Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology

ISSN No:-2456-2165

Oral Premalignant Lesions

Dr. Indushree D

Abstract:- This paper provides an general overview of  Dyskeratosis congenita

oral premalignant lesions and conditions , reasons and  Lupus erythematosus
causes behind this premalignant lesions and conditions
and how to identify these conditions and differentiate
them from other non cancerous lesions and this paper
also provides information on early signs and Symptoms
along with signs and symptoms during the later stages
and complications associated and also provides
information on etiopathogenesis and as of how to
diagnose these lesions clinically and by different
laboratory tests and also gives an overview on
management a of these lesions.

I. INTRODUCTION

Precancerous lesion, It is an applied state of tissue

often, but not always has a high potential to undergo
malignant transformation. Some benign lesions or
conditions for varying length of time, also generally precede
oral cancer. Interestingly, these lesions or conditions share Fig 1 Showing Histological Chances In Different Grades Of
same etiological factors with oral cancer, particularly the use Cancer
of tobacco and exhibit same habit and relationship .Many of
them show high potential to become cancer and are, II. PRECANCEROUS LESIONS
therefore, termed as precancerous lesion.
 Stages of Precancerous Lesions
It is especially important to remember that a
premalignancy is not guaranteed to eventually transform
into cancer ,as is often but erroneously believed. Individual
with oral precancer has 69 times greater risk of developing
oral cancer as compared to tobacco users who do not have
precancer.

 Definition
 Precancerous lesion: It is defined as a morphologically
altered tissue in which cancer is more likely to occur,
than its apparently normal counterparts.
 Precancerous condition: It is defined as a generalized
state or condition associated with significantly increased
risk for cancer development.

 Some of oral precancerous lesions are:

 Leukoplakia
 Erythroplakia
 Mucosal changes associated with smoking habits
 Carcinoma in situ
 Bowen disease
 Actinic keratosis, cheilitis and elastosis.

 Some of precancerous conditions are :

 Oral submucous fibrosis
 Syphilis
 Sideropenic dysplasia
 Oral lichen planus Fig 2 Showing Types And Aetiology Of Oral Cancer.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
III. LEUKOPLAKIA

 Definition
It is defined as any white patch on mucosa, which
cannot be rubbed or scraped off and which cannot be
attributed to any other diagnosable disease.

 Who Definition
It is a whitish patch or plaque that cannot be
characterized, clinically or pathologically, as any other
disease and which is not associated with any other physical
or chemical causative agent except use of tobacco.

The term Leukoplakia originates from two greek words

leuko means white and plakia means a patch and the white
colour of mucosa results from the thickened surface of the
keratin layer.

Fig 4 Showing Non Homogeneous Leukoplakia

 Erythroleukoplakia- leukoplakiai is present in

Association with Erythroplakia.
 According to etiology
 Tobacco induced
 Non tobacco induced

Fig 3 showing Leukoplakia of palate.  According to High risk of future development of oral
cancer
 Clinical Aspects ● High Risk Sites
 Floor of mouth
Pre leukoplakia is defined as a low-grade or very mild  Lateral or ventral surface of tongue
reaction of oral mucosa, appearing as a grey or greyish  Soft Palace
white ,but never completely white area with slightly lobular
pattern and with indistinct borders blending into adjacent ● Low Risk Site
normal mucosa (Pindborg, et al,1968) Classification  Dorsum of tongue.
 Hard palate
 According to clinical description:
 Homogenous ● Intermediate Group
 Flat : It has a smooth surface.  All other sites or oral mucosa.
 Corrugated: like a beach at ebbing tide.  According to Histology
 Pumice like :with pattern of fine fines  Dysplastic
 Wrinkled: like dry, craked mud surface.  Non dysplastic
 Non Homogenous  According to extent
 Nodular or speckled,- characterized by white specks or
nodules on erythematous base .  Localised
 Verrucous-slow growing papillary proliferations above  Diffused
the mucosal surface that may be heavily keratinized.
Extensive lesions of this type is known as oral florid  Etiopathogenesis
papillomatosis.  Local Factors Local Factors Include
 Ulcerated- lesions exhibit red area at the Periphery of  Tobacco
which white patches are present.  Alcohol
 Sanguinaria

