The Salivary Glands diseases

Clinical Anatomy of the Salivary Glands

Minor salivary glands

Use of saliva as diagnostic fluid Change in sal composition and flow rate Sialadenitis –Na &Cl secretion increases . Sjol gren syndrome –increased Na Cl cons ,decreased phosphate and IgA is increased. rate of flow is reduced . Cirrhosis liver Ca, K, of protein ,and amylase concentration are increased rate of saliva is also increased.

Cont Xerostomia –flow rare decreased Sialorrhoea Flow rate increased. Salivary IgA is higher in subject with more dental caries. Cystic fibrosis causes decreased secretion with marked increased in salivary Ca from sub lingual ,sub mental and minor salivary glands . Ca and Phosphrous conc in saliva is raised in hyperparathyrodism.

Reactive lesions Mucocele is a clinical term that includes mucus extravasation phenomenon and mucus retention cyst.

Mucocele Etiology Extravasation type Physical-traumatic injury to minor gland excretory duct Mucus extravasation into periductal soft tissue produces a local inflammatory response and granulation tissue “encapsulation.”

Clinical Presentation Lower lip most common site; also buccal mucosa, anterior ventral tongue Painless bluish hue when mucin is near surface Often waxes and wanes in size Microscopic Findings Mucus pool surrounded by granulation tissue Macrophage and neutrophil response to free mucin Focal chronic sialadenitis

Differential Diagnosis Presentation Microscopic findings Differential Diagnosis Hemangioma Pyogenic granuloma Salivary neoplasm Connective tissue neoplasm

Treatment Excision with associated local minor salivary glands Prognosis Occasional recurrence

Mucus Retention Cyst Etiology Represents dilatation of salivary excretory duct due to obstruction Duct obstruction may be due to a mucous plug or sialolith formation

Clinical Presentation Major or minor salivary glands affected in adulthood Asymptomatic, soft mucosal swelling Can occur at any intraoral minor salivary gland site, especially upper lip

Differential Diagnosis Microscopic Findings Thin, dilated, epithelial-lined salivary excretory duct Lining is cuboidal to columnar with occasional mucus-producing cells present Adjacent salivary gland lobules minimally altered but may show obstructive inflammatory changes Diagnosis Microscopic findings Differential Diagnosis Extravasational mucocele Salivary gland neoplasm, especially mucoepidermoid carcinoma

Treatment Prognosis Excision of cyst with adjacent gland(s) Recurrence is rare.

Necrotizing Sialometaplasia Etiology Local ischemic injury of salivary gland lobules May be preceded by trauma or local anesthetic injury, or it may appear spontaneously

Clinical Presentation Both major and minor salivary glands can be affected. Hard palate most common site, usually unilateral Initially a painful to dysesthetic submucosal swelling Ultimately, a central necrotic crater develops. May extend to and involve deep soft tissue and palatal bone

Microscopic Findings Salivary gland inflammation and lobular necrosis (necrosis is not always demonstrable on biopsy) Ductal squamous metaplasia (bland cytology) Lobular architecture of salivary glands persists

Differential Diagnosis Microscopic findings Differential Diagnosis Salivary gland neoplasm Squamous cell carcinoma Granulomatous disease

Treatment Follow-up only Prognosis Excellent

Ranula Etiology Obstruction of the sublingual (usually) or submandibular salivary gland by a sialolith or by trauma Secondary to obstruction, extravasation of saliva into the soft tissue of the floor of the mouth

Clinical Presentation Unilateral, fluctuant, soft tissue mass on the floor of the mouth Usually has a bluish, slightly translucent quality When above the mylohyoid muscle, presentation is intraoral. If extravasation extends below the mylohyoid muscle, a plunging ranula forms. Occlusal radiographs may demonstrate a suspected sialolith.

Clinical picture

Plunging ranula An unusual clinical variant, the plunging or cervical ranula, occurs when the spilled mucin dissects through the mylohyoid muscle and produces swelling within the neck.

