Release of Matrix Metalloproteinases by Macrophages in Radicular Cysts and Residual Radicular Cysts.

INTRODUCTION: Radicular cysts (RCs) and residual radicular cysts (RRCs) are the sequelae of dental caries and that leads to proliferation of epithelial rests of Malassez in periapical tissues. OBJECTIVES: The aim was to evaluate the relationship between Langerhans cells, macrophages, matrix metalloproteinases (MMP-9, MMP-13), and tumor necrosis factor-alpha (TNF-α) in the capsule and lining epithelium of cystic lesions. MATERIALS AND METHODS: Twenty RCs and 20 RRCs were submitted to immunohistochemical analysis with anti-CD68, anti-CD1a, anti-MMP-9, anti-MMP-13, and anti-TNF-α antibodies. The Mann-Whitney test and the Spearman correlation test were used for analysis of the data (P<0.05). RESULTS: The immunoexpression of MMP-13 and CD68 was significantly higher in RCs when compared with RRCs (P=0.011 and 0.012, respectively). The presence of an intense inflammatory infiltrate was significantly correlated with the immunoexpression of CD68 in RCs (P=0.025). Expression of CD68 showed a significant positive correlation with MMP-13 (P=0.015). A moderate correlation was observed between MMP-9 and MMP-13 (P=0.010). TNF-α expression was more common in RCs (P=0.001). CD1a was more frequently expressed in atrophic epithelium (P=0.041) and was significantly correlated with TNF-α (P=0.014). CONCLUSION: Langerhans cells induce a greater release of TNF-α which, in turn, is responsible for the stimulation of M1 macrophages. Higher immunoexpression of MMP-13 and MMP-9 is observed in the early stages of RCs compared with RRCs. Therefore, the toxins of microorganisms present in highly inflamed RCs are the main factors triggering a proinflammatory immune response and greater cystic expansion in the early stages of these lesions.

Langerhans Cells Correlate With Macrophages for Defense Mechanisms in the Atrophic Epithelium of Radicular Cysts.

Langerhans cells (LCs) play important roles in cell-mediated immune reactions, as well as in the pathogenesis of periapical lesions. The aim of this study is to evaluate the role of LCs in the proliferative epithelium of radicular cysts (RCs) and the release of the proinflammatory cytokine tumor necrosis factor α (TNF-α) associated with epithelial thickness. Thirty cases of RCs and 30 cases of residual RCs were randomly selected. Morphologic analysis was performed to evaluate the association between the inflammatory infiltrate, cystic epithelial thickness and lesion size, in addition to immunohistochemical assessment of CD1a, CD68, and TNF-α. The highest macrophage percentages and TNF-α scores were found in RCs (P=0.038 and 0.017, respectively). The largest number of LCs was observed in RCs (P=0.021), especially those exhibiting atrophic epithelium (P=0.05). In addition, LCs were positively correlated with the number of macrophages in both RCs and residual RCs (P=0.033 and 0.002, respectively). In contrast to LCs, the largest number of macrophages was detected in cases with an intense inflammatory infiltrate (P=0.022). In addition, the highest TNF-α scores were associated with an intense inflammatory infiltrate (P=0.024) when analyzed in the capsule of RCs (P=0.017). In conclusion, LCs participate in defense mechanisms and were present in all cases evaluated. Along with macrophages, these cells release proinflammatory cytokines such as TNF-α, which is responsible for inducing the continued proliferation of cystic epithelium.