The Central Giant Cell Lesion is very interesting pathologically, as it is one of the few disease processes that we can alter minimize with something other than surgery. I have been fortunate to treat a number of cases, both with direct excision as well as with steroids and calcitonin. I hope that this presentation is useful to you.
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Central Giant Cell Lesion Guide
1. George P. Hatzigiannis DMD, MD®
Central Giant Cell Lesion
George P. Hatzigiannis DMD, MD
Diplomat, American Board of Oral & Maxillofacial Surgery
Dr. George PC
2. George P. Hatzigiannis DMD, MD®
History
Initially considered identical to the giant cell tumor of
long bones
1953 - Jaffe introduced term giant cell reparative
granuloma
No longer considered reparative
Pathogenesis unclear
Alternatively called giant cell granuloma, giant cell lesion,
giant cell tumor
Will refer to as giant cell lesion
3. George P. Hatzigiannis DMD, MD®
Introduction
Benign but aggressively destructive osteolytic lesions,
likely of osteoclastic origin
Accounts for 7% of all benign jaw lesions
60% of cases occur before age 30
Female predilection 2-3:1
70% of cases in mandible, usually anterior to 1st molar;
may be present in posterior
Many cross midline
4. George P. Hatzigiannis DMD, MD®
Clinical Presentation
Painless clinical expansion that may have short (2 week -
2 month) ascendancy
Occasionally, rapid expansion can stretch periosteum
and cause pain
Reactive to unknown stimulus
May appear blue because of cortical and mucosal
thinning
Aggressive and nonaggressive subtypes
5. George P. Hatzigiannis DMD, MD®
Subtypes
Aggressive Nonaggressive
Mean age 10.7 years
Higher number of giant cells,
larger
Greater fractional surface area
occupied by giant cells
Even distribution of giant cells
Recognizable mitotic figures
Evidence of root resorption
Cortical perforation
Paresthesia, pain
Recurrence after curettage
Size > 5 cm
Mean age 22.5 years
Presence of osteoid
More often in anterior maxilla
Irregularly shaped giant cells
6. George P. Hatzigiannis DMD, MD®
Radiographic Findings
Unilocular or multilocular radiolucency
Ill-defined or corticated borders
Often has cortical thinning
Root resorption, cortical perforation in aggressive lesions
May scallop inferior border, displace teeth, resorb interradicular bone
7. George P. Hatzigiannis DMD, MD®
Differential
Dentigerous cyst
Odontogenic
keratocyst
Ameloblastoma
Ameloblastic fibroma
Myxoma
Brown tumor of
hyperparathyroidism
Aneurysmal bone cyst
Langerhans cell
histiocytosis
Cherubism
8. George P. Hatzigiannis DMD, MD®
Work-Up
Needle aspiration to rule out high-pressure
vascular lesion
Imaging determines extent of lesion, cortical
perforation, relation to teeth and
neurovascular bundle
Serum calcium to distinguish
hyperparathyroidism; also obtain PTH and
serum phosphorus
9. George P. Hatzigiannis DMD, MD®
Histopathology
Red-brown friable tissue
Cellular stroma with spindle-shaped fibroblasts
Multinucleated giant cells of osteoclastic origin, irregularly distributed
Extravasated erythrocytes
Hemosiderin
Ostoid or bony trabeculae
Cannot be distinguished from lesions of hyperparathyroidism,
aneurysmal bone cysts, or cherubism
10. George P. Hatzigiannis DMD, MD®
Surgical Treatment
Curettage
Resection if pathologic fracture or recurrent lesion
Lesion does not invade soft tissue; requires bone for existence
Recurrence as high as 50%, usually around teeth and neurovascular
bundle in large lesions
Adjunctive Carnoy solution and endodontic therapy do not reduce
recurrence rate
11. George P. Hatzigiannis DMD, MD®
Steroid Treatment
First establish diagnosis with biopsy
Use based on assumed inflammatory etiology of CGCL (this may be
reflective of angiogenic nature)
Steroids inhibit osteoclasts
Allows for reduction in size prior to enucleation
Weekly steroid injections x 6 weeks - 1:1 mixture of 10 mg/mL
triamcinolone and .5% bupivicaine with 1:200,000 epinephrine,
injecting 1 cc of mixture per cm of lesion
May also be definitive therapy
Case reports of lesions becoming more aggressive following steroids
12. George P. Hatzigiannis DMD, MD®
Calcitonin Treatment
Based on histologic similarity to brown tumor
of hyperparathyroidism
CGCL have calcitonin receptors, giant cells are
osteoclasts
200 units salmon calcitonin QD via nasal spray
Quiescence versus resolution
Minimal adverse reactions
13. George P. Hatzigiannis DMD, MD®
Interferon Treatment
Based on belief that CGCG, as a rapidly proliferating vascular lesion,
can be treated as a hemangioma
Hemangiomas overexpress angiogenic proteins b-FGF and VEGF
Interferon alpha inhibits b-FGF and VEGF
Initial dose is 3 million units / m2 SC QD, 12-24 months and adjust for
efficacy and adverse reactions
Urine b-FGF trend not consistent
Response in as little as three weeks
Adjunct to surgical therapy, after conservative enucleation
Occasionally severe reactions
Monitor CBC & LFTs every six weeks
14. George P. Hatzigiannis DMD, MD®
Relation to Giant Cell Tumor
Controversial
GCT seldom metastasizes, GCGC does
not metastasize
Inconsistent histopathologic
differences
May represent a spectrum of disease
15. George P. Hatzigiannis DMD, MD®
Prognosis
Recurrence 10-50%
Recurrence greater around teeth and
neurovascular bundle
Recurrence usually within 12-18 months
Greater recurrence with cortical perforation
Minimal malignant potential
16. George P. Hatzigiannis DMD, MD®
References
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17. George P. Hatzigiannis DMD, MD®
References
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20. George P. Hatzigiannis DMD, MD®
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21. George P. Hatzigiannis DMD, MD®
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