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Chronic irritation
 Candidiasis
 Electromagnetic reaction or galvanism

 Regional Systemic Factors

 Syphilis
 Vitamin deficiency
 Nutritional deficiency
 Xerostomia
 Hormones
 Drugs
 Virus
 Idiopathic

Fig 6 Showing Pathogenesis Of Candida Leukoplakia.

 Sharp Staging
 Stage 1 -Earliest lesion non palpable faintly translucent
white discoloration.
 Stage 2- Localized or diffuse slightly elevated plaque of
irregular outline.
 It is opaque white and me have fine granular texture.
Fig 5 Chart Showing Etiology Of Leukoplakia.
 Stage 3-Thickened white lesion showing induration and
feasuring.
 Clinical Features
 Sex and age distribution- It occurs more commonly in  Diagnosis
older age group I e 35 to 45 years and above males are
 Clinical Diagnosis
more frequently affected than female, due to direct
Clinically any white patch with a history of tobacco
consequence of tobacco habit.
chewing which cannot be rubbed of is a Diagnostic indicator
 Common site- It can occur anywhere on the oral mucosa, for leukoplakia.
buccal mucosa and comissure are more commonly
involved, lip lessons are more common in male and
 Laboratory Diagnosis
tongue lesions are more common in females.
In biopsy hyperorthokeratosis of epithelium, epithelial
 Extent -The extent of involvement may vary from small dysplasia, liquefaction degeneration, Basal cell hyperplasia
well localized irregular patches to diffuse lesions can be seen ,scanning electron microscopy will show
involving a considerable portion of oral mucosa, epithelial dysplastic changes.
multiple areas of involvement are not uncommon.
 Colour- Lesson maybe white or a yellowish white but
with heavy use of tobacco it may assume brownish
colour.
 Symptoms -Some patients may report a feeling of
increase thickness of mucosa, those with ulcerated and
nodular type may complain of burning sensation,
enlarged cervical lymph nodes maybe single occurrence
of metastasis.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
IV. GUIDELINE FOR MANAGEMENT OF
LEUKOPLAKIA

Fig 7 Chart Staging of Leukoplakia.

 Malignant Potential
It is higher in women i e 6% than men i e 3.9% due to
involvement of endogenous factors.

 Differential Diagnosis
 Lichen planus
 Chemical burn
 White sponge nevus
 Discoid lupus erythematosus
 Psoriasis
 Leukoedema
 Hairy leukoplakia
 Cheek biting lesion
 Electro Galvanic white lesion.

 Management
 Elimination of Etiological Factors
 Prohibition of smoking
 Removal of chronic irritant
 Elimination of other etiological factors

 Conservative Treatment
 Vitamin therapy
 Vitamin A + vitamin E
 13 cis retinoic acid Fig 8 Showing Management of Leukoplakia.
 Antioxidant therapy
 Vitamin A palmitate
 Nystatin therapy
 Vitamin B complex
 Antibiotic preparation
 Estrogen

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Erythroplakia  Extent- unlike leukoplakia and erythroplakia is seldom
It is also called as erythroplasia of Queyrat, multiple and seldom covers extensive areas of mouth
erythroplasia is a persistent velvety red patch. Reddish ,also unlike leukoplakia, erythroplakia seldom expand
colour results from absence of surface keratin layer and due laterally after initial diagnosis ,because most lesions are
to presence of connective tissue papillae containing enlarged completely removed or destroyed immediately after
capillaries projected close to the surface. formal diagnosis .

 Definition
It is applied to any area of red and velvet textured
mucosa that cannot be identified on the basis of clinical and
histopathological examination as being caused by
inflammation or any other disease process.

