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Giant cell lesion’s of jaw

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Giant cell lesion’s of jaw

  1. 1. GIANT CELL LESIONS OF THE JAWS DR KRISHNA KISHOR DEPT OF ORAL & MAXILLOFACIAL SURGERY SGT DENTAL COLLEGE
  2. 2. CONTENTS DEFINITION OF GIANT CELLS ORIGIN CLASSIFICATION OF GIANT CELL LESIONS GIANT CELL GRANULOMA / TUMOR ANEURYSMAL BONE CYST TRAUMATIC BONE CYST OSTEOID OSTEOMA / OSTEOBLASTOMA CHERUBISM BROWN TUMOR OF HYPERPARATHYROIDISM HISTIOCYTOSIS
  3. 3. DEFINITION 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.
  4. 4. ORIGIN Giant cells are derived from the cells of mononuclear phagocyte system. Originate from precursor cell in the bone marrow and also closely related cells of bone marrow origin. They are transported in blood as monocytes, which are pool of immature cells.
  5. 5. Monocytes invade areas of damage & inflammation, where they differentiate into macrophages. When the macrophages fail to deal with particles to be removed they fuse together to form multinucleated giant cells.
  6. 6. CLASSIFICATION OF GIANT CELL LESION Inflammatory / Reactive: • Peripheral Giant Cell Granuloma • Central Giant Cell Granuloma • Aneurysmal Bone Cyst • Traumatic Bone Cyst Metabolic: • Hyperparathyroidism • Cherubism • Histiocytosis Neoplastic: • Central Giant Cell Tumor • Osteoid osteoma / Osteoblastoma
  7. 7. CENTRAL GIANT CELL GRANULOMA • Was 1st described in jaws by Jaffe (1953). • Designated as Giant Cell Reparative Granuloma. • Waldron & Shafer (1966)
  8. 8. • Classified on the basis of biologic behavior as: Non-aggressive & Aggressive. Etiology: • Reactive lesion • Trauma • Origin from odontoclasts
  9. 9. Clinical Features: • Male : female ratio of 1:2 • Age: 11-30yrs • Present almost exclusively in jaws • Mandible > maxilla • Frequent site in mandible is the ant. region not crossing midline.
  10. 10. • Non-aggressive type: Asymptomatic, slow expansion of the affected bone. • Aggressive type: Painful, rapid growth, root resorption, perforation of cortical bone, paraesthesia.
  11. 11. Radiographic Features: • Solitary unicystic radiolucency, as it grows it becomes multilocular with soap-bubble appearance. • Multilocular > unilocular • Root displacement / resorption • Loss of lamina dura • Expansion of cortical plate
  12. 12. Histologic Features: • Proliferation of spindle cells in collagenous stroma. • Numerous small vascular channels. • Giant cells with 15-20 nuclei present throughout the stroma, adjacent to capillaries.
  13. 13. Treatment: Intralesional steroids: • Triamcinolone – 20 mg/cc once per wk for 6 wks • Suppresses inflammatory component of lesion Calcitonin – s.c. inj.: • Dose – 20 IU O.D. • Antagonizes bone resorption by inhibiting Giant cells. JOMS 61:649-53,2003
  14. 14. CASE REPORT (JOMS 61:649-53,2003)
  15. 15. α-Interferon – s.c. inj.: • Dose – 30 lac IU O.D. • Suppresses angiogenic component of lesion. Surgical: • Curettage • Enucleation
  16. 16. Surgical technique (JOMS 60:756-61;2002 ) • Incisions placed (1cm away from radiographic extent of the lesion) • mucoperiosteal flap raised • Buccal bone overlying lesion removed • Through curettage is done
  17. 17. • Peripheral ostectomy may be done  Doesn’t spread via perineural spread so preserve neurovascular bundle  Through debribment of bony cavity • Control of hemorrhage • Flap repositioned & sutured
  18. 18. Preserve teeth in area of lesion  With good prognosis (adequate bone support)  Treat endodontically before surgery Extract teeth in area of lesion  With poor prognosis (poor bone support)  Compromising access to the lesion
  19. 19. Recurrence • Varies from 10 – 50 % • Higher for Locally aggressive lesion • Recurrent lesion respond well to further curettage, aggressive lesions may require more radical surgery for cure. • Incomplete removal
  20. 20. GIANT CELL TUMOR • Very rarely found in jaws. • Aggressive – variant of low grade osteosarcoma • H/F: similar to CGCG, except that the giant cells are larger with more nuclei and are more evenly spread. • Treatment: Resection ( high recurrence rate)
  21. 21. 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. C/F: • Age: 5th 0r 6th decade of life. • Common in females. • Mandible is affected more often.
