WHAT IS A TUMOUR? · Verruca vulgaris (Common wart) • Def. is a benign epithelial enlargement of...

WHAT IS A TUMOUR?

a swelling

inflammatory – abscess

neoplasm – growth- hamartoma

NEOPLASM

• Def.:✓ New growth which is self autonoumous (its growth is

uncoordinated with that of the surrounding normaltissues), progressive and persists after removal ofinitiating factors

✓ By definition is NOT reversible✓ Terms: Tumor, Neoplasia, Hyperplasia, metaplasia,

Reactive lesions , Hamartoma, Ectopia (heterotopia,choristoma), Differentiation

Reactive and neoplastic conditions

Reactive (Hyperplastic)lesion

Neoplastic lesion

Has definite etiologic factors as inflammation, infection,

trauma or excessive functional demands.

No definite cause or may be caused by irradiation, chemical carcinogens or specific type of

viruses.

Their rate of growth is directly related to the stimulus.

No relation between the rate of growth and the stimulus.

Lesions regress after cessation of the causative stimulus.

Their growth persists in the same excessive manner after the cessation of the causative

stimulus.

Classification of neoplasms according to the tissue of origin(Histogenesis)

1. Epithelial origin.

2. Mesenchymal origin.

3. Neoplasms of debatable origin.

Classification of neoplasms according to the behavior

1. Benign

2. Malignant

3. Neoplasms of intermediate behaviour (Locally aggressive).

Benign neoplasms Malignant neoplasm

Mode of growth

expansion Invasion

Rate of growth

slow rapid

Metastasis No metastasis blood or lymphaticmetastasis

Recurrence No recurrence after surgical excision.

Recurrence after surgical excision.

Clinical picture

• No ulceration orhemorrhage unlesstraumatized.

• capsulated• Soft in consistency• Smooth edges• Not fixed to the

surrounding tissues

• Frequent ulceration andhemorrhage

• Not capsulated• Hard• Irregular edges• fixed

Benign neoplasms Malignant neoplasm

Histopathology:1. Differentiation

2. Dysplasia3. Mitosis

well differentiated.

No dysplasiaNormal mitosis

range from well to poorly differentiated

DysplacsticAbnormal mitosis

Metastasis: is the ability of the primary tumor to develop secondary tumor deposits in distant sites.

Differentiation: is the degree of resemblance of the tumor to the tissue of origin both histologically and functionally.

Terminology

• Benign tumors The cell of origin + omaChondroma

Fibroma

• Benign tumors of surface epithelium Papilloma

• Benign tumors of glandular epithelium Adenoma .

• Benign-sounding malignancies: lymphoma, melanoma, mesothelioma, seminoma

Benign tumors of Surface epithelium

Hamartoma:Nevi

True neoplasms:1- Squamous cell papilloma.2- Kertaoacanthoma

Reactive lesions:1-Verruca Vulgaris.2- Condyloma auminatum3- Verruciform Xanthoma4- Heck’s disease.

Papilloma

• Def.

• Etiology

• Clinically

Squamous cell papilloma

• Def:

A benign neoplasm of surface epithelium.

Etiology:

True neoplasm caused by HPV 6,11

Papilloma

Squamous cell papilloma

• Clinically:

firm, non-painful, pedunclated

It has a rough white cauliflower or warty surface with numerous fingerlike processes.

It arises from the surface stratified squamous epithelium, is exophytic, and it does not invade underlying tissue.

