oral Potential malignant

disorders
OPMDS
DONE BY: DR.Omnia Sami
• Potential malignant lesion:
• A benign lesion with morphologically altered tissue which has a
GREATER THAN NORMAL RISK of malignant transformation

• Potential malignant condition:

• A disease or patient habit that does not necessarily altered the
clinical appearance of local tissue but is associated with a GREATER
THAN NORMAL RISK of of malignant transformation
• Potential malignant lesions:
• 1-leukoplakia
• 2-erythroplakia
• 3-nicotinic stomatitis
• 4-Smokeless Tobacco Keratosis
• 5-Candidiasis
• Potential malignant conditions:
• erosive lichen planus
• Actinic keratosis
• Submucous fibrosis
• Syphilis
• Discoid lupus erythematosus
• dyskeratosis congenita
• epidermolysis bullosa
• Paterson–Kelly syndrome (sideropenic dysphagia; Plummer–Vinson
syndrome)
• Xeroderma pigmentosua
• Nutritional deficiency ( vitamin A,B,C deficiency)
• Immuonosuppresive disease( AIDS)
Potential malignant lesions
leukoplakia
• A predominantly white lesion of the oral mucosa that cannot be
characterized clinically or histologically as any other definable lesion.
• The exact etiology is unknown. But some predisposing factors can be
identified. PREDISPOSING FACTORS ARE BEST REMEMBERED AS 6 S
• Smoking
• Spirit
• Sharp tooth
• Spicy food
• Syphilis
• Sepsis
Etiology
• Tobacco. Most important causative factor.
• Alcohol. Heavy consumption of alcohol is second most important risk
factor, it acts synergistically with tobacco.

• Candida infection. Candida albicans infection (chronic hyperplastic

candidiasis) may play a role in the etiology of leukoplakia.
• Human papilloma viruses.

• Vitamin Deficiency. Vit A deficiency will cause metaplasia and

keratinization of epithelial structures (particularly glands
Histopathology
• Leukoplakia is purely a clinical terminology and histopathologically it
is reported as epithelial dysplasia.
• WHO in 2005 proposed five grades of epithelial dysplasia
• 1-Squamous Hyperplasia
• 2-Mild Dysplasia – better prognosis
• 3-Moderate Dysplasia
• 4-Severe Dysplasia
• 5-Carcinoma in-situ – poor prognosis.
Epithelial dysplasia: histological features.

• Drop-shaped rete ridges

• Nuclear hyperchromatism
• Nuclear pleomorphism
• Altered nuclear/cytoplasmic ratio
• Excess mitotic activity
• Loss of polarity of cells.
• Deep cell keratinization
• Disordered or loss of differentiation
• Loss of intercellular adherence
Carcinoma in situ
Clinical Types:

• HOMOGENOUS
• Uniform white patch lesion with smooth or corrugated surface sometimes,
slightly raised mucosa. Usually plaque like, some are smooth, may be wrinkled or
crossed by small crack or fissure.

• Malignant transformation – 1 to 7%.

• NON-HOMOGENOUS LEUKOPLAKIA TYPES

• Ulcerative or Erosive
• Verrucous or Nodular----white/,(proliferative verrucous leukoplakia)…speckled
• Speckled (High malignant transformation)erythroleukoplakia
• The rate of dysplastic or malignant alterations in oral leukoplakia has
been reported to be between 15.6% and 39.2%. Leukoplakia usually
occurs about 5 years earlier than OSCC.

• Leukoplakia exhibiting moderate to severe dysplasia need complete

removal by, cryosurgery or laser ablation. Leukoplakia not exhibiting
dysplasia usually is not excised, but clinical assessment every 6
months is recommended.
mangement
• Surgery is the obvious option for the management of leukoplakia,
certainly for patients with high predisposition to malignant
transformation
• Resection with a scalpel or CO laser excision seems to have advantage
over the use of a scalpel

• Topical anticancer drugs or retinoids can induce regression of

leukoplakia and are generally well-tolerated and effective
• Topical treatment of leukoplakia with podophyllin solution or
bleomycin has induced some regression

