Association between MTHFR C677T polymorphism and non-traumatic osteonecrosis of the femoral head: An update meta-analysis

Abstract

Objective To investigate the correlation between MTHFR C677T polymorphism and non-traumatic osteonecrosis of the femoral head.Methods Open published studies relevant to MTHFR C677T polymorphism and non-traumatic osteonecrosis of the femoral head were electronic systematic searched in the databases of cochrane central register of controlled trials, EMBSE and CNKI. The correlation between MTHFR C677T polymorphism and non-traumatic osteonecrosis of the femoral head was calculated by odds ratio (OR) and corresponding 95% confidence interval (95%CI). The publication bias for the included studies were assessed by Begg’s funnel plot and Egger’s line regression text.Results After systematic searching the electronic databases, 11 original studies were finally included the present work. The I2 test indicated significant statistical heterogeneity (I2=53.5%, P=0.018) across the included 11 publications. The polled results indicated that subjects of Caucasians with CC genotype had decreased risk of developing non-traumatic osteonecrosis of the femoral head (OR=0.65,95%CI: 0.44-0.96, P=0.031). However, there was no correlations between MTHFR C677T polymorphism and non-traumatic osteonecrosis of the femoral head in American Jewish and East Asian races(p>0.05). Sensitivity analysis indicated the pooled ORs were not sensitive to any included single study. The Begg’s funnel plot was generally left and right symmetrical which indicated no obviously publications. The Egger’s line regression test also demonstrated no statistical publication bias (t=1.57, P=0.15).Conclusion According to the present evidence, MTHFR C677T polymorphism was correlated with non-traumatic osteonecrosis of the femoral head especially for Caucasians race. Subjects of Caucasians race with CC genotype had decreased risk of developing non-traumatic osteonecrosis of the femoral head.

Osteonecrosis of the Jaws in Patients with Hereditary Thrombophilia/Hypofibrinolysis—From Pathophysiology to Therapeutic Implications

“…Moreover, the hereditary thrombophilia/hypofibrinolysis state is nowadays recognized as an important contributor to the osteonecrosis of the hip and knee. While much evidence has been provided supporting the involvement of FV Leiden [ 100 , 101 , 102 , 103 ], deficiencies in protein C and/or S [ 114 , 115 ], APCR [ 115 , 116 ] and high FVIII levels [ 162 , 163 , 164 , 165 ] in the pathogenesis of ONFH and ONK, other hereditary anomalies of coagulation possibly have no influence (e.g., the 20210A polymorphism in the prothrombin gene [ 100 , 101 , 119 , 120 ]) or show contradictory results (e.g., the MTHFR C677T gene polymorphism [ 102 , 119 , 120 , 124 , 125 , 126 ]) in relation to the osteonecrosis of large joints. The hereditary hypofibrinolysis traits strongly associated with the osteonecrosis of the hip and knee were 4G4G homozygosity of the PAI-1 gene [ 127 , 148 , 149 , 150 ] and, in some studies, high Lp(a) levels [ 100 , 105 , 152 ].…”

“…The MTHFR C677T gene polymorphism’s role in osteonecrosis is still under debate. While some studies positively correlated the MTHFR C677T gene polymorphism with ONFH [ 102 , 119 , 120 , 124 ], others did not confirm this association [ 125 , 126 ]. Similarly, the relationship between the polymorphism of the MTHFR C677T gene and ONK has little and contradictory evidence [ 127 , 128 ].…”

Osteonecrosis of the Femoral Head in Patients with Hypercoagulability—From Pathophysiology to Therapeutic Implications

“…In an analysis of different ethnic groups, MTHFR C677T gene polymorphism was associated with ONFH, especially in Caucasian subjects. Caucasians with the CC genotype had a lower risk for ONFH than subjects with CT+TT genotype, with an OR = 0.65 [86].…”

Avascular Necrosis of Femoral Head in the Republic of Bashkortostan: a Clinical and Epidemiological Study

“…Однако большинство случаев АНГБК -мультифакториальные. Наиболее часто выявляются ассоциации с аллельными вариантами генов, участвующих в свертывании крови (V плазменного фактора свертывания -FVL, протромбина -PRT, 5,10-метилен-тетрагидрофолатаредуктазы -MTHFR, ингибитора-1 активатора плазминогена -PAI-1, тканеспецифического активатора плазминогена -TPA) [9][10][11][12][13][14]. Это говорит о вероятной роли коагулопатии в патогенезе болезни.…”