A chronic red mucosal macule which cannot be given

any other specific Diagnostic name and cannot be attributed
to traumatic, vascular or inflammatory causes

Fig 10 Showing Erythroplakia.

 Diagnosis
 Clinical Diagnosis
 Red well demarcated patch with no sign of infection and
inflammation give rise to diagnosis of erythroplakia.
 Toluidine blue test -Differentiation of erythroplakia with
malignant changes and early squamous cell carcinoma,
Fig 9 Showing Erythroplakia. from benign inflammatory lesions of oral mucosa is
enhanced by use of 1% toluidine blue test. Laboratory
 Classification Diagnosis.
 Homogeneous  Biopsy exhibits epithelial changes ranging from mild
 These commonly occur on buccal mucosa with a well dysplasia to carcinoma In Situ and even invasive
demarcated margin. carcinoma.

 Erythroleukoplakia  Differential Diagnosis

 Erythroplakia interspersed with leukoplakia.  Candidiasis
 Granular or speckled these are elevated lesions.  Denture stock
 Tuberculosis
 Etiology  Histoplasmosis
 Idiopathic  Area of mechanical irritation
 Alcohol and smoking  Macular haemangioma
 Candida infection.  Telangiectasia
 Traumatic lesion
 Clinical Features
 Age and sex- Male prediliction is seen and most  Management
common in 6th and 7th decades of life.  Removal of suspected irritate
 Site- Occurs on all mucosal surface of head and neck  Incisional Biopsy
area, half of all cases however are found on the  Surgical stripping
vermillion or intra oral surfaces, with the rest being  Destructive techniques such as laser electro
eventually divided between larynx and pharynx. coagulation, cryotherapy have also proven to be
 Symptoms -As name obviously implies is asymptomatic effective.
 Clinical follow up

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
V. CARCINOMA IN SITU

Also called intra epithelial carcinoma .Severe

dysplastic changes in a white lesion indicate considerable
risk of development of Cancer. The most severe grade of
dysplasia merges with the condition known as carcinoma
Insitu. It is more common on skin but can also occur on
mucous brane.

Fig 12 Histological Image Showing Carcinoma Insitu.

 Management
● Surgical removal: Lesions may be surgically excised,
cauterized and even exposed to solid carbon dioxide.

VI. PREMALIGNANT CONDITION LICHEN

PLANUS

The term lichen planus is derived since the lesion looks

like lichen on rocks and planus stands for flat, various
mucosal surfaces may be involved either independently or
concurrently with cutaneous involvement or serially.
Fig 11 Showing Histological Chances In Carcinoma Insitu
And Cancer.  Definition
Lichen planus is a common inflammatory disease of
 Clinical Features skin presenting with characteristic violaceous, polygonal,
 Age and sex -Male predilection ia seen and occurs more pruritic papules. The disease may also affect the mucosa,
commonly in elderly person. hair and nails.
 Site- Common site are floor of mouth, tongue and lips.
 Appearance- Appearance of lesion maybe like It is a relatively common dermatological disorder
leukoplakia and erythroplakia. occurring on skin and oral mucous membrane refers to the
Lace -like pattern produced by symbiotic algae and fungal
 Diagnosis colonies on the surface of rocks in nature. Prevalence of
 Clinical diagnosis clinically cannot be differentiated lichen planus in general population is about 0.9% to 1.2%
and prevalence of oral lichen is reported in between 0.1%
from leukoplakia.
and 2.2%
 Laboratory diagnosis

In biopsy keratin may or may not be present on the

surface of lesion but if present if more apt to be parakeratin
rather than Orthokeratin, loss of orientation of cell and loss
of polarity .Sharp line of division between normal and
altered epithelium extending from surface down to
connective tissue rather than blending of epithelium and
increase in nuclear cytoplasmic ratio nuclear
hyperchromatism are sometimes seen.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Types
 Reticular
 Papular
 Atrophic
 Classical
 Plaque
 Erythematous
 Ulcerative
 Hypertrophic
 Erosive
 bullous
 Hypertrophied
 Annular
 Actinic
 follicular
 linear
Fig 13 Showing Lichen Planus Of Lip.

