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SALIVARY GLAND NEOPLASMS
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STRUCTURAL ELEMENTS OF THE SALIVARY GLAND UNIT
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ETIOLOGY Not fully understood. Two theories predominate: (A) Bicellular stem cell theory (B) Multicellular theory Bicellular stem cell theory : Tumors arise from 1 of 2 undifferentiated stem cell (A) Excretory duct reserve cell-squamous cell and mucoepidermoid carcinomas, (B) Intercalated duct reserve cell- pleomorphic adenomas, oncocytomas, adenoid cystic carcinomas, adenocarcinomas, and acinic cell carcinomas. -
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CONTD Multicellular theory:Each tumor type arises from a specific differentiated cell within the salivary gland unit. Squamous cell carcinomas - excretory duct cells, pleomorphic adenomas -intercalated duct cells oncocytomas -striated duct cells, acinic cell carcinomas -acinar cells.
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RISK FACTORS Radiation –Mucoepidermoid carcinoma(mc among malignant),Warthins (mc among benign) Viral –EBV-lymphoepithelial carcinoma Tobacco smoking- Warthin tumors Increased incidence of second primary tumor in patient with thyroid cancer treated with radioiodine. Controversy:mobile phones- electromagnetic waves-H/N neoplasm
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CONTD. Occupational exposure – Silica dust - 2.5-fold increased risk of cancer Rubber workers( nitrosamines) Iatrogenic-Radiation therapy to the head and neck Latency period - 11 years for malignant tumors and 21.5 years for benign Possible protective effect - Diet high in polyunsaturated fatty acids
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GENETIC ALTERATION AND SALIVARY GLAND NEOPLASM Tumor suppressor genes- p53 family Increased expression- p63 and p73( Benign salivary neoplasms, pleomorphic adenomas, myoepitheliomas, and basal cell adenomas). Overexpression of MDM2(Murine double minute 2 ) along with high-mobility group protein gene (HMGIC) - carcinoma ex pleomorphic adenoma.
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CONTD. PLAG1, translocations,band 8q12-pleomorphic adenomas. Allelic loss of 19q -adenoid cystic carcinoma Mucoepidermoid carcinomas -loss of chromosomal arms 2q, 5p, 12p, and 16q. Increased expression of erb-2 is associated with salivary gland neoplasm.
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CONTD. Matrix metalloproteinase-1, tenascin-C, and beta-6 integrin help in tissue invasion by malignant tumors. In adenoid cystic carcinoma, increased immunoreactivity for nerve growth factor and tyrosine kinase A -correlated with perineural invasion.
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INCIDENCE Relatively uncommon 2% of head and neck neoplasms Distribution Parotid: 80% overall; 80% benign Submandibular: 15% overall; 50% benign Sublingual/Minor: 5% overall; 40% benign
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MINOR SALIVARY GLAND DISTRIBUTION
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PATIENT EVALUATION Clinical Features Both benign or malignant tumors of the parotid gland -painless swelling. Benign tumors have a slow growth rate. A rapid increase in size -suspicion of malignant transformation Mass in the parotid->Metastasis-from skin cancer (melanoma)- >So examination of facial skin and scalp is mandatory.
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EXAMINATION Benign tumors of the parotid gland -usually well-defined, nontender, and freely mobile. Locates in the "tail" of the parotid gland-superficial or deep lobe. Dumbbell tumor :Extend from the superficial to the deep lobe through stylomandibular tunnel. Deep lobe and dumbbell tumor -> parapharyngeal space extension-> medial displacement of oropharyngeal wall
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DUMBBELL TUMOR
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DEEP LOBE TUMORS OF PAROTID
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SUBMANDIBULAR GLAND TUMOR LOCATION Benign tumors of the submandibular gland painless, mobile mass in the submandibular triangle.
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SUSPICION OF MALIGNANCY Facial nerve paresis Ipsilateral weakness or numbness of the tongue indicates involvement the hypoglossal or lingual nerves(malignant tumor of SMG) pain Fixation of the mass to the overlying skin or underlying structures (to the mandible in malignant tumor of SMG) Cervical adenopathy
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SUSPICION OF MALIGNANCY
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FINE-NEEDLE ASPIRATION BIOPSY BENIGN TUMORS: sensitivity -85.5% to 99% specificity -96.3% to 100%. Ultrasound-guided FNAB enhance the overall diagnostic accuracy. MALIGNANT LESION: Accuracy is less in comparision to benign lesion. Sensitivity-60% to 73%
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FNAB MIMICRY Basal cell adenomas- Adenoid cystic carcinoma particularly the solid (anaplastic) type. Mucoepidermoid carcinoma-Benign salivary gland duct obstruction. Large cell epithelial lesions of low nuclear grade: oncocytic proliferations and acinic cell carcinoma.
