Pathology PosterNeoplasia

In The Floor Of The Mouth

Mohamed Ahmed

PREMALIGNANT LESIONS

ErythroplakiaDescription :clinical term to describe any erythematous (red) area on a mucous membrane. Although often the terms erythroplasia and erythroplakia are used synonymously, some sources distinguish them, stating that the latter is macular (flat) while the former is papular (bumpy). It appears as a red macule or plaque with well-demarcated borders. The texture is characterized as soft and velvety. An adjacent area of leukoplakia may be found along with the erythroplakia. it is soft on palpation and does not become indurated until an invasive carcinoma develops in it . It is often asymptomatic, although some patients may complain of a sore, burning or metallic sensation.

X-Ray: No X-ray Picture

Etiology :Erythroplakia has an unknown cause but researchers presume it to be similar to the causes of Squamous cell carcinoma. Carcinoma is found in almost 40% of erythroplakia. It is mostly found in elderly men around the ages of 65 - 74. It is commonly associated with smoking.Alcohol and tobacco use have been described as risk factors.

DD: Non-homogeneous leukoplakia-Erosive lichen planus-Acute atrophic candidiasis-Invasive oral cancer-Pemphigus-Lupus erythematosus-Denture induced stomatitis-Haemangioma

Treatment: Persons with erythroplakia should be advised to stop tobacco/alcohol habits, and should be encouraged to take a diet rich in vegetables and fruits. In view of the high malignant potential of these lesions the recommended treatment is surgical excision, including laser.

Histopathology: Erythroplakia harbours carcinoma in about 51% of cases, severe dysplasia or CIS in 40% and mild to moderate dysplasia in 9% . The red appearance is due to the thin atrophic epithelium with prominent subepithelial vascularity and inflammation. Almost all erythroplakic lesions contain dysplastic cells. The histopathology may be mild or moderate epithelial dysplasia, severe dysplasia or carcinoma in-situ. Carcinoma in-situ is characterized by a complete disorganization of cells throughout all layers of the epithelium, with no keratin pearls. In other words, the entire thickness of the epithelium is occupied by dysplastic cells, with an intact and well-defined basement membrane. Rete pegs are frequently bulbous or tear-drop shaped, often with secondary proliferations or projections of abnormal cells. Nuclei are typically hyperchromatic and enlarged, with the amount of cytoplasm diminished. Mitotic activity is pronounced and abnormal mitotic figures may be noted. The basement membrane should be carefully examined for areas of micro-invasion.

Oral LeukoplakiaDescription :Leukoplakia is a white or gray patch. The patch may have developed slowly over weeks to months and be thick, slightly raised, and may eventually take on a hardened and rough texture. It usually is painless, but may be sensitive to touch, heat, spicy foods, or other irritation.

X-Ray: No X-ray Picture

DD: Candidiasis – Lichen Planus – White Sponge Nevus – chemical Burn - Morsicatio buccarum (habitual cheek biting)Psoriasis.

Treatment: Leukoplakia is usually harmless. lesions usually clear in a few weeks or months after the source of irritation is removed.

Histopathology: Basic microscopic characteristics of oral LKP include hyperkeratosis of ortho- or parakeratotic type and acanthosis of the epithelium, with various degrees of chronic inflammatory infiltrates in lamina propria. Also, various degrees of epithelial dysplasia may occur. Some of the most important microscopic characteristics of dysplasia are: loss of polarity of basal cells, increased nuclear cytoplasmic ratio, irregular epithelial stratification, increased number of abnormal mitotic figures and their presence in the superficial epithelium, cellular and nuclear pleomorphism, keratinization of single cell groups.

Malignant Potentiality: malignant potential of LKP does not exceed 4%, but some authors found that even 16% LKP with some degree of dysplasia, have a potential to transform to carcinoma.LKP is the most common oral mucosal lesion (evident in 3% of adults). At the same time, up to 85% of all precancerous lesions are manifested as LKP.

