Salivary gland pathology

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Oral Pathology II
Forth Year

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Salivary gland pathology

  1. 1. Februray 29, 2009 Salivary Glands Classification, General Considerations & Tumors Like Conditions By Louay Jaber DDS, MSc, MSD, PhD
  2. 2. The Normal Salivary Gland  The system is comprised of major & minor salivary glands    Major: Parotid, submandibular & sublingual. Minor: They produce the fluid that constitute oral saliva    Parotid: serous Submandibular: serous & mucous Sublingual: mucous & serous     Palate: mucous Tongue: mucous & serous Lip: mucous Buccal mucosa: mucous Oral mucosa Acinus Intercalaetd-Striated-Excretory “ducts”
  3. 3. The Normal Salivary Gland (Cont.) “Parotid gland” Lymph node Serous Acini & striated duct Facial nerve
  4. 4. The Normal Salivary Gland (Cont.) “Submandibular, sublingual & minor glands” Submandibular Sublingual Minor
  5. 5. Mucocele 70% in the lower lip  The remainders   floor of the mouth, tongue & buccal mucosa Third decades of life  Men > women (slight)  Small dome-shaped swelling  Size 0.2-1.0 cm  Mucoceles of the floor of the mouth can be a large size (several centimeters-Ranula)  Mucocele Ranula
  6. 6. Mucocele     Pts might report a fluctuation in size related to meals or rupture They are generally soft & fluctuant (older becomes firmer) They are painless They develop rapidly within hours to days Ruptured mucocele Mucocele
  7. 7. Mucocele Microscopically Pool of mucus  It is a rounded pool of mucus within fibrous connective tissue  Inflammatory reaction (Macrophages that contain phagocytized mucus) Phagocytic macrophages
  8. 8. Mucus Retention Cyst  Etiology: It results from obstruction of salivary flow because of sialolith, periductal scar or impinging tumor  Clinical features: it is commonly found in the upper lip, palate, cheek and floor of the mouth. It represents asymptomatic swelling Microscopically  Retention cyst: Epithelial-lined fibrous tissue wall surrounds the mucus pool  Little or no inflammatory reaction (no epithelial rupture Cuboidal epithelium
  9. 9. Ranula    It is a clincial term that includes mucus extravasation phenomenon and mucus retention cyst Occur specifically in the floor of t he mouth Etiology:  Trauma & ductal obstruction   Clinical features:   Sialolith: represents precipitation of calcium salts around the central nidus of cellular debris it is fluctuant, unilateral soft tissue mass in the floor of the mouth Histopathology:  It is similar to mucus retention cyst
  10. 10. Necrotizing Sialometaplasia       Clinically It is a reactive inflammatory condition of the salivary glands Average age is 46 years Male predominence 2:1 Palatal location preference Deep crater-like ulcer, develops rapidly & slow to heal Size 1-5 cm. Unilateral ulcer of necrotizing sialometaplasia
  11. 11. Necrotizing Sialometaplasia  Pathogenesis: Ischemic necrosis or infarction       Traumatic injury Dental injection Denture use Adjacent tumor & cyst Surgery Upper respiratory infection or allergy Swelling but no ulceration of necrotizing sialometaplasia
  12. 12. Necrotizing Sialometaplasia  Histologically The principle characteristics are:     Lobular coagulative necrosis of acini Squamous metaplasia of ducts Pseudoepitheliomatous hyperplasia inflammation Acini necrosis Necrotizing sialometaplasia
  13. 13. Necrotizing Sialometaplasia Necrotic mucous acini & mild inflammatory infiltrate Squamous metaplasia (ducts)
  14. 14. Infectious Conditions  Mumps:  It is an infectious , acute viral sialadenitis primarily affected the parotid glands  It is the most common salivary gland diseases  Etiology:  The causative agent is a paramyxovirus  2-3 weeks incubation period  Transmission by direct contact with salivary droplets
  15. 15. Mumps  Clinical features:  Fever  Malaise  Headache  Chills  Preauricular pain  Parotid swelling  Male = female  Young adults & children
