Botryoid odontogenic cyst. Exploration of proliferative activity, apoptosis and expression of TP53 and BCL2 compared to the histologically identical lateral periodontal and gingival cysts

Abstract

The botryoid odontogenic cyst (BOC) is a rare, locally more aggressive variant of the usually indolent lateral periodontal cyst (LPC) and gingival cyst (GC). A recent case of BOC provided an opportunity for an exploratory study on the causes of its more aggressive behavior. The limited objective was to see if the BOC was sufficiently different from the other cysts to warrant an investment in a large study. Sections of neutral buffered formalin fixed, paraffin-embedded tissues from the BOC and archival specimens of four GCs, four LPCs and three odontogenic keratocysts (OKCs) were stained using immunohistochemistry for Ki-67, a marker of proliferating cells, caspase-3, a marker of cells undergoing apoptosis, tumor suppressor p53, and the apoptosis inhibitor BCL2. The mean labeling index (LI) of immunoreactive cyst epithelial cells was computed for each antibody and type of cyst. Compared to the LPCs and GCs, the BOC exhibited a moderately larger Ki-67/caspase-3 LI difference, which indicates that the BOC had a net higher rate of growth. We found a much higher level of LI, therefore likely dysregulation of p53. We also found a much higher LI of BCL2. The LIs of p53 and BCL2 in the BOC were similar to and more than twice that of the OKCs, respectively. Although meaningful statistical analysis was precluded by our use of only one case of BOC and a small number of the other cysts, the high p53 and very high BCL2 labeling indices of the BOC offer a potential explanation for its reportedly more aggressive behavior that clearly is worthy of further investigation.

Key words:

• apoptosis
• BCL2
• botryoid odontogenic cyst
• gingival cyst
• immunohistochemistry
• lateral periodontal cyst
• odontogenic keratocyst
• p53
• proliferation

Acknowledgments

We thank Lyvouch Filkoski, Pathology and Laboratory Service, DCVAMC, for assistance with the immunohistochemistry. Our work was supported by the U.S. Department of Veterans Affairs and the Institute for Clinical Research, Inc., Washington, DC.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.