CAJ | 학술논문

二膦酸盐与骨组织有着高度的亲和力，对骨组织的药理作用取决其与骨组织的亲和力和对破骨细胞的抑制作用，各代二膦酸盐的性能差别使其临床疗效存有差异。一定剂量的二膦酸盐可防止牙槽骨密度降低，且对牙槽嵴高度降低有一定的预防作用，可促进炎性根尖周组织的血管重建和骨缺损修复。含氮二膦酸盐通过抑制法尼基焦膦酸合成酶的活性抑制破骨细胞的破骨作用。核因子-κB受体活化因子配体（RANKL）和骨保护蛋白（OPG）的相对比值决定着骨代谢的方向和骨吸收的程度，两者比值上升则骨吸收增加，反之则骨吸收抑制。二膦酸盐可致RANKL与OPG的比值明显降低。二膦酸盐可竞争性地抑制基质金属蛋白酶活化，减少活性基质金属蛋白酶造成的局部细胞外基质破坏。骨特异性碱性磷酸酶（BAKP）水平降低可造成牙槽骨高度降低，而二膦酸盐可防止BAKP水平的降低，有效地降低炎性反应，降低牙槽骨高度降低速率。
이련산염여골조직유착고도적친화력，대골조직적약리작용취결기여골조직적친화력화대파골세포적억제작용，각대이련산염적성능차별사기림상료효존유차이。일정제량적이련산염가방지아조골밀도강저，차대아조척고도강저유일정적예방작용，가촉진염성근첨주조직적혈관중건화골결손수복。함담이련산염통과억제법니기초련산합성매적활성억제파골세포적파골작용。핵인자-κB수체활화인자배체（RANKL）화골보호단백（OPG）적상대비치결정착골대사적방향화골흡수적정도，량자비치상승칙골흡수증가，반지칙골흡수억제。이련산염가치RANKL여OPG적비치명현강저。이련산염가경쟁성지억제기질금속단백매활화，감소활성기질금속단백매조성적국부세포외기질파배。골특이성감성린산매（BAKP）수평강저가조성아조골고도강저，이이련산염가방지BAKP수평적강저，유효지강저염성반응，강저아조골고도강저속솔。
Bisphosphonates?can?bind?to?hydroxyapatite?crystals?in?a?mineralized?bone?matrix?and?increase?bone?resistance?against?osteoclasts.?The?relative?contributions?of?these?properties?differ?among?individual?bisphosphonates,?and?can?help?determine?their?clinical?behavior?and?effectiveness.?Appropriate?doses?of?bisphosphonates?appear?to?prevent?the?loss?of?alveolar?bone?on?density?and?height,?and?promote?angiogenesis?and?bone?tissue?repair.?The?anti-resorptive?effects?of?nitrogen-containing?bisphosphonates?on?osteoclasts?appear?to?result?from?their?properties?as?potent?inhibitors?of?farnesyl?pyrophosphate synthase. Bisphosphonates can decrease the relative ratio of the receptor activator of nuclear factor-κB ligand/osteoprotegerin,?which?determines?the?progress?of?bone?metabolism?and?degree?of?bone?resorption.?Some?studies?have?shown?that?bisphosphonates?can?decrease?matrix?metalloproteinase?expression?in?the?periapical?area,?and?inhibit?bone?resorption.?Other?studies?demonstrated?that?bisphosphonates?can?maintain?the?levels?of?bone-specific?alkaline?phosphatase(BAKP)?in?alveolar?bone,?and?the?decrease?in?BAKP?in?periodontitis?can?exacerbate?the?inflammatory?response?and?periodontal?tissue?damage.