BENIGN TUMORS OF EPITHELIAL ORIGIN

DR. ABHAY KUMAR

INTRODUCTIONCharacteristics: 1) Slow rate of growth and longer duration2) Well defined mass of regular smooth outline (possesses a fibrous capsule ) 3) Swelling and pressure effect on surrounding structures 4) Smaller compared to malignant tumors 5) Displacement of adjacent normal tissues 6) Usually painless

Benign Epithelial Tissue Lesions: 1) Papilloma 2) Keratoacanthoma 3) Squamous Acanthoma

SQUAMOUS PAPILLOMA

• A benign exophytic papillary growth of stratified squamous epithelium

• 4th most common oral mucosal mass • 3-4% of all biopsied oral soft tissue lesions• Associated with papilloma virus (HPV type 6 and 11)• Low virulence and infectivity rate• Clinically and microscopically indistinguishable from

Verruca Vulgaris (virus-induced focal papillary hyperplasia of the epidermis)

Clinical Features:- Exophytic growth made up of numerous fingr like projections (roughened , verrucous or cauliflower surface)

- <1cm in greatest diameter

- Sessile or pedunculated and white(keratinized) or pink (nonkeratinized) , mostly solitary

- Occurs on the soft palate, uvula , and ventral and dorsal surfaces of the tongue , gingiva and buccal mucosa

- Painless , white or pink in colour

- Occurs at any age

- Papilloma like or papillomatous lesions as well as ‘pebbly’ lesions and fibromas of various sites in the oral cavity are recognized as manifestation of multiple hamartoma and neoplasia syndrome (Cowden’s syndrome)

HISTOLOGICAL FEATURES:- Long , thin , finger-like projections extending above the

surface of the mucosa Each made up of continous layer of stratified squamous

epithelium Contains a thin , central connective tissue core (supports

nutrient blood vessels)

- Proliferation of the spinous cells in papillary pattern

- May show basilar hyper plasia and mild mitotic activity

(SHAFER’S)

• A thick papillary layer of keratinized or non-keratinized squamous epithelium

• A central core of fibrovascular connective tissue (characteristic)

• Long and finger –like or short , rounded and blunt(papillary projections)

• Normal maturation pattern shown by epithelium

• Mild degree of basilar hyperplasia (SAPP)

Differential diagnosis:Verruca vulgarisOral condyloma acuminatumFocal epithelial hyperplasia (Heck disease)

Treatment :- Surgical excision of the base of lesion and small area

of surrounding normal tissue- Recurrence is uncommon

Squamous Acanthoma

Description :- - Uncommon Lesion - Represents reactive phenomenon of epithelium - Not true neoplasm

- Tomich and Shafer described lesion

Clinical features:-Age :- Older Adults

Site of Occurance:- - Any site on oral mucosa- Appears small flat or elevated- White , sessile or pedunclated lesion on mucosa

Causes :- Trauma

H/P features:- Elevated or Umblicated epithelial proliferation

- Thickened layer of orthokeratin and underlying spinous layer of cells

T/P:- Excision - No case of recurrence after excision

KERATOACANTHOMA

• Self –healing carcinoma ,molluscum pseudo-carcinomatosum , molluscum sebaceum , verrucoma

• A benign endophytic epithelial growth appearing as a well-circumscribed keratin-filled crater on sun-exposed skin

• Low grade malignancy , originates in pilosebaceous glands

• Variant of invasive SCC (considered)

- Occurs on: Hair-bearing skin (cheeks , nose , eyelids , ears ) Lower lip- Arises from hair follicle epithelium above sebaceous

glands- Lower lip – arises from superficial epithelium of

sebaceous ducts or from the hair follicle epithelium of adjacent skin

Etiological factors:- Trauma , chemical carcinogens , human papilloma virus ,

genetic factors and immunocompromised status

Clinical Features:- Seen above >50yrs of age- Male:female – 2:1- Less common in dark skinned individuals- Occurs in sun exposed areas- Face,neck,and dorsum of the upper extremities are

common sites- 8.1% cases occurred on lips( vermilion border of both upper

and lower lips are equally affected)

