Potentially Malignant Lesions and Conditions
-
Upload
naleena-joseph -
Category
Documents
-
view
234 -
download
0
Transcript of Potentially Malignant Lesions and Conditions
-
8/3/2019 Potentially Malignant Lesions and Conditions
1/24
POTENTIALLY MALIGNANT LESIONS AND
CONDITIONS
PRESENTED BY
NALEENA JOSEPH
CTAHBDS029KMCT DENTAL COLLEGE
1
-
8/3/2019 Potentially Malignant Lesions and Conditions
2/24
2
-
8/3/2019 Potentially Malignant Lesions and Conditions
3/24
3
-
8/3/2019 Potentially Malignant Lesions and Conditions
4/24
POTENTIALLY MALIGNANT LESION
Definition:
A morphologically altered tissue in which cancer is more likely to occur
than its normal counterpart
- Shafer
1) Leukoplakia
2) Erythroplakia
3) Palatal Keratosis associated with reverse smoking4) Actinic Keratosis, Cheilitis, & Elastosis
POTENTIALLY MALIGNANT CONDITION
Definition:
A generalized state or condition associated with significantly increased risk
of cancer development
- Shafer
1) Oral Submucous Fibrosis
2) Oral Lichen Planus
3) Discoid Lupus Erythematosus
4) Dyskeratosis Congenita
5) Sideropenic Dysphagia
6) Syphilitic Glossitis
7) Xeroderma Pigmentosum8) Epidermolysis Bullosa
4
-
8/3/2019 Potentially Malignant Lesions and Conditions
5/24
LEUKOPLAKIA
DEFINITION:
A white patch or plaque that cannot be characterized clinically or
pathologically as any other lesion
-WHO
A predominantly white lesion of the oral mucosa that cannot be
characterized as any other definable lesion. Some oral leukoplakia will
transform into cancer.
-Axell 1996
A predominant white lesion of oral mucosa that cannot be characterized as
any other definable lesion
- Pindborg 1997
EPIDEMIOLOGY
Risk of malignant transformation is 4-6%
Global prevalence of 2.6%
Common in patients above 50 yrs of age
Common in men
5
-
8/3/2019 Potentially Malignant Lesions and Conditions
6/24
ETIOLOGY
TOBACCO
- Smoking form- Smokeless form
ALCOHOL
CHRONIC IRRITATION
SANGUINERIA
CANDIDIASIS
VIRAL INFECTION
NUTRITIONAL DEFICIENCY
DRUGS
IDIOPATHIC
CLASSIFICATION
LEUKOPLAKIA
1) Mild / Thin Leukoplakia
2) Homogenous Leukoplakia
3) Non homogenous Leukoplakia
HOMOGENOUS LEUKOPLAKIA
Well-defined white patch, localized or extensive, that is slightly elevated and
that has a fissured, wrinkled, or corrugated surface on palpation, these
lesions may feel leathery to dry, or cracked mud-like
NON HOMOGENOUS LEUKOPLAKIA
White patches or plaque intermixed with red tissue elements. Also called
Erythroleukoplakia and speckled leukoplakia
NODULAR
VERRUCOUS
PROLIFERATIVE VERRUCOUS
ULCERATED
ERYTHROLEUKOPLAKIA
6
-
8/3/2019 Potentially Malignant Lesions and Conditions
7/24
NODULAR LEUKOPLAKIA
Keratotic white nodules or patches are distributed over an Erythematous
background. Associated with higher rate of malignant transformation
VERRUCIFORM LEUKOPLAKIA
Presence of thick white lesions with papillary surfaces in the oral cavity.
These lesions are usually heavily keratinized and are most often seen inolder adults in the sixth to eighth decades of life. Some of these lesions may
exhibit an exophytic growth pattern.
PROLIFERATIVE VERRUCOUS LEUKOPLAKIA (PVL)
Extensive papillary or Verrucoid white plaques that tend to slowly involve
multiple mucosal sites in the oral cavity and to inexorably transform into
Squamous cell carcinomas over a period of many years. PVL has a very high
risk for transformation to dysplasia, Squamous cell carcinoma or verrucous
carcinoma .Verrucous Carcinomas is a slow growing and well-differentiated
lesion that seldom metastasizes.
