二氧化矽(silica)為具有良好生物相容性之生物醫學材料，可應用於骨組織工程與人工關節，這些材質常與骨組織接觸進而刺激破骨細胞分化，而破骨細胞會分解二氧化矽材料導致人工骨組織腐蝕或鬆動，臨床上已發現游離輻射有抑制破骨細胞活性的作用，然而使用二氧化矽為骨組織材料之病患接受輻射治療時，其破骨細胞之生物效應則甚少研究。
本研究取齧齒類單核球細胞株(Raw 264.7)與安全劑量範圍之二氧化矽顆粒共同培養，觀察二氧化矽顆粒之生物效應。實驗中，細胞分成對照組、二氧化矽處理組、輻射(5 Gy)處理組及二氧化矽合併輻射處理組等四組。本實驗驗分析破骨細胞活性酵素抗酒石酸酸性磷酸酶(tartrate resistant acid phosphatase; TRAP)之相對產量與破骨細胞之分化數目等相關參數，並以細胞凋亡染劑(Annexin-V-FITC)評估破骨細胞凋亡百分比。結果顯示，二氧化矽顆粒可促進代表破骨細胞活性之TRAP 產量與破骨細胞之分化數目，而輻射照射可促進破骨細胞凋亡，進而抑制二氧化矽顆粒所誘發之破骨細胞分化。結論：輻射可促進二氧化矽誘發分化的破骨細胞凋亡而降低破骨細胞之活性與數目。

Silica is a biomedical material with excellent biological compatibility applicable in bone tissue engineering and artificial joints. The silica materials usually contact with bone tissues and stimulate the differentiation of osteoclasts. On the other hand, the differentiated osteoclasts can further decompose the silica materials resulting in corrosion or loosening of artificial bone tissues. Clinically, radiation has been found able to inhibit the activity of osteoclasts. However, the biological effect of radiation on osteoclasts is seldom investigated for the patients with bone tissues using silica materials.
Monocytes from RAW 264.7 cell line were cultured with safe dose of silica particles to investigate the biological effect of silica on monocytes in this research. Four groups including the control, silica treatment, radiation treatment (5 Gy) and a combinative treatment of silica and radiation were divided in the experiment. In this research, relative concentration of produced tartrate resistant acid phosphatase (TRAP) and the number of differentiated osteoclasts were evaluated. Osteoclasts were stained by Annexin-V-FITC kit to analyze the apoptotic cells. Silica particles were found able to stimulate the production of TRAP representing the activity of osteoclasts and increase the number of differentiated osteoclasts. However, radiation was discovered promotive to apoptosis of osteoclasts yet suppressive to the differentiation of osteoclasts. The results concluded that radiation was able to increase the apoptosis of osteoclasts induced by silica and decline the activity and amount of osteoclasts.