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Oral Pre Cancer Lesion &

Oral Cancer Lesion


DRG. ROCHMAN MUJAYANTO, SP.PM
FAKULTAS KEDOKTERAN GIGI UNIVERSITAS ISLAM SULTAN AGUNG
iNTRODUCTION

 tobacco chewing is a major risk factor for oral leukoplakia, OSMF, and
erythroplakia,
 tobacco smoking may be a risk factor for oral leukoplakia.
 Alcohol drinking may increase the risk by 1.5-fold for oral leukoplakia, by 2-
fold for OSMF, and 3-fold for erythroplakia

 alcohol drinking and tobacco chewing may possibly be risk factors for
multiple oral premalignant lesions,
 smoking was not associated with the risk of multiple oral premalignant
lesions.
early diagnosis:
1. symptomatic and/or non-symptomatic non-healing lesions of oral mucosa;
2. history of smoking, chewing tobacco, alcohol consumption, oral HPV
infection, drug use, long-term exposure to sunlight;
3. advanced age;
4. the presence of immunodeficiency;
5. the presence of genetic disease; and
6. poor oral hygiene.
Early detection of premalignant lesions and oral cancer is very important. Therefore,
miscellaneous modalities such as :

 oral cavity examination,  Raman spectroscopy,


 supravital staining,  fluorescence imaging,
 Oral cytology and optical technologies  optical coherence tomography,
including spectroscopy,
 narrow-band imaging,
 fluorescence spectroscopy,
 multimodal optical imaging may be used
 elastic scattering (reflectance)
spectroscopy,
Oral Cavity Exmination

 WHO

Figure 1B: Oral examination using head mirror.


Figure 1C: Oral examination with torch and wooden spatula.

WHO
Figure 1A: Physical examination under bright daylight.
Figures 2: Examination of the lips.

Figure 3: Examination of the labial mucosa.


Oral Pre Cancer

 In a World Health Organization Workshop, held in 2005, the


terminology, definitions and classifications of oral lesions with a
predisposition to malignant transformation have been discussed
and recommended to use the term “potentially malignant
disorders” to eliminate terminological confusion.

 The etiology of precancerous lesions of oral mucosa is not well-


known

 Some risk factors such as tobacco chewing, tobacco smoking, and


alcohol
 oral precancerous lesions are :
 oral leukoplakia,
 oral submucous fibrosis (OSMF),
 oral erythroplakia
 Actinic cheilitis
ORAL LEUKOPLAKIA

 Leukoplakia is defined as “A white plaque of questionable risk


having excluded (other) known diseases or disorders that carry no
increased risk for cancer”
 Histopathologically, two distinct appearances may be seen as
dysplastic or non-dysplastic leukoplakia

 Although leukoplakia can occur at any age, it often occurs in


individuals under the age of 40
 Leukoplakia is seen six times more among smokers than among
non-smokers
 leukoplakia may be affect any part of the oral and oropharyngeal
cavity
 Homogenous lesions are characterized by uniformly flat, thin,
uniformly white in colour and shows shallow cracks of the
surface keratin
 Non-homogenous lesions have been defined as a white and
red lesion (known as erythroleukoplakia) that may be either
irregularly flat (speckled) or nodular .
 Verrucous leukoplakia (multifocal presentation), has a strong
potential for malignant transformation and is resistance to
treatment.
 HOMOGENOUS LEUKOPLAKIA
 NON HOMOGENOUS LEUKOPLAKIA
differential diagnosis oral leukoplakia

 aspirin burn, chemical injury,  papilloma and allied lesions,


 oral pseudomembranous and  mucous patches in secondary syphilis,
hyperplastic candidiasis,
 tobacco-induced lesions,
 frictional lesions,  smoker’s palate (nicotinic stomatitis),
 oral hairy leukoplakia,  stuff-induced lesion,
 leukoedema,
 white sponge nevus,
 linea alba,  oral lichen planus (OLP)
 lupus erythematosus,  Oral lichenoid reaction
 morsicatio buccarum,
 Oral leukoplakia should be  Non-surgical treatment modalities might
confirmed by mucosal biopsy. be considered in selected patients.
 But before biopsy, some staining  Carotenoids (β-carotene, lycopene),
methods used methylene blue  vitamins [L-ascorbic acid (vitamin C),
 αtocoferol (vitamin E),
 The most commonly preferred  retinoic acid (vitamin A), and
treatment options are surgical fenretinide], and
excision or CO2 laser therapy.
 bleomycin may be used in patients
 In widespread lesions,
with oral leukoplakia
photodynamic therapy may be
considered
ORAL ERYTHROPLAKIA