Diagnosis Diagnosis Demonstration of sialolith Soft tissue imaging (T2-weighted magnetic resonance image) Aspiration of mucinous salivary fluid Excised tissue with granulation tissue lining around mucin pool

Differential Diagnosis Dermoid cyst Salivary gland tumor Soft tissue tumor Cystic hygroma Thymic cyst

Treatment Treatment Prognosis Marsupialization as an initial procedure Excision of the involved gland (extravasation type) Sialolithectomy (in obstructive type) Prognosis No recurrence with sialadenectomy Recurrence risk with sialolithectomy secondary to duct scarring or reformation of stone

Sialolithiasis Etiology Sialoliths are calcified structures that develop within the salivary ductal system. They are believed to arise from deposition of calcium salts around a nidus of debris within the duct lumen. This debris may include inspissated mucus, bacteria, ductal epithelial cells, or foreign bodies. The cause of sialoliths is unclear, but their formation can be promoted by chronic sialadenitis and partial obstruction. Their development is not related to any systemic derangement in calcium and phosphorus metabolism.

Salivary obstruction from stones, mucous plugs, and mucous extravasation phenomenon.

Clinical Presentation Sialolithiasis can form in all of the salivary glands, including minor salivary glands, but the gland that most commonly produces such stones is the submandibular gland. The so‐called stones that form in the parotid duct system are rarely calcified and are actually mucous plugs that do not appear on radiographs. Stones that form in the submandibular duct system are almost always radiopaque because they are composed of calcium carbonate and calcium phosphate.

C/F They can occur along any part of the duct and are most frequent at anatomic bends. In the submandibular duct, stones are often found at the duct's bend around the posterior edge of the mylohyoid muscle. When sialoliths form, they will obstruct the duct either partially or completely. Therefore, individuals present with a painful swelling of the gland and usually with signs of secondary infection, including a suppurative exudate from the duct, fever, and mild to moderate leukocytosis . Individuals will report an increase in pain and swelling upon eating. The gland will be palpably firm and anywhere from mildly tender to very painful.

ClinicaI presentation

Diagnosis Diagnosis CT scan with 2‐ to 3‐mm cuts to identify the location of the stone. Most obstructed submandibular glands will have both inflammation and fibrosis in a homogeneous pattern throughout the gland.

Differential Diagnosis Calcified lymph nodes from previously resolved tuberculosis Phleboliths (particularly if an old cavernous hemangioma were present) Tonsoliths Calcifications of the carotid bifurcation.

Treatment Treatment Stones that are accessible in the floor of the mouth are removed via a direct approach, and the damaged duct is sutured to the mucosa of the floor of the mouth (sialodochoplasty). Parotid stones usually do not produce a long‐term clinical problem. Most are passed with parotid flow, and a few require removal from the duct with either a repair or duct transposition.

Prognosis Prognosis If the sialolith has been present for a short time, the gland may recover after sialolith removal. If the sialolith is of long standing, the gland may harbor irreversible inflammation and fibrosis, so that it cannot recover even if the sialolith is removed.

Sialorrhea (Sialosis) Etiology Varied; may include idiopathic paroxysmal sialorrhea, parkinsonism, stomatitis (acute), newly inserted oral appliances, expectorants, neostigmine, and others

Clinical Presentation Excess saliva resulting in drooling Angular cheilosis Diffuse parotid/submandibular salivary gland enlargement

Clinical presentation

Diagnosis Diagnosis Direct observation and analysis of history Flow-rate measurement

Treatment Treatment Prognosis Scopolamine If related to medication use, an alternate medication should be chosen, if possible. Prognosis Guarded/indeterminate

Adenomatoid hyperplasia Etiology It is a nonneoplastic enlargement of the minor salivary glands of the hard palate. The cause is unknown, although there is some evidence to suggest that trauma plays a role.

Clinical Presentation The palate is the chief site of involvement of this salivary gland hyperplasia. There is a male predominance, and age ranges from 24 to 63 years. The clinical presentation is a unilateral swelling of the hard and/or soft palate. This lesion is asymptomatic, broad based, and covered with intact mucosa of normal color and quality.

Differential Diagnosis Salivary neoplasms Lymphoma Extension of nasopharyngeal or sinonasal disease into the oral cavity.

Treatment Treatment Prognosis Subsequent to identification by means of an incisional biopsy, no treatment is necessary, given the purely benign nature of this process. Prognosis There is no neoplastic potential.

