Osteoprotegerin (OPG) is a key factor in bone remodelling (inhibitor of
osteoclastogenesis), a member of the tumour necrosis factor receptor family, and also
a decoy receptor for the receptor activator of nuclear factor kappa-B ligand (RANKL)
and tumour necrosis factor- related apoptosis inducing ligand (TRAIL) was recently
implicated in human atherogenesis. OPG could be produced by cells of the
cardiovascular system, including coronary artery smooth muscle cells and endothelial
cells and may operate in vascular physiopathology regulating vascular calcification,
apoptosis and immune defense raising the possibility that alterations of OPG serum
levels may be associated with coronary artery disease (CAD). The present work was
intended to assess the possible role of serum OPG and s-TRAIL in the pathology of
CAD. Since OPG acts by neutralizing TRAIL we hypothesized that serum levels of
TRAIL are also altered in vascular disease. Eighty male subjects were included in this
study categorized into three groups: 28 patients with acute myocardial infarction
(AMI), 32 patients with established stable CAD and 20 healthy males serving as
control subjects. All groups were matched for age and body mass index. Following
clinical evaluation, blood samples were withdrawn for serum OPG & s-TRAIL
determination using enzyme linked immunosorbent assay (ELISA). In the present study,
both AMI and stable CAD groups exhibited significantly higher serum OPG levels
compared to control subjects. On the other hand, both AMI and stable CAD groups
showed significantly lower serum s-TRAIL levels compared to control
subjects.Furthermore, in the AMI group there was a significantly higher serum OPG
and lower s-TRAIL levels compared to stable CAD group. Also, it was found that there
is a progressive increase in serum OPG levels and decrease in s-TRAIL levels as the
number of affected coronary vessels increase in both AMI and stable CAD groups. In
conclusion, the present data showed a close association between raised serum OPG
and reduced s-TRAIL in patients with CAD (both AMI and stable CAD). In view of the
pro-apoptotic effects of TRAIL on vascular smooth muscle and endothelial cells, an
elevation of circulating OPG levels may represent a crucial compensatory mechanism
to limit further vascular damage.