• Develops rapidly over a period of 1to2months

• Soliatry and benign as firm, round ,skin coloured or reddish papules

• Rapidly progress to dome-shaped nodules with a smooth shiny surface and a central crateriform ulceration or keratin plug (projects like horn)

• Appears elevated umblicated or crateriform(with depressed central core or plug)

• 1 to 1.5cm in diameter

• Painful often and regional lymphaedopathy present

Differential diagnosis:Actinic keratosisMolluscum contagiosumMuir-Torre syndromeSCCVerrucous carcinoma

Histological features:- Hyperplastic squamous epithelium growing in underlying

connective tissue

- Parakeratin or orthokeratin covers the surface with central plugging

- Dysplastic features seen – occasionally (peripheral zone formed by squamous cells with atypical

mitotic figures , hyperchromatic nuclei and loss of polarity )

- Pseudocarcinomatous infiltation typically presents a smooth , regular , well-demarcated front that does not extend beyond the level of the sweat glands

- Connective tissue – shows chronic inflammatory cell infiltration

- Characteristic features – seen at margins , normal adjacent epithelium elevated towards the central portion of crater (abrupt change in epithelium occurs as hyperplastic acanthotic epithelium is reached)

(SHAFER’S)

Features :- Central plug of keratin surrounded by a sharply demarcated

- Cup-shaped buttress of normal epidermis

- Epithelium represents pseudocarcinomatous growth pattern

- Epithelium composed of well-differentiated spinous cells with abundant cytoplasm, minimal pleomorphism , infrequent mitotic figures , absence of abnormal mitotic figures

TREATMENT:- Surgical excision- Recurrent tumors may require more aggressive

therapy

Benign pigmented lesion

- Depending on amount and distribution of melanin in skin or mucosa, different color ranges seen

- Brown - Basal cells

- Black - keratin and Spinous cells

- Dark blue – Deeper Connective Tissue

ORAL NEVI

• Oral melanocytic nevus , nevocellular nevus , mole , mucosal melanocytic nevi

• Ackermann and field reported 1st case in 1943

• Benign proliferation of nevus cells either in epithelium or connective tissue

• Benign , Pigmented ,acquired lesion* of skin or mucosa

• Focal collection (nests) of rounded melanocytes (nevus cells)

• Histologic location ,acquired nevi classified in 3 types :1) Junctional Nevi: - Nevus cells limited to basal cell layer of epithelium2) Compound Nevus: - Epidermis and dermis3) Intradermal Nevus: - Nests of nevus cells in connective tissue

*Nevi can be classified as congenital or acquired (Buchner and hansen)

• Blue nevus :- A true mesodermal structure- Composed of dermal melanocytes

- Spitz nevus (spindle cell or epitheloid cell nevus) :- known as juvenile melanoma

- Common mucosal type : Intramucosal Nevus- 2nd common mucosal type : Blue Nevus

• Junctional and compound nevus : 3-6% of all oral nevi

• Oral acquired melanocytic nevi evolve through stages Junctional Nevi

(infants , children & young adults)

matures Compound Nevi

Intramucosal Nevi

Congenital Nevi• Ainsworth and her colleagues divided congenital

nevi of skin :1) Small Nevi: >1cm diameter (3-5 cm)2) Garment Nevi : >10cm in diameter - covers large areas of skin- 1 to 2.5% of neonates - Flat , pale tan macules to elevated , verrucous,

hairy lesions- Approx 15% - skin of head and neck- Intraoral occurrence is rare

• Acquired nevi are common• Eight month of life and in number with age• Number of nevi as one ages • Clark stated “number of nevi a person has is

genetically determined”

• 85% - young patients (<40 years) 55% - white patients 23% - black patients

Mean age for:1) Junctional /Compound Nevi – 22 – 24 yrs2) Intramucosal / Blue Nevi – 35-38yrsPredominant in women than in man

Site of occurrence:- hard palate -40% buccal mucosa – 20% Vermillion border of lip & labial mucosa gingiva – 10% Tongue and floor of mouth – 1 case reported