Hairy LeukoplakiaDescription :"Hairy" leukoplakia of the mouth is an unusual form of leukoplakia (caused by the Epstein-Barr virus) that is seen only in people who are infected with HIV, have AIDS, or AIDS-related complex. Irregular white patches on the inside of your tongue and may occasionally appear in other places in your mouth and your tongue.The irregular white patches look folded or corrugated in appearance.Running along the folds there will be tiny hair-like protrusions, which you can see best when you stick out your tongue, stretched to the side.The lesions cannot be dislodged or moved.

X-Ray: No X-ray PictureEtiology :It is thought that hairy leukoplakia is caused by the Epstein-Barr virus which is a virus that is related to herpes. It is an oral infection. It is a very common human virus and occurs worldwide. During a person’s lifetime, almost everyone becomes infected with this virus.This is the same virus that can also cause infectious mononucleosis if the infection with this virus happens during young adulthood or adolescence.Hairy leukoplakia is frequently associated with an immune system that has been compromised which is why is often happens in people who have moderate to severe immune system damage or HIV.DD: Geographic tongue -Squamous cell carcinoma-Pseudo–hairy leukoplakia -Tobacco-associated leukoplakia- Lichen planus-Candidiasis- Condyloma Accuminatum

Treatment: Hairy leukoplakia requires treatment with an antiviral Medication.

Histopathology: In oral hairy leukoplakia, the mucosa displays mild papillary acanthosis . Hyperkeratosis and marked parakeratosis of the superficial epithelial layer is a prominent feature . Superficial infections of the hyperkeratinized epithelium with bacteria or Candida may also be seen. The acanthosis is caused by ballooning koilocyte-like cells. The nuclei of these have a homogenous ground-glass appearance and may contain intranuclear inclusions.

Special studies for oral hairy leukoplakiaDiagnosis requires demonstration of EBV DNA, RNA, or protein within the epithelial cells of the lesion. In-situ hybridisation for EBV is usually performed for confirmation of the diagnosis.

BENIGN LESIONS

Adult RhabdomyomasDescription :The lesion usually presents as a smooth, movable, solitary (but occasionally multifocal), asymptomatic, round, or polypoid nodule in the head and neck region, or as a circumscribed intramuscular mass in the tongue, the sublingual region, lips, cheek, orbit, or submandibular region that is neither tender nor painful. However, it may compress or displace the tongue. Rhabdomyomas are slowly growing, and the lesions vary in size from a few millimeters to 15 cm .

DD: granular cell tumor(S-100 positivity ) - salivary gland tumors, namely, acinic cell carcinoma or oncocytoma- rhabdomyosarcoma.

Treatment: The treatment of choice for rhabdomyoma is surgical excision.

Histopathology: Histologically, the adult rhabdomyoma type is characterized by a sheet-like proliferation of tightly packed, large polygonal to round cells with abundant, deeply eosinophilic, granular cytoplasm with one or two peripherally placed vesicular nuclei; prominent nucleoli may occasionally be identified. Many cells show cytoplasmic vacuolization due to intracytoplasmic glycogen accumulation. Some cells have a small central acidophilic cytoplasmic mass connected by thin strands of cytoplasm to a condensed rim of cytoplasm at the periphery. These so-called “spider-cells” are more prevalent in cardiac rhabdomyomas than in extracardiac rhabdomyomas. Cross-striations are usually readily identifiable. Mitoses and necrosis are absent

Cavernous HemangiomasDescription :

Cavernous hemangiomas are composed of large, irregular, deep dermal and subcutaneous blood-filled channels that impart a purplish discoloration to the overlying skin. They are typically soft, poorly defined, and readily blanch with compression, giving them a characteristic "bag of worms" feel. The lesion may expand and darken with crying, when agitated, or when placed in a dependent position. Often, a capillary component overlies a cavernous component, and it may be difficult to distinguish these components histologically. Cavernous and mixed hemangiomas demonstrate the same patterns of proliferation as those of capillary lesions. However, involution is often incomplete, depending on the location and the presence of associated arteriovenous malformations.