Sjögren’s Syndrome Etiology An autoimmune disease resulting in exocrine gland dysfunction secondary to mononuclear cell infiltration Increased prevalence of human leukocyte antigen DR/DQ alleles Autoantibody production against nuclear antigens SS-A and SS-B No specific agent identified; postulations include the following: Potential role for viruses/retroviruses as cofactors Possible role of cytokine and hormonal influence on signal transduction and secretion

Clinical Presentation Decrease in exocrine gland function Xerostomia Xerophthalmia/keratoconjunctivitis sicca Salivary and lacrimal gland enlargement (one-third of cases) Secondary effects of exocrine dysfunction are as follows: Dental caries Oral candidiasis Ocular/corneal discomfort Primary form: exocrine dysfunction dominates Secondary form: exocrine dysfunction; other associated autoimmune conditions—usually rheumatoid arthritis, less often lupus erythematosus

Sialography

Diagnosis Diagnosis Demonstration of objective xerostomia and xerophthalmia Serologic demonstration of associated SS-A or SS-B antibodies Correlation of clinical and serologic findings with labial salivary gland biopsy; demonstration of presence of periductal lymphocytic sialadenitis

Differential Diagnosis Differential Diagnosis (Xerostomia/Parotid Gland Swelling) • Sarcoidosis • Depression • HIV- associated • Autonomic neuropathy exocrinopathy • Graft-versus-host disease • Drug side effects • Alcoholism • Lymphoma • Diabetes mellitus • Bulimia

Treatment Directed at associated connective tissue or autoimmune disease Systemic corticosteroids if acute symptoms arise Frequent dental/ophthalmic examinations

Treatment Usually symptomatic and preventative therapies are used, including the following: Reduction of oral dryness Pilocarpine Cemiveline Oral moisturizing agents (saliva substitutes) Gustatory stimulation Ocular moisture replacement Saline Synthetic glycoprotein solutions Carboxymethylcellulose sodium Ocular punctual occlusion

Prognosis Guarded High risk of lymphoma compared with risk in those without autoimmune disease.

Salivary Gland Neoplasms Benign Neoplasms Malignant Neoplasms Controversial Issues

Salivary Gland Neoplasms Diverse histopathology 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

Tumors of the salivary glands Benign tumors. Pleomorphic adenoma Warthins tumors . Basal cell adenoma Canalicular adenoma Oxyphilic adenoam Myepithelial ductul adenoma

Tumors of the salivary glands Malignant tumors ( major and minor salivary glands .} Mucoepidermoid carcinoma . Adenoid cystic carcinoma Malignant mixed tumour Acinic cell carcinaoma.

Pleomorphic adenoma (mixed tumor) More than 50% of all tumors and 90%of benign tumors. Major and minor salivary glands but commonly parotid gland Both epithelial and connective tissue elements so it is mixed tumor. Clinical features Parotid and minor salivary gland tumor of palate,lip.

Pleomorphic Adenoma

Pleomorphic adenoma (mixed tumor) Less frequently affects submandibular glands. Between 4 th to 6 th decade of life . More common in female. Small painless nodule either at the angle on mandible of beneath the ear lobe. Slowly growing ,intermittent growth ,firm in consistency ,well circumscribed encapsulated ,may show area of degenerations.

Pleomorphic adenoma Intra oral pleomorphic adenoma are noticed early because of location on the palate . May show fixity to underlying bone but does not invade the bone. D/D Hyperplastic lymph nodes Neurilemmoma of facial nerve .