CLINICAL FEATURES
Asymptomatic
Common sites buccal mucosa, lower lip, Gingiva
Less common sites palate, retro molar area
Lesions on the floor of mouth and lateral borders of tongue are high
risk sites for malignant transformation
HISTOPATHOLOGY
7
-
8/3/2019 Potentially Malignant Lesions and Conditions
8/24
Epithelial hyperplasia and surface hyperkeratosis
Mild to moderate epithelial dysplasia
Chronic inflammatory changes
DIAGNOSIS
1) Elimination of possible causes
2) Biopsy (gold standard test)
3) Toluidine blue staining
4) Exfoliative cytology (Limited value)
MANAGEMENT
1) MEDICAL topical vitamin A / Retinoid (single and combination
dosages of vitamins A, C, and E; beta carotene; analogues of vitamin A; anddiets that are high in antioxidants and cell growth suppressor proteins (fruits
and vegetables).
2) SURGICAL
Cold knife surgical excision
Laser ablation & cryosurgery - preferred because of their
Precision and rapid healing
MANAGEMENT OF LEUKOPLAKIA
PROVISIONAL CLINICAL DIAGNOSIS
Elimination of possible causes No possible causes
(2-4 weeks observation) (Definitive clinical diagnosis)
---------------------------------
Biopsy
Good response No response
(Definitive clinical diagnosis)
___________________________
Definable lesion
8
-
8/3/2019 Potentially Malignant Lesions and Conditions
9/24
(Management accordingly) No definable lesion Definable lesion
(Treatment/ (Management
Observation/ accordingly)
Follow up)
PROGNOSIS
Long term follow up necessary
Malignant changes occur 2-4 yrs after onset
ERYTHROPLAKIA
DEFINITION
A fiery red patch that cannot be characterized clinically or pathologically as
any other definable lesion - Pindborg 1997
Less common than Leukoplakia
High frequency of pre-malignant & malignant changes
Often associated with heavy smoking with or without concomitant
alcohol use
CLASSIFICATION
ERYTHROPLAKIA
- Homogenous Erythroplakia
- Granular / Speckled Erythroplakia
- Erythroleukoplakia
CLINICAL FEATURES
Seen in older men
Irregular outline
Common sites floor of mouth, Ventral aspect of tongue, soft palate
Histopathology lack of Keratin production and Atrophic Epithelium
Treatment same as Leukoplakia
Recurrent rate less than 5%
9
-
8/3/2019 Potentially Malignant Lesions and Conditions
10/24
PALATAL CHANGES ASSOCIATED WITH REVERSE SMOKING
Peak incidence 55-64 yrs
CLINICAL CHANGES
Keratosis Diffuse whitening of entire Palate
Patches Well defined, elevated white Plaques
Excrescences 1-3mm elevated white Plaques
Red areas Well defined reddening of the Palatal Mucosa
Ulcerated areas Crater like areas covered by Fibrin
Non pigmented areas Areas of Palatal Mucosa that are devoid of
Pigmentation
HISTOLOGICAL FINDINGS
Hyperorthokeratosis
Epithelial Dysplasia
Inflammatory cells in connective tissue
Melanin deposits in Lamina Propria
Malignant changes were seen in 0.3% of the palatal lesions
ACTINIC KERATOSIS
Also called Solar Elastosis, Senile Elastosis or Actinic Elastosis
It is Dermatological disease which is a degenerative condition of skin Also called Sailors or Farmers skin
ETIOLOGY
1. Hereditary factors skin pigmentation or its absence
10
-
8/3/2019 Potentially Malignant Lesions and Conditions
11/24
2. Exposure to elements sunlight and wind
CLINICAL FEATURES
Common in elderly patients
Site lips
Affected skin appears wrinkled, dry, atrophic and flaccid
On lips there is mild Keratosis and subtle blending of the lip
vermillion with skin surface
HISTOPATHOLOGY Increase in amount of elastic connective
tissue fibers
TREATMENT No treatment
ORAL SUBMUCOUS FIBROSIS
DEFINITION
A insidious and chronic disease affecting mucosa of any part of oral cavityand occasionally extend into pharynx and esophagus ,although sometimes
preceded by and / or associated with vesicle formation . It is always
associated with a juxta epithelial inflammatory reaction followed by fibro-
elastic change of lamina propria with epithelial atrophy leading to stiffness
of oral mucosa causing trismus and inability to eat.