Occlusal Radiographs – Computed Tomography.

Etiology :The causes of vasoformative tumors are unknown. One hypothesis postulates that placental cells, such as the trophoblast, may be the cell of origin for hemangiomas.DD:The diagnosis of hemangiomas is straightforward from the history and the clinical examination, and the differential diagnosis is limited. For intraosseous lesions, the differential diagnosis can be more challenging, with the radiographic appearance being similar to that of a giant cell lesion or an ameloblastoma.

Treatment: Treatment COMPLETE SURGICAL EXCISON OF THE LESION

Histopathology: Irregular Dilated Vascular Spaces Lined By Flattened Endothelial Cells In Fibrous Connective Tissue stroma. Endothelium lined vascular spaces are engorged with large aggregates of erythrocytes.

Cystic HygromaDescription :

Cystic hygromas are abnormal growths that usually appear on a baby’s neck or head. They consist of one or more cysts and tend to grow larger over time. The main symptom of a cystic hygroma is the presence of a soft, spongy lump. This lump most commonly appears on the neck.

Radiography : CT Scan Etiology :Cystic hygromas can develop due to genetic disorders or environmental factors. One or more growths may be present at the time of diagnosis.Common environmental causes of cystic hygromas are:1-viral infections passed from the mother to the baby during pregnancy2-exposure to drugs or alcohol during pregnancyCystic hygromas are seen more often in infants with genetic diseases. They are particularly common in infants with chromosomal abnormalities. Some genetic conditions associated with hygromas include:Turner’s syndrome — where female children have one X chromosome instead of twoTrisomy 13, 18, or 21 — conditions where children have an extra copy of a chromosomeNoonan syndrome — a disorder caused by a mutation (change) in one of seven particular genesDD: Branchial cleft cyst -Thyroglossal duct cyst -Ranula -Goiter -Soft tissue tumors -Neck abscess

Treatment: The first step of treatment is surgery.

Histopathology: 1-Large, irregular vascular spaces lined by flattened, bland epithelial cells with fibroblastic or collagenous stroma .2-Stroma may contain lymphocytes .

LipomaDescription :A lipoma can usually be diagnosed by its appearance alone. They present as slow growing asymptomatic lesions with yellowish color and soft, doughy feel, generally with no gender predilection.

X-Ray: No X-ray Picture

Etiology :The cause of lipomas is not completely understood, but the tendency to develop them is inherited. A minor injury may trigger the growth.

DD: Other connective tissue lesions such as granular cell tumor, neurofibroma, traumatic fibroma, and salivary gland lesions (mucocele and mixed tumor).- Normal Fat – Well-differentiated Liposarcoma

Treatment: Lipomas usually are not treated, because most of them don't hurt or cause problems. It might remove the lipoma if it is painful, gets infected, or bothers the patient.

Histopathology: Sections show mature adipose tissue. The fat contains few small capillaries within thin fibrous strands. A thin fibrous capsule is often seen. Fat necrosis and other inflammatory changes may be seen when lipomas are traumatised.

NeurofibromaDescription :Neurofibroma is an uncommon benign tumor of the oral cavity derived from the cells that constitute the nerve sheath. Neurofibroma is seen either as a solitary lesion or as part of the generalized syndrome of neurofibromatosis (usually neurofibromatosis type 1 [NF-1], also called von Recklinghausen disease of the skin). Patients usually present with an uninflamed, slowly enlarging, asymptomatic lesion that varies greatly in size from tiny nodules to large pendulous masses. The lesion is rarely painful; however, patients may experience pain if the lesion is secondarily traumatized due to its location. Oral neurofibromas usually present as submucosal, nontender, discrete masses that range in size from a few millimeters to several centimeters. The lesions are typically pedunculated or sessile, usually painless, but occasionally pain or paresthesia is reported due to nerve compression.