  22. 22. • Occurs exclusively on gingiva, edentulous alveolar ridge. • Reddish or bluish nodule, most lesions smaller than 2cm in diameter. • May be ulcerated due to trauma.
  23. 23. H/F: • Fibroblast are the basic element. • Giant cells are scattered throughout the stroma. • Foci of hemorrhage, liberation of hemosiderin pigment.
  24. 24. R/F: • May or may not be present • Larger lesion may exhibit superficial erosion of the cortical bone • May demonstrate widening of adjacent PDL spaces Treatment: Local surgical excision down to the underlying bone
  25. 25. Differential diagnosis • CGCG • Pyogenic granuloma
  26. 26. ANEURYSMAL BONE CYST • First described by Jaffe & Lichtenstein in 1942. • First case in jaw was reported by Bhaskar & Bernier in 1958. • Is a non-neoplastic, reactive lesion of bone generally consisting of several cavities filled with blood and deprived of an endothelial lining. • Not a true cyst, sinusoidal blood filled space.
  27. 27. • Word “Aneurysm” was used to describe the blown out appearance of the contour of the affected area. • Exist in two clinico-pathologic forms: 1. Primary 2. Secondary – arising in other osseous conditions like Fibrous Dysplasia, Ossifying Fibroma, CGCG, Osteoblastoma, Osteosarcoma, Ameloblastoma
  28. 28. Etiology: Cause is controversial, the theories put forth regarding the pathogenesis of the lesion are: - Trauma - Local changes in haemodynamics - Reparative response to the hematoma
  29. 29. C/F: • Occurs below 20 yrs of age. • Predilection towards female. • Mandible > maxilla, molar region is the most common site. • Slow growing, may expand the cortical plate, does not destroy them. • Aggressive lesions may perforate cortical plate with soft tissue extension.
  30. 30. • Teeth may be tender, missing or displaced. • Pain is occasional complaint. • On palpation: egg-shell crackling, non-pulsatile. • On surgical exploration: ‘welling up’ of blood. • Gross examination: blood-soaked sponge.
  31. 31. R/F: • Well defined radiolucency • Extreme expansion of cortical plates - honey - comb or soap - bubble appearance • Can displace teeth • Cortex may be destroyed
  32. 32. H/F: • Consist of a fibrous connective tissue stroma containing of many sinusoidal blood filled spaces. • Fibroblast are numerous as well multinucleated giant cells. • Vascular spaces lack any endothelial lining, and giant cells form part of their walls.
  33. 33. Treatment: • Surgical curettage & partial resection are primary means of treatment. • Cryotherapy. • Recurrence rate is high, ranging from 19% to about 50%. • Follow up is necessary.
  34. 34. • Differencial diagnosis • CGCG • Hyperparathyroidism • Cherubism
  35. 35. TRAUMATIC BONE CYST Etiology: • Trauma → Failure of organization of blood clot → Degeneration of clot → Empty cavity within bone. C/F: • Young persons (<20 yrs). • Male predilection. • Mandible frequently affected.
  36. 36. • Asymptomatic, pain or tenderness rarely present. • Rarely expansion of jaw. • Teeth - vital, No tipping / migration. • Aspiration – negative. • On surgical exploration – usually empty cavity, sometimes filled with little straw colored fluid.