• Treatment with photodynamic therapy, in which a light- sensitizing

dye is given to the patients, and light shone on the lesion to activate
the dye and cause necrosis of the path- ological tissue
Hairy leukoplakia
• Clinical features
• Male predilection. Most common in 40 – 60 years of age (Recent
studies show higher incidences in young adults). It occurs on the
lateral margins of the tongue often bilaterally. The lesions are white,
sometimes corrugated and may be proliferative to produce a shaggy
carpet like appearance
• Hairy leukoplakia is associated with Epstein-Barr virus (EBV) and
occurs primarily in HIV-positive individuals.
Homogenous leukoplakia
Nodular leukoplakia
Speckled leukoplakia
verrucous leukoplakia
proliferative verrucous leukoplakia
Erosive leukoplakia
erythroplakia
• WHO definition A predominantly RED lesion of the oral mucosa that
cannot be characterized clinically or histologically as any other
definable lesion
• Clinically, erythroplakia is classified into three types: homogeneous,
granular, and speckled

• According to Shafer and Waldron, 51% of erythroplakias transformed

into SCC, 40% were carcinoma in situ and 9% showed mild to
moderate dysplasia.
• Diagnosis:
• Appearance
• History of tobacco/alcohol use
• Biopsy results
• Microscopically, the tissue exhibits severe epithelial dysplasia,
carcinoma-in-situ, or invasive squamous cell carcinoma.
• There is an absence of keratin production and a reduced number of
epithelial cells.
• Differential Diagnosis: Erythematous (atrophic) candidiasis • Kaposi’s
sarcoma • Ecchymosis • Contact stomatitis • Vascular malformation •
Squamous cell carcinoma • Geographic tongue

• Treatment. The treatment is same as that for invasive carcinoma or

carcinoma-in-situ like surgery, radiation and cauterisation.
Nicotinic stomatitis(Palatal Keratosis associated with
Reverse Smoking)
• Reverse smoking is seen in patients of low socioeconomic class and is
more common in females (91.3%), especially after the third decade of
life

• risk of malignant transformation in oral lesions of reverse smokers

was 19 times more than that of nonsmokers.

• the percentage of epithelial dysplasia is 83.3% and OSCC is 12.5% of

reveres smokers
Smokeless Tobacco Keratosis (Snuff Dipper’s Lesion)

• Smokeless tobacco keratosis is characterized by a white plaque in the

buccal or labial vestibule where the tobacco is held.
• The degree of mucosal alteration depends on the quality and type of
tobacco, the frequency of tobacco use and host susceptibility

• Epithelial dysplasia has been found in this lesion and the risk of
developing OSCC is four times greater in smokeless tobacco users
compared to non-users.
• breaking the habit leads to a normal mucosa within 2 to 6 weeks. A
lesion that remains more than 6 weeks should be considered a true
leukoplakia or carcinoma and should be biopsied
Candida Leukoplakia (, Chronic Hyperplastic Candidiasis)

• Leukoplakia with candidal infection has a higher rate of malignant

transformation than uninfected leukoplakia.
• Candida can then produce carcinogenic compounds, like
nitrosamines, N-nitrosobenzylmethylamine.
• Carcinogenic compounds then can bind with DNA causing miscoding
or irregularities with DNA replication.

• Thus results in oncogene formation and initiating cancer development

Potenial malignant conditions
erosive lichen planus

• LP involves epithelial damage immunologically mediated by cytotoxic

T cells directed against basilar keratinocytes and resulting in vacuolar
degeneration and lysis of basal cells.
• . There is the accumulation of T lymphocytes beneath the epithelium
of the oral mucosa and increase in the rate of differentiation of
stratified squamous epithelium, causing hyperkeratosis and erythema
with or without ulceration.

• LP and especially lichenoid lesions have a small malignant potential –

probably of the order of 1–3%, and predominantly in non-reticular
lesions
Carcinoma arising in lichen planus
Erosive lichen planus resembling lupus erythematosus
Actinic cheilosis

• Actinic cheilosis (AC) is a potential malignant condition frequently

associated with long term exposure to sun radiation and may be found on
the vermilion border of the lips as well as other exposed skin surfaces.