Also called Atrophica Idiopathica Mucosae Oris , idiopathic
scleroderma of mouth, diffuse oral submucous fibrosis
ETIOLOGY
a) Areca nut chewing
b) Chillies
c) Genetic
11
-
8/3/2019 Potentially Malignant Lesions and Conditions
12/24
d) Tobacco
e) Autoimmune disorders
PATHOGENESIS
Alkaloids like Arecolin modulate matrix metallo proteins, lysyl
oxidases & collagenases which the affects collagen metabolism and
leads to increased fibrosis
Increased fibrosis results in decrease in water retaining proteoglycans
which favor increased collagen type 1 production
Polymorphism in gene coding for TNF
Aberrations of TGF beta and Interferon gamma
CLINICAL FEATURES
Age group 4-75 yrs
Common in middle & old age
Female predilection
3.3% risk of malignant transformation
PRODROMAL SYMPTOMS/ EARLY OSF
Burning sensation while consuming spicy food
Blisters ,ulcerations ,altered salivary flow, defective gustatory
sensation
Appearance of vesicles, petechiae, pain
ADVANCED OSF
Blanching of mucosa and appearance of white fibrous vertical bands
Buccal mucosa and lips are affected first
Dense fibrosis of Pterygomandibular raphe results in trismus
Restricted tongue movements and depappilation also seen
12
-
8/3/2019 Potentially Malignant Lesions and Conditions
13/24
OTHER SYMPTOMS
Obstruction of Eustachian tube
Nasal intonation of speech
TMJ pain Inability to blow
HISTOPATHOLOGY
Early stage there is Epithelial Hyperplasia and later stage there is
epithelial atrophy
Sub-mucosal deposition of extremely dense and avascular collagenous
tissue also seen
Chronic inflammatory cells seen in connective tissue such as
Lymphocytes and Plasma cells
DIAGNOSIS
Clinical examination and history of betel chewing habit
At least one of the following should be present
Palpable fibrous band
Mucosa tough and leathery
Blanching of mucosa and Histopathological features
TREATMENT
PREVENTION By stoppage of chewing habits
EXERCISE In mouth opening
MEDICAL Topical or systemic steroids
- Vitamin and nutrient supplements
- Placentrex
- Fibrinolytic agents
- Colloidal Iodine- Antioxidants
SURGICAL
- Surgical excision of bands
- Surgical removal of affected mucosa
followed by repair with grafts
13
-
8/3/2019 Potentially Malignant Lesions and Conditions
14/24
ORAL LICHEN PLANUS
Oral Lichen Planus (OLP) is a common chronic immunologic inflammatory
mucocutaneous disorder that varies in appearance from Keratotic (reticular
or plaque like) to Erythematous and ulcerative. The skin lesions are flat
violaceous papules with a fine scaling on the surface. Unlike oral lesions,
skin lesions are usually self-limiting, lasting only 1 year or less.
ETIOLOGY
Cell mediated immune response
Autoimmune disease
Stress
Hepatitis C Virus
CLINICAL FEATURES
Radiating white or grey, velvety, thread like papules in a linear,
annular or retiform arrangement with Wickhams striae
0.3-3% rate of malignant transformation. Common in erosive and
atrophic form
The Buccal mucosa is the most common site.
TYPES OF LICHEN PLANUS
a) RETICULAR
b) PLAQUE
c) ERYTHEMATOUS
d) BULLOUSe) PAPULAR
f) EROSIVE
RETICULAR-Fine white striae or lines which form a network or annular
pattern with peripheral Erythematous Zoneand usually seen bilaterally in
buccal mucosa.