Radiology :Neurofibroma in the floor of the mouth. Coronal contrast-enhanced CT (a) and coronal STIR MR (b) images show a large cystic lesion ( * ) located cephalad to the mylohyoid muscle (arrowhead). The lesion has penetrated the genio- glossus-geniohyoid muscle complex (arrows).  Etiology :The cause of these lesions is unknown; however, neurofibromatosis syndrome or the disseminated form is inherited as an autosomal dominant trait and may present with a variety of lesions, including a highly variable number of neurofibromas.DD: Granular cell tumor -Fibroma -Scar tissue -Neurilemmoma (schwannoma) -Leiomyoma –Rhabdomyoma.

Treatment:Solitary oral neurofibromas are usually treated by surgical excision, depending on the extent and the site.

Histopathology: Microscopy revealed that the circumscribed tumor consisted of interlacing bundles of spindle cells with hyperchromatic nuclei. Spindle cells were intermixed with foci comprising dense bundles of collagen fibers.

Pleomorphic AdenomaDescription :

Pleomorphic adenoma is a benign salivary gland tumor that exhibits wide cytomorphologic and architectural diversity. Pleomorphic adenoma usually presents as a slow-growing, painless mass, which may be present for many years. On gross examination, a pleomorphic adenoma is a single firm, mobile, well-circumscribed mass. Its color may vary from whitish-tan to gray to bluish, and its size may range from a few millimeters to quite large or even giant. Pleomorphic adenomas are irregularly shaped and have a bosselated surface.

Computed-tomography (CT) images showed a distinct radiolucent, homogeneous lesion extending anteriorly in the area where the left sublingual gland (sublingual sulcus) normally lies Etiology :Although the etiology of pleomorphic adenoma is unknown, the incidence of this tumor has been found to increase 15-20 years after exposure to radiation. One study suggests that the simian virus (SV40) may play a causative role in the development of pleomorphic adenoma.

DD: other salivary gland tumors of submandibular/minor salivary glands.- lymphomas, non-neoplastic entities of salivary glands such as ranulas, retention cysts, sialolithiasis, sialadenitis, and cystic lesions of the floor of the mouth such as dermoid cysts.

Treatment: Early total surgical resection of the sublingual gland and its neoplastic mass in normal margins for benign tumors is the treatment of choice to avoid recurrences.

Histopathology: Microscopic satellite tumor nodules, pseudopodia, and capsular penetration may be seen beyond the capsule . This may be the cause of recurrence of pleomorphic adenomas in cases that were treated with simple enucleation or in cases in which surgical resection was performed with inadequate surgical margins. The epithelial component consists of epithelial and myoepithelial cells with divergent growth patterns, including trabecular, tubular, solid, cystic, and papillary architecture. Pure epithelial cells are mainly cuboidal. Cells that exhibit myoepithelial features

may have plasmacytoid, epithelioid, spindle, oncocytic, or clear cell morphology. In some studies, the most common myoepithelial cell type that was encountered displayed plasmacytoid cell morphology; the spindle cell type was the next most common type. All cellular elements appear cytologically bland, with no significant mitotic activity.The ducts and tubules seen in pleomorphic adenomas usually exhibit a lining comprising 2 cell types—that is, an inner cuboidal epithelial cell layer and an outer myoepithelial cell layer (or layers) tend to merge into the surrounding stromal component, which also contains dispersed or grouped modified myoepithelial cells . The cuboidal epithelial cells occasionally have a clear cytoplasm; the myoepithelial cell cytoplasm ranges from deeply eosinophilic to clear.The stromal component is a product of the modified myoepithelial cells and may appear mucoid, myxoid, hyaline, chondroid, myxochondroid, or even osseous

Schwannoma (Neurilemmoma)Description :

Schwannomas are usually solitary lesions; however, some are seen as multiple lesions as part of Neurofibromatosis type I. The solitary neurilemoma is a slow growing, encapsulated tumor that typically arises in association with a nerve trunk. As it grows it pushes the nerve aside. Usually the mass is asymptomatic, although tenderness or pain may occur in some instances.