  16. 16. Mumps  Complications:  Serious complication in adults can occur:  Oophoritis  Orchitis  Widspread involvement can include  Liver  Pancreas  Kindney  Nervous system
  17. 17. Mumps  Differential diagnosis  Bacterial infection (suppurative parotitis)  Salivary calculi  Lymphoma  Lymphoepithelial lesion  Metabolic diseases
  18. 18. Mumps  Treatment & Prognosis  Symptomatic therapy  Bed rest  Analgesics  Corticosteroids (variable success)  Vaccination is now available
  19. 19. Metabolic Conditions Sialadenosis  It is non-neoplastic & non-inflammatory salivary gland enlargement  It is related to metabotic factor or secretory dysfunction Painless bilateral swellings Peak incidence: 5th & 6th decades of life  Slight female predominence  Swelling develops slowly, painless & accompanied by decreasing salivary secretion  
  20. 20. Metabolic Conditions Sialadenosis  It is usually associated with systemic conditions:      Diabetes mellitus Malnutrition Liver cirrhosis (Chronic Alcoholism) Hyperlipidemia Acromegaly Enlargement of parotid associated with chronic alcoholism & liver cirrhosis
  21. 21. Metabolic Conditions Sialadenosis Microscopically  As the disease persistsAtrophy of the paranchymal tissue but compensatory increase in the amount of adipose tissue  Inflammatory cell infiltrates are absent Atrophy of parotid parenchymal tissue & increase of intraglandular fat
  22. 22. Sjögren Syndrome  It is the expression of an autoimmune process that principally results in  Rheumatoid arthritis  Dry eyes (keratoconjunctivitis sicca)  Dry mouth (xerostomia)  Lymphocytic replacement of lacrimal and salivary glands
  23. 23. Sjögren Syndrome   Clinical features:  Peak age: 50 yo  Parotid gland enlargment Treatment:  Artificial saliva and tears & preventive oral measures
  24. 24. Sjögren Syndrome Focal aggregates of lymphocytes, periductal lymphocytes & dilated ducts
  25. 25. Mixed Tumors “Pleomorphic Adenoma”  It is the most common benign neoplasm of salivary glands origin  It represents 45-74% of all salivary gland tumors  Slow growing & asymptomatic,  Average age is about 43 yo.  Recurrent lesion occurs as multiple nodules & are less mobile than initial lesion.
  26. 26. Mixed Tumors “Pleomorphic Adenoma”  CT revealed a mixed tumor medial to the mandibular ramus  It has prominent cartilagenous & osseous elements that led initially to diagnosis of osteochondroma
  27. 27. Mixed Tumors “Pleomorphic Adenoma”  The most common intraoral site is the palate followed by the upper lip & buccal mucosa  Mobility is limited for palatal tumors.  Large intraoral tumors are susceptible to trauma
  28. 28. Mixed Tumors “Pleomorphic Adenoma” Submandibular Small glistening capsular surface  Gross finding: It is irregular round to ovoid mass & well defined borders Parotid Homogeneous tan or tan white surface
  29. 29. Mixed Tumors “Pleomorphic Adenoma” Gross findings Translucent central zone represents myxochondroid tissue The presence of multiple individual nodules are typical of recurrent mixed tumor
  30. 30. Mixed Tumors “Pleomorphic Adenoma” Microscopic findings  Composed of epithelial & mesenchymal like tissue  Present or absent of fibrous capsule
  31. 31. Mixed Tumors “Pleomorphic Adenoma” Cystic degeneration Prominent osseous differentiation in mixed tumor Epithelial cell in mixed tumor Cytokeratin immunoteactivity in epithelial cells
  32. 32. Mixed Tumors “Pleomorphic Adenoma” Microscopic findings  In the absence of surgical intervention, viable epithelial cells within necrotic tissue suggest a malignant transformation  Rarely tumor cells are seen within vascular spaces
  33. 33. Mixed Tumor “Treatment”  Parotidectomy & excision of the scar tissue with preservation of the facial nerve are recommended (specially recurrent)  Long term follow up is recommended more than 5 years  The risk of malignant degeneration increases with time  Radiotherapy has been found by some investigators to be useful in some recurrent mixed tumor