14
-
8/3/2019 Potentially Malignant Lesions and Conditions
15/24
PLAQUE TYPE- Homogenous well demarcated white plaque. Common in
smokers
ERYTHEMATOUS FORM- Homogenous red area and striae seen in
periphery
BULLOUS FORM Appear as bullous structures surrounded by a reticular
network
PAPULAR FORM- seen in initial phase of disease, small white dots are
seen which intermingle with reticular form
EROSIVE FORM disabling form of OLP, fibrin coated ulcers surrounded
by an Erythematous zone with radiating white striae
HISTOPATHOLOGY
Hyperparakeratosis
Saw tooth rete pegs
Subepithelial band of mononuclear infiltrate
Civatte bodies degenerated basal Keratinocytes
Max-Joseph space
TREATMENT
Topical and systemic steroids
Calcineurin inhibitors (Cyclosporine & Tacrolimus)
Retinoid & UV phototherapy
DYSKERATOSIS CONGENITA
Also called Cole Engman Syndrome
Rare Genodermatosis, inherited as x-linked recessive trait
characterized by
Cutaneous reticulated hyper-pigmentation
Nail dystrophy
15
-
8/3/2019 Potentially Malignant Lesions and Conditions
16/24
Pre-malignant leukoplakia of oral mucosa
Progressive pancytopenia
Striking male predilection is seen
ETIOLOGY
Mutations in DKC1 gene
CLINICAL FEATURES
First manifestation is nail changes that is Dystrophic and shedding of
nails at the age of 5yrs
Grayish brown pigmentation appear at same time in trunk, neck and
thighs
Skin becomes atrophic & teleangiectactic.
Face becomes red
OTHER MINOR FEATURES
Frail skeleton
Mental retardation
Small Sella Turcica
Dysphagia
Transparent tympanic membrane, deafness
Eyelid infections
ORAL MANIFESTATIONS
Mucosal Leukoplakia buccal mucosa, tongue & oropharynx
Can become verrucous or ulcerative
Dysphagia and Dysuria
Increased incidence of malignant neoplasms,dental caries,and tooth
loss
HISTOLOGICAL FINDINGS
16
-
8/3/2019 Potentially Malignant Lesions and Conditions
17/24
Mild hyperkeratosis
Epidermal atrophy
Teleangiectasia of superficial BV
TREATMENT
Allogenic bone marrow transplant
DISCOID LUPUS ERYTHEMATOSUS
Chronic, scarring, atrophy producing, Photosensitive Dermatosis
ETOLOGY Genetic predisposition
PATHOGENESIS - heat shock proteins is induced in Keratinocyte
following UV exposure or stress and this protein act as target for T
cell mediated epidermal cell cytotoxicity
CLINICAL FEATURES
Third and fourth decade of life and common in women Common sites are face, oral mucous membrane,chest,back and
extremities
Slightly elevated red or purple macules covered by grey or yellow
scales
Carpet tack lesions caused by forceful removal of scales
Malar rash
ORAL MANIFESTATIONS
Begin as Erythematous raised or depressed area, without indurations
and with white spots
Superficial painful ulceration with crusting or bleeding is seen
Central healing result in scar formation
Common site are vermillion border of lower lips
17
-
8/3/2019 Potentially Malignant Lesions and Conditions
18/24
Malignant transformation can occur
TREATMENT
Corticosteroid Therapy
Pulse intravenous Cyclophosphamide regimen followed by quarterly
infusion for maintenance is the mainstay of modern therapy
EPIDERMOLYSIS BULLOSA
Heterogenous group of inherited mucocutaneous disorders
4 broad categories
* Simplex
* Junctional
* Dystrophic
* Hemidesmosomal
ETIOLOGY
Mutation of gene coding for keratins 5 and 14 causes simplex type
Recurrent nonsensense mutation in the LAMB3 gene causes
junctional type
Mutation of gene encoding for type 4 collagen COL7A1 causes
dystrophic type
CLINICAL FEATURES
EPIDERMOLYSIS BULLOSA SIMPLEX