Computed Tomography :Computed tomography scan in axial view showed a well-defined heterodense mass with specks of calcification in the right sublingual region.

Etiology :The cause of these neoplasms is unknown. Neurilemmoma can be associated with von Recklinghausen disease; when this is the case, multiple tumors often are present.

DD: Lipoma – Fibroma –Neurofibroma - Rhabdomyoma - Leiomyoma

Histopathology: The histological finding of the present case consists of a well-defined fibrous capsule having two patterns.Antoni ‘A’ areas are composed of compact spindle-shaped cells with twisted nuclei, indistinct cytoplasmic borders and occasional clear intranuclear vacuoles arranged in bundles or inter lacing fascicles. In the Antoni ‘A’ areas there was nuclear palisading, whirling of cells and Verocay bodies formed by two compact rows of well aligned nuclei separated by fibrillar cell processes. Antoni ‘B’ areas were far less orderly and cellular. The spindle or oval cells were arranged haphazardly in the loose textured matrix, which was punctuated by microcystic change, inflammatory cells and delicate collagen fibres. These tumors may undergo degenerative changes in the form of cyst formation, hyalinization, calcification, hemorrhage, and nuclear atypism, but, are nonetheless benign.Diagnostic Tools :S-100 is strongly expressed by most cells in Schwannoma in contrast to cells of neurofibromas, which variably expresses the antigen. Although the expression of S-100 is diminished in Antoni B areas.

Immunohistochemistry

White Sponge NevusDescription :Clinically, white sponge nevus of the oral cavity is characterized by the presence of asymptomatic, bilateral, soft, white and “spongy” plaques . The surface of the plaque is thick, folded and may peel away from the underlying tissue. Lesions are asymptomatic and rough to palpation. The condition may involve the entire oral mucosa as to leave little normal mucosa visible, or may be distributed unilaterally as discrete white patches.

Etiology :White sponge nevus (WSN) is an inherited disorder exhibiting autosomal-dominant transmission with no sex predilection mutations. The mutations affecting keratin protein interfere with intermediate filament assembly.

DD: oral lesions of leukoplakia, chemical burns, trauma, syphilis, tobacco and betel nut use. White sponge nevus may also be confused with candidiasis, but fungal examination, the histology of biopsy specimens, and the response to antifungal agents will be the differentiating factors. Cheek- biting, lichen planus, lupus erythematosus should also be excluded.

Treatment: Treatment with vitamins, antihistaminics and mouth rinses have been recommended, but none has been successful. Penicillin was reported to succeed to a little extent in the management of WSN.

Diagnosis :. The diagnosis is made more certain if there is a positive family history and other mucous membranes are affected. In case of any suspicion, biopsy should be performed.

Prognosis: The lesions on mucous membranes persist through life, but the condition is benign.

Histopathology: When viewed microscopically, the tissue exhibits acanthosis or a heavy thickening of the prickle cell layer of the epithelium. This promotes the thick white appearance that is very characteristic of WSN. Another feature noted is the cytoplasmic clearing of the epithelial cells that a pathologist will recognize.

MALIGNANT LESIONS

Adenoid Cystic Carcinoma

Description :The clinical course is characterized by an initial period of slow and indolent growth that is usually asymptomatic. In most cases the tumor goes unnoticed until it has invaded local nerves and structures causing varying symptoms depending on location. Thus, most patients will present with locally invasive disease.The tumor is typically a firm, poorly circumscribed, and unencapsulated mass. Tumor size typically averages from 1 to 8 cm in maximum dimension. Tumor size greater than 3 cm has been associated with increased rates of distant metastasis. The cut surface is white to gray-white with a solid appearance. Hemorrhage and necrosis are rare features and should raise the suspicion of high-grade transformation into dedifferentiated ACC.

