy)
Treatment of erythroplakia:
1. Removal of the suspected irritants
2. Surgical excision
3. Laser ablation
4. Cryotherapy
5. Long-term clinical follow up (Every 3months for 1st postoperative
year, then every 6months for an additional 4 years).