Head and Neck Bony Tumors


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Any dental board exam will ask about bony tumors of the head and neck. I created this study aid when studying for three different dental board examinations.

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Head and Neck Bony Tumors

  1. 1. BENIGN TUMORSODONTOGENIC TUMORS AMELOBLASTOMA: Benign but aggressive and infiltrative. Of epithelial origin (dental lamina and dentalorgan). Most common epithelial odontogenic tumor. Unicystic in adolescents. Others 20 to 40 years.Honeycomb, soap bubble appearance. Typically lower third molars but can be anywhere, maxilla andmandible. Unicystic – 6% Multicystic – 92% Peripheral – 2% Can go malignant to: MALIGNANT AMELOBLASTOMA – Metastatic lesions resemble 1° lesion AMELOBLASTIC CARCINOMA – Metastatic lesions do not resemble 1° lesion ADENOMATOID ODONTOGENIC TUMOR (AOT) / ADENOAMELOBLASTOMA Benign, non-invasive but will displace teeth.. Technically a harmartoma. Mild swellingwith clinically missing tooth. Originates from residual odontogenic epithelium of the dental follicle.Called the “two thirds” tumor. Occurs in second and third decade (12 to 20 yo.) 90% incisor region (2/3 maxilla, 1/3 mandible) 2/3 females 2/3 Follicular (associated with impacted tooth) 1/3 Extra-follicular (w/o impacted tooth) CALCIFYING EPITHELIAL ODONTOGENIC TUMOR (CEOT) / PINDBORG TUMOR Originates from reduced enamel epithelium of stratum intermedium. Benign but locallyinvasive and expansive. 50% associated with unerupted teeth. 66% mandible. Premolar/molar area.Mixed radiolucent and radiopaque foci. Snow driven appearance.
  2. 2. ODONTOGENIC MYXOMA / MYXOFIBROMA Benign but invasive and destructive. Looks the same clinically as Ameloblastoma.Almost exclusively in jaw bones. Originates from mesenchymal tissue. Radiographically, fineintralesional trabeculation with soap bubble or tennis racket appearance. Can cause exopthalamos ifinvades the maxilla. AMELOBLASTIC FIBROMA Benign but expansive. Unilocular or bilocular. 70% under 20 y/o. A Mixed tumor arisingfrom both epithelial and mesenchymal tissues. Premolar/molar area associated with missing tooth.Looks the same as unicystic ameloblastoma. AMELOBLASTIC FIBRO-ODONTOMA Benign well encapsulated tumor. Pericoronal to imbedded tooth. Initially radiolucent butdevelops radiopaque foci as hard tooth structures begin to develop. Most under 20 y/o. Premolars. COMPLEX ODONTOMA Associated with an unerupted tooth. Sunburst radiopacities. Do not resemble teeth butare made of tooth structure. Histodiferentation but not morphodifferentation. Demarcated borders. Nopain. Benign. Lower Posterior teeth. COMPOUND ODONTOMA Most common odontogenic tumor. Upper anterior teeth. Morphodifferentation.“Toothlets”. Associated with unerupted tooth. AMELOBLASTIC ODONTOMA / ODONTOAMELOBLASTOMA Combined ameloblastoma and compound odontoma. Missing tooth. Less than 20 y/o.Boys, mandible. CEMENTOBLASTOMA Benign derived from PDL. Lower first molar. Vital tooth. Well defined radiopacityattached to root of tooth. NOT a cementoma.
  3. 3. NON-ODONTOGENIC TUMORS OSTEOMA Originate from cartilage and periosteum. Exclusive to skull. Mandible on side of ramusand inferior border. Seen in Gardners Syndrome. HEMANGIOMA Benign tumor. Female mandible, body and ramus. Loose and migrating teeth. Bruae areheard. Traumatic in origin. Radiographically – Soap bubble / honeycomb. Sun ray, sunburst. CHONDROMA Benign tumor of cartilagenous origin. Locally invasive. Can resorb teeth. ATRIOVENOUS FISTULA Vascular defect. Pulse is felt. Surgical repair. NEUROLEMMOMA / SCHWANNOMA Originates from neuroectodermal Schwann cells. Round or oval radiolucent lesionposterior to the mental foramen. Parasthesia distal to and pain at site. NEUROMA / TRAUMATIC NEUROMA / AMPUTATION NEUROMA Not a neoplasm. Overgrowth of severed nerve. Painful. Radiolucent. NEUROFIBROMA Originates from both Schwann cells and peripheral nerves including axons. Malignantpotential. Enlarges inferior alveolar and mental nerve foramen.