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IMAGING CT-SCAN MRI-SCAN USG MRI is better than CT(Dental artifacts obscure vital details of gland in CT-scan) Pleomorphic adenoma-calcification (CT-SCAN) Tumor composition better defined in T2 than T1.
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IMAGING CT better than MRI in defining cortical bony involvement Disadvantage of CT-ionizing radiation and requiring contrast for vascular detail. Disadvantage of MRI: Bony-soft tissue interface is often not clearly distinguishable
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Deep lobe tumors Dumb-bell tumors Parotid tumors with facial weakness Indication of malignancy Congenital parotid masses SMG tumors with mandibular fixation Tumors of the palate with suspected involvement of nose or maxillary antra Any tumors with clinically ill defined margins. INDICATIONS OF CT/MR IMAGING MAJOR GLANDS MINOR GLANDS
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MR SCAN SHOWING PLEOMORPHIC ADENOMA OF DEEP LOBE OF PAROTID
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PLEOMORPHIC ADENOMA Most common of all salivary gland neoplasms 70% of parotid tumors 50% of submandibular tumors 45% of minor salivary gland tumors 6% of sublingual tumors 4 th -6 th decades F:M = 1.4:1(overall) 1.7:1(SMG)
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PLEOMORPHIC ADENOMA Slow-growing, painless mass Parotid: 80% in superficial lobe, most in tail of gland Minor salivary gland: most common site- palate. second most common site -upper lip. Other sites – buccal space base of tongue retropharyngeal space pterygopalatine fossa lateral nasal wall nasal septum maxillary bone facial skin trachea lung breast
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PLEOMORPHIC ADENOMA Despite the abundance of minor salivary glands in the lower lip, pleomorphic adenoma is very rare. Pleomorphic adenoma is the most common benign tumor of the lacrimal gland.
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Gross pathology Smooth Well-demarcated Solid Cystic changes Myxoid stroma Capsule:present (major salivary glands) absent (minor salivary glands ) PLEOMORPHIC ADENOMA Histology Mixture of epithelial, myopeithelial and stromal components Epithelial cells: nests, sheets, ducts, trabeculae Stroma: myxoid, chrondroid, fibroid, osteoid Tumor pseudopods
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PLEOMORPHIC ADENOMA GROSS PATHOLOGY
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PLEOMORPHIC ADENOMA Treatment: complete surgical excision Parotidectomy with facial nerve preservation Submandibular gland excision Wide local excision of minor salivary gland Avoid enucleation and tumor spill
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RECURRENT PLEOMORPHIC ADENOMA One fourth of pleomorphic adenomas demonstrate pseudopodia from thin capsules. A cuff of normal tissue should be excised for complete removal of these pseudopods. Failure to remove these pseudopods –a high chance of recurrence. Multicentric pattern is characteristic of recurrent pleomorphic adenoma.
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MR SCAN OF RECURRENT PLEOMORPHIC ADENOMA
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RECURRENT PLEOMORPHIC ADENOMA Progesterone receptors are present. Potential target for hormone treatment. Increased risk for facial nerve injury with revision surgery. Neutron radiotherapy
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BASAL CELL ADENOMA 96% in the parotid gland and 4% in the other salivary glands painless and slow growing. 7 th decade M:F =1:1 Upper lip mc site of the minor salivary gland basal cell adenomas
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BASAL CELL ADENOMA Four histologic growth patterns : solid, trabecular, tubular, and membranous. Basal cell adenoma may be difficult to distinguish from the solid variety of adenoid cystic carcinoma. Treatment is surgical excision with a cuff of normal surrounding tissue
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CANALICULAR ADENOMA 7 th decade F:M – 1.8:1 Most common in minor salivary glands of the upper lip (74%) Painless submucosal mass
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CANALICULAR ADENOMA Histology Tubular structures lined by columnar or cuboidal cells Vascular stroma TREATMENT: Enucleation or surgical excision can be done. Recurrence is rare
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WARTHIN’S TUMOR AKA: papillary cystadenoma lymphomatosum 6-10% of parotid neoplasm M:F=1.5:1 10% bilateral or multicentric 3% with associated neoplasms(mc with Pleomorphic Adenoma) Development:neoplastic proliferation of ectopic salivary gland ducts within intraparotid and periparotid lymph nodes during encapsulation of the parotid gland. T- and B-cell markers positivity support this pathogenetic origin.