Cont- Most common of all salivary gland neoplasms 4th-6th decades 70% of parotid tumors 50% of submandibular tumors 45% of minor salivary gland tumors 6% of sublingual tumors 4th-6th decades F:M = 3-4:1

Pleomorphic Adenoma Slow-growing, painless mass Parotid: 90% in superficial lobe, most in tail of gland Minor salivary gland: lateral palate, submucosal mass Solitary vs. synchronous/metachronous neoplasms

Pleomorphic Adenoma Gross pathology Smooth Well-demarcated Solid Cystic changes Myxoid stroma

Pleomorphic Adenoma Histology Mixture of epithelial, myopeithelial and stromal components Epithelial cells: nests, sheets, ducts, trabeculae Stroma: myxoid, chrondroid, fibroid, osteoid No true capsule Tumor pseudopods

Pleomorphic Adenoma

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. Irradiation is contra indicated. (radio resistant

Warthin’s Tumor AKA: papillary cystadenoma lymphomatosum 6-10% of parotid neoplasms Older, Caucasian, males 10% bilateral or multicentric 3% with associated neoplasms Presentation: slow-growing, painless mass

Warthin’s Tumor Gross pathology Encapsulated Smooth/lobulated surface Cystic spaces of variable size, with viscous fluid, shaggy epithelium Solid areas with white nodules representing lymphoid follicles

Warthin’s Tumor Histology Papillary projections into cystic spaces surrounded by lymphoid stroma Epithelium: double cell layer Luminal cells Basal cells Stroma: mature lymphoid follicles with germinal centers

Warthin’s Tumor

Oncocytoma Rare: 2.3% of benign salivary tumors 6th decade M:F = 1:1 Parotid: 78% Submandibular gland: 9% Minor salivary glands: palate, buccal mucosa, tongue

Oncocytoma Presentation Technetium-99m pertechnetate scintigraphy Enlarging, painless mass Technetium-99m pertechnetate scintigraphy Mitochondrial hyperplasia

Oncocytoma Gross Histology Encapsulated Homogeneous, smooth Orange/rust color Histology Cords of uniform cells and thin fibrous stroma Large polyhedral cells Distinct cell membrane Granular, eosinophilic cytoplasm Central, round, vesicular nucleus

Oncocytoma Electron microscopy: Mitochondrial hyperplasia 60% of cell volume

Monomorphic Adenomas Basal cell, canalicular, sebaceous, glycogen-rich, clear cell Basal cell is most common: 1.8% of benign epithelial salivary gland neoplasms 6th decade M:F = approximately 1:1 Caucasian > African American Most common in parotid

Basal Cell Adenoma Solid Most common Solid nests of tumor cells Uniform, hyperchromatic, round nuclei, indistinct cytoplasm Peripheral nuclear palisading Scant stroma

Basal Cell Adenoma Trabecular Cells in elongated trabecular pattern Vascular stroma

Basal Cell Adenoma Tubular Multiple duct-like structures Columnar cell lining Vascular stroma

Basal Cell Adenoma Membranous Thick eosinophilic hyaline membranes surrounding nests of tumor cells “jigsaw-puzzle” appearance

Monomorphic Adenomas Canalicular adenoma 7th decade F:M – 1.8:1 Most common in minor salivary glands of the upper lip (74%) Painless submucosal mass

Canalicular Adenoma Histology Well-circumscribed Multiple foci Tubular structures line by columnar or cuboidal cells Vascular stroma

Myoepithelioma <1% of all salivary neoplasms 3rd-6th decades F>M Minor salivary glands > parotid > submandibular gland Presentation: asymptomatic mass

Myoepithelioma Histology Spindle cell Plasmacytoid cell More common Parotid Uniform, central nuclei Eosinophilic granular or fibrillar cytoplasm Plasmacytoid cell Polygonal Eccentric oval nuclei

Mucoepidermoid Carcinoma Most common salivary gland malignancy 5-9% of salivary neoplasms Parotid 45-70% of cases Palate 18% 3rd-8th decades, peak in 5th decade F>M Caucasian > African American

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 Tori

Mucoepidermoid Carcinoma Gross pathology Well-circumscribed to partially encapsulated to unencapsulated Solid tumor with cystic spaces

Mucoepidermoid Carcinoma Histology—Low-grade Mucus cell > epidermoid cells Prominent cysts Mature cellular elements

Mucoepidermoid Carcinoma Histology—Intermediate- grade Mucus = epidermoid Fewer and smaller cysts Increasing pleomorphism and mitotic figures

Mucoepidermoid Carcinoma Histology—High-grade Epidermoid > mucus Solid tumor cell proliferation Mistaken for SCCA Mucin staining