Computed Tomography

Etiology : No strong genetic or environmental risk factors have been identified. Damage to the DNA genome occurs in the development of ACC, as it does in all cancers studied to date. Various studies have shown chromosomal abnormalities and genetic deletions occurring in samples of ACC. There is some evidence that the p53 tumor suppressor gene is inactivated in advanced and aggressive forms of this neoplasm.

DD: benign mixed tumor, mucoepidermoid carcinoma and polymorphous low-grade adenocarcinoma (PLGA). Treatment: Surgery

Histopathology:The microscopic appearance of the tumor is heterogeneous, consisting of varying amounts of 3 distinct growth patterns; however, the cytology of the tumor cells themselves is relatively uniform. The cells of the tumor display a basaloid appearance with angulated, hyperchromatic nuclei and scant, clear to eosinophilic cytoplasm. Three growth patterns for ACC have been described: cribriform, tubular, and solid. The cribriform subtype is the most frequent. It is composed of islands of basaloid cells surrounding variably sized cystlike spaces forming a “Swiss cheese” or sieve like pattern.The cystlike spaces are referred to as “pseudocysts” because they do not represent true glandular lumina and are contiguous with the surrounding stroma. The pseudocysts contain basophilic glycosaminoglycans and/or eosinophilic, periodic acid-Schiff–positive basal lamina material.Rare, true glandular lumina composed of cuboidal cells showing ductal differentiation can also be found scattered throughout and their presence greatly aids in diagnosis.

The tubular pattern shows similar cytology with the tumor cells arranged in nests surrounded by variable amounts of eosinophilic, often hyalinized stroma. Occasionally, the stroma component is increased, compressing the tumor cells into thin strands, forming a “trabecular” pattern. Well-formed ducts with recognizable inner epithelial and outer myoepithelial layers are more prominent than in the cribriform pattern. The continuity of the pseudocysts with the surrounding stroma is also more prominent.The solid pattern contains aggregates of basaloid cells without tubular or cystic formation. Although the basaloid cytology of the tumor cells is retained, the tumor cells may be larger and nuclear pleomorphism may be more pronounced. Mitotic figures and comedonecrosis may also be seen. As in the cribriform pattern, true ducts will occasionally be seen scattered among the sheets of cells. This feature, along with accompanying areas of cribriform or tubular growth, can aid in differentiation from other basaloid neoplasms.

Ewing SarcomaDescription :

ES is a poorly differentiated neuroectodermal tumor with small, round and blue cells. Swelling, pain, increased CRP, leukocytosis, and elevated temperature may be the first signs of oral ES, occurring also in odontogenic infections . Also there is apical osteolysis, loss of sensibility and loosening of teeth.

Axial MRI scan revealing a bone destroying mass of approximately 7 × 8 × 6 cm 3 surrounding the mandible and massively infiltrating the soft tissue of the floor of the mouth and the tongue. Etiology :More than 90% of cases show a characteristic translocation t(11;22)(q24;q12) resulting in the fusion of the EWS and FLI-1 genes. This gene rearrangement causes a fusion product which functions as an oncogenic aberrant transcription factor with structural variability and potentially prognostic impact . Immunoreactivity against FLI-1 and CD 99 can help to confirm the diagnosis Treatment:

Treatment of ES should include wide surgical resection and (neo-)adjuvant chemotherapy .

Histopathology:Histologically, the tumour was composed of uniform small round cells with indistinct cytoplasm and round nuclei with finely dispersed chromatin. There is a Lack of reticulin fibres. Finally, the characteristic translocation (11;22)(q24;q12) was detected using Fluorescence in situ Hybridisation.

