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Non odontogenic tumors


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A lecture for fifth stage dentistry college (oral and maxillofacial surgery department )

Published in: Health & Medicine
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Non odontogenic tumors

  1. 1. Non odontogenic tumors Dr .mohammed Rhael ali Tikrit dentistry college
  2. 2. Classification according to its origin  A. gaint cell lesion  Gaint cell reparative granuloma  Brown tumor of hyperparathyroidism  Cherubism  B. Vascular  Vascular tumor  Vascular malformation  C. Hematopoietic-reticuloendothelial  eosinophilic granuloma  hand-schuller –christian disease  letterer –siwe disease  D.Neurogenic  neurofibroma  shwannoma
  3. 3. giant cell lesions
  4. 4. • Giant cells are very large, multinucleate, modified macrophages which may be formed by coalescence of mononuclear cells or by nuclear division without cytoplasmic division of monocytes, particularly in response to the presence of a foreign body.
  5. 5. Giant cell lesions include : • aneurysmal bone cyst • chondroblastoma • simple (traumatic) bone cyst • osteoid osteoma • osteoblastoma • osteosarcoma • giant-cell reparative granuloma • brown tumor of hyperparathyroidism • cherubism
  6. 6. central gaint cell granuloma • Mandible more than maxilla • Female more than male • Young more than old • Mostly in anterior region of lower jaw. • Mainly Asymptomatic ,may cause expansion perforation of cortex • Present almost exclusively in jaws
  7. 7. central gaint cell granuloma Classified on the basis of biologic behavior as :  Non-aggressive :  Asymptomatic, slow  expansion of the affected Bone  Aggressive type:  Painful, rapid growth, root resorption  perforation of cortical bone  paraesthesia Etiology :  Reactive lesion  Trauma
  8. 8.  Treatment conservatively by local curettage • Recurrence may occure Recurrence , Varies from 10 – 50 % • Use of liquid nitrogen after curretage decrease the reccurance rate  Intralesional steroids: • • Triamcinolone – Suppresses inflammatory component of lesion  Calcitonin – s.c. inj.: • Antagonizes bone resorption by inhibiting Giant cells.  α-Interferon  bisphosphonates such as Zoledronate • Recurrent and aggressive type treated by surgical resection  Management of associated teeth : • Preserve teeth in area of lesion : when have adequate bone support , Treat endodontically before surgery . • Extract teeth in area of lesion : When have poor prognosis (poor bone support or Compromising access to the lesion Treatment
  9. 9. PERIPHERAL GIANT CELL GRANULOMA • Common tumor like growth in the oral cavity • Does not represent a true neoplasm but a reactive lesion • Arising from periosteum or PDL membrane. Often called as peripheral giant cell reparative granuloma.
  10. 10. C/F: Age: 5th 0r 6th decade of life. Common in females. Mandible is affected more often. Occurs exclusively on gingiva Reddish or bluish nodule, most lesions smaller than 2cm in diameter. May be ulcerated due to trauma. Treatment: Local surgical excision down to the underlying bone Differential diagnosis ; CGCG • Pyogenic granuloma
  11. 11. Parathormone (PTH) is normally produced by parathyroid glands, which regulates the Ca+ metabolism. Hyperthyroidism may be : Primary : due to over production of parathyroid hormones Secondary : due to decrease calcium level in the blood (as in chronic renal disease) Brown tumor of hyperparathyroidism
  12. 12. BROWN TUMOR OF HYPERPARATHYROIDISM C/F  Predilection for females.  Jaw - not as frequent as in long bones and skull.  Vague aches, severe bone pain, tenderness following fractures.  Mobility of teeth R/F: • Generalized loss of lamina dura. • Ground glass appearance. • Cortical plate may be thinned or lost. • There is a cystic type of radiolucency. Treatment: • Primary: – Surgical excision of parathyroid adenoma .. Bone lesions resolve spontaneously. • Secondary: – Management of kidney disorders.