Mucoepidermoid Carcinoma Treatment Influenced by site, stage, grade Stage I & II Wide local excision Stage III & IV Radical excision +/- neck dissection +/- postoperative radiation therapy

Adenoid Cystic Carcinoma Overall 2nd most common malignancy Most common in submandibular, sublingual and minor salivary glands M = F 5th decade Presentation Asymptomatic enlarging mass Pain, paresthesias, facial weakness/paralysis

Adenoid Cystic Carcinoma Gross pathology Well-circumscribed Solid, rarely with cystic spaces infiltrative

Adenoid Cystic Carcinoma Histology—cribriform pattern Most common “swiss cheese” appearance

Adenoid Cystic Carcinoma Histology—tubular pattern Layered cells forming duct-like structures Basophilic mucinous substance Histology—solid pattern Solid nests of cells without cystic or tubular spaces

Adenoid Cystic Carcinoma Treatment Complete local excision Tendency for perineural invasion: facial nerve sacrifice Postoperative XRT Prognosis Local recurrence: 42% Distant metastasis: lung Indolent course: 5-year survival 75%, 20-year survival 13%

Acinic Cell Carcinoma 2nd most common parotid and pediatric malignancy 5th decade F>M Bilateral parotid disease in 3% Presentation Solitary, slow-growing, often painless mass

Acinic Cell Carcinoma Gross pathology Well-demarcated Most often homogeneous

Acinic Cell Carcinoma Histology Solid and microcystic patterns Most common Solid sheets Numerous small cysts Polyhedral cells Small, dark, eccentric nuclei Basophilic granular cytoplasm

Acinic Cell Carcinoma Treatment Prognosis Complete local excision +/- postoperative XRT Prognosis 5-year survival: 82% 10-year survival: 68% 25-year survival: 50%

Adenocarcinoma Rare 5th to 8th decades F > M Parotid and minor salivary glands Presentation: Enlarging mass 25% with pain or facial weakness

Adenocarcinoma Histology Heterogeneity Presence of glandular structures and absence of epidermoid component Grade I Grade II Grade III

Adenocarcinoma Treatment Prognosis Complete local excision Neck dissection Postoperative XRT Prognosis Local recurrence: 51% Regional metastasis: 27% Distant metastasis: 26% 15-year cure rate: Stage I = 67% Stage II = 35% Stage III = 8%

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

Carcinoma Ex-Pleomorphic Adenoma 2-4% of all salivary gland neoplasms 4-6% of mixed tumors 6th-8th 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

Carcinoma Ex-Pleomorphic Adenoma Gross pathology Poorly circumscribed Infiltrative Hemorrhage and necrosis

Carcinoma Ex-Pleomorphic Adenoma Histology Malignant cellular change adjacent to typical pleomorphic adenoma Carcinomatous component Adenocarcinoma Undifferentiated

Carcinoma Ex-Pleomorphic Adenoma Treatment Radical excision Neck dissection (25% with lymph node involvement at presentation) Postoperative XRT Prognosis Dependent upon stage and histology

Carcinosarcoma Rare: <.05% of salivary gland neoplasms 6th decade M = F Parotid History of previously excised pleomorphic adenoma, recurrent pleomorphic adenoma or recurring pleomorphic treated with XRT Presentation

Carcinosarcoma Gross pathology Poorly circumscribed Infiltrative Cystic areas Hemorrhage, necrosis Calcification

Carcinosarcoma Histology Biphasic appearance Sarcomatous component Dominant chondrosarcoma Carinomatous component Moderately to poorly differentiated ductal carcinoma Undifferentiated

Carcinosarcoma Treatment Prognosis Radical excision Neck dissection Postoperative XRT Chemotherapy (distant metastasis to lung, liver, bone, brain) Prognosis Poor, average survival less than 2 ½ years

Squamous Cell Carcinoma 1.6% of salivary gland neoplasms 7th-8th decades M:F = 2:1 MUST RULE OUT: High-grade mucoepidermoid carcinoma Metastatic SCCA to intraglandular nodes Direct extension of SCCA

Squamous Cell Carcinoma Gross pathology Unencapsulated Ulcerated fixed

Squamous Cell Carcinoma Histology Infiltrating Nests of tumor cells Well differentiated Keratinization Moderately-well differentiated Poorly differentiated No keratinization

