Immunoexpression of TNF-α and TGF-β in central and peripheral giant cell lesions of the jaws
Article first published online: 13 SEP 2011
© 2011 John Wiley & Sons A/S
Journal of Oral Pathology & Medicine
Volume 41, Issue 2, pages 194–199, February 2012
How to Cite
de Matos, F. R., de Moraes, M., Nonaka, C. F. W., de Souza, L. B. and de Almeida Freitas, R. (2012), Immunoexpression of TNF-α and TGF-β in central and peripheral giant cell lesions of the jaws. Journal of Oral Pathology & Medicine, 41: 194–199. doi: 10.1111/j.1600-0714.2011.01075.x
- Issue published online: 1 FEB 2012
- Article first published online: 13 SEP 2011
- Accepted for publication August 4, 2011
- central giant cell lesion;
- peripheral giant cell lesion;
J Oral Pathol Med (2012) 41: 194–199
Background: Peripheral giant cell lesion (PGCL) is a reactive process associated with a local irritating factor that shows low recurrence after treatment, especially if the irritating factor is eliminated. On the other hand, central giant cell lesion (CGCL) presents a variable clinical behavior ranging from slow and asymptomatic growth without recurrence to rapid, painful and recurrent growth. Our aim was to compare the immunoexpression of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) in CGCL and PGCL.
Methods: Twenty CGCL and 20 PGCL were selected for analysis of the immunoexpression of TNF-α and TGF-β in multinucleated giant cells (MGC) and mononucleated cells (MC).
Results: The PGCL showed lightly higher expression of TNF-α than CGCL. In comparison with PGCL, the CGCL showed higher expression of TGF-β in MC and MGC (P < 0.05) and in total cells (P < 0.05). Significant positive correlation was found between expressions of TGF-β and TNF-α in CGCL (P < 0.05).
Conclusions: Our results suggest that, in CGCL, coordinated interactions between TGF-β and TNF-α may be important for osteoclastogenesis and bone resorption. PGCL occasionally cause bone resorption but to a lower extent, a fact that might be explained by the lower expression of TGF-β in these lesions.