42 association between the T-786C enos polymorphism and idiopathic osteonecrosis of the hip.
Abstract
Nitric oxide (NO) regulates bone turnover by osteoblasts-osteoclasts. NO production is impaired by T-786C eNOS and stromelysin 1 5A6A polymorphisms that lead to vasoconstriction, platelet aggregation, reduced angiogenesis, and bone formation, all of which may be associated with osteonecrosis (ON) of the hip. eNOS and stromelysin polymorphisms were compared in 95 hip ON cases (54 idiopathic [18 smokers], 41 secondary [9 smokers]) and 72 healthy normal adult controls. TT eNOS homozygosity was present in 11 of 54 (20%) idiopathic ON cases versus 1 of 51 (2%) race-/gender-/age-matched controls, TC heterozygosity in 28 of 54 (52%) cases versus 17 of 51 (33%) controls, and CC (wild-type normal) in 15 of 54 (28%) cases versus 33 of 51 (65%) controls, p = .0001. The eNOS mutant allele frequency in idiopathic ON was 50 of 108 (46%), higher than in race-/gender-/age-matched controls, 19 of 102 (19%), p .7) or for the 6A allele frequency (p > .4). The eNOS T-786C polymorphism is associated with and may contribute to the pathogenesis of idiopathic ON.
How strong is the evidence?
Evidence Hub reads this as a case-control. Its evidence level is 4 of 5 (Low · observational). Observational designs can show an association but not prove cause.
Read the paper
Related studies
- Irisin Enhances Osteoblast DifferentiationIn Vitro
- Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo
- Interaction between Schwann Cells and Osteoblasts In Vitro
- Administration of cinnamaldehyde promotes osteogenesis in ovariectomized rats and differentiation of osteoblast in vitro
- The Effect of the Major Components of Fructus Cnidii on Osteoblasts In Vitro
- Estrogen depletion alters osteogenic differentiation and matrix production by osteoblasts in vitro
Go deeper in Evidence Hub
Evidence Hub adds a study data sheet (design, sample size, evidence level, key numbers), an AI summary and a chat grounded in the paper's text.