https://www.ncbi.nlm.nih.gov/pubmed/30116976
Curr Osteoporos Rep. 2018 Oct;16(5):554-560. doi: 10.1007/s11914-018-0469-1.
The Effects of Homocysteine on the Skeleton.
Homocystinuria is a congenital metabolic disorder in which cystathionine β-synthase (CBS) deficiency
results in a prominent increase in homocysteine (Hcy) (serum levels
> 100 μM), causing mental retardation, atherosclerotic cerebral
infarction, and osteoporosis accompanied by fragility fractures.
Encountering a case with excessive homocysteinemia such as that seen in
hereditary homocystinuria is unlikely during usual medical examinations.
However, in individuals who have vitamin B or folate deficiency,
serum homocysteine concentrations are known to increase. These
individuals may also have a polymorphism in methylenetetrahydrofolate
reductase, MTHFR (C677T: TT type), which regulates homocysteine
metabolism. These changes in homocysteine levels may elicit symptoms
resembling those of homocystinuria (e.g., Alzheimer's disease,
atherosclerosis, osteoporosis).
RECENT FINDINGS:
High serum homocysteine has been shown to have detrimental effects on neural cells, vascular endothelial cells, osteoblasts, and osteoclasts. Homocysteine is also known to increase oxidative stress, disrupt cross-linking of collagen molecules, and increase levels of advanced glycation end products, which results in reduced bone strength through a mechanism that goes beyond low bone density and increased bone resorption. Therefore, high serum homocysteine may be regarded as a factor that can reduce both bone mass and impair bone quality. In this review, we outline the epidemiology and pathophysiology of osteoporosis associated with hyperhomocysteinemia.
KEYWORDS:
RECENT FINDINGS:
High serum homocysteine has been shown to have detrimental effects on neural cells, vascular endothelial cells, osteoblasts, and osteoclasts. Homocysteine is also known to increase oxidative stress, disrupt cross-linking of collagen molecules, and increase levels of advanced glycation end products, which results in reduced bone strength through a mechanism that goes beyond low bone density and increased bone resorption. Therefore, high serum homocysteine may be regarded as a factor that can reduce both bone mass and impair bone quality. In this review, we outline the epidemiology and pathophysiology of osteoporosis associated with hyperhomocysteinemia.
KEYWORDS:
Advanced glycation end products; Bone quality; Collagen; Cross-links; Fracture risk; Homocysteine; Pentosidine
- PMID:
- 30116976
- DOI:
- 10.1007/s11914-018-0469-1
https://www.ncbi.nlm.nih.gov/pubmed/19860214
Rinsho Byori. 2009 Sep;57(9):876-83.
[Bone quality markers: pentosidine, homocysteine, and MTHFR polymorphism].
[Article in Japanese]
Saito M1. Abstract
Bone
quality is thought to encompass the structural and material properties
of bone that are affected by the turnover rate. Evidence has accumulated
that collagen cross-links play important roles in bone strength. We
have demonstrated that the quantitative and qualitative deterioration of
lysyl oxidase control and non enzymatic cross-links (advanced glycation
end products, AGEs, pentosidine) of collagen in patients with
osteoporotic femoral neck fracture might be affected by
hyperhomocysteinemia, oxidative stress, and vitamin
B6 insufficiency.
Recently, Shiraki et al. demonstrated that a functional polymorphism in methylenetetrahydrofolate reductase (MTHFR) polymorphism, T allele (C677T), may be a risk factor for future fracture in addition to the traditional risk factors.
Further, we reported that a higher urinary pentosidine level was an independent risk factor for vertebral fracture in a 5-year prospective study involving Japanese women.
If confirmed in large, prospective trials, measurements of serum homocysteine and serum or urine levels of pentosidine might be characterized as markers reflecting bone collagen deterioration.
Recently, Shiraki et al. demonstrated that a functional polymorphism in methylenetetrahydrofolate reductase (MTHFR) polymorphism, T allele (C677T), may be a risk factor for future fracture in addition to the traditional risk factors.
Further, we reported that a higher urinary pentosidine level was an independent risk factor for vertebral fracture in a 5-year prospective study involving Japanese women.
If confirmed in large, prospective trials, measurements of serum homocysteine and serum or urine levels of pentosidine might be characterized as markers reflecting bone collagen deterioration.
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