Palate, lip, tongue

Single

D.D: Verruca vulgaris, condyloma acuminatum, verruciform xanthoma

Squamous cell papilloma

Verruca vulgaris (Common wart) • Def.is a benign epithelial enlargement of skin and mucosa • Etiologycaused by human papilloma virus 2,4,40. • ClinicallyLesions usually found on the labial mucosa, anterior tongue and vermillion borderIt is asymptomatic, exophytic, and has a broad base (Sessile). The surface is white, rough, and warty. Verrucae may spread to other body surfaces by autoinoculation.Sometimes they resolve spontaneously. Usually multiple

Verruca vulgaris

Sessile with broad base

Squamous cell papilloma

• Histologically:

- Multiple finger like projections made up of stratified squamous cell epithelium that shows acanthosis and contain a core of connective tissue containing dilated capillaries

- The mass may exhibit hyperkeratosis depending on the site o the lesion and the amount of friction

Squamous cell papilloma

• Histologically:- Koilocytes: squamous

epithelial cell infected with HPV. They have perinuclear halo and pyknotic nuclei. They may be present or absent.

- Chronic inflammatory cells may be found within the connective tissue

Squamous cell papilloma

Verruca vulgaris

Histologically:• elongated rete ridges tend

to converge toward the center of the lesion, producing a "cupping" effect.

• abundant koilocytes.

• Eosinophilic intranuclearviral inclusions may sometimes be noted within the cells of the granular layer.

Verruca vulgaris

Histologically:

Verruca vulgaris

Squamous cell papilloma vs Verruca vulgaris

Squamous cell papilloma

• Caused by HPV 6, 11 (not found in malignant lesions)

• not infectious

• Only mucosal

• Pedunclated and Short rounded projection

• Pink or white

• Mostly soiltary

• No cupping effect

• may or may not have koilocytes

Verruca vulgaris

• Caused by HPV 2,4,40

• Contagious and may be transmitted to other parts by autoinoculation

• Common in skin and may appear in mucosa

• sessile and pointed surface projections

• White

• Multiple or clustered

• elongated rete ridges tend to converge toward the center of the lesion, producing a "cupping" effect

• abundant koilocytes.

Squamous cell papilloma vs Verruca vulgaris

Squamous cell papilloma

• No eosinophilic intranuclearviral inclusions can be noted within the cells of the granular layer

• squamous cell papilloma does not regress with time and require excision

• squamous cell papilloma dose not transform to malignacy

Verruca vulgaris

• Eosinophilic intranuclearviral inclusions may sometimes be noted within the cells of the granular layer.

• verruca vulgaris undergo spontaneous regression

• verruca vulgaris can be transformed into malignant lesion

Condyloma acuminatumVenereal wart

• Def:virus induced proliferation of stratified squamous cell epithelium of the genitalia, perianal region, mouth and larynx

• Etiology:HPV 6, 11, 16, 18 (high risk types)Tansmission by AutoinoculationOr venereal • Clinically:Lip, tongue ,palateSessile, pink, painless, exophytic with short blunted projectionsMultiple, mulberry like with red surface

Condyloma acuminatum

• Verruca vulgaris is shaped like a series of inverted V's.

• Condylomaacuminata are shaped like a series of C's placed on their sides.

• Papillomas are pedunculated like the letter P.

• Histopathology:

Hyperplastic stratified squamous epithelium with mildly keratotic papillary projections which are more blunted and broader than those of squamous cell papilloma and verruca vulgaris giving keratin filled crypts between prominences

Keratin is sparse

Koilocytes are much more common than those of squamous cell papilloma

Retepegs are short bulbous and of even length

Condyloma acuminatum

Focal epithelial hyperplasiaHeck’s disease

• Def:Multiple oral papilloma induced by HPV 13 & 32• Clinically:Labial, oral mucosa and tongue.

Multiple, non-tender, soft rounded or flat-like papule

Usually normally coloured mucosa but may be pale or white Cobble stone or fissured appearance as lesions develop in clusters

Focal epithelial hyperplasia

focal epithelial hyperplasia similar to multiple papillary lesions develop in AIDS pts

Focal epithelial hyperplasia

• Histopathology:

The hallmark is abrupt acanthosis

The thick mucosa extend upwards so the lesionalreteridges are at the same level as the adjacent

Koilocytes

“Mitosoid bodies”, are nuclei with coarse clumped heterochromatin resembling a mitotic figure.

