Abstract

Osteoporosis is a growing healthcare burden that affects the quality of life in the aging population. Vitamin E is a potential prophylactic agent that can impede the progression of osteoporosis. Various in vivo studies demonstrated the antiosteoporotic potential of vitamin E, but evidence on its molecular mechanism of action is limited. A few in vitro studies showed that various forms of vitamin E can affect the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling and their molecular targets, thus preventing the formation of osteoclasts in the early stage of osteoclastogenesis. Various studies have also shown that the effects of the different isoforms of vitamin E differ. The effects of single isoforms and combinations of isoforms on bone metabolism are also different. Vitamin E may affect bone metabolism by disruption of free radical-mediated RANKL signaling, by its oestrogen-like effects, by its effects on the molecular mechanism of bone formation, by the anti-inflammatory effects of its long-chain metabolites on bone cells, and by the inhibition of 3-hydroxyl-3-methyglutaryl coenzyme A (HMG-CoA). In conclusion, the vitamin E isoforms have enormous potential to be used as prophylactic and therapeutic agents in preventing osteoporosis, but further studies should be conducted to elucidate their mechanisms of action.

Highlights

  • Osteoporosis is a metabolic disease of the skeletal system, characterized by low bone mass and deterioration of the microarchitecture of bone, leading to fragility and subsequent fractures [1]

  • The major cause of osteoporosis in women is due to the presence of a phase of accelerated bone loss during menopause, which accounts for 20–30% loss of cancellous bone and for 5–10% loss of cortical bone

  • Vitamin E, either together or separated into its various isomers, has enormous potential to be developed as an antiosteoporotic agent

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Summary

Introduction

Osteoporosis is a metabolic disease of the skeletal system, characterized by low bone mass and deterioration of the microarchitecture of bone, leading to fragility and subsequent fractures [1]. With the global shift of distribution of death from younger to older ages and from communicable to noncommunicable causes [3], osteoporosis presents a growing disease burden especially in developing countries [4] Both men and women suffer from osteoporosis, but the prevalence of osteoporosis, as indicated by osteoporotic fractures, is lower in males than in their female counterpart. According to an estimate by Burge et al, the economic cost of osteoporosis (inclusive of long-term care cost) in the United States was more than 16.9 billion dollars This cost was projected to increase to 25.3 billion dollars (an increment of 48% compared to the year 2005) by the year of 2025 due to the increase in the age of the population and bone fracture incidence [8]. Data for health economic burden of osteoporosis in Malaysia is currently not available

RANKL Signaling and Osteoclastogenesis
Therapy for Osteoporosis
Vitamin E and Its Bone Protective Properties
The Effects of Vitamin E on RANKL Signalling
Potential Areas of Interest in Vitamin E-Mediated Bone Remodeling
Findings
Conclusion
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