Porphyromonas gingivalis has been implicated as an important periodontophathic bacterium in the etiology and progression of periodontal diseases. It has been reported that P.gingivalis may mediate periodontal destruction not only directly through its virulence factors, but also indirectly by including complex host mediated inflammatory reponses. The purpose of this study was t o evaluate the effects of P.gingivalis on the bone formation and resorption by osteoblasts. For this purpose, after determining the concentration below which sonicated P.gingivalis extracts (SPEs) have no cytotoxicity on mouse calvarial primary osteoblastic (POB) cells, we investigated the effects of SPEs on the alkaline phosphatase (ALP) activity, matrix metalloproteinase (MMP) expression (MMP-2, -9, 13), and prostaglandin $E_2$ ($PGE_2$) release in POB cells by treatment with SPEs below that concentration. The results were as follows; 1. SPEs showed no cytotoxic effect on POB cells up to a concentration of 1 ${mu}m$/ml. 2. The treatment with SPEs reduced ALP activity in a dose-dependent manner in POB cells, In addition, when we investigated the effect of SPEs (1 ${mu}m$/ml) on ALP activity for different exposure periods, statistically significant inhibition of ALP activity was shown at 2 days of exposure, and further significant inhibition occurred by extending the periods of exposure. 3. The treatment with SPEs stimulated the gene expression of MMP-9 in POB cells. 4. The pre-treatment with SPEs increased the amount of $PGE_2$ released in POB cells. In summary, the present study shows that P.gingivalis could inhibit osteogenesis and stimulate bone resorption not only by reducing ALP activity but also by increasing MMP-9 mRNA expression in osteoblasts, possibly through an endogenous $PGE_2$ pathway. In addition, our results suggest that if P.gingivalis affects osteoblasts in early differentiation stage, such effects by P. gingivalis could be irreversible.