Kirsch Thorsten
Musculoskeletal Research Laboratories, Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Curr Opin Rheumatol. 2006 Mar;18(2):174-80. doi: 10.1097/01.bor.0000209431.59226.46.
Physiological mineralization is necessary for the formation of skeletal tissues and for their appropriate functions during adulthood. Pathological or ectopic mineralization of soft tissues, including articular cartilage and cardiovascular tissues, leads to morbidity and mortality. Recent findings suggest that the mechanisms and factors regulating physiological mineralization may be identical or similar to those regulating ectopic mineralization. Therefore, the purpose of this review is to describe the current knowledge of mechanisms and determinants that regulate physiological mineralization and how these determinants can be used to understand ectopic mineralization better.
Recent findings have indicated that physiological and pathological mineralization are initiated by matrix vesicles, membrane-enclosed particles released from the plasma membrane of mineralization-competent cells. An understanding of how these vesicles initiate the physiological mineralization process may provide novel therapeutic strategies to prevent ectopic mineralization. In addition, other regulators (activators and inhibitors) of physiological mineralization have been identified and characterized, and evidence indicates that the same factors also contribute to the regulation of ectopic mineralization. Finally, programmed cell death (apoptosis) may be a contributor to physiological mineralization, and if occurring after tissue injury may induce ectopic mineralization and mineralization-related differentiation events in the injured area and surrounding areas.
This review describes how the understanding of mechanisms and factors regulating physiological mineralization can be used to develop new therapeutic strategies to prevent pathological or ectopic mineralization events.
生理性矿化对于骨骼组织的形成及其在成年期的正常功能至关重要。包括关节软骨和心血管组织在内的软组织发生病理性或异位矿化会导致发病和死亡。最近的研究结果表明，调节生理性矿化的机制和因素可能与调节异位矿化的机制和因素相同或相似。因此，本综述的目的是描述目前关于调节生理性矿化的机制和决定因素的知识，以及如何利用这些决定因素更好地理解异位矿化。
最近的研究结果表明，生理性和病理性矿化均由基质小泡引发，基质小泡是具有矿化能力的细胞的质膜释放的膜包被颗粒。了解这些小泡如何启动生理性矿化过程可能会为预防异位矿化提供新的治疗策略。此外，已鉴定并表征了生理性矿化的其他调节因子（激活剂和抑制剂），有证据表明相同的因素也参与异位矿化的调节。最后，程序性细胞死亡（凋亡）可能是生理性矿化的一个促成因素，如果在组织损伤后发生，可能会在损伤区域及其周围诱导异位矿化和矿化相关的分化事件。
本综述描述了如何利用对调节生理性矿化的机制和因素的理解来开发新的治疗策略，以预防病理性或异位矿化事件。