Occurs shortly after birth. Formation of vesicles and
bullae on hands and feet at sites of friction or trauma. Heals in 2-10 days
18
-
8/3/2019 Potentially Malignant Lesions and Conditions
19/24
without scarring or pigmentation (generalized form) Localized form occur in
later childhood.Bullae also seen in oral cavity
JUNCTIONAL EPIDERMOLYSIS BULLOSA
Onset at birth with absence of scarring or pigmentation and death occurs
within 3 months of age . Oral bullae are frequent, extremely fragile and
produce feeding problems. Severe disturbance in enamel and dentin
formation of deciduous teeth are also seen
DYSTROPHIC EPIDERMOLYSIS BULLOSA ( DOMINANT )
Blisters develop in ankles, knees, elbows, feet and
head and it heals with scarring/ keloid. Dystrophic nails, palmar plantar
keratosis with hyperhidrosis and hypertrichosis are also seen. Oral bullae
also present
DYSTROPHIC EPIDERMOLYSIS BULLOSA ( RECESSIVE )
Classical form of the disease withonset at birth and
spontaneous bullae formation at sites of trauma, friction or pressure. It also
exhibits Nikolskys sign and heals by scarring. Also dystrophic nails and
sparse hair. Oral bullae initiated by nursing or any simple dental operative
procedure. Scar formation can obliterate sulcus and restrict tongue
movements. It can also result in hoarseness and Dysphagia and dental
defects like congenitally absent teeth, hypoplastic teeth and rudimentary
teeth seen
TREATMENT
Mild form- topical and intralesional steroids
Tetracycline and doxycycline to control desquamative gingivitis
Dapsone therapy
19
-
8/3/2019 Potentially Malignant Lesions and Conditions
20/24
Long term systemic steroids and immunosuppresive therapy.
XERODERMA PIGMENTOSUM
Genetically determined disorder
Defective DNA repair mechanism due to excessive chronic UV
damage leads to subsequent development of sun related skin tumors
including melanoma
CLINICAL FEATURES
Increased tendency to sunburn and skin changes like atrophy and
freckled pigmentation
Development of Actinic keratosis which progress to squamous cell or
basal cell carcinoma. Melanoma also develops
Oral manifestation squamous cell carcinoma of lower lip and tip of
tongue
TREATMENT
Avoid sun exposure and use protective clothing
Topical chemotherapeutic agents like 5 -Flurouracil to treat actinic
keratosis
Nonmelanoma skin cancers excised conservatively
Genetic counselling
SIDEROPENIC DYSPHAGIA
Also called Plummer Vinson syndrome or Patterson Kelly syndrome
Characterized by iron deficiency anemia, glossitis and dysphagia
20
-
8/3/2019 Potentially Malignant Lesions and Conditions
21/24
CLINICAL FEATURES
Seen in Scandinavian women between 30-50 yrs of age
Burning sensation of tongue and oral mucosa
Severe angular chelitis Abnormal bands of tissue in esophagus- esophageal web
Koilonychia
TREATMENT
Dietary iron supplements
Esophageal dilation
SYPHILLITIC GLOSSITIS
Seen in tertiary stage
Surface of tongue gets broken up by fissures due to atrophy and
fibrosis of tongue musculature and hyperkeratosis
Exclusively seen in males
High rate malignant transformation
Treatment by intensive antibiotic treatment using Penicillin or
Erythromycin or Tetracycline
21
-
8/3/2019 Potentially Malignant Lesions and Conditions
22/24
22
-
8/3/2019 Potentially Malignant Lesions and Conditions
23/24
23
-
8/3/2019 Potentially Malignant Lesions and Conditions
24/24
REFERENCE
BURKETS ORAL MEDICINE 11TH EDITION-
GREENBERG,GLICK,SHIP
TEXTBOOK OF ORAL PATHOLOGY 6TH EDITION- SHAFER
ORAL AND MAXILLOFACIAL PATHOLOGY 3RD EDITION
NEVILLE, DAMM, ALLEN, BOUQUOT