Mitosoid bodies are characteristic but not specific for focal epithelial hyperplasia.

KeratoacanthomaSelf healing carcinoma,

pseudocarcinoma• Def:A true neoplasm thought to arise from epithelium of hair follicleA self-limiting epithelial proliferation that is similar clinically and histologically to well-differentiated SCC

• Etiology:Sun damageHPVCarcinogens as smoking habitsGenetic factorsImmunosuppression

• Clinically:WhiteMen < femaleOld ageSun exposed skin including upperlip

It appears as a firm non-tendersessile dome-shaped nodulewith a central plug of keratin

❑Course:

• Rapid growth followed byslow involution .

• Brownish or reddish dome-shaped lesion then centraldepression appear filled withkeratin (cup-shaped lesion)

Keratoacanthoma(Self healing carcinoma)

Keratoacanthoma(Self healing carcinoma)

• Similarities with SCC:

1- Clinical appearance

2- Rapid growth

3- Histopathology

• Difference:

1- Spontaneous disappearance without ttt.

Keratoacanthoma(Self healing carcinoma)

• Histopathology:HyperkeratosisAcanthosisKeratinized clefts and penetrating squamous reteprocessesDeep keratin pearlsDense inflammatory infilterateAbrupt change between normal and affected epithelium at tumor edgePseudoepithelomatous hyperplasiaDense inflammatory infilterate in the underlying connective tissue.

Keratoacanthoma(Self healing carcinoma)

Keratoacanthoma(Self healing carcinoma)

Keratoacanthoma

Keratoacanthoma

Papillary hyperplasia of palate

Papillary hyperplasia

• Def.Asymptomatic nodular or papillary mucosal lesion seen in the palate of pts who wear dentures. • EtiologyMost pts wear ill-fitting dentures, war denture continuously or have poor denture hyagiene.It appears in non-denture wearer due to xerostomiaor pts with high arched palateFlorid presentation occur in immunsupressed ptsand HIV infection

• Histopathology:

1. Hyperplasia of epithelium and underlying fibrous tissue.

2. Parakeratinization or less commonly ortho.

3. Rounded or sharply defined reteprocesses.

4. May be pseudoepitheliomatous hyperplasia with keratin pearl.

DD: Focal epithelial hyperplasia, verruciformxanthoma and HIV-induced papillomatosis

Papillary hyperplasia of palate

Papillary hyperplasia of palate

Papillary hyperplasia of palate

Verruciform xanthoma

• Hyperplastic condition (papillary lesion)of the mouth with lipid ladden histocytes beneath the epithelium

• Etiology:Unusual reaction or immune response to epithelial trauma or damage. This hypothesis is supported by cases of verruciformxanthoma that developed in association with disturbed epithelium (eg Lichn planus, lupus erythrematosus)• Clinically:Soft painless sessile slightly elevated mass with papillary or rough surface.White, yellow-white or red colorMultiple lesions may occur

Lesion of the ventral tongue with biphasic appearaneWide arrow: white lesionNarrow arrow: less keratinized

Verruciform xanthoma

• Histopathology:

1. Hyperkeratosis

2. Papillary acanthotic surface projections

3. Clefts between surface epithelium are filled with keratin

4. Elongated reteridges with uniform depth.

5. Large macrophages with foamy cytoplasm in ct papillae (xanthoma cells) containing lipid

Verruciform xanthoma

Verruciform xanthoma

Verrucal papillary lesions

• Reactive lesions:

1. Verruca vulgaris 2. Condyloma acuminatum3. Papillary hyperplasia 4. Focal epithelial hyperplasia

• True neoplasms:

1. Squamous cell papilloma 2. Keratoacanthoma3. Verrucous carcinoma

• Unknown etiology:

1. Verruciform xanthoma

• Premalignant lesions:

1. Verrucous leukoplakia

Melanocytic nevus

• Hamartoma

• Nevi

• Types of nevi:

1. Keratotic nevi: white spongy nevus

2. Vascular nevi

3. Pigmented nevi

Melanocytic nevus

• Physiology of melanocytes.