 Erythroplakia is defined as “A fiery red patch that cannot be


characterized clinically or pathologically as any other definable
disease”.
 It mainly occurs in the middle aged and the elderly.
 Male gender is most frequently affected.
 Etiopathogenesis is not known exactly Chewing tobacco and
alcohol use are the possible etiologic factors for the development
erythroplakia.
 Clinical appearance is characterized by flat or even depressed
erythematous change of the mucosa without a patch lesion.

 Mostly, a solitary lesion occurs over the surface of any part of the
oral cavity. But the most commonly affected areas were reported
as the soft palate, the floor of the mouth, and the buccal mucosa

 Clinically, typical lesion of oral erythroplakia is less than 1.5 cm in


diameter, but it also be less than 1 cm and larger than 4 cm
 Histopathologically, moderate or severe dysplasia was usually seen
in lesion with erythroplakia.

 Malignant transformation rates is very high (vary from 14% to 50%),


so it needs to be treated expeditiously

 Surgical excision may be used in lesions with severe epithelial


dysplasia or carcinoma in situ
differential diagnosis oral erythroplakia

 Oral candidiasis,  lingual varices,


 oral histoplasmosis,  Kaposi’s sarcoma,
 oral tuberculosis,  early squamous cell carcinoma,
 atrophic OLP,  local irritation,
 lupus erythematosus,  mucositis,
 Pemphigus & pemphigoids,  drug reaction,
 amelanotic melanoma,  median rhomboid glossitis
 haemangioma,
 telangiectasia,
Oral Lichen Planus

 OLP is a T-cell mediated autoimmune disease

 Prevalence of OLP varies mainly occurs among female gender and


the age of onset is usually between third and sixth decade

 fine white striae known as “Wickham’s striae” most commonly affected


areas are dorsum of the tongue, buccal mucosa, and gingiva

 Typically, lesions present symmetrically and bilaterally,


 Clinically, OLP may be seen as six types including
 Reticular  “Wickham’s striae” and usually asymptomatic
 Papular  “Wickham’s striae” with papular pattern, which is rarely
seen, is characterized by small, white, raised papules with fine white
striation at the periphery of the lesion.
 plaque-like  “Wickham’s striae” with Plaque type clinically resembles
leukoplakia
 bullous type  “Wickham’s striae” with bullae formation range from a
few millimeters to several centimeters in diameter
 Atrophic  “Wickham’s striae” with Atrophic pattern presents as a red
lesion.
 Erosive  “Wickham’s striae” with irregular erosion or ulceration
covered with a fibrinous plaque or pseudomembrane.

 atrophic and erosive pattern are generally associated with a burning


sensation and pain that exacerbated by trauma and hot, spicy or acidic
foods.
 Diagnostic histologic features include liquefactive degeneration of
the basal cells, colloid bodies (known as Civatte bodies),
homogenous infiltrate of lymphocytes in a dense, band-like pattern
along the epithelium-connective tissue interface in the superficial
dermis, cytologically normal maturation of the epithelium,
sawtooth rete ridges, and hyperkeratosis

 Increased malignant transformation risk occurs greater in erosive


and atrophic forms and in cases of lesions of lateral border of the
tongue
LICHEN PLANUS
 Patients with reticular and other
asymptomatic OLP can be followed
without treatment.

 But if there are any symptoms and/or


potential malignant risk, lesions should
be treated.
ORAL SUBMUCOUS FIBROSIS

 Oral submucous fibrosis is chronic and potentially malignant disorder


characterized by juxtaepitelial fibrosis of the oral cavity.

 Fibroelastic change of the lamina propria and epithelial atrophy occur in


consequence of juxta epitelial inflammatory reaction, and eventually,
stiffness of oral mucosa, trismus and an inability to eat develops

 OSMF is usually seen in Asians population (particularly Indians) from the


southern states and Taiwanese.
 Predominantly, it occurs in the second and third decade, and both sexes
may be affected
 Its etiology is not well-known and thougt to be multifactorial

 The strongest risk factor for OSMF is the chewing of betel quid
containing areca nut.
 Symptoms such as burning sensation and/or intolerance to spicy
food are the most common symptoms in the initial phase of the
disease.
 Over time, it gradually progresses and fibrosis develops that can
affect mouth opening.
 Three current treatment modalities including surgical,physical, and
medical are available for the management of OSMF.

