Meghji, Sajeda; (1994) Periapical infection and the inflammatory radicular cyst. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Much attention has focused on the activity of lipopolysaccharides (LPS), in periapical lesions; however, the surface associated material (SAM) from oral bacteria was found to be 100-1000 times more potent in inhibiting mammalian cell division. SAM also significantly inhibited DNA and collagen synthesis by murine calvaria and isolated osteoblasts and had potent bone resorbing activity. However, where the radicular microbial component is small and contained by the local immune response the outcome appears to be a chronic granuloma or a cyst. To test this hypothesis, cyst fluids were investigated for the presence of endotoxin, microorganisms and cytokines. The results showed significantly high concentrations of endotoxin in radicular cyst fluids. All were sterile. Immunoassay showed IL-1a and β in the inflammatory radicular cysts, whereas the developmental keratocysts and follicular cysts only showed IL-1a. All the cyst fluids contained IL-6 and none contained any TNF. The influence of endotoxin and these cytokines on the epithelial cell rests was explored. Endotoxins, IL-1, IL-6 and TNF significantly stimulated keratinocyte proliferation. PGE2 had no effect except at 10μM where it induced cytotoxicity. As epithelial cell rests are undoubtedly influenced by the adjacent connective tissue, the role of fibroblasts was also explored. Fibroblast culture media were shown to have a dose related proliferative effect on keratinocytes. Antibodies against the cytokines IL-1, TNF, IL-6, were used to localise these molecules histochemically in cysts. All radicular cyst epithelia showed positive staining for IL-1 a and ? and IL-6. Keratocysts revealed the presence of IL- 1a and IL-6. It is postulated that growth of radicular cysts involves endotoxin stimulation of the epithelium, the autocrine stimulation of cyst epithelial cell division by IL-1 and IL-6 and the paracrine activity of these cytokines on the fibroblast component of the cyst wall. The consequence of this is osteolysis by fibroblast/inflammatory cell factors such as the eicosanoids.

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