Mechanisms of Bone Remodeling Disorder in Hemophilia

被引：10

作者：

Wang, Hanshi ^{[1
]}

Bai, Xizhuang ^{[1
]}

机构：

[1] China Med Univ, Peoples Hosp, Dept Sports Med & Joint Surg, 33 Wenyi Rd, Shenyang 110016, Peoples R China

来源：

SEMINARS IN THROMBOSIS AND HEMOSTASIS | 2021年 / 47卷 / 01期

基金：

中国国家自然科学基金;

关键词：

hemophilia; factor VIII; factor IX; osteoporosis; osteogenesis; osteoclastogenesis; PROTEINASE-ACTIVATED RECEPTOR-2; QUALITY-OF-LIFE; FACTOR XIII-A; MINERAL DENSITY; OSTEOCLAST DIFFERENTIATION; FACTOR-VIII; TRANSGLUTAMINASE ACTIVITY; MACROPHAGE POLARIZATION; OSTEOBLASTIC CELLS; PLASMA FIBRONECTIN;

D O I：

10.1055/s-0040-1718890

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hemophilia is caused by a lack of antihemophilic factor(s), for example, factor VIII (FVIII; hemophilia A) and factor IX (FIX; hemophilia B). Low bone mass is widely reported in epidemiological studies of hemophilia, and patients with hemophilia are at an increased risk of fracture. The detailed etiology of bone homeostasis imbalance in hemophilia is unclear. Clinical and experimental studies show that FVIII and FIX are involved in bone remodeling. However, it is likely that antihemophilic factors affect bone biology through thrombin pathways rather than via their own intrinsic properties. In addition, among patients with hemophilia, there are pathophysiological processes in several systems that might contribute to bone loss. This review summarizes studies on the association between hemophilia and bone remodeling, and might shed light on the challenges facing the care and prevention of osteoporosis and fracture in patients with hemophilia.

引用

页码：43 / 52

页数：10

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