  34. 34. Carcinoma Ex-Mixed Tumor “Clinical Features”  It arises from a benign mixed tumor (diagnosis requires identification of mixed tumor)  20% of patients had previous operation for mixed tumor  The risk for malignant transformation correlates with the duration of mixed tumor  Painless mass or sometimes associated with facial nerve pain or palsy  Tumor is freely movable or sometime fixed to underlying tissue (especially with recurrent tumors)
  35. 35. Carcinoma Ex-Mixed Tumor “Microscopic Findings” Capsular invasion Myxochondoid bening elements & carcinomatous elements
  36. 36. Carcinoma Ex-Mixed tumor “Treatment”  38-53% develop recurrence  Distant metastasis to lung, bone, brain, liver & subcutaneous tissue  Radiotherapy alone has proven ineffective, although it may have a beneficial role when combined with surgery
  37. 37. Basal Cell Adenoma   It is composed of cells predominantly of one type Basal cell adenoma:  Occurs mainly in parotid  Slow growing & painless  Can be multinodular  Age 35-80  Male predominence Well circumscribed mass near the inferior pole of the parotid
  38. 38. Basal Cell Adenoma Solid Trabecular Solid
  39. 39. Basal Cell Adenoma Immunostaining for cytokeratin Histology: Ultrastructure shows ductal cells
  40. 40. Basal Cell Adenoma Basal cell adenoma usually lack cribriform pattern Histology: Adenoid cystic carcinoma with clear cytoplasm & angular nuclei
  41. 41. Basal Cell Adenoma  Treatment & prognosis: Conservative surgical excision including a margin of normal uninvolved tissue  Prognosis is good and recurrence rate is so low  Small cells in the periphery of the epithelial islands And larger cells adjacent to the tumor islands
  42. 42. Malignant Epithelial Tumors “Mucoepidermoid Carcinoma”  It is the most common malignant salivary glands tumor  It represents 15.5% of all benign & malignant tumors at all sites resemble a mucoceles. Size varies from 1-12cm  
  43. 43. Mucoepidermoid Carcinoma  It is believed to arise from salivary duct system Normal duct-lining epithelium Neoplastic transformation
  44. 44. Mucoepidermoid Carcinoma  Ionizing radiation increases the risk for its developing  Occurrence:   7% Submandibular gland  1% Sublingual gland   45% Parotid gland 21% in the palate and 19% for the rest of the minor salivary glands. Mean age is about 47 years with the age range between 8 to 92 yo.  Women > men
  45. 45. Mucoepidermoid Carcinoma  Typically, it is a solitary painless mass  2/3 of pts. are asymptomatic  if growing rapidly, usually accompanied with pain & mucosal ulceration, and sometimes a discharge of fluid resemble abscess.  6 years average between onset & diagnosis (high grade lesions demonstrate a 1.5-year interval before diagnosis).
  46. 46. Mucoepidermoid Carcinoma  According to cytologic features, it is divided into: - Low - Intermediate - High grade types.  All grades of this neoplasm are carcinomas and have the potential to metastasize.  They are epithelial mucin-producing tumor
  47. 47. Mucoepidermoid Carcinoma (Central)   This lesion may also arise centrally within the mandible (Differential diagnosis: giant cell granuloma & odontogenic tumors).  Asymptomatic radiolucencies  Mandibule > maxilla  Third molar region is the most likely to be involved
  48. 48. Mucoepidermoid Carcinoma (Central) It arises from either: Ectopic salivary gland tissue Neoplastic transformation of epithelial lining of odontogenic cysts Glandular odontogenic cyst Mayer’s mucicarmine stain highlights numerous mucus cells in a dentigerous cyst
  49. 49. Mucoepidermoid Carcinoma  Treatment & Prognosis:  low grade usually follow a benign course. However, in several instances low grade lesions have metastasize widely.  High grade metastasize widely (60% of cases).  Surgical, or surgery plus postoperative radiotherapy (high grade)  Central mucoepidermoid carcinoma is usually of low grade (40% recurrence rate).