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WARTHIN’S TUMOR Gross pathology Encapsulated Smooth/lobulated surface Cystic spaces of variable size, with viscous fluid Solid areas with white nodules representing lymphoid follicles
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WARTHIN’S TUMOR
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Histology Papillary projections into cystic spaces surrounded by lymphoid stroma (Papillary cystadenoma lymphomatosum) Eithelium : double cell layer Luminal cells Basal cells Stroma: mature lymphoid follicles with germinal centers
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WARTHIN’S TUMOR
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Basal cuboidal cells contain small dark nuclei and abundant granular pink cytoplasm (oncocyts). The granular eosinophilia of oncocytes is due to abundant mitochondria present in the cytoplasm. Oncocytes selectively incorporate technetium (Tc)-99m pertechnetate and appear as hot spots on radionucleotide scintigraphy
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(TC)-99M PERTECHNETATE
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WARTHIN’S TUMOR Treatment :surgical excision, parotidectomy with facial nerve preservation.
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ONCOCYTOMA Rare: 2.3% of benign salivary tumors 6 th decade M:F = 1:1 Parotid: 78% Submandibular gland: 9% Minor salivary glands: palate, buccal mucosa, tongue
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ONCOCYTOMA Presentation Enlarging, painless mass Technetium-99m pertechnetate scintigraphy Mitochondrial hyperplasia Gross Encapsulated Homogeneous, smooth Orange/rust color
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ONCOCYTOMA Electronmicroscopy Mitochondrial hyperplasia 60% of cell volume
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ONCOCYTOMA A true oncocytoma contains no lymphoid tissue. Although histologically benign, they have a destructive potential Treatment of choice for benign oncocytomas is surgical excision
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MYOEPITHELIOMA <1% of all salivary neoplasms 3 rd -6 th decades No gender predilection Minor salivary glands > parotid > submandibular gland Presentation: asymptomatic mass
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MYOEPITHELIOMA Histology Spindle cell Uniform, central nuclei Eosinophilic granular or fibrillar cytoplasm Plasmacytoid cell Polygonal Eccentric oval nuclei
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MYOEPITHELIOMA D/D based on histology: plasmacytomas Any tumors with spindle cells neurilemoma fibroma meningioma leiomyoma. Treatment is surgical excision
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SIALOADENOMA PAPILLIFERUM Rare, benign salivary gland tumor Resembles skin tumor syringocystadenoma papilliferum on gross pathologic and microscopic examination. Major and minor salivary glands, men >60 years cell of origin -pluripotential myoepithelial cell.
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SIALOADENOMA PAPILLIFERUM D/D-papillary lesions like squamous papilloma, verrucous hyperplasia, or carcinoma Distinguished from other intraoral minor salivary gland tumors because it is exophytic and not a smooth, mucosa- covered mass. Treatment is surgical excision
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INVERTED DUCTAL PAPILLOMA Originates from the excretory ducts of the minor salivary glands different entity from the inverted oral papilloma M=F Lesions are raised but not ulcerated Treatment is surgical excision
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HEMANGIOMAS Most common tumors of infancy 10% of all births Rapid growth phase -1 to 6 months Involution phase-1 to 12 years. Hemangiogenesis :somatic mutation in one or more components of critical vascular growth-regulatory pathways (VEGFpathway)
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HEMANGIOMAS Both hemangiomas and placental microvessels shows immunoreactivity for Erythrocyte-type glucose transporter GLUT1 Lewis Y antigen Merosin INFERENCE:placenta as a potential site of origin of hemangiomas.
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TREATMENT Steroids -2 to 4 mg/kg per day. Response to steroids is usually immediate and often dramatic. Unfortunately, the response rate to steroids is only 40% to 60%. In such patients, interferon is an option.