• Epidemal melanin unit

• Importance of melanin:

1- Melanin provides maximalprotection from damagingultraviolet light.

2-Melanin also has beenshown to be a free oxygen–radical scavenger

• Def.Benign proliferation of nevus cells (representmelanocytes or first cousins of melanocytes).• Nevus cells are altered melanocytes characterized

with:1- Rounded cytoplasm with lack of dendriticprocesses.2- No contact inhibition and formation of nest orclusters called theques.3- Ability to migrate into the submucosa.4- Three types: A(epithelioid type), B (Lymphocyte-like) and C (spindle-shaped).

Melanocytic nevus

• Oral nevi are rare. Most commonly on hardpalate and gingiva.

• More than one in five intraoral nevi lack clinicalpigmentation

• Nevi may be congenital or acquired

• The acquired melanocytic nevus (mole) isprobably the most common of all human"tumors," and white adults have an average of10 to 40 cutaneous nevi per person.

Melanocytic nevus

• Types of acquired melanocytic Nevi (common mole):1. Junctional nevus2. Compound nevus3. Intradermal nevus (intramucosal in case of oral

nevi) (most common type of oral nevus) (>one half of oral nevi).

Other variants of acquired melanocytic nevi:1. Blue nevus (second most common type of oral

nevus)2. Juvenile melanoma3. Halo nevus

Melanocytic nevus

General clinical features:

• Age: Acquired melanocytic nevi begin to developon the skin during childhood. Most cutaneouslesions are present before 35 years of age.

• Sex: men and women, although women usuallyhave a few more than men.

• Race: Racial differences are seen. Whites havemore nevi than Asians or blacks.

• Site: above the waist, and the head and neckregion is a common site of involvement.

Melanocytic nevus

General Histopathologic FeaturesThe acquired melanocytic nevus is characterized by abenign, unencapsulated proliferation of small , ovoid cells(nevus cells).The lesional cells have small, uniform nuclei and a moderateamount of eosinophilic cytoplasm, with indistinct cellboundaries.These cells demonstrate a variable capacity to producemelanin , with the pigment primarily evident in thesuperficial aspects of the lesion .Nevus cells typically lack the dendritic processes thatmelanocytes possess.A characteristic microscopic feature is that the superficialnevus cells tend to be organized in to small roundaggregates theques.

Melanocytic nevus

General Histopathologic Features▪ The superficial cells typically appear larger and

epithelioid with abundant cytoplasm, Frequentintracellular melanin , and a tendency to cluster intotheques.

▪ Nevus cell s of the middle portion of the lesion haveless cytoplasm. are seldom pigmented . and appearmuch like lymphocytes.

▪ Deeper nevus cells appear elongated and spindleshaped. much like Schwann cells or fibroblasts.

▪ Some authorities classify these variations as type A(epithelioid), type B (lymphocyte- like) and type C(spindle-shaped) nevus cells.

Melanocytic nevus

Junctional nevus• Clinically:

➢ Sharply demarcated macule, brown to black.

➢ It occurs in palms of hands and soles of feet.

➢ It is devoid of hair.

➢ Less than 6 mm in diametre

Junctional nevus

• Histologically:

Nests of nevus cell located at the dermo-epidermal junction.

After 20 ys, it denotes malignant transformation

Junctional activity: increased mitosis, abnormal proliferation, pleomorphism and hyperchromatism.

Dropping effect: The cells appear to be dropping from the surface epithelium

Compound nevus• Definition:

A type of pigmented nevus thatcontains both junctional andintradermal parts.