  50. 50. Adenoid Cystic Carcinoma Oral mucosa overlying this palatal mucosa is ulcerated Clinical Features  50-70% starts in the minor salivary glands.  If major salivary gland (parotid is the most affected)  Age: 5th and 7th decades This tumor appears deceptively well circumscribed
  51. 51. Adenoid Cystic Carcinoma  No gender predilection  (slight female predominance).  Unilocular mass  Firm on palpation  Occasional pain or tenderness  Slow growth rate  Bone invasion occurs  Lung metastasis Sublingual gland tumor.
  52. 52. Adenoid Cystic Carcinoma  Treatment & prognosis:  Surgery is the treatment of choice  Radical resection is justified to obtain surgical margins that are free of tumor  Multiple-agent chemotherapy showed some promise for postoperative treatment  High recurrence rate
  53. 53. Acinic Cell Carcinoma Clinical features  Age: 5th to 6th decades of life  No gender predilection  It represents 14% of parotid gland tumor  9% of total salivary gland carcinoma of all sites  50% of cases, the clinical appearance is a benign lesion
  54. 54. Acinic Cell Carcinoma    Usually less than 3 cm in diameter Pain The interval between the initial appearance & treatment is 6 months to 5 years The origin is the ductal cells
  55. 55. Acinic Cell Carcinoma  Treatment & prognosis:  Surgery is the preferred treatment  Seldom metastasize  Tendency to recur
  56. 56. Polymorphous Low-Grade Adenocarcinoma        It is considered to be low grade malignancy and low risk of metastasis Age: 5th to 8th decades No gender predilection Occurs in minor salivary glands (palate) Firm, non-ulcerated & non tender Size between 1-4 cm Slow growth Well circumscribed mass at the junction of the hard & soft palate
  57. 57. Polymorphous Low-Grade Adenocarcinoma Partially circumscribed but lack encapsulation
  58. 58. Polymorphous Low-Grade Adenocarcinoma  Treatment & prognosis:   Conservative surgical excision Prognosis is good
  59. 59. Carcinoma Ex-Mixed Tumor “Microscopic Findings” The carcinomatous elements appeared separated from benign element Apparent malignant transformation
  60. 60. Carcinomatous & benign Components of ExMixed  w
  61. 61. Mucoepidermoid Carcinoma  Fluctuant because of cyst formation Mucin filled cystic spaces
  62. 62. Mucoepidermoid Carcinoma   Microscopic features: The name is a contraction of epidermoid and mucus-secreting carcinoma A close association of mucous & epidermoid cells Mayer’s mucicarmine hightlights the extracellular & Intracytoplasmic mucin
  63. 63. Mucoepidermoid Carcinoma Mucoepidermoid carcinoma incites secondary lymphoid proliferation The lymphoid response extends along the periphery of the tumor
  64. 64. Mucoepidermoid Carcinoma Low grade. Note Intracystic spaces Intermediate grade. hyperchromatic nuclei & several microcystic spaces High grade Focal necrosis
  65. 65. Epidermoid & mucus cells Epidermoid cells solid & infiltrative Central Mucoepidermoid Carcinoma Cyst Solid & cystic neoplastic area Characteristic variety of cell types
  66. 66. Adenoid Cystic Carcinoma Tubular pattern in the top & bottom. A cribriform pattern in the center Epithelial cells have a clear Cytoplasm, poorly defined border & irregular shaped nuclei Immunoreactivity of the tumor cells for cytokeratin
  67. 67. Adenoid Cystic Carcinoma Mitotic figures The tumor appears well circumscribed Myoepithelial & ductal cells
  68. 68. Adenoid Cystic Carcinoma Neural invasion Comedo-type necrosis
  69. 69. Acinic Cell Carcinoma  Well differentiated acinar cell  Cytoplasmic granules.  Slightly basophilic cytoplasm  Eccentricaly located nuclei Acinar cells
  70. 70. Acinic Cell Carcinoma Papillary cystic growth pattern Follicular pattern