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MUCOEPIDERMOID CARCINOMA Most common salivary gland malignancy 5-9% of salivary neoplasms Parotid 45-70% of cases Palate 18% 3 rd -8 th decades, peak in 5 th decade F>M
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MUCOEPIDERMOID CARCINOMA Presentation Low-grade: slow growing, painless mass High-grade: rapidly enlarging, +/- pain **Minor salivary glands: may be mistaken for benign or inflammatory process Hemangioma Papilloma
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MUCOEPIDERMOID CARCINOMA Gross pathology Well-circumscribed to partially encapsulated to unencapsulated Solid tumor with cystic spaces
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MUCOEPIDERMOID CARCINOMA Histology—Low-grade Mucus cell > epidermoid cells Prominent cysts Mature cellular elements
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MUCOEPIDERMOID CARCINOMA Histology— Intermediate- grade Mucus = epidermoid Fewer and smaller cysts Increasing pleomorphism and mitotic figures
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MUCOEPIDERMOID CARCINOMA Histology—High- grade Epidermoid > mucus Solid tumor cell proliferation Mistaken for SCCA Mucin staining
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MUCOEPIDERMOID CARCINOMA Features of high grade mucoepidermoid CA: 1.Four or more mitotic figures per 10 high power fields 2. Neural invasion 3. Necrosis 4. Intracystic component <20% 5. Cellular anaplasia
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MUCOEPIDERMOID CARCINOMA Treatment Influenced by site, stage, grade Stage I & II Wide local excision Stage III & IV Radical excision +/- neck dissection +/- postoperative radiation therapy postoperative irradiation for patients with positive margins, nodal metastasis, and high-grade malignancies.
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ADENOID CYSTIC CARCINOMA Overall 2 nd most common malignancy Most common in submandibular, sublingual and minor salivary glands Perineural invasion(typical) Hard palate-mc site M = F 5 th decade Presentation Asymptomatic enlarging mass Pain, paresthesias, facial weakness/paralysis
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ADENOID CYSTIC CARCINOMA Gross pathology Well-circumscribed Solid, rarely with cystic spaces infiltrative
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ADENOID CYSTIC CARCINOMA Histology— cribriform pattern Most common Good prognosis
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Histology—tubular pattern Layered cells forming duct- like structures Basophilic mucinous substance Intermediate prognosis ADENOID CYSTIC CARCINOMA Histology—solid pattern Solid nests of cells without cystic or tubular spaces poorer prognosis
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ADENOID CYSTIC CARCINOMA Eibling and others found that involvement of nerves with diameters >3 mm correlated with recurrent disease. Exhibits a neurotropic spread, recurrences at the skull base after surgical and radiation treatment. cervical metastases rare Distant metastasis: lung
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ADENOID CYSTIC CARCINOMA Treatment Complete local excision Tendency for perineural invasion: facial nerve sacrifice Postoperative RT Prognosis Local recurrence: 42% Indolent course: 5-year survival 75%, 20-year survival 13%
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RECENT EVIDENCE Epidermal growth factor receptor (EGFR) +vity in 85% tumor EFGR antagonists can be used in case of pts with distant metastasis. VANDETANIB is a small molecule inhibitor of VEGFR-2 and EFGR tyrosine kinase activity. Its antitumor efficacy in vitro and in mouse model has already been proved.
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ACINIC CELL CARCINOMA 2 nd most common parotid malignancy 5 th decade F>M Bilateral parotid disease in 3% Presentation Solitary, slow-growing, often painless mass
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ACINIC CELL CARCINOMA Histologic subtypes solid (38%) microcystic (33%) papillary cystic (25%) follicular (4%),
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ACINIC CELL CARCINOMA Primary treatment is complete surgical resection with neck dissection Postoperative radiation:Not routinely advocated for low- grade malignancies but may be used for advanced or high- grade tumors. Prognosis 5-year survival: 82% 10-year survival: 68% 25-year survival: 50%
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SQUAMOUS CELL CARCINOMA 0.3-1.5%of salivary gland neoplasms 7 th -8 th decades M:F = 2:1 MUST RULE OUT: High-grade mucoepidermoid carcinoma Metastatic SCCA from skin(scalp),aerodigestive tract,ear canal Gross pathology Unencapsulated Ulcerated fixed
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SQUAMOUS CELL CARCINOMA Treatment Radical excision Neck dissection Postoperative RT Prognosis 5-year survival: 24% 10-year survival: 18%
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MALIGNANT MIXED TUMORS Carcinoma ex-pleomorphic adenoma Carcinoma developing in the epithelial component of preexisting pleomorphic adenoma Carcinosarcoma True malignant mixed tumor—carcinomatous and sarcomatous components Metastatic mixed tumor Metastatic deposits of otherwise typical pleomorphic adenoma sixth decade 5% to 12% of salivary gland malignancies