  37. 37. R/F: • Well defined, scalloped margin. • Oval / round shape. • No root resorption. • Lamina dura intact. • Usually located above mandibular canal.
  38. 38. H/F: • Thin connective tissue membrane. • No epithelial lining. • Presence of giant cells. Treatment: • Curettage • Re-establish bleeding into the lesion.
  39. 39. OSTEOBLASTOMA • It is a benign neoplasm of bone that arises from osteoblasts. • Osteid osteoma is thought to represent a smaller version of the same tumor. C/F: • Occurs mostly in young persons (<30yrs). • Slight male predilection. • Affects both the jaws, more in post region. • Characterized by Pain and swelling at tumor site. • Size: 2-4cm ,but may be larger than 10cms, measuring <1.5cm is osteoid osteoma.
  40. 40. R/F: • Well circumscribed. • Radiolucent - mixed - radiopaque pattern. • A thin radiolucency may be surrounding calcified central tumor mass. • Occasional sun-ray appearance - resembling osteosarcoma.
  41. 41. H/F: • Irregular trabeculae of osteoid & immature bone within the stroma. • Prominent vascular network. • Actively proliferating osteoblasts & moderate no. of multinucleated giant cells.
  42. 42. Treatment : • surgical excision. • Recurrence is rare. • Malignant transformation into osteosarcoma has also been reported.
  43. 43. • Differential diagnosis Cementoblastoma Ossifying fibroma Fibrous dysplasia
  44. 44. CHERUBISM • Rare developmental jaw condition. • The condition is named due to the facial appearance -plump cheeked little angels with upward directed look depicted in renaissance painting. Etiology: • Inherited as an autosomal dominant trait. • Gene for cherubism present on chromosome 4p16.3.
  45. 45. • Disturbance in development of permanent II & III molars. • Dysregulation of mesenchymal bone formation and development of giant cell granulomas. C/F: • Occurs between the age of 2-5yrs. • Progressive, painless, symmetric swelling of the jaws- mandible or maxilla.
  46. 46. • Cherub like facies arise from bilateral involvement of posterior mandible that tends to include the angles & rami region - angelic chubby cheeks. • Eyes ‘up turned to heaven’ appearance – due to b/l maxillary involvement.
  47. 47. • Lesion grows slowly but no perforation of cortex. • Marked cervical lymphadenopathy. • Premature shedding of deciduous teeth. • Permanent dentition – teeth missing, failure of teeth eruption, teeth displacement. • Speech difficulty. • Bony lesions regresses after puberty.
  48. 48. R/F: • B/L expansion & thinning of cortical plates. • Multilocular cystic appearance – teeth floating in spaces. • Numerous unerupted & displaced teeth.
  49. 49. H/F: • Consists variable number of multinucleated giant cells. • Foci of extravasated blood are commonly present. • Cuff like deposits surrounding small blood vessels throughout the lesion.
  50. 50. Treatment: • The lesions tend to show varying degree of remission after puberty. • By 4th decade facial feature approach normalcy. • Early surgical intervention for cosmesis has given good results. • Some studies showed the use of calcitonin, but still not proved.
  51. 51. BROWN TUMOR OF HYPERPARATHYROIDISM • Parathormone (PTH) is normally produced by parathyroid glands, which regulates the Ca+ metabolism. • Excessive production of PTH results in a condition known as Hyperparathyroidism. • It is an exaggerated form of ‘Osteitis fibrosa cystica’ discovered by von Recklinghausen in 1891.
  52. 52. Three types: • Primary hyperparathyroidism • Secondary hyperparathyroidism • Tertiary hyperparathyroidism
  53. 53. C/F: • Incidence: 1 in 500 • Predilection for females. • Describes the features - ‘Stones , Bones, Abdominal Groans & Psychic Moans’ • Metastatic calcifications - Nephrocalcinosis, blood vessels.