  71. 71. Acinic Cell Carcinoma Cluster of neoplastic epithelial cells & numerous electron dense cytoplasmic granules
  72. 72. Polymorphous Low-Grade Adenocarcinoma The nuclei are round or ovoid & have a slightly irregular contour Tumor cells are often concentrically arranged
  73. 73. October 11, 2005 Oral Pathology II 0701441 Connective Tissue Lesions
  74. 74. Connective Tissue Lesions  Fibrous lesions:  Reactive hyperplasia: Fibrous hyperplasia or exuberant proliferation of granulation tissue  Peripheral fibroma  Generalized gingival hyperplasia  Denture induced fibrous hyperplasia  Neoplasms: heterogeneous that form complex collection of disease  Myxoma  Fibrosarcoma
  75. 75. Connective Tissue Lesions “Fibrous Lesions”  Peripheral fibroma  Etiology: Reactive (secondary to overexuberant repair)  Origin: Connective tissue of the submucosa  Clinical features:  Predilection for young adults  Female>male  Location: commonly at the gingiva anterior to molars  Similar in color to the surrounding tissue
  76. 76. Connective Tissue Lesions “Fibrous Lesions”  Peripheral Odontogenic fibroma
  77. 77. Connective Tissue Lesions “Fibrous Lesions”  Focal fibrous hyperplasia:  It is common in frequently traumatized area
  78. 78. Connective Tissue Lesions “Fibrous Lesions”  Peripheral fibroma  Histopathology:  Focal fibrous hyperplasia: Highly collagenous and relatively avascular  Mild to moderate inflammatory cell infiltrate  Subtypes:  Peripheral ossifying fibroma  Peripheral odontogenic fibroma  Giant cell fibroma  Differential diagnosis: Pyogenic granuloma & peripheral giant cell granuloma  Treatment: Local excision
  79. 79. Connective Tissue Lesions “Fibrous Lesions”  Peripheral Ossifying Fibroma
  80. 80. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:  Definition: Overgrowth of the gingiva  Etiology:  Non-specific: Response to chronic inflammation associated with local factor  Hormonal changes (imbalance)  Drugs (Phenytoin, Cyclosporine, Nifidipine)  Leukemia
  81. 81. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:  Clinical features: Increase in the bulk of free and attached gingiva.     Stippling is lost Color: red to blue Associated inflammation: non-specific factors & hormonal imbalance appears more inflamed than drug induced hyperplasia Histopathology:      Abundance in collagen Increased number of fibroblasts Various degree of chronic inflammation Increased capillaries (hormonal) Immature & atypical white blood cells with leukemic type
  82. 82. Connective Tissue Lesions “Fibrous Lesions”  Gingival fibromatosis
  83. 83. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:   Treatment: Attentive oral hygiene is necessary Gingivoplasty or gingivectomy in combination with prophylaxis
  84. 84. Connective Tissue Lesions “Fibrous Lesions”  Denture-induced fibrous hyperplasia  Etiology: Chronic trauma produced by an ill-fitting denture  Clinical features: Occurs in the vestibular mucosa  Overexuberant fibrous connective tissue reparative response  Painless folds of fibrous tissue  Treatment: Surgical excision is usually required
  85. 85. Epulis Fissuratum
  86. 86. Connective Tissue Lesions “Fibrous Lesions”  Neoplasms:  Myxoma: Benign proliferation of spindle cells  Clinical features: It is a soft neoplasms composed of gelatinous material  Slow growing  Asymptomatic  Location: Palate  Occurs at any age Soap bubble multilocular area
  87. 87. Connective Tissue Lesions “Fibrous Lesions”  Myxoma:  Histopathology:  Not encapsulated (may exhibit infiltration into surrounding soft tissue)  Dispersed stellate & spindle-shaped fibroblasts  Loose myxoid stroma
  88. 88. Connective Tissue Lesions “Fibrous Lesions”  Myxoma:  Treatment: Surgical excision  Recurrence is not uncommon
