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Abstract：
Osteonecrosis of the jaw is the progressive loss and destruction of bone affecting the maxilla or mandible in patients treated with antiresorptive and antiangiogenic agents without receiving prior radiation therapy. The pathogenesis involves the inflammatory pathway of receptor activator of nuclear factor NF-kB ligand and the macrophage colony-stimulating factor, essential for osteoclast precursors survival and proliferation and acting through its receptor c-Fms. Evidence has shown the role of non-coding RNAs in the pathogenesis of osteonecrosis of the jaw and this finding might be useful in diagnosis since these small RNAs could be considered as biomarkers of apoptotic activity in bone. Interestingly, it has been proved that miR-29 and miR-31-5p, acting on specific targets such as CALCR and RhoA, promote programmed-cell death and consequently the necrosis of bone tissue. Specific long non-coding RNAs, instead, have been detected both at reduced levels in patients with multiple myeloma and osteonecrosis, and associated with suppression of osteoblast differentiation, with consequences in the progression of mandible lesions. Among non-coding genic material, circular RNAs have the capability to modify the expression of specific mRNAs responsible for the inhibition of bisphosphonates activity on osteoclastogenesis.
摘要：
颌骨坏死是在未接受事先放射治疗的情况下接受抗吸收和抗血管生成剂治疗的患者中，影响上颌骨或下颌骨的骨骼的进行性丢失和破坏。其发病机制涉及核因子NF-kB受体活化因子配体和巨噬细胞集落刺激因子的炎症通路,对破骨细胞前体存活和增殖至关重要，并通过其受体c-Fms发挥作用。证据表明非编码RNA在颌骨坏死的发病机理中的作用，这一发现可能对诊断有用，因为这些小RNA可以被认为是骨骼中凋亡活性的生物标志物。有趣的是,已经证明miR-29和miR-31-5p,作用于特定靶标，如CALCR和RhoA，促进程序性细胞死亡，从而促进骨组织坏死。特定的长链非编码RNA，相反，在多发性骨髓瘤和骨坏死患者中都检测到水平降低，并与成骨细胞分化的抑制有关，影响下颌骨病变的进展。在非编码基因材料中，环状RNA具有修饰负责抑制双膦酸盐对破骨细胞生成活性的特定mRNA的表达的能力。