• Clinically:

nevus cells proliferate over aperiod of years to produce

a slightly elevated, soft papulewith a relatively smooth surface(compound nevus). The degree ofpigmentation becomes less; mostlesions appear brown or tan.

Compound nevus• Histologically:

As the nevus cells proliferate. groups of cells begin to dropoff in to the underlying dermis or lamina propria. Becausecells are now present both along the junctional area andwithin the underlying connective tissue, it is termedcompound nevus

The junctional elementmay show junctionalactivity.

Intradermal nevus• It is the most common type• Clinically:➢ As time passes, the nevus

gradually loses its pigmentation,➢ the surface may become

somewhat papillomatous, and hairs may be seen growing from the center (intradermal nevus)

➢ Throughout the adult years, many acquired melanocytic nevi will involute and disappear ; therefore, fewer of these lesions can be detected in elderly persons.

Intradermal nevus

Intradermal nevus

• Histologically:

Oval or ellipsoid nevus cells located intradermallyand contain melanin pigmentation.

Nevus cells may fuse to form Touton giant cells.

Juvenile melanoma(Spitz nevus)

Def.: an uncommon type of melanocytic nevus that shares many histopathologicfeatures with melanoma.

Clinical FeaturesSite: the skin of the extremities or the face during childhood. shape: appears as a solitary, dome-shaped, pink to reddish-brown papule,Size: usually smaller than 6 mm in greatest diameter. Theyoung age at presentation and the relatively small size of the Spitz nevus are useful features to help distinguishit from melanoma.

Juvenile melanoma(Spitz nevus)

Histologically:▪ The Spitz nevus has the overall microscopic

architecture of a compound nevus▪ lesional cells are either spindle-shaped or

plump (epithelioid), and the two types often are intermixed.

▪ The epithelioid cells may be multinucleated and appear somewhat bizarre, often lacking cell cohesiveness. Mitotic figures, all normal in appearance, may be seen in the superficial aspects of the lesion.

Ectatic superficial blood vessels, which probably impart much of the reddish color of some lesions, are seen frequently.

Halo nevus

• Def.: It is pigmented macule withsurrounding depigmentation.

• Clinically: It is characterized clinicallybe appearance of depigmentationaround a nevus. Complete regressionmay occur leaving a depigmentedmacule

• Histologically, it is a compoundnevus with dense lymphocyticinflammation around and infiltratesthe nevus cell population that leadsto destruction of melanocytes

Blue nevus

Blue nevus owes its unique color to :1- the abundance of melanin transmitting from the deep location offset by the color of the normal surrounding skin. 2- The blue color of this melanin-producing lesion can be also explained by the Tyndall effect , which relates to the interaction of light with particles in a colloidal suspension. Melanin particles are deep to the surface, so that the light reflected back has to passthrough the overlying tissue. Colors with long wavelengths (reds and yellows) tend to be more readily absorbed by the tissues; the shorter-wavelength blue light is more likely to be reflected back to the observer's eyes.

Def: Blue nevus is an uncommon, benign proliferation ofdermal melanocytcs, usually deep within subepithelialconnective tissue.

Blue nevus(Mongolian spot)

Clinically:Site: dorsa of the handsand feet, the scalp, and theface. Oral lesions are foundalmost always on thepalate.Age: children and youngadultsSex: female predilection isseen.Shape: macular or domes-haped, blue or blue-blacklesion smaller than I cm indiameter

Blue nevus

TTT & Prognosis

• No treatment is indicated for a cutaneous melanocyticnevus unless:

1- it is cosmetically unacceptable.2- is chronically irritated by clothing.3- a change in size or color.• the risk of transformation of a particular acquired

melanocytic nevus to melanoma is approximately I in Imillion.

• The risk of transformation increases withapproximating the sun exposure. So, junctional nevusand junctional component of compound nevus is themost dangerous.

• Pseudoepitheliomatous hyperplasia.

• Verrucal papillary lesions

• Types of nevi