  89. 89. Pluripotential Mesenchymal Stem Cells
  90. 90. Connective Tissue Lesions “Fibrous Lesions”  Fibrosarcoma: It is a malignant spindle cell tumor showing interlacing fascicular pattern  Clinical features  Can arise in bone  Young adults most commonly affected  It is considered as infiltrative neoplasms
  91. 91. Connective Tissue Lesions “Fibrous Lesions”  Fibrosarcoma:  Histopathology:  Collagen sparse  Frequent mitotic figures  Ill defined periphery
  92. 92. Connective Tissue Lesions “Fibrous Lesions”  Treatment of Fibrosarcoma  Wide surgical excision  Recurrence is not uncommon  Metastasis is infrequent  5 years survival rate is 3050%
  93. 93. Vascular Lesion   Reactive & Congenital Lesions Lymphangioma   Etiology:  It is regarded as congenital lesion  Appears within the first 2 decades of life Clinical features:  Painless nodular, vesicle like swelling  Crepitant sound  Tongue is the most common intraoral site
  94. 94. Vascular Lesion  Histopathology:  Endothelium-lined lymphatic channels  Eosinophilic lymph that occasionally include red blood cells  Lymphatic channels directly adjacent to overlying epithelium  Treatment: Surgical removal but because of lack of encapsulation, recurrences are common
  95. 95. Vascular lesion   Neoplasms: Angiosarcoma  It is a neoplasm of endothelial cell origin  Scalp is the usual location  The lesion consists of an unencapsulated proliferation of endothelial cells enclosing irregular luminal spaces  It has an aggressive clinical course and poor prognosis
  96. 96. Neural lesions   Reactive lesion: Traumatic neuroma:  Etiology: It is caused by injury of peripheral nerve  Oral surgery procedure  Local anesthetic injection  Accident  Clinical features:  Pain  Wide age range  Mental foramen is the most common location
  97. 97. Neural lesion  Traumatic neuroma (Cont.)  Histopathology:  Bundles of nerves admixed with dense collagenous fibrous tissue  Treatment: Surgical excision
  98. 98. Neural Lesion  Neoplasms:  Granular cell tumors  Etiology: It is an uncommon benign tumor of unknown cause  The granular cell that make this tumor is believed to originate from Schwann cells Clinical features:  Wide age range  Tongue is the most common location  Uninflamed asymptomatic mass  < 2 cm in diameter  Overlying epithelium is intact 
  99. 99. Neural lesion   Neoplasms: Granular cell tumors  Histopathologically:  Unencapsulated sheets of large polygonal cells with pale granular or grainy cytoplasm  Pseudoepitheliomatous hyperplasia   Treatment: Surgical removal
  100. 100. Neural lesion   Neoplasms: Schwannoma:   Etiology: It is derived from schwann cells Clinical features:  It is an encapsulated submucosal mass  Asymptomatic lump  Occurs at any age  Tongue is the most common location  Bony lesion produce a well-defined radiolucent lesion  Slow growing but may undergoe a sudden increase (hemorrhage)
  101. 101. Neural lesion   Neoplasms: Schwannoma:  Histopathology:  Spindle cells either organized (palisaded waves) or haphazardly distributed  Treatment: Surgical excision
  102. 102. Neural lesion   Neoplasms: Neurofibroma:    It mat appear as solitary or multiple lesions Etiology: - Solitary type is unknown - Neurofibromatosis is inherited Clinical features: Solitary type  Uniflamed asymptomatic submucosal mass  Location: Tongue, vestibule & buccal mucosa
  103. 103. Neural lesion Neurofibroma
  104. 104. Neural lesion  Neurofibroma:  Clinical features: Neurofibromatosis:  Multiple  Café-au-lait macules  Bone abnormalities (cortical erosion or medullary resorption)  Central nervous system changes  Pain or parasthesia may be seen  Malignant degeneration into neurogenic sarcoma is seen in 5% to 15%
