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June 25-28 International Association for Dental Research 2014

Document Type

Conference Proceeding

Publication Date



Central giant cell granulomas (CGCG) account for 7% of all benign tumors of the jaw while peripheral giant cell granulomas (PGCG) occur on the gingiva (Table 1). The underlying pathophysiology of CGCG and PGCG is not known. Therefore there are studies attempting to identify biomarkers to increase understanding the pathogenesis of CGCG and PGCG. Some authors consider CGCG in jaw bones similar to giant cell tumors of long bones while others believe them to be reactive or non-neoplastic lesions. Recurrence of these lesions following conservative treatment is attributed to matrix metalloproteinases, namely MMP9. Recent studies have shown an increase in levels of MMP9 in central and peripheral giant cell granulomas as in aneurysmal bone cysts (ABC). De-ubiquitinating enzymes play an important role in cellular processes, though their precise role in normal physiology is not fully understood. USP6 is the first de-ubiquitinating enzyme recognized as an oncogene. Recently studies have described the USP6 translocation in CGCG as transforming this lesion to a neoplasm. This retrospective study analyzed two cases of CGCG and one PGCG for the USP6 translocation.


USP6, Giant cell granuloma

USP6 Translocation in Giant Cell Granulomas of the Jaws