• clinical presentations of AC are diffuse poorly-defined atrophic, erosive,

ulcerative or keratotic plaque.

• AC is one of the main causes of lip cancer,6-10% evolve into SSC

• There a recent study, demonstrated that lip SCC originating from AC is

more prone to metastasis
management
• There are various treatment methods for AC, including
• cryotherapy,
• electrosurgery,
• topical retinoids,
• 5-flurouracil cream
• photodynamic therapy, CO2 laser ablation
• vermilionectomy
dyskeratosis congenita Cole-Engman Syndrome or
Zinsser-Cole-Engman Syndrome)

• Dyskeratosis congenita is a rare genetic form of bone marrow failure,.

Its presented as:
• 1-reticular pigmentation of skin
• 2-dystrophic nails
• 3-oral leukoplakia
• Oral lesions, as white keratotic patches, occur in about 80% of cases
• There is no effective treatment for DC. However, surgery and
treatment with bleomycin, vitamin A, steroids have been
recommended
Xeroderma pigmentosa
• Xeroderma pigmentosum (XP) is a rare autosomal recessive disease,
which is associated with cutaneous malignant transformation.
• Oral involvement is usually observed in patients under 20.4
• Squamous cell carcinoma of the lower lip and tongue has been
reported in patients with XP
• caused by mutations in genes that are involved in repairing damaged
DNA. DNA
• Patients with XP are advised to avoid sunlight, and to wear
appropriate protective clothing and sunscreens if they cannot avoid
sun exposure
Submucous fibrosis

• Oral submucous fibrosis (OSF) is a chronic, progressive, scarring,

potential malignant which is characterized by mucosal rigidity.
• It has been associated with long-lasting dipping of betel-nut
• The most frequently affected sites in the oral cavity are buccal
mucosa, retromolar area, tongue and soft palate
• Clinical signs and symptoms of OSF are vesicles, ulcerations,
petechiae, melanoses, xerostomia, burning sensation, and limitation
in jaw movement.
• Overall, patients with OSF are at least 19 times more likely to develop
OSCC than healthy people.
Discoid lupus erythematosus
• Discoid lupus erythematosus (DLE) is a chronic, scarring, immunologically
mediated , mucocutaneous disease, causes scarring, hair loss,
hyperpigmentation changes in the skin and peripheral telangiectasia
•
• Clinically characterized by white keratinized plaques with elevated borders
and radiating white striae
• Oral discoid lesions are seen in 20% of patients.

• Malignant transformation of DLE into SCC is usually observed on the lower

lip, 5.5% of lower lip SCCs arise from lesions of DLE.
Plummer-Vinson syndrome
• The Plummer-Vinson syndrome, called sideropenic dysphagia, is
characterized by dysphagia, iron deficiency, anemia and the presence
of Postcricoid web,
• it has been identified as a risk factor for developing squamous cell
carcinoma of the upper gastrointestinal tract.
epidermolysis bullosa

• blistering disease of the skin and mucosa

• There are three types of EB: simplex, junctional and dystrophic
• Oral involvement has been reported in the junctional and dystrophic forms
of the disease, which is characterized by bulla and vesicle formation
following mild physical trauma
• Malignancy usually develops in areas of chronic ulceration during the
second to third decades of life
• EB is even at risk for developing basal cell carcinoma (BCC) and malignant
melanoma.
• Topical or systemic corticosteroids are usually recommended for
management of EB.
• The 3 main types of EB are:

• epidermolysis bullosa simplex (EBS) – the most common type, which

tends to be milder with a low risk of serious complications
• dystrophic epidermolysis bullosa (DEB) – which can range from mild
to severe
• junctional epidermolysis bullosa (JEB) – the rarest and most severe
type
junctional epidermolysis bullosa
dystrophic epidermolysis bullosa
• There is no cure for EB. However, significant research, including gene
therapy and cell-based therapy, continue in the aim to improve
quality of life.

• Most current treatment is symptomatic. The primary aim is to protect

the skin and stop blister formation, promote healing, and prevent
complications.
references
• 1-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439658/

• 2-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4091702/

• 3-Oral and_Maxillofacial Medicine The Basis of diagnosis and

treatment ,scully ,third edition