Squamous Cell Carcinoma Treatment Radical excision Neck dissection Postoperative XRT Prognosis 5-year survival: 24% 10-year survival: 18%

Polymorphous Low-Grade Adenocarcinoma 2nd most common malignancy in minor salivary glands 7th decade F > M Painless, submucosal mass Morphologic diversity Solid, glandular, cribriform, ductular, tubular, trabecular, cystic

Polymorphous Low-Grade Adenocarcinoma Histology Isomorphic cells, indistinct borders, uniform nuclei Peripheral “Indian-file” pattern Treatment Complete yet conservative excision

Clear Cell Carcinoma AKA glycogen-rich Palate and parotid 6th-8th decade M = F Histology Uniform, round or polygonal cells Peripheral dark nuclei Clear cytoplasm Treatment Complete local excision

Epithelial-Myoepithelial Carcinoma < 1% of salivary neoplasms 6th-7th decades, F > M, parotid ? Increased risk for 2nd primary Histology Tumor cell nests Two cell types Thickened basement membrane Treatment Surgical excision

Undifferentiated Carcinoma Lymphoepithelial Eskimos: parotid, F > M, familial Asian: submandibular, M > F Large-cell Bimodal peaks M > F Parotid Small-cell 6th-7th decades M:F = 1.6:1 parotid

Controversial Issues Management of the N0 Neck Recurrence in the neck = low likelihood of salvage Parotid: clinical neck disease, 16% N- disease = 74% 5-year survival N+ disease = 9% 5-year survival Submandibular: clinical neck disease, 8% N- disease = 41% 5-year survival

Management of the N0 Neck Increase risk of occult neck metastasis **High-grade malignancies **Advanced primary tumor stage (T3-T4) High risk histology Undifferentiated, SCCA, adenocarcinoma, high-grade mucoepidermoid, salivary duct carcinoma Tumor size > 3cm Patient > 54 years of age Facial paralysis Extracapsular, perilymphatic spread

Management of the N0 Neck Neck Dissection Advantages Pathologic staging Improved counseling and prediction of prognosis Disadvantages Longer OR time, increase complications, increased cost Functional deficits, cosmetic effects Type Parotid: levels II-IV Submandibular: levels I-III

Management of the N0 Neck Radiation Therapy Advantage Avoids surgical sequlae Disadvantages Radiation effect on normal tissue Radiation induced malignancies Proponents argument: the same factors that increase the risk of occult neck disease also increase the risk for local recurrence and necessitate postoperative XRT to the primary so it is reasonable to treat the neck with XRT as well

Fine-Needle Aspiration Biopsy Efficacy is well established Accuracy = 84-97% Sensitivity = 54-95% Specificity = 86=100% Safe, well tolerated

Fine-Needle Aspiration Biopsy Opponents argument: Doesn’t change management Surgery regardless of reported diagnosis Obscuring final pathologic diagnosis Frequency of “inadequate” sampling, requires multiple biopsies, prolongs course until definitive treatment, increases cost

Fine-Needle Aspiration Biopsy Proponent’s argument: Important to distinguish benign vs. malignant nature of neoplasm Preoperative patient counseling Surgical planning Differentiate between neoplastic and non-neoplastic processes Avoid surgery in large number of patients

Bicellular Theory Intercalated Ducts Excretory Ducts Pleomorphic adenoma Warthin’s tumor Oncocytoma Acinic cell Adenoid cystic Excretory Ducts Squamous cell Mucoepidermoid

Multicellular Theory Striated duct—oncocytic tumors Acinar cells—acinic cell carcinoma Excretory Duct—squamous cell and mucoepidermoid carcinoma Intercalated duct and myoepithelial cells—pleomorphic tumors

Tumorigenesis Contradictory evidence: Luminal cells are readily capable of replication Acinar cells participate in gland regeneration Immunohistochemical staining of S-100 protein Present in many salivary gland neoplasms Not present in normal ductal cells

Conclusions Hugely diverse histopathology Accurate pathologic diagnosis does influence management Relatively rare malignancies Utilize preoperative studies when indicated Don’t believe everything you read!