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 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 The Normal Salivary Gland (Cont.) “Parotid gland” The Normal Salivary Gland (Cont.) “Submandibular, sublingual & minor glands” Mucocele Mucocele Mucocele 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 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  Sialolith: represents precipitation of calcium salts around the central nidus of cellular debris
  2. 2. Clinical features:   it is fluctuant, unilateral soft tissue mass in the floor of the mouth Histopathology:   It is similar to mucus retention cyst 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. Necrotizing Sialometaplasia Pathogenesis: Ischemic necrosis or infarction        Traumatic injury Dental injection Denture use Adjacent tumor & cyst Surgery Upper respiratory infection or allergy Necrotizing Sialometaplasia Histologically  The principle characteristics are:     Lobular coagulative necrosis of acini Squamous metaplasia of ducts Pseudoepitheliomatous hyperplasia inflammation Necrotizing Sialometaplasia 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 Mumps
  3. 3.          Clinical features: Fever Malaise Headache Chills Preauricular pain Parotid swelling Male = female Young adults & children Mumps    Complications: Serious complication in adults can occur:  Oophoritis  Orchitis Widspread involvement can include  Liver  Pancreas  Kindney  Nervous system Mumps       Differential diagnosis Bacterial infection (suppurative parotitis) Salivary calculi Lymphoma Lymphoepithelial lesion Metabolic diseases Mumps       Treatment & Prognosis Symptomatic therapy Bed rest Analgesics Corticosteroids (variable success) Vaccination is now available Metabolic Conditions Sialadenosis Metabolic Conditions Sialadenosis It is usually associated with systemic conditions:   Diabetes mellitus
  4. 4.     Malnutrition Liver cirrhosis (Chronic Alcoholism) Hyperlipidemia Acromegaly Metabolic Conditions Sialadenosis 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  Sjögren Syndrome      Clinical features: Peak age: 50 yo Parotid gland enlargment Treatment: Artificial saliva and tears & preventive oral measures Sjögren Syndrome 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. 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  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. 
  5. 5.  Large intraoral tumors are susceptible to trauma Mixed Tumors “Pleomorphic Adenoma” Gross finding: It is irregular round to ovoid mass & well defined borders  Mixed Tumors “Pleomorphic Adenoma” Gross findings Mixed Tumor “Treatment” Carcinoma Ex-Mixed Tumor “Clinical Features” Carcinoma Ex-Mixed Tumor “Microscopic Findings” Carcinoma Ex-Mixed tumor “Treatment” Basal Cell Adenoma Basal Cell Adenoma Malignant Epithelial Tumors “Mucoepidermoid Carcinoma” Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma (Central) Mucoepidermoid Carcinoma (Central) Mucoepidermoid Carcinoma Adenoid Cystic Carcinoma Adenoid Cystic Carcinoma Adenoid Cystic Carcinoma Acinic Cell Carcinoma
  6. 6. Acinic Cell Carcinoma Acinic Cell Carcinoma Polymorphous Low-Grade Adenocarcinoma Polymorphous Low-Grade Adenocarcinoma Polymorphous Low-Grade Adenocarcinoma Mixed Tumors “Pleomorphic Adenoma” Microscopic findings   Composed of epithelial & mesenchymal like tissue Present or absent of fibrous capsule 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 Mixed Tumors “Pleomorphic Adenoma” Carcinoma Ex-Mixed Tumor “Microscopic Findings” Carcinomatous & benign Components of Ex-Mixed Basal Cell Adenoma Basal Cell Adenoma Basal Cell Adenoma Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma Mucoepidermoid Carcinoma Adenoid Cystic Carcinoma Adenoid Cystic Carcinoma Adenoid Cystic Carcinoma Acinic Cell Carcinoma Acinic Cell Carcinoma Acinic Cell Carcinoma
  7. 7. Polymorphous Low-Grade Adenocarcinoma October 11, 2005 Connective Tissue Lesions 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  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 Connective Tissue Lesions  “Fibrous Lesions” Peripheral Odontogenic fibroma Connective Tissue Lesions “Fibrous Lesions”  Focal fibrous hyperplasia: It is common in frequently traumatized area  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
  8. 8. Peripheral odontogenic fibroma Giant cell fibroma Differential diagnosis: Pyogenic granuloma & peripheral giant cell granuloma Treatment: Local excision     Connective Tissue Lesions “Fibrous Lesions” Peripheral Ossifying Fibroma  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 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 Connective Tissue Lesions  “Fibrous Lesions” Gingival fibromatosis Connective Tissue Lesions “Fibrous Lesions” Generalized gingival hyperplasia:    Treatment: Attentive oral hygiene is necessary Gingivoplasty or gingivectomy in combination with prophylaxis Connective Tissue Lesions “Fibrous Lesions”   Denture-induced fibrous hyperplasia Etiology: Chronic trauma produced by an ill-fitting denture
  9. 9.   Clinical features: Occurs in the vestibular mucosa  Overexuberant fibrous connective tissue reparative response  Painless folds of fibrous tissue Treatment: Surgical excision is usually required Epulis Fissuratum 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 Connective Tissue Lesions “Fibrous Lesions” Myxoma:   Histopathology:  Not encapsulated (may exhibit infiltration into surrounding soft tissue)  Dispersed stellate & spindle-shaped fibroblasts  Loose myxoid stroma Connective Tissue Lesions “Fibrous Lesions”    Myxoma: Treatment: Surgical excision Recurrence is not uncommon Pluripotential Mesenchymal Stem Cells 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
  10. 10. Connective Tissue Lesions “Fibrous Lesions”   Fibrosarcoma: Histopathology:  Collagen sparse  Frequent mitotic figures  Ill defined periphery Connective Tissue Lesions  “Fibrous Lesions” Treatment of Fibrosarcoma 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 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 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 Neural lesions
  11. 11.     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 Neural lesion    Traumatic neuroma (Cont.) Histopathology:  Bundles of nerves admixed with dense collagenous fibrous tissue Treatment: Surgical excision 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 Neural lesion    Neoplasms: Granular cell tumors Histopathologically: Unencapsulated sheets of large polygonal cells with pale granular or grainy cytoplasm  Pseudoepitheliomatous hyperplasia    Treatment: Surgical removal 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
  12. 12.  Bony lesion produce a well-defined radiolucent lesion  Slow growing but may undergoe a sudden increase (hemorrhage) Neural lesion     Neoplasms: Schwannoma: Histopathology:  Spindle cells either organized (palisaded waves) or haphazardly distributed Treatment: Surgical excision 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   Neural lesion Neurofibroma Neural lesion Neurofibroma:   Clinical features: Neurofibromatosis:  Multiple  Café-au-lait macules Café  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% Neurofibromatosis
  13. 13. (JADA, 1988) 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 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 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 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  Appears at any age Muscle Lesions   Leiomyoma Histopathology:
  14. 14. Immunohistochemical demonstration of actin and desmin protein expression can confirm diagnosis  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 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  The neoplastic cells mimic their normal counterpart (adult)  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  Muscle Lesions Rhabdomyosarcoma  Histopathology: Embryonal type (children) consists of primitive round cells in which striations are rarely found  Immunohistochemistry demonstrates desmin, actin and myogenin  Muscle Lesions Rhabdomyosarcoma  Treatment: Combination of surgery, radiation and chemotherapy  Survival rate incraese from 10% to 70% with this aggressive treatment approach
  15. 15. 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  Fat Lesion Lipoma:   Well circumscribed, lobulated mass of mature fat cells 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 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