Osteogenic sarcoma is primary malignant bone tumor. It can arise de novo or from the benign precursors lesions, like Paget’s disease, giant cell tumor, chronic osteomyelitis, osteoblastoma, and fibrous dysplasia. Here, we present a case of osteogenic sarcoma arising from florid osseous dysplasia appearing as a rapidly growing bony bulging mass in 44‐year‐old Korean female who had at first been non‐symptomatic, but later suffered from the numbness of chin and lower lip. The radiologic images revealed the mixed radiopaque‐ radiolucent intraosseous lesions throughout the mandible, which were diagnosed as florid osseous dysplasia pathologically. But only after 6 months, the lesions were substituted by the radiological ill‐defined diffuse bony sclerotic lesion with bone destruction, accompanying the interrupted periosteal bone formation, which were pathologically diagnosed as osteogenic sarcomas. These serial clinicopathologic changes imply the malignant progression of florid osseous dysplasia rather than the collision of benign condition, florid osseous dysplasia and malignant tumor, osteogenic sarcoma. The possibility for fibro‐osseous lesion of the jaw as premalignant lesion should not be overlooked; therefore, periodic check‐ups for the lesions are necessary. Proper evaluation and interpretation for clinical neural symptom and radiologic change of bone density may lead to the correct differential diagnosis and therapeutic intervention.

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a naturally occuring polyphenol compound which present in the skin of grapes and red wine has been considered to posses chemopreventive and antioxidant properties. However, little is known about the cellular actions by which resveratrol mediates its therapeutic effects. In this study, the effect of resveratrol on cell proliferation and induction of apoptosis in human osteogenic sarcoma (HOS) cells was investigated. IC50 value was determined to be approximately 60μg/mℓ. Chromosomal DNA framgmentation analysis showed the appearance degraded DNA in time-and dose-dependent manner upon treatment of resveratrol. In order to observe the molecular mechanism involved in resveratrol-induced apoptosis, Western blot analysis was performed. We observed the decrease in the level of procaspase-3, the zymogen form of active caspase-3 in resveratrol-treated cells. This result implies that caspase-3 is activated upon treatment of resveratrol. The activation of caspase-3 was confirmed by the cleavage of poly(ADP-ribose) polymerase. Taken together, our data demonstrate that resveratrol has anti-proliferative effect on HOS cells and induced apoptosis through activation of caspase-3 and PARP cleavage.