  4. 4. NEUROFIBROMATOSIS Von Recklinghausens disease. Generic. Neurofibromas, Cafe au Lait spots and freckledin armpits. KERATOCANTHOMA Sebaceous gland tumor of skin. Self healing cancer. BENIGN TUMORS OF SALIVARY GLAND TISSUE PLEOMORPHIC ADENOMA Most common salivary gland tumor. At tail of the parotid gland. When in minorsalivary glands, hard palate is most common site. Mixed tumor (epithelial and connective tissuecomponents). Benign ADENOLYMPHOMA / WARTHINS TUMOR / PAPILLARY CYSTADENOMALYMPHOMATOSUM Parotid. Well encapsulated. Contains multiple cysts. Benign. INTRADUCTAL PAPILLOMA Small, tan, smooth lesion found in submucosal layer. ONCOCYTOMA / OXYPHIL ADENOMA Small, slow growing spherical masses in parotid of females over 50 y/o. HEMANGIOMA Most common SGT in children. Parotid. Rapid growth age 1 to 6 months.Spontaneous involution ages 1 to 12 years. LYMPHANGIOMA / CYSTIC HYGROMA Parotid and submndibular of infants and children. From embryonic lymph ducts.They are spongy, multiloculated masses with a yellowish or bluish surface and are formed byendothelial-lined spaces
  5. 5. LIPOMA From fat cells. Smooth round yellow masses. NECROTIZING SIALOMETAPLASIA Painless solitary lesion of hard palate. Benign and self healing. LYMPHOEPITHELIAL HYPERPLASIA / SICCA SYNDROME / MIKULICZDISEASE This disorder can manifest as a diffuse enlargement of all or part of the parotidgland, or it may manifest as a discrete mass. 40 to 50 y/o.FIBRO-OSSEOUS LESIONS FIBROUS DYSPLASIA Benign skeletal developmental deformity of bones. Maxilla. Replaces medullary bonewith fibrous tissue. Expansion and weakening of bone. Seen in Albrights syndrome along withendocrine disorders (Precocious Puberty) and skin pigmentation. NO radiation therapy. FIBROUS DYSPLASIA OSSIFICANS PROGESSIVA / MYOSITIS OSSIFICANSPROGRESSIVA Fibrous tissue (muscle, tendon and ligaments) are ossified without injury in predictablepatterns. Genetic disorder. Stone Man Disease. Deformed big toe. MYOSITIS OSSIFICANS Fibrous tissue (muscle, tendon and ligaments) are ossified as a result of trauma. CHERUBISM Inherited fibro-osseous disease of only the jaws. Bilateral mandibular involvement.Disease of kids. Starts 2-6 y/0. Multiple cyst like radiolucencies. Displaces lower 7 and 8s. Prematureloss of baby teeth. CEMENTIFYING FIBROMA, OSSIFYING FIBROMA – only one bone
  6. 6. CEMENTOOSSIFYING FIBROMA A tumor of fibroblastic tissue containing masses of cementum-like tissue, usually in themandible of older person. Overgrowth of gingival tissues containing microscopically fibrous tissue andmineralized products (bone, cementum) CEMENTOOSSEOUS DYSPLASIA Originates from odontogenic cells in PDL. The following are the same pathological process. PERIAPICAL CEMENTOOSSEOUS DYSPLASIA / CEMENTOMA / PERIAPICALOSTEOFIBROSIS Apexes of lower anterior teeth. Black females over 40. Vital teeth. Early stageradiolucent. Late stage radiopaque. FOCAL CEMENTOOSSEOUS DYSPLASIA Lower premolar and molar. Single lesions. Caucasians. Margins not so discrete. FLORID CEMENTOOSSEOUS DYSPLASIA Multiple sclerotic symmetrical masses. Blacks 90%. GIGANTIFORM CEMENTOMA Rare. Young Children. InheritedMALIGNANT INTRAORAL TUMORS: SQUAMOUS CELL CARCINOMA 90% of oral carcinoma is SCC. Epithelial origin. Posterior lateral border of tongue andlower lip. Older men. METASTATIC CARCINOMA Most common malignant tumor in skeleton. Mandible, premolar. Metastasize from otherareas in body.