 Etiology
 Cell mediated immune response
 Auto immunity
 Immune deficiency
 Genetic factors
 Infection
 Psychogenic factor
 Habit.

Fig 15 Showing Lichen Planus Involving Skin.

 Clinical Features
 Age and sex- It occurs in adulthood with age range for
males is 35 to 44 years and females is 45 to 54 years, it
has more female prediction
 Oral and other mucous membrane symptoms -chief
complaint is usually of intense pruritus, itching
associated with lichen planus usually provokes rubbing
of lesion, rather than scratching.
 Signs- Lesions have characteristic violet hue. They are
flat topped Shiny polygonal papules and plaques.

Fig 14 Showing Etiology And Management Of Lichen

Planus.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Laboratory Diagnosis
There is hyper orthokeratosis, hyperparakeratosis,
acanthosis with intercellular oedema of spinous cells.
Biopsy also shows civatte bodies in spinous and basal cell
layers and lamina propria saw tooth appearance of rete pegs
is seen.
Immuno fluorescent study- Positive IgA and IgM and
IgG Antisera.

 Differential Diagnosis
 leukoplakia
 candidiasis
 Pemphigus
 Lupus Erythematosus
 Drug induced lesions
 Ectopic Geographic tongue
 Cheek biting
 Lichenoid drug reaction

 Management
 Removal of a cause
 Steroids
 Steroid spray
Fig 16 Showing Lichen Planus of Buccal Mucosa.  Steroid coating in soft custom tray
 Topical delivery regimen
VII. ORAL LICHEN PLANUS  Topical application of fluocinolone acetonide
 Site- Common sites are buccal mucosa (84% )and to  combination of prednisolone and levamisole
lesser extent tongue, lips, gingiva, floor of mouth and  Topical application of antifungal agent
palate  Vitamin A therapy
 Symptoms- Patient may report with burning sensation of  Cyclosporin
oral mucosa  surgical therapy and psychotherapy
 Appearance -oral lesion is characterized by radiating  Dapsone therapy
white or grey velvety thread like papules in a linear,  PUVA therapy
angular or retiform arrangement forming typical lacy
reticular patterns, rings and streaks over buccal mucosa VIII. ORAL SUBMUCOUS FIBROSIS
and to a lesser extent on lip, tongue and palate.
It Is A Chronic High Risk Precancerous Condition,
 Malignant potential- The incidence of malignant
Prevalent In Days Of Sushruta.
transformation ranges from 0.4% to 12.3% .In India the
incidence of malignant transformation is 0.4%
 Definition
.Carcinoma development is more common in women
An Insidious, chronic disease affecting any part of the
than in men. Atrophic, erosive and ulcerative lesion
oral cavity and sometimes pharynx. Although occasionally
showing Erythroplakia components and tobacco are
preceded by and or associated with a vesicle formation. It is
indicated to be more cancer prone.
always associated with juxta epithelial inflammatory
reaction followed by fibro elastic changes of lamina propria
 Clinical Scoring System For Oral Lichen Planus
with epithelial atrophy leading to stiffness of oral mucosa
and causing trismus and inability to eat.
 0= No lesions.
 1= White striae only.
 2= White striae and erosions less than 1 cm square.
 3=white striae and ulceration more than 1 cm square.
 4=white striae and ulceration less than 1 cm square.