Melanoma Description :Oral melanomas arise silently, with few symptoms until progression has occurred. Most people do not inspect their oral cavity closely, and melanomas are allowed to progress until significant swelling, tooth mobility, or bleeding causes them to seek care. Pigmented lesions 1.0 mm to 1.0 cm or larger are found.On physical examination, the pigmentation of these lesions varies from dark brown to blue-black ; however, mucosa-colored and white lesions are occasionally noted, and erythema is observed when the lesions are inflamed.

Etiology :The cause of oral melanoma or melanoma of any mucosal surface remains unknown. In contrast, cutaneous lesions are linked directly to fair-skinned and blue-eyed persons with a history of blistering sunburns, and the incidence has increased dramatically (approximately 4-6% per year) over the same period.  However, mucosal exposure to sunlight is unlikely, and, therefore, cutaneous melanoma and mucosal melanoma are different diseases.

DD : Haemangioma -Melanotic macule-Oral mucosal nevi-Amalgam tattoo-Kaposi Sarcoma

Histopathology:The melanoma cells have large nuclei, often with prominent eosinophilic nucleoli, and show nuclear pseudoinclusions due to nuclear membrane irregularity (see the following image). The abundant cytoplasm may be uniformly eosinophilic or optically clear. Fine and coarse intracytoplasmic pigment may be evident. Occasionally, the cells become spindled (sarcomatoid) or neurotize in areas. In the oral mucosa, the prognosis is dismal for patients with any architectural type (spindled, pleomorphic, plasmacytoid, undifferentiated) of cell. Metastatic spread to the cervical and supraclavicular lymph nodes is a common finding.

Squamous Cell CarcinomaDescription :

The most common presentation of cancer of the floor of the mouth is a painless inflamed superficial ulcer with poorly defined margins. Preexistent or coincident leukoplakia can be observed in adjacent tissues in approximately 20% of cases. The presence of erythroplasia strongly suggests an invasive tumor. A small ulceration or nodular lesion may remain asymptomatic for long periods, so the patient may not seek medical attention. Vague symptoms of soreness in the regional mucosa could be attributed to an aphthous ulcer. In fewer than 50% of cases, the ulcer is localized only to the floor of the mouth on initial presentation. If the tumor has grown with relatively few symptoms or if the patient has neglected its initial signs, the patient may first present with a neck mass, by which time the tumor has metastasized.

Etiology :Tobacco and alcohol have additive effects on oral cancer. Tobacco includes smokeless tobacco derivatives, such as snuff and betel nut. Some people seem to be more vulnerable than others to the effect of these irritants. The nature of the increased vulnerability may be genetic, familial, or acquired (eg, immunosuppression, syphilis, Plummer-Vinson syndrome, chronic candidiasis). These risk factors and the underlying pathogenesis do not disappear following surgical excision or radiation therapy for the cancer. The organs remain susceptible. DD: Lymphoma – Adenoid cystic carcinoma – Adenocarcinoma – Mucoepidermoid Carcinoma – Liposarcoma –Rabdomyosarcoma – Ranula - Infected Teeth – Radionecrosis of mandibular soft tissues.

Treatment : Various therapeutic measures are available for managing localized carcinomas of the oral cavity, including surgical excision, radiation therapy, electrodesiccation, cryotherapy, laser-beam excision, chemotherapy, and a combination of these methods.

Histopathology:Typical SCC has nests of squamous epithelial cells arising from the epidermis and extending into the dermis. The malignant cells are often large with abundant eosinophilic cytoplasm and a large, often vesicular, nucleus. Variable keratinisation (keratin pearls etc) is present.Typically SCC is graded as: 1-Well differentiated2-Moderately differentiated3-Poorly differentiatedGrading of SCC depends on how easy it is to recognise the characteristics of squamous epithelium (eg. intracellular bridges, keratinisation), pleomorphism and mitotic activity. There is considerable inter-observer variation in grading SCC.

Well Differentiated

Moderately Differentiated

Poorly Differentiated

Thank You

Mohamed Ahmed