Ibe Izuchukwu K, Sahlstrom Adam, White Andrew, Henderson Shasta E, Lee Francis Y
Instr Course Lect. 2019;68:547-556.
Metastatic bone disease is a substantial driver of morbidity and mortality in many cancers. The presence of bone metastases often indicates a worse prognosis for patients. The mechanisms underlying bone metastases and bone loss are complex and involve interaction between the local factors controlling bone remodeling, systemic regulators, cancer cells, the immune system, and pharmaceutical agents. Cancer cells hone to and initiate interactions with bone cells, thereby resulting in an increase or decrease of local bone mass. Osteolytic metastases are clinically important because they place patients at risk of skeletally related events. In the era of precision medicine and targeted therapies, several pathways have been identified that can serve as targets for new drugs. Therefore, it becomes necessary to understand the molecular mechanisms governing normal bone homeostasis and cancer-induced bone loss to optimally use available and emerging therapeutic modalities for the benefit of patients with skeletal metastases. When pharmacologic or radiation therapies do not block the pathogenesis of metastatic cancer-induced bone loss, surgical stabilization and reinforcement procedures are performed based on size of the lesion, location, degree of osteolysis, and pain. These interventions are performed with the goal of improving patient function and overall outcome.
转移性骨病是许多癌症发病和死亡的重要驱动因素。骨转移的存在往往预示着患者预后较差。骨转移和骨质流失的潜在机制很复杂,涉及控制骨重塑的局部因素、全身调节因子、癌细胞、免疫系统和药物之间的相互作用。癌细胞趋向于与骨细胞相互作用并引发这种相互作用,从而导致局部骨量增加或减少。溶骨性转移在临床上很重要,因为它们会使患者面临骨相关事件的风险。在精准医学和靶向治疗时代,已经确定了几种可作为新药靶点的途径。因此,有必要了解调节正常骨稳态和癌症诱导的骨质流失的分子机制,以便最佳地利用现有的和新兴的治疗方式,使骨转移患者受益。当药物治疗或放射治疗不能阻止转移性癌症诱导的骨质流失的发病机制时,会根据病变大小、位置、溶骨程度和疼痛情况进行手术稳定和强化手术。这些干预措施的目的是改善患者功能和总体预后。