 Surgical treatments may be used to improve mouth opening and


movements.

 Physical treatment including physical exercise regimen, splints or


other moutopening devices, and microwave diathermy may be
usefuin some patients with OSMF.
ACTINIC CHEILITIS

 Actinic cheilitis is a potentially malignant disease of the lip caused by


exposure solar radiation.

 It is commonly seen the surface area of the lower lip due to the anatomic
proximity.

 In addition to solar rays, tobacco use, lip irritation, poor oral hygiene, and ill-
fitting dentures

 The disease predominantly occurs in men compared to the women


 actinic cheilitis shows erythema and edema
 in the early stages diffuse scaling, thickened epithelium with small
greyish-white plaques (known as leukoplakia), inflammatory areas
(known as erythroleukoplakia),
 in the late stages of the disease  linear fissures may present
 Diagnosis should be confirmed by biopsy to evaluate the degree
of dysplasia.

 Histopathologically, hyperplasia, acanthosis or atrophy of the


epithelium, thickening of the keratin layer, and/or dysplasia, which
may range from mild to severe, may be shown.

 In addition to these epithelial changes, in connective tissue,


basophilic degeneration of collagen fibers, known as solar elastosis
 In treatment,
 5-fluorouracil,
 scalpel vermillionectomy
 chemical peel,
 electrosurgery,
 cryosurgery,
 CO2 laser,
 imiquimod,
 photodynamic treatment,
 diclofenac 0.3% gel
ORAL CANCER

 Oral cancer is more common after the age of 50 years, and


incidence increases with age.

 Most studies suggest that 4–6% of oral cancers occur in patients


under 40 years
Etiology:

 Tobacco and alcohol are the most important risk factors and account for 75–
90% of oral cancers
 The other risk factors associated with oral carcinogenesis include poor oral
hygiene, chronic irritation from ill-fitting dentures or sharp teeth, viral
infections, nutritional deficiencies, ultraviolet light, immunosuppression, prior
exposure to radiation and genetic susceptibility.
Clinical Signs and Symptoms:
 Oral cancers in early stages are often asymptomatic and may present as
reddish areas, small mucosal growths or ulcerations. Sometimes, there may
be some discomfort and irritation.

 Initially, these lesions appear as a change in a preexisting precancerous


lesions with induration, ulceration or growth, or present as de-novo hard
indurated nodule, ulcer or growth, or as a cauliflower-like exophytic growth
or ulcero-infiltrative lesion, or as a warty verrucous growth.
 In advanced stages patients complain of ulceration or growth in the oral
cavity, loosening of teeth, pain, malodour (halitosis), excessive salivation,
bleeding, difficulty in speaking and swallowing, referred pain to the ear,
swelling and ulceration of the face and neck swelling.

 Regional lymph node involvement worsens the prognosis

 More than 95% of oral cancers are squamous cell carcinomas.


 Squamous cell carcinoma is an invasive epithelial neoplasm showing varying
degrees of squamous differentiation

 Squamous differentiation, seen as keratinisation with “pearl” formation and


an invasive growth is a prerequisites for the diagnosis of squamous cell
carcinoma.
TREATMENT ORAL CANCER

 Treatment of Early-Stage Oral Cancer (Stages I and II) : Surgery and


radiotherapy are widely used for the treatment of early oral
cancer, either as single modalities or in combination.

 Treatment of Locally Advanced Tumors of the Oral Cavity (Stages III


and IV) : surgery, radiotherapy with or without chemotherapy
Oral Complications of Cancer Therapy
Oral Complications of Cancer Therapy
Oral Complications of Cancer Therapy
REFFERENCE

 http://screening.iarc.fr/atlasoral.php
 Epstein_et_al-2012-CA__A_Cancer_Journal_for_Clinicians.pdf
 Lalla et al, Management of Oral Mucositis in Patients with Cancer, Dent
Clin North Am. 2008 January ; 52(1): 61–viii
 Yardimci G, Kutlubay Z, Engin B, Tuzun Y. Precancerous lesions of oral
mucosa. World J Clin Cases 2014; 2(12): 866-872
 Cancer / editors, Hellen Gelband, Prabhat Jha, Rengaswamy
Sankaranarayanan, Susan Horton. 2015

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