Association between plasminogen activator inhibitor gene polymorphisms and osteonecrosis of the femoral head susceptibility

Abstract

This study aimed to analyze the correlation of the plasminogen activator inhibitor (PAI-1) gene polymorphisms (rs6092 and rs7242) with susceptibility of osteonecrosis of the femoral head (ONFH).This case-control study included 106 ONFH patients and 151 healthy controls. PAI-1 polymorphisms were genotyped by polymerase chain reaction (PCR) with direct sequencing. The genotype distribution of polymorphism in the control group was checked with the status of Hardy–Weinberg equilibrium (HWE). The χ2 test was applied to compare the genotypes of polymorphisms between the case and control groups. The association intensity between PAI-1 polymorphisms and ONFH risk was estimated by odds ratios (ORs) and 95% confidence intervals (95% CI). The linkage disequilibrium of PAI-1 polymorphisms was analyzed by Haploview.We found that the genotypes and alleles of PAI-1 rs6092 and rs7242 polymorphisms had no obvious association with the risk of ONFH (P >.05). But the strong linkage disequilibrium existed between rs6092 and rs7242 polymorphisms and haplotype G-T was significantly associated with the decreased risk of ONFH occurrence (OR = 0.666, 95%CI = 0.445–0.998).PAI-1 rs6092 and rs7242 polymorphisms are not associated with ONFH development, but haplotype G-T may be a protective factor of ONFH.

Germline VWF/MPRIP and somatoplasm FGA variants synergically confer susceptibility to non-traumatic osteonecrosis of the femoral head

“…The most common pathophysiological abnormalities of non-traumatic ONFH include intravascular coagulation and microcirculation thrombosis 23 . Hypercoagulation and low fibrinolysis are common in patients with ONFH, which jointly contribute to thrombosis occlusion of blood vessels in the femoral head, and thus aggravating avascular necrosis of osteocytes 24 . VWF and FGA variants may promote platelet’s degranulation and activation.…”

Germline VWF/MPRIP and somatoplasm FGA variants synergically confer susceptibility to non-traumatic osteonecrosis of the femoral head

“…The most common pathophysiological abnormalities of non-traumatic ONFH include intravascular coagulation and microcirculation thrombosis [23] . Hypercoagulation and low brinolysis are common in patients with ONFH, which jointly contribute to thrombosis occlusion of blood vessels in the femoral head, and thus aggravating osteocyte avascular necrosis [24] . VWF and FGA variants may promote platelet degranulation and activation.…”

A Molecular Troika of Angiogenesis, Coagulopathy and Endothelial Dysfunction in the Pathology of Avascular Necrosis of Femoral Head: A Comprehensive Review

“…Coagulopathy is the condition of disturbed homeostasis of procoagulant and anticoagulant factors that promotes excessive clot formation and demotes thrombolysis [ 7 ]. It exaggerates ischemia and internal bleeding because of reduced production of fibrinolytic enzymes such as tissue plasminogen activator (tPA) [ 8 ]. Furthermore, coagulopathy participates in the formation of intravascular and microvascular thrombi, thereby obstructing the blood flow, exacerbating the tissue ischemia and delaying the tissue repair [ 9 ].…”