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CARCINOMA EX- PLEOMORPHIC ADENOMA Malignant degeneration can occur in 3% to 7% of pleomorphic adenomas. 6 th -8 th decades Parotid > submandibular > palate Risk of malignant degeneration 1.5% in first 5 years 9.5% after 15 years Presentation Longstanding painless mass that undergoes sudden enlargement
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CARCINOMA EX-PLEOMORPHIC ADENOMA Gross pathology Poorly circumscribed Infiltrative Hemorrhage and necrosis
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CT-SCAN CARCINOMA EX-PLEOMORPHIC ADENOMA
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CARCINOMA EX- PLEOMORPHIC ADENOMA Treatment Radical excision Neck dissection (25% with lymph node involvement at presentation) Postoperative XRT Prognosis Dependent upon stage and histology
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ADENOCARCINOMA Rare 5 th to 8 th decades F > M Parotid and minor salivary glands Presentation: Enlarging mass 25% with pain or facial weakness
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ADENOCARCINOMA Histology Heterogeneity Presence of glandular structures and absence of epidermoid component Variants are Mucinous adenocarcinoma (low grade) Papillary cystadenocarcinoma(low grade) Trabecular adenocarcinoma Clear cell adenocarcinoma Sebacous adenocarcinoma
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ADENOCARCINOMA Histlogical Grade based upon: Mitotic rate Cellular pleomorphism, Stromal invasion Salivary duct variant –worst prognosis Treatment Complete local excision Neck dissection Postoperative XRT
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POLYMORPHOUS LOW- GRADE ADENOCARCINOMA 2 nd most common malignancy in minor salivary glands Palate>lip>buccal mucosa 7 th decade F > M Painless, submucosal mass Histology Isomorphic cells, indistinct borders, uniform nuclei Peripheral “Indian-file” pattern Treatment conservative excision
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LYMPHOMA 1.7% of all salivary neoplasms. parotid >submandibular >minor salivary glands. B-cell lymphpma> T-cell, mucosa-associated lymphoid tissue (MALT)> Hodgkin's lymphomas Sjögren's disease -40 times greater risk primary lymphoma prognosis of primary lymphoma is better than systemic lymphomas Treatment:Chemotherapy except MALTOMA(surgery)
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METASTATIC CANCER Skin of H/N region>Lung >Kidney >Breast >Nasopharynx >Colorectal >Thyroid
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PROGNOSTIC FACTORS IN SALIVARY GLANDS MALIGNANCY Tumor histology Histological grade Anatomic site of origin Clinical stage Age Facial nerve paralysis Experience of the surgeons
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STAGING
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PRINCIPLES OF MANAGEMENT OF BENIGN SALIVARY GLAND NEOPLASMS Small adenomas in the tail of the parotid gland only dissection of the lower division of the facial nerve with removal of the tumor and the surrounding parotid tissue Larger tumors of the superficial lobe -complete superficial parotidectomy. Deep lobe tumors -total parotidectomy with facial nerve preservation. Parapharyngeal tumors -cervical-parotid approach and with or without a mandibulotomy.
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The skin incision is placed in a preauricular crease and extends superiorly to the level of the root of the helix. The incision extends inferiorly around the lobule of ear over the mastoid tip. It gently curves down along the sternocleidomastoid muscle and then slightly forward in a natural skin crease in the upper neck. The preauricular portion of the incision passes on or just inside the tragal margin. The incision is then carried below the lobule of the ear, turns posteriorly over the mastoid, and is then extended within the hairline INCISIONS modified Blair's incision Modified "facelift" incision for parotidectomy
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TYPES OF SURGERY IN MALIGNANT PAROTID TUMOR Superfical parotidectomy Total conservation parotidectomy Total radical parotidectomy Extended Radical parotidectomy
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TOTAL CONSERVATION PAROTIDECTOMY INDICATION: Benign neoplasm of deep lobe. Recurrent pleomorphic adenoma. Certain malignant tumors Facial nerve is preserved.
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Total conservation parotidectomy +Sacrifice of facial nerve. TOTAL RADICAL PAROTIDECTOMY
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SURAL NERVE GRAFT
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EXTENDED RADICAL PAROTIDECTOMY Radical parotidectomy +removal of adjacent structures like ascending ramus of mandible,zygomatic arch,temporalis muscle,sternomastoid muscle(anterior part),EAM and mastoid process. Radical neck dissection is usually performed along with this procedure. Larger defect is closed with PMMF.
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NECK DISSECTION Elective neck dissection for N0 neck indicated in high grade mucoepidermoid carcinoma,SCC and adenocarcinoma of parotid. MND type-1 usually performed.
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PORT AND SURVIVAL
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