  105. 105. Neurofibromatosis (JADA, 1988)
  106. 106. Neural lesion  Neurofibroma:  Histopathology:  Spindle-shaped cells in connective tissue matrix  It may be well circumscribed or blended into surrounding connective tissue  Mast cells are scattered  Immunohistochemistry with S-100 is a useful tool to confirm diagnosis  Treatment: Surgical excision for solitary lesion Lack of encapsulation
  107. 107. Neural lesion  Malignant peripheral nerve sheet tumor  The cell of origin is believed to be the schwann cells and possibly other nerve sheath cells  It appears as expansile mass (soft tissue)  Asymptomatic  Dilation of the mandibular canal (bone)  Pain or parasthesia
  108. 108. Neural lesion  Malignant peripheral nerve sheet tumor  Histopathologically:  Abundant spindle cells  Mitotic figures  Nuclear pleomorphism  Treatment: Wide surgical exicion  Recurrence is common  Metastases are frequently seen
  109. 109. Muscle Lesions  Neoplasms (Leiomyoma & leiomyosarcoma):    Smooth muscle neoplasms are relatively common They may arise anywhere in the body Leiomyoma     Leiomyomas are commonly arise in the muscularis of the gut and uterus Oral leiomyoma is slow growing & asymptomatic submucosal masses Appears in the tongue, hard palate or buccal mucosa Spindle cells Appears at any age Pterygo-mandibular space
  110. 110. Muscle Lesions  Leiomyoma  Histopathology:  Immunohistochemical demonstration of actin and desmin protein expression can confirm diagnosis Obvious vascular origin Vascular leiomyoma Limited & uniform proliferation around each of the vascular spaces
  111. 111. Muscle Lesions   Neoplasms Leiomyosarcoma      It is commonly arise in the retroperitoneum, mesentery, or subcutaneous and deep tissue of the limbs It may appear at any age Immunohistocemistry can be a valuable diagnostic tool Treatment: wide surgical excision Metastasis is not uncommon Blunt ended nuclei
  112. 112. Muscle Lesions  Rhabdomyoma:      Predilection for the soft tissues of the head and neck  Floor of the mouth, soft palate, tongue & buccal mucosa Mean age: 50 years (children to older adults) Asymptomatic Well defined submucosal mass Well demarcated but unencapsulated The neoplastic cells mimic their normal counterpart (adult) Large eosinophilic granular cell with peripheral nuclei
  113. 113. Muscle Lesions  Rhabdomyosarcoma:     When occurs in head and neck is primarily found in children It is a rapidly growing mass May cause pain and parasthesia Common location: Tongue and soft palate
  114. 114. Muscle Lesions Rhabdomyosarcoma  Histopathology:  Embryonal type (children) consists of primitive round cells in which striations are rarely found  Immunohistochemistry demonstrates desmin, actin and myogenin
  115. 115. Muscle Lesions Rhabdomyosarcoma  Treatment: Combination of surgery, radiation and chemotherapy  Survival rate incraese from 10% to 70% with this aggressive treatment approach
  116. 116. Fat Lesion  Lipoma:     Location: Buccal mucosa, tongue & floor of the mouth Asymptomatic, yellowish submucosal mass Overlying epithelium is intact Superficial blood vessels are usually evident
  117. 117. Fat Lesion  Lipoma:  Well circumscribed, lobulated mass of mature fat cells
  118. 118. Fat Lesion  Lipomyosarcoma:      It is a lesion of adulthood It may occur at any site Slow growing (mistaken for a benign process) Treatment: surgery or radiation Prognosis is fair to good Well differentiated Myxoid type
  119. 119. Mumps   It is an acute viral sialadenitis affecting primarily the parotid glands Etiology & pathogenesis:   Paramyxovirus, incubation period is 2-3 weeks Transmission is by direct contact with salivary droplets

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