There are many important factors in periodontal idlammation. IL-1 p, PGE and collagenase are predorminantly key factors. These inflammatory mediators induce gingival tissue and alveolar bone destruction. For the prevention and treatment of periodontal disease, it is necessary to inhibit IL-1 p, PGE production and collagenase activity. Ursodeoxycholic acid(UDCA) has immunomodulatory properties, and there is evidence that some natural extracts show antiinflammatory activity to some degree. L'he purpose of this study was to assess the inhibitory effect of UDCA and its mixture with natural extracts on IL-1 p, PGF.p production and collagenase activity. Accordingly we assessed the effect of UDCA and its mixture combined with some natural extracts on inhibition of IL-1 p, PGEg production and collagenase activity. For the IL-1p inhibition study, cultwed cells were exposed to 25 pg/ml LPS. IL.-1 p activity was measured by IL-Ip enzyme immunoassay system. Human gingival fibroblasts were prepared and cells (105/well) were seeded into culture plates. rhIL-1p was added to induce PGE. The amount of PGE in sample media was measured using enzyme immunoassay system. Crude collagenase was prepared from Porphyromonas gingivalis and collagenolytic activity was determined using a Collageno kit CLN-100. The test inhibitor was added to the assay mixture consisting of 0.1ml of 50mM Tris buffer(pH 7.5) and 0.2ml of substrate solution. UDCA and UDCA combined with natural extracts generally inhibited IL-1 p production. Groups above 0.01% UDCA strongly inhibited IL-1p synthesis. Both groups inhibited IL-1p-induced synthesis of PGE. In low concentration, the degree of inhibition was as same as prednisolone. In high concentration, each group was superior to prednisolone. UDCA group and UDCA mixture group exerted a moderate inhibition ofcollagenolytic enzyme. The present study suggested that UDCA and its mixture with natural extracts could be further investigated as antiinflammatory drug For periodontal disease.