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Staphylococcus aureus (S. aureus) is one of the most common bacterial pathogens, causing approximately 80% of all cases of osteomyelitis with a broad host range in coagulase-positive staphylococci and is one of the leading causes of infections in oral and maxillofacial regions1, 2. Moreover, the rapidly increasing frequency of antibiotic-resistant bacteria has caused considerable alarm within the dental and medical community3, 4. Infections associated with this organism are extremely common and often life threatening; therefore, there is serious potential for S. aureus to cause increased morbidity and mortality in oral and maxillofacial regions3-6. To cause the infection, the bacteria do the followings: adhere and enter the host, multiply on or in the host tissues, resist host defences, and damage the host. All four processes must be accomplished in order to produce an infectious disease, and each is complex, involving several determinants. Bacterial attachment and penetration into underlying tissues play an important role in the initiation of infection. Some bacteria may penetrate tissue surfaces by producing lytic substances that break down the tissue surface, easing penetration to the deeper tissues, and other bacteria can penetrate through epithelial cells. It is likely that a variety of mechanisms are used by different organisms to penetrate the various tissue surfaces that they use as their portal of entry7. However lately, many authors have demonstrated the capability of the bacteria to attach on and invade the internal space of non-phagocytic eukaryotes8-13. On the other hand, it has been suggested that the continuous process of actin filament elongation provides the driving force for bacterial propulsion in infected cells or cytoplasmic extracts14-16. Several unrelated intracellular bacterial pathogens, including Listeria monocytogenes (L. monocytogenes), Shigella flexneri, Rickettsiae and Vaccinia virus, are known to share the ability to use actin polymerization as a driving force for intracellular movement, cell-to-cell spread and dissemination within infected tissues. While S. aureus has not traditionally been considered to be an intracellular pathogen, previous studies have revealed that S. aureus may be actively internalized by phagocytosis and are capable of intracellular survival in epithelial and endothelial cells17, 18. It has also been suggested that S. aureus interact with or binds to the cell surface of bovine

Some therapeutic agents and medicines such as phenytoin(PHT), nifedipine and cyclosporine may lead to adverse effects causing pathologic changes in tissue, especially on the gingivae1-8). The common histological finding is a marked gingival hyperplasia, with proliferation of gingival fibroblasts and an increase of collagen fibers in connective tissue. PHT-induced human gingival overgrowth may be genetically programmed for increased synthesis of collagen9). PHT-induced gingival overgrowth was preceded by the inflammation of gingivae10-11). Previous studies reported that PHT, nifedipine and cyclosporine increased the cell activity of human gingival fibroblasts12-17). Some differentiation factors such as glycyrrhetinic acid(GA), retinoic acid, ursolic acid and oleanolic acid inhibited18-25). Previous studies reported that GA inhibited intercellular communication between human fibroblasts26-27). Glycyrrhizin(GL), a major component of licorice (Glycyrrhiza glabra L.), is ingested orally as a sweetener or as an ingredient in oriental medicine. GL has a steroid-like action and anti-viral activity (Pompei et al., 1979). Indeed, use of GL to treat chronic viral hepatitis has shown that it can reduce hepatocellular injury by immunopathologic mechanisms and hepatotoxins, possibly through its ability to inhibit phospholipase A2 activity preventing liver lysosome labilization29-30). GL is metabolized to GA, and then 3-epi-18-GA via 3-keto-18-GA by human intestinal flora31). GA shows pronounced antiinflammatory activity and anti-estrogenic action via alteration of cortisol metabolism32-35). GA inhibits the growth and stimulates melanogenesis in cultured melanoma cells36). There are many reports about the use of differentiation factors for the resolution of uncontrolled growth such as in tumors, but there are few report about its use in the dental field including gingival hyperplasia. The purpose of this study was to investigate the 대한치주과학회지 : Vol. 28, No. 3, 1998