• Asymptomatic , incidental finding on routine dental check up

• Melanotic macules,amalgam tatoos , physiologic ethnic pigmentation , smoke’s melanosis or pigmented lesion

• Differences :- - melanotic macules and amalgam tatoos are flat

while nevi are elevated from mucosal surface

• 85% of oral nevi - pigmented - brown to black or blue• Nevi - well circumsribed ,round or oval , raised (65-80%)

Anatomic distribution closely follows histologic type - 2/3rd of blue nevi – palate - Intramucosal : hard palate -25% buccal mucosa – 25% gingiva – 17% vermilion border of lip – 17% labial mucosa – 9%

• H/P features:-- Large ovoid, rounded or spindle –shaped cells with

pale cytoplasm- Vesicular nucleus- Granules of melanin pigment in cytoplasm- Group in sheets or cords (nests or theques)

• Intramucosal (Intradermal) Nevus: - common mole - common lesion of oral mucosa

Clinical features:-- Young patients- Asymptomatic, pigmented – brown to black- Smooth flat lesion or elevated above surface- Hard palate or gingiva- Grows slowly - Measures <1cm in diameter

H/P features:-- Nests , cords or sheets of nevus cells within

connective tisssue- Multinuclested giant cells seen- Spindles cells may be present- Seperated from epithelium by well – defined

band of connective tissue - Free of nevus cells

• Junctional Nevus:-- Benign , brown –black- Skin , oral mucosa (occasional)- Hard Palate or Gingiva

H/P features:-- No zone of demarcation - Nevus cell in contact and blend with surface

epithelium- Overlying epithelium is thin ,irregular and shows

cells crossing junction & growing down into connective tissue

- Known abtropfung or dropping off effect- Feature showing malignant transformation

( junctional activity)

• Compond Nevus:-- Lesion Composed of two elements- Common in skin than in oral mucosa- Pigmented papulae or macule on hard palate or

gingiva

H/P features:-- Combined characteristic seen ( intramucosal +

junctional nevus) (nevus cells in basal region of epithelium and

adjacent connective tissue)- Nests of nevus cells dropping off from

epidermis

• Blue Nevus:-- True mesodermal structure- Consisting of dermal melanocytes- Rarely undergo malignant transformation- Present at birth and early childhood- Remains unchanged throughout life

- Appears as big pigmented lesion- Dark blue , dome shaped papule or flat macule on skin or mucosa- Smooth and exhibit hair growing from surface- Color :– - Due to melanocytes resides deep in connective

tissue overlying vessels dampen brown coloration of

melanin BLUE tint seen

• H/P features:-- Two types : 1) Common Blue Nevus 2) Cellular Blue nevus

1) Common Blue Nevus:- Elongated melanocytes with long branching

dendritic process lie in bundles- Parallel to epidermis- Middle and lower third of dermis- No junctional activity seen

2) Cellular Blue Nevus:-- Large , round or spindle cell with pale

vacuolated cytoplasm- Alveolar pattern arrangement seen

• Spitz Nevus:-- Children : on face or extremities- 15% reported in adults- Solitary , dome-shaped , pink to reddish

brown papulae- Size < 6mm

H/P features :-- Composed of Pleomorphic cells of three types 1) spindle cells 2) oval 3) epitheloid cells- Mononuclear and multinucleated giant cell- Arranged in cicumscribed sheets - Junctional activity seen

Treatment and Prognosis:-1) Acquired Pigmented Nevus : - common occurrence - removal adviced – occur in area irritated by clothing (belt or collar

line) or increase in size, deepen in colour or ulceratedTrauma to intradermal nevus doesnot induce

malignancy

2) Congenital pigmented Nevus:- - Great risk for transformation to malignant

melanoma - Clark and Coworkers described

B-K mole Syndrome (autosomal dominant condition)

- large pigmented nevi - higher risk for development of melanoma - not intraoral

• Conclusion:-Surgical excision of all intraoral pigmented nevi advicedDue to chronic irritation of mucosa in all intraoral sites ( eating , toothbrushing)

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