This document discusses various giant cell lesions of the jaws. It defines giant cells and describes their origin from monocytes/macrophages. Giant cell lesions are classified as inflammatory/reactive, aneurysmal bone cyst, metabolic like hyperparathyroidism, or neoplastic like central giant cell tumor. Central giant cell granuloma is described in detail with regards to etiology, clinical features, radiographic appearance, histology, and treatment involving intralesional steroids, calcitonin or surgery. Other giant cell lesions discussed include peripheral giant cell granuloma, aneurysmal bone cyst, traumatic bone cyst, osteoid osteoma/osteoblastoma, cherubism, and brown tumor of hyperparathyroidism

1. GIANT CELL LESIONS
OF THE JAWS
Abhishek Roy
II MDS
1

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
2

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.
3

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.
4

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.
5

6. 6

7. CLASSIFICATION OF GIANT CELL LESION
Chatterjee et al, 2015
Inflammatory / Reactive:
• Peripheral Giant Cell
Granuloma
• Central Giant Cell
Granuloma
Aneurysmal Bone Cyst•
Metabolic:
•
•
•
•
•
Hyperparathyroidism
Cherubism
Histiocytosis
Neoplastic:
Central Giant Cell Tumor
Osteoid osteoma /
Osteoblastoma
7

8. CENTRAL GIANT CELL GRANULOMA
• Was 1st described in jaws by Jaffe (1953)
• Designated as Giant Cell Reparative Granuloma.
• Waldron & Shafer (1966)
8

9. • Classified on the basis of biologic behavior as:
Non-aggressive & Aggressive.
Etiology:
• Reactive lesion
• Trauma
• Origin from odontoclasts
9

10. Clinical Features:
• Male : female ratio of 1:2
• Age: 11-30yrs
• Present almost exclusively in jaws
• Mandible > maxilla
• Frequent site in mandible is the anterior region usually
crossing midline.
10

11. • Non-aggressive type:
Asymptomatic, slow
expansion of the affected
bone.
• Aggressive type:
Painful, rapid growth, root
resorption, perforation of
cortical bone, paraesthesia. 11

12. 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

13. 13

14. 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.
14

15. 15

16. 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.
16

17. CASE REPORT
(JOMS 61:649-53,2003)
17

18. α-Interferon – s.c. inj.:
• Dose – 30 lac IU O.D.
• Suppresses angiogenic component of lesion.
Surgical:
• Curettage
• Enucleation
18

19. Surgical technique
• Incisions placed (1cm away from radiographic
extent of the lesion)
• Mucoperiosteal flap raised
• Buccal bone overlying lesion removed
• Through curettage is done
19

20. • 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
20

21. 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
21

22. 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
22

23. 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 or 6th decade of life.
Common in females.
•
•
• Mandible is affected more often.
23

24. • Occurs exclusively on
gingiva, alveolar ridge
• Reddish or bluish nodule,
most lesions smaller than
•
2cm in diameter.
May be ulcerated
due to trauma.
24

25. H/F:
• Fibroblast are the basic element.
• Giant cells are scattered throughout the stroma.
• Foci of hemorrhage, liberation of hemosiderin pigment.
25

26. 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
26

27. 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

28. • 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

29. 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

30. 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

31. • 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

32. R/F:
• Well defined radiolucency
• Extreme expansion of cortical
plates - honey - comb or
soap - bubble appearance
• Can displace teeth
• Cortex may be destroyed
32

33. H/F:
• Consist
tissue
of a fibrous
stromaconnective
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

34. 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

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.
35

36. • Asymptomatic, pain or tenderness
rarely present.
• Rarely expansion of jaw.
• Teeth - vital, No tipping / migration.
• Aspiration – air
• On surgical exploration – usually empty cavity, sometimes
filled with little straw colored fluid.
36

37. R/F:
• Well defined, scalloped
margin.
• Oval / round shape.
• No root resorption.
• Lamina dura intact.
• Usually located above
mandibular canal.
37

38. H/F:
• Thin connective tissue
membrane.
• No epithelial lining.
• Presence of giant cells.
Treatment:
• Curettage
• Re-establish bleeding into the lesion.
38

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.
39

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.
40

41. H/F:
• Irregular
osteoid &
trabeculae of
immature bone
within the stroma.
• Prominent vascular network.
• Actively proliferating
osteoblasts & moderate no.
of multinucleated giant
cells.
41

42. Treatment :
• surgical excision.
• Recurrence is rare.
• Malignant transformation into osteosarcoma has also been
reported.
42

43. 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
43

44. • 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.
44

45. • 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.
45

46. • 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.
46

47. R/F:
• B/L expansion & thinning of cortical plates.
• Multilocular cystic appearance – teeth floating in spaces.
• Numerous unerupted & displaced teeth.
47

48. 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.
48

49. 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.
49

50. BROWN TUMOR OF HYPERPARATHYROIDISM
• Parathormone (PTH) is normally produced by parathyroid
glands, which regulates the Ca2+ 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.
50

51. Three types:
• Primary hyperparathyroidism
• Secondary hyperparathyroidism
• Tertiary hyperparathyroidism
51

52. C/F:
‘Stones , Bones, Abdominal
• Incidence: 1 in 500
• Predilection for females.
• Describes the features -
Groans & Psychic Moans’
• Metastatic calcifications - Nephrocalcinosis, blood vessels.
52

53. 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.
53

54. R/F:
• Sub-periosteal erosion of
middle phalanges is the
hallmark.
• Very rarely jaw affected
first.
• Generalized loss of lamina
dura.
• Ground glass appearance.
54

55. • 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”
55

56. 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
56

57. Treatment:
• Primary:
– Surgical excision of parathyroid adenoma.
– Bone lesions resolve spontaneously.
• Secondary:
– Management of kidney disorders.
• Tertiary:
– Oral Ca supplement
– Vit. D analogue
57

58. 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)
58

59. 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.
59

60. • May cause bony swelling
and involve overlying soft
tissue.
• Gingival bleeding, pain &
ulceration.
• Loosening
often occurs
of the teeth
after
destruction of alveolar
bone.
60

61. 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.
61

62. H/F:
• Sheets of Histiocytes.
• Histiocytes coalesce to
form Giant cells.
• Early lesion – large no.
of eosinophils.
• Mature lesion – fibrosis,
eosinophils decrease.
Treatment:
• Curettage
62

63. 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
63

64. • 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.
64

65. R/F:
• Individual lesions – sharply
outlined.
• Jaw lesions – more diffuse.
• Destruction of alveolar bone
with tooth displacement.
65

66. 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
66

67. Treatment:
• Spontaneous regression – approx. half of the pts.
• Curettage / excision
• Radiotherapy – inaccesible lesions
• Chemotherapy – vinblastine
cyclophosphamide
• Prognosis – good
67

68. 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
68

69. • 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.
69

70. 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.
70

71. Advances in surgical treatments
• Laser
• Cryosurgery
• Electrosurgery
• Radiofrequency Ablation
• Mohs micrographic surgery
71

72. REFERENCES
Textbook of OMFS – Peterson
Textbook of OMFS – Laskin
Oral Pathology – Shafer
Textbook on Cysts - Shear
•
•
•
•
Internet
•
•
•
•
72

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