Symptomatic residual radicular cysts

The clinical, radiological and histological characteristics of 31 symptomatic residual radicular cysts are compared and contrasted with 39 asymptomatic residual cysts. Differences in size and site incidence are demonstrated along with an inversely proportional relationship between radiographic cortication and degree of acute inflammation in the cyst wall. A number of possible aetiological factors, to account for initiation of active inflammation in deeply placed residual cysts have been examined and excluded, but explanation, in most cases, remains paradoxical.     

Symptomatic residual radicular cysts

The clinical, radiological and histological characteristics of 31 symptomatic residual radicular cysts are compared and contrasted with 39 asymptomatic residual cysts. Differences in size and site incidence are demonstrated along with an inversely proportional relationship between radiographic cortication and degree of acute inflammation in the cyst wall. A number of possible aetiological factors, to account for initiation of active inflammation in deeply placed residual cysts have been examined and excluded, but explanation, in most cases, remains paradoxical.     

Age changes in residual radicular cysts

Histological and radiographic study of 33 uninfected residual radicular cysts has shown that there is a slow increase in mineralised deposits within the cyst lumen with time. This becomes prominent histochemically in those cysts more than 8 years old and radiographically 6 years later. It would appear that mineralisation in these elderly cysts is due to dystrophic calcification of deucnerate cellular material within the cyst lumen. Inflammation in all cysts, apart from mild granulomatous reactions related to cholesterol within cyst walls, was minimal. Overall reduction of cyst size with increasing epithelial atrophy and loss of hyaline bodies and mucous cells, has been shown to occur with increasing cyst age. It is suggested that the majority of radicular cysts heal spontaneously following extraction of the associated tooth. Furthermore, lesions that persist as residual radicular cysts will also undergo slow resolution if inflammation is not a prominent feature.     

Age changes in residual radicular cysts

Histological and radiographic study of 33 uninfected residual radicular cysts has shown that there is a slow increase in mineralised deposits within the cyst lumen with time. This becomes prominent histochemically in those cysts more than 8 years old and radiographically 6 years later. It would appear that mineralisation in these elderly cysts is due to dystrophic calcification of degenerate cellular material within the cyst lumen. Inflammation in all cysts, apart from mild granulomatous reactions related to cholesterol within cyst walls, was minimal. Overall reduction of cyst size with increasing epithelial atrophy and loss of hyaline bodies and mucous cells, has been shown to occur with increasing cyst age. It is suggested that the majority of radicular cysts heal spontaneously following extraction of the associated tooth. Furthermore, lesions that persist as residual radicular cysts will also undergo slow resolution if inflammation is not a prominent feature.     

Lactate dehydrogenase isoenzymes in human radicular cysts

Lactate dehydrogenase (LDH) isoenzymes of 15 clinically dormant radicular cysts were examined. A fragment from each cyst was homogenized, centrifuged and the LDH isoenzymes in the supernatant were separated by cellulose acetate paper electrophoresis. The strongest bands of the cysts were LDH-5 and LDH-4.     

Apoptosis in epithelial cells of apical radicular cysts

AIM: To investigate the occurrence of apoptotic cell death in the epithelium of radicular cysts and to compare its frequency in lesions presenting a distinct functional state. METHODOLOGY: Twenty radicular cysts were selected and arranged into two groups with 10 lesions in each group: atrophic (quiescent) and hyperplastic (active) epithelium. Morphologic investigations of apoptosis were conducted by means of optic microscopy in haematoxylin and eosin slides. Immunohistochemical techniques to detect the bcl-2 protein were carried out by streptavidin-biotin-peroxidase assay. In both instances, 30 sequential high-power microscopic fields were observed to determine apoptotic (AI) and bcl-2 immunostaining (bcl-2I) indexes. The presence of AI and bcl-2I within the two groups was compared using the t-test. Correlation between the AI and the bcl-2I was investigated using the Spearman test. RESULTS: Apoptosis was detected in the epithelium of all cysts. Higher AI levels were found in lesions with an atrophic (0.17 +/- 0.19) rather than a hyperplastic (0.10 +/- 0.10) epithelium. The same was found for the bcl-2I levels (0.06 +/- 0.03 vs. 0.04 +/- 0.01, respectively). However, these differences were not statistically significant. A positive and significant correlation was found between AI and bcl-2I. CONCLUSIONS: Apoptosis was always present in the epithelium of the lesions and was more frequent in lesions with atrophic (quiescent) epithelium.     

Immunohistochemical localization of cyclooxygenase-2 in radicular cysts

AIM: The purpose of this study was to investigate the expression of cyclooxygenase-2 (COX-2) in radicular cysts. METHODOLOGY: Thirty biopsy specimens of radicular cysts were examined using immunohistochemistry. A peroxidase-labelled streptavidin-biotin technique was used for identification of the COX-2. Fisher's exact test (two-tail) was used for statistical analysis of the results. RESULTS: The result demonstrated that COX-2 expression was significantly higher in radicular cysts with higher levels of inflammatory infiltrates. COX-2 stain was detected in the lining epithelium, subepithelial fibroblasts, macrophages and endothelial cells in all specimens. CONCLUSIONS: COX-2 expression is significantly higher in radicular cysts. COX-2 may play an important role in the pathogenesis of radicular cysts.     

Heparanase expression in periapical granulomas and radicular cysts

Heparanase is an endo-β-d-glucuronidase enzyme which degrades heparan sulfate glycosaminoglycan side chains of proteoglycans in the extracellular matrix and in basement membranes. The aim of this study was to evaluate the expression of heparanase in periapical granulomas (PGs) and radicular cysts (RCs). Immunohistochemistry was used to assess heparanase expression in PGs and RCs. Parameters including stain intensity, location and cell type were used to characterize heparanase expression in the periapical lesions. Ordered categories (from weak to strong) were used to compare the level of heparanase staining in the PG and RC groups. Both epithelial cells and inflammatory cells were positive for heparanase. The relative staining of the epithelial cells was strong, whereas the relative staining of the inflammatory cells was weak. Significant differences in immunohistochemical staining of epithelial cells were observed between RCs and PGs (p = 0.002). The relative expression of heparanase in epithelial cells in RCs was strong. In PGs, lesions with few or no epithelial cells, heparanase was predominantly expressed weakly by inflammatory cells. PGs and RCs have the same infectious origin. Therefore, the different cellular sources of heparanase in these periapical lesions may imply that this enzyme has specific pathogenetic functions in RCs and PGs.