  54. 54. • Jaw - not as frequent as in long bones and skull. • Vague aches, severe bone pain, tenderness following fractures. • Swelling develops, firm in consistency, tender. • Mobility of teeth.
  55. 55. R/F: • Sub-periosteal erosion of middle phalanges is the hallmark. • Very rarely jaw affected first. • Generalized loss of lamina dura. • Ground glass appearance.
  56. 56. • Cortical plate may be thinned or lost. • There is a cystic type of radiolucency. • On gross examination-Vascularity, hemorrhage & deposits of haemosidrin imparts a dark reddish brown color to the lesion –”Brown Tumor”
  57. 57. H/F: • Giant cells of osteoclastic origin scattered over the fibrovascular stroma in which foci of hemosiderin are present. Lab. investigations: • Serum calcium level, alkaline phosphatase & PTH level will be raised
  58. 58. Treatment: • Primary: – Surgical excision of parathyroid adenoma. – Bone lesions resolve spontaneously. • Secondary: – Management of kidney disorders. • Tertiary: – Oral Ca supplement – Vit. D analogue
  59. 59. 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)
  60. 60. Eosinophilic granuloma C/F: • Occurs in older children & young adults. • Male > female • May be asymptomatic – incidental finding on R/F. • Affects skull & mandible, also long bones. • Local pain, swelling, tenderness. • General malaise and fever occasionally accompany.
  61. 61. • May cause bony swelling and involve overlying soft tissue. • Gingival bleeding, pain & ulceration. • Loosening of the teeth often occurs after destruction of alveolar bone.
  62. 62. 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.
  63. 63. H/F: • Sheets of Histiocytes. • Histiocytes coalesce to form Giant cells. • Early lesion – large no. of eosinophils. • Mature lesion – fibrosis, eosinophils decrease. Treatment: • Curettage
  64. 64. 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. Hand-Schuller-Christian Disease
  65. 65. • 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 mimicking advanced periodontal disease – characteristic.
  66. 66. R/F: • Individual lesions – sharply outlined. • Jaw lesions – more diffuse. • Destruction of alveolar bone with tooth displacement.
  67. 67. H/F: • Proliferative histiocytic phase: eosinophils scattered throughout sheets of histiocytes. • Vascular – granulomatous phase: histiocytes + eosinophils + Foam cells • Diffuse xanthomatous phase: abundance of Foam cells • Healing phase: fibrosis
  68. 68. Treatment: • Spontaneous regression – approx. half of the pts. • Curettage / excision • Radiotherapy – inaccesible lesions • Chemotherapy – vinblastine, cyclophosphamide • Prognosis – good
  69. 69. Letterer-Siwe Disease C/F • Occurs in infants (age < 3 yrs). • Initially – skin rash of trunk, scalp & extremities. • Low-grade fever, malaise, irritability. • Splenomegaly • Hepatomegaly
  70. 70. • Lymphadenopathy • Nodular or Diffuse involvement of visceral organs – Lungs & GIT. • Diffuse involvement of skeletal system. • Ulcerative lesions of oral mucosa. • Gingival hyperplasia. • Loosening & premature loss of teeth.
  71. 71. H/F: • Histiocytic proliferation with or without eosinophils. • Foam cells – not prominent. • No fibrosis. Treatment: • Chemotherapy – only few pt. respond. • Poor prognosis. • Rapid course of disease – terminates fatally in short time.
  72. 72. REFERENCES • Textbook of OMFS – Peterson • Textbook of OMFS – Laskin • Oral Pathology – Regezi • Oral Pathology – Shafer • Surgical Pathology – Cawson • J Craniomaxfac Surg 2005: 33,61-68 • Oral Surg Oral Med Oral Patho 2005: 99,464-70 • J Oral Maxillofac Surg 2002: 60,1103-11 • Am J Otolaryngol 2006: 27,281-86 • J Craniomaxfac Surg 1998: 26,56-62

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