 Diagnosis
 Clinical Diagnosis
The interlacing white striae appearing bilaterally
presence of Wickham striae and koebner phenomenon is
also diagnostic.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Clinical Features
 Age and sex distribution- It affects both the sexes. The
age group varies although majority of patients are
between 20 and 40 years of age.
 Site Distribution- The most frequent location of osmf
retro molar area, it also commonly involves soft palate
,palatal fauces, tongue and labial mucosa, sometimes it
involves floor of mouth and Gingiva.
 Prodromal symptoms- The onset of condition is
insidious and is often of 2 to 5 years of duration the most
common initial symptom is burning sensation of oral
mucosa, aggravated by spicy food followed by either
hyper salivation or dryness of mouth. Vesiculation,
ulceration pigmentation, recurrent stomatitis and
defective sensation have also been indicated as early
symptoms.
 Late symptoms – Trismas, difficulty in swallowing,
difficulty protrusion of tongue, referred pain, blanching
of mucosa, fibrous band formation
Fig 17 Showing Decreased Mouth Opening In Osmf.  Soft palate and uvula- Involvement of soft palate is
marked by fibrotic changes, uvula when involved is
 Epidemiology shrunken and in extreme cases it becomes bud like or
OSMF is very common in India and in Indian hockey stick appearance.
subcontinent and other Asian people ,the prevalence rate of
oral Fibrosis in India, Burma ,South Africa ranges from 0 to
1.2%, in India overall incidence is 0.2 0.5% .Its incidence is
high in southern parts of India, where the incidence of oral
cancer is also high.

IX. ETIOPATHOGENESIS

 Chillies - Capsaicin in chillies act as local irritants.

 Tobacco
 Lime
 Betel nut
 Nutritional deficiency
 Defective iron metabolism
 Bacterial infection
 Collagen and disorders
Fig 19 Showing Decreased Mouth Opening In OSMF Case.
 Immunological disorders
 Altered salivary composition
 Clinical Stages Of Oral Submucous Fibrosis
 genetic susceptibility
 Stage of stomatitis and vesiculation.
 Stage of Fibrosis.
 Stage of sequelae and complication.

 Diagnosis
 Clinical Diagnosis
 Clinically reduced mouth opening with palpable fibrous
bands is enough to make a diagnosis.

 Laboratory Diagnosis
 Oral epithelium is markedly atrophic which exhibits
intracellular edema, signet cells and epithelial atypia.
The inflammatory cells are mostly mononuclear;
eosinophils and occasional plasma cells may be seen.
Fig 18 Showing Vertical Bands On Buccal Mucosa In
OSMF Case.

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Volume 8, Issue 1, January – 2023 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Malignant Potential REFERENCES
 The carcinoma patients exhibiting osmf have a
frequency which exceed 1.2% of submucous Fibrosis in [1]. Textbook of Oral Medicine By Dr Anil Ghom.
a General population. [2]. Text of Oral Pathology By Dr Shafer.
[3]. Text of Oral And Maxillofacial Surgery By Dr
Neelima Malik.
[4]. Https://Www.Ncbi.Nlm.Gov
[5]. Https://Maaom.Memberclicks.Net
[6]. Https://Www.Tandfonline.Com
[7]. International Journal on Precancerous Lesions of Oral
Cavity by Chris De Souza, Uday Pawar, Pankaj
Chaturvedi.
[8]. Https://Www.Tandfonline.Com.
[9]. Article By Dr Jerry Boquot, Deot of Oral Maxillofacial
Surgery, West Verginia.

Fig 20 Showing Correlation of Mouth Opening With Grade

of OSMF.

 Management
 Restriction of habit and behavioural therapy
 Medicinal therapy
 Supportive treatment
 Vitamin rich diet
 Iodine B- Complex preparation
 Steroids
 Local Hydrocortisone injection
 Systemic therapy with Hydrocortisone 25 mg tablets in
doses of 100 mg per day .
 Placental extract
 Hyaluronidase
 Lycopene (Tab lycopene , OD for 3 months)
 Vitamin E therapy
 Other therapies include vasodilator injection and
injection of Gamma interference, laser therapy,
cryosurgery ,oral
 Physiotherapy and diathermy.

X. CONCLUSION

Prompt diagnosis of Oral premalignant lesion itself

reduces the chance of conversion or progression of lesion
into malignant lesion by more than fifty percent further
more immediate identification of the cause and correction of
the cause can further aid in control of progression of the
lesion into malignant lesion.

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