Incidence of central giant cell granuloma of the jaws with clinical and histological confirmation: an archival study in Northern India

Peripheral and central giant cell lesions: etiology, origin of giant cells, diagnosis and treatment

“…Although there is not enough evidence that this lesion promotes reparative process, it was denominated reparative giant cell granuloma (2,(25)(26)(27)(28)(29)(30) . Based on differences in their histological pattern and clinical behavior, Jaffe separated maxillary CGCL from long bone giant cell tumor.…”

“…This lesion affects patients aged 2 to 80 years, although most cases are below 30 years of age. The female gender is the most affected, possibly due to hormonal factors (pregnancy and estrogen) despite the fact that the lesions rarely express estrogen receptors (26,30,37) . CGCL are more common in the anterior portion of the mandible and often cross the midline (6-8, 22, 25, 27, 30) .…”

“…The latter lesions cause pain and exhibit rapid growth, usually larger than five centimeters, producing expansion and perforation of the cortical bone, displacement of teeth and root resorption. Besides, there is a high recurrence rate, which generally ranges between 37.5% and 70% (7,8,14,15,25,26,29,30,32,37) .…”

“…It is debatable whether the lesions that have a greater number of giant cells with multiple nuclei and densely cellular stroma are more aggressive and more likely to relapse after surgical treatment (13,14,21,27) . By means of histomorphometric analysis, Reddy et al (30) revealed significant differences in the number of giant cells in aggressive and non-aggressive lesions, although there was no statistically Recently, a strong expression of nuclear factor of activated T cells (NFATc1), a factor of osteoclastogenesis probably involved in bone resorption, has been observed in giant cells from CGCL, cherubism and brown tumor of hyperparathyroidism (10,18) . In a simplified view of osteoclastogenesis, osteoclast precursor cells from bone marrow are involved in osteoclast differentiation by intranuclear accumulation of NFATcI.…”

“…There is also the possibility that the mutation in the gene SH3BP2 may exert some influence on the MSX-1 gene involved in regulating dental development. Accordingly, the development of CGCL may be associated with an imbalance of MSX-1, which could lead to a failure in osteoclast differentiation (25,30) .…”