  7. 7. MALIGNANT TUMORS OF SALIVARY GLANDS 50% Sub mandibular gland. MUCOEPIDERMOID CARCINOMA Most common salivary gland tumor in children. Three cell types – mucous cells,intermediate cells and squamous cells. The more mucous cells in the tumor the better. ADENOCYSTIC CARCINOMA Well differentiated and slow growing. Specific to salivary glands. Most commonmalignant SGT in palate area. Also called Cylindroma. Honeycomb ans Swiss cheese histologicalpatterns. ADENOCARCINOMA Tumor of glands. Epithelial in origin. Malignant cells have secretory properties. MALIGNANT MIXED TUMOR SARCOMAS Bone tumors. Origin within connective tissue. Spread through blood stream. OSTEOGENIC SARCOMA / OSTEOSARCOMA Second most common tumor of long bone. Young (under 20) and very old. Motheaten, sunburst, onion peel. Widened PDL space. CHONDROSARCOMA Cartilaginous origin. Third most common tumor of long bone. Maxilla males.Increasing gap between adjacent teeth.
  8. 8. FIBROSARCOMA Periosteal / endosteal origins. Mandible. Seen in Pagets disease. EWINGS SARCOMA Male teenagers. Round cell tumor of bones. Onion skin appearance. LEUKEMIAS Children less than 5 years old. gingival hyperplasia. Loosening of teeth. BURKITTS LYMPHOMA / BURKITTS LEUKEMIA B-lymphocyte malignancy. Epstein Barr Virus association. African variety. Jawbone. Gross distortion of face. Starry Sky. Loss of lamina dura. MULTIPLE MYELOMA Cancer of plasma cells (white blood cells) in bone marrow. Men 40 to 70 y/o.Bence Jones protein. Posterior mandible. Punched out radiolucencies. Migration of teeth. Punched outradiolucencies in premolar area of lower jaw. Cartwheel and checkerboard patterns histologically.REACTIVE LESIONS CENTRAL GIANT CELL GRANULOMA (CGCG) Benign. Age less then 20 y/o. Female. Intraosseous lesion usually mandibleanterior to 1st molar. Crosses symphysis. Expansive. Parasthesia is common. The aggressive versionresorbs roots and moves teeth. Multilocular radiolucencies. Soap Bubble. Contains giant cells. OSTEITIS DEFORMANS / PAGETS DISEASE Slow virus infection (paramyxovirus). Disordered bone metabolism. Results inenlarged and deformed bones. Over 40 years old and mostly men. Osteogenic Sarcoma is a RARE
  9. 9. complication. Cotton wool appearance on radiographs. Migration of teeth, dentures dont fit. Loss oflamina dura and hypercementosis. Increased alkaline phosphatase on blood tests. OSTEOPETROSIS/ MARBLE BONE DISEASE Rare, inherited. Increased bone density. Osteoclastic dysfunction. Narrowmarrow space. Delayed tooth eruption. Poorly calcified teeth. Early loss of crowns. Brittle bones,stunted growth. Anemia. Very radiopaque dental x-rays. SCLEROSTEOSIS Generalized skeletal overgrowth, mostly pronounced in the skull and largemandible; facial distortion; tall stature; syndactyly; radial deviation of the terminal phalanges – cigarshaped; dysplastic or absent nails. INFANTILE CORTICAL HYPEROSTOSIS / CAFFEY – SILVERMAN DISEASE Self limiting within 6 to 9 months.. Mandible, clavicle. Bone changes, soft tissueswelling and irritability. Increased ESR.