Ovariectomy Exacerbates Apical Periodontitis in Rats with an Increase in Expression of Proinflammatory Cytokines and Matrix Metalloproteinases.

INTRODUCTION

The aim of this study was to evaluate the gene expression of proinflammatory cytokines, matrix metalloproteinases (MMPs), and cathepsin K in apical periodontitis (AP) and the volume of lesions in ovariectomized and sham-operated rats.

METHODS

Twenty 12-week-old female Wistar rats were subjected to ovariectomy (OVX) or sham surgery. After 9 weeks, access cavities were prepared in the maxillary and mandibular first molars, pulp tissue was removed, and canals were exposed to the oral environment during 21 days for the induction of AP. The groups were as follows: sham, OVX, sham+AP, and OVX+AP. Animals were euthanized, and blocks containing the maxillary first molar and the surrounding bone were removed for quantification of proinflammatory cytokines cathepsin K and MMP genes by real-time polymerase chain reaction. The hemimandibles containing the mandibular first molars were used for analysis of the AP lesion volume by micro-computed tomographic imaging.

RESULTS

AP in OVX rats showed an increased expression of interleukin 1 beta, tumor necrosis factor alpha, interleukin 6, MMP-8, and MMP-13 (P < .05). OVX alone, without AP induction, did not affect the expression of the evaluated genes. Additionally, AP induced an increase in cathepsin K expression, without significant differences between AP in the sham and OVX groups (P > .05). Micro-computed tomographic imaging showed a significantly greater AP lesion mean volume in OVX compared with sham animals (P < .05).

CONCLUSIONS

AP lesions in ovariectomized rats are larger and have an increased expression of proinflammatory cytokines and MMPs, indicating that the infection combined with ovariectomy has an important role in the regulation of these signaling molecules and enzymes during the development of AP. Based on that, it may be assumed that the hypoestrogenic condition aggravates inflammation and degradation of extracellular matrix components in AP, which may provide insight into understanding the development of AP in female postmenopausal patients.