  13. 13. Benign Mesenchymal tumors (Fibrous dysplasia )
  14. 14. Benign Mesenchymal tumors (Fibrous dysplasia )
  15. 15. Benign Mesenchymal tumors (Fibrous dysplasia )
  16. 16. Benign Mesenchymal tumors (Fibrous dysplasia ) • Replacemnt of bone by immature bone with extensive vascular fibrous element • Affect children • Appear usually as painless enlargment of maxilla of affected side leading to facial asymmetry • Ground glass appearance is the typical radiographical feature treatment Self limited , usually disappear after completion of skeletal growth If disfiguaration occure then surgical shaving and recontouring may done
  17. 17. Benign Mesenchymal tumors (cherubism )
  18. 18. Benign Mesenchymal tumors (cherubism )
  19. 19. Benign Mesenchymal tumors (cherubism )  It consider as familial inherted type of fibrous dysplasia  affect mandible more than maxilla  Clinically Appear as painless slow growing of angle of mandible bilaterally ,early exfoliation of deciduous teeth  Multiple missing and impacted permanent teeth  Radiographically appear as multilocular radiolucency Treatment : • shaving and Surgical contouring • better done after skeletal maturation , but if disfugaration huge or affect on airway or causing social problem to the patient so treatment can do early
  20. 20. Vascular lesions • vascular tumors : hemangiomas which demonstrating endothelial hyperplasia. • Vascular Malformations : lesions with normal endothelial turnover.
  21. 21. Hemangiomas • The word "hemangioma" comes from the Greek haema-, "blood"; angeio , "vessel"; -oma , "tumor". • A hemangioma is a benign and usually self- involuting tumor of the endothelial cells that line blood vessels, and is characterised by increased number of normal or abnormal vessels filled with blood. • Exhibits rapid early growth until 6-8 months of age, followed by regression by 5-9 years of age.
  22. 22. Vascular Malformations  Vascular malformations are present at birth and unlike hemangiomas, do not go through a “rapid proliferative phase”  not “involute”.  They grow constantly with the patient growth  Approximately 31% of these malformations are found in the head and neck region.  Abnormal development of either arterial or the venous side of vascular network during this phase of development  Trauma, infection, and hormonal fluctuation (pregnancy or puberty) may stimulate increased growth of the vascular malformation.  The mechanism of growth is not increased endothelial proliferation - which is within a normal range in these lesions, “but alteration in the flow dynamics within and around the lesion”.  This results in recruitment of “collateral vessels” and dilatation of involved vessels.
  23. 23. Classified in to : 1. low flow :  Cappillary malformation  Venous malformation  Lymphatic malformation 2. High flow :  Arterial malformation , Arteriovenous Malformations Vascular Malformations
  24. 24. Capillary Malformations ( portwine stain) • appear as reddish-pink macules over facial dermatomes may be smooth initially but become more “ pebble – like” as the patient grows.
  25. 25. Venous Malformations • Venous malformations are bluish, soft and easily compressible, • auscultation reveals no bruits. The clinical absence of “pulsations or a thrill” generally indicates a low flow Venous vascular malformation  Thrill : Feeling of the mass by finger  Bruit . Auscalt the mass by stethoscope
  26. 26. Lymphatic Malformations • Low- flow lesions • Within the oral cavity the LMs are more commonly found on the anterior 2/3 of tongue, followed by palate,gingiva, and oral mucosa. • Predilection for head and neck and the axilla, where embryonic lymph sacs are located
  27. 27.  MICROCYSTIC LM (Lymphangioma) • In the oral cavity appear as multiple translucent non- compressible cysts or vesicles  Macrocystic LMs (cystic hygroma) • usually presents as multiple cysts of >2 cm and are commonly found in the neck, and in the cervical area just below the angle of the mandible. They clinically appear as localized painless non-pulsatile swelling with no bruit or thrill, having a rubbery compressible consistency, and covered by normal appearing skin unless hemorrhage or communication with venous malformations produce a blue discolouration. Positive to transillumination . Lymphatic Malformations
  28. 28. MICROCYSTIC LM (Lymphangioma)
  29. 29. Macrocystic LMs
  30. 30. Transillumination of cystic hygroma
  31. 31. Arterial / Arteriovenous Malformations • “High-flow lesions • create a direct communication between the arterial and venous systems, • AVM is present at birth, but become clinically apparent only during the 4-5th decade of life and is often misdiagnosed due to delay in clinical presentation. • The most common site for AVM is the brain, followed by the head, neck, limbs, trunk, and viscera. • They appear as purple-blue raised painful macule, are pulsatile with thrill and bruit, warm to touch • do not empty fully on compression, and refill quickly on reliving digital pressure. • They are associated with embolism, pain, bleeding, ulceration, and congestive cardiac failure due to increased cardiac load. • Often a patient presents with severe bleeding as the first sign that a high flow- lesion is present. They may also complain of recurrent gingival bleeding and loose or depressible teeth.
  32. 32.  DIAGNOSIS of vascular lesions : • History • Clinical examination • MRI • Doppler Ultrasound • CT • Arteriography
  33. 33. Treatment of vascular lesions Hemangioma : • Self limited ,usually disappear after 12 y age • Treatment indicated when the lesion interfer with development (obstructive vision,recurrent bleeding ,ulcerations,interfere with vocal cords function. • Treatment options : • Steroid (systemic or intralesional injection) • Interferone • Laser • Surgical excision
  34. 34. Treatment of vascular lesions Cappillary malformatios:  Laser venous malformations 1.Injection of sclerosing agents ( absolute alcohol,sodium tetradecyle sulphate(std), and bleomycin. 2. Surgical excision Arterio-venous malformations  pre-opertative embolization or ligation of feeding artery followed by surgical resection
  35. 35. Treatment of vascular lesions Lymphatic malformations: 1.Aggressive surgical debulking may be necessary in vary large lesions. 2. Infections such as upper respiratory infections often cause dramatic and painful swelling of the lesion and should treated aggressively by antibiotic and drainge to avoid obstructions of airway 3. Injection of sclerosing agents or OK423 4. Surgical excision
  36. 36. Neurogenic tumors • NEUROFIBROMAS. -It may occur as solitary cutaneous lesions (neorfibroma ) , in which case one finds no café-au-lait spots and no family history of the disease. -Multiple cutaneous lesions w/café- au- lait spots, dominantly inherited, referred as neurofibromatosis that starts to be manifested since childhood
  37. 37. • LANGERHANS CELL HISTIOCYTOSIS Results from abnormal proliferation of Langerhans cells or their precursors. Langerhans cells are specialized cells of the histiocytic cell line that normally are found in the skin. Types :  Eosinophilic granuloma (Solitary)  Hand Schuller Christian disease (Chronic disseminated)  Letterer Siwe disease (Acute disseminated) Hematopoietic-reticuloendothelial lesions
  38. 38. Esonophilic granuloma C/F: • Occurs in older children & young adults. • Male > female • May be asymptomatic – incidental finding on radiograph • Affects skull & mandible, also long bones. • Local pain, swelling, tenderness. • General malaise and fever occasionally accompany. • May cause bony swelling and involve overlying soft tissue. • Gingival bleeding, pain & ulceration. • Loosening of the teeth often occurs after destruction of alveolar bone.
  39. 39. • R/F: • Single or multiple irregular radiolucent lesions. • Well circumscribed. • Usually involving superficial alveolar bone. • Cortex often destroyed. • Tooth ‘floating in air’ appearance. • Pathologic fractures may occur • Treatment: • Curettage Esonophilic granuloma
  40. 40. hand-schuller –christian disease C/F: • Occurs in early life (Age < 5 yrs) • Widespread skeletal & extra-skeletal lesions. • Chronic clinical course • Classic triad of: 1. Multiple ‘punched-out’ lesions of skull. 2. U/L or B/L Exophthalmos. 3. Diabetes insipidus with or without Dyspituitarism. • Oral manifestations – earliest signs of diseases. Stomatitis, Gingivitis, Halitosis • Loose teeth, premature exfoliation. • Failure of healing of post-extraction sockets. • Loss of supporting alveolar bone ,advanced periodontal disease
  41. 41. Treatment: • Spontaneous regression – approx. half of the patients. • Curettage / excision • Radiotherapy – inaccesible lesions • Chemotherapy • Prognosis – good
  42. 42. letterer – siwe disease C/F • Occurs in infants (age < 3 yrs). • Diffuse involvement of skeletal system. Ulcerative lesions of oral mucosa. • Gingival hyperplasia. • Loosening & premature loss of teeth.
  43. 43. Treatment: • Chemotherapy – only few pt. respond. • Poor prognosis. • Rapid course of disease – terminates fatally in short time.
  44. 44. Thank you for listening