These findings reveal a new paradigm by which IGF-1 influences chondrocyte metabolism, by reversing the IL-1-mediated catabolic pathway through up-regulation of its decoy receptor.
In nearly all areas, repair tissue appeared to integrate well with the margins of the remaining normal cartilage.
I think this is important, I also think that after cartilage is formed perhaps prp may enhance its ability to differentiate into more hyaline like tissue. The manufacturers website states they develop hyaline tissue; nonetheless fibro cartilage is still functional aslong as it doesn't wear away, and treatments with FGF-18 may prevent that. I'm really positive about this drug which may be due for release in USA by 2021, not far away. Obviously OA is a slow moving process in most cases; I have read studies wherby moderate hip OA doesn't progress for a period of 8 years, so hopefully just have to bind our time Read More...
Yes I feel BMP-7 is a powerful drug and just grows anything. There was a company advert which highlighted how excess cartilage from BMP7 had to be removed from the joint (in animal study), but thats the power if it growing tissue. I suppose the trouble in an OA joint is in some parts we have bone where we want cartilage and it may cause excessive bone growth in these areas. Perhaps with surgical intervention, i.e microfracture it may come into it's own, but again just an opinion Read More...
I think its saying that as we age we have reduced response to dea(1-3), but this doesn't change the fact that we have increased response to des(1-3) IGF-1 in the OA joint, it summarizes with "the mechanism of the reduced response with age cannot be attributed to changes in IGFBP. Age-related changes in IGF receptors or, more likely, age-related alterations in intracellular signal transduction may also be involved."
So my theory is ( and it is just a theory ) that des(1-3)IGF-1 is better for joints than IGF-1; this may also be the case with LR3-IGF1. But Des(1-3) is readily available Read More...
yes that's correct, you note that "IGF-1 directly to the joint through fibrin constructs (18–20) have been promising, but rapid clearance of IGF-1 from the joint has prevented intra-articular injections of IGF-1 without a carrier from being effective (9), and has been a limiting factor in delivery methods proposed to date," also IGF1-LR3 has half life of about 20–30 hours (relative to IGF-1's half-life of about 12–15 hours).
Not sure what implications this has yet
The consequences of these modifications are that IGF-1 LR3 retains the pharmacological activity of IGF-1 as an agonist of the IGF-1 receptor, has very low affinity for the insulin-like growth factor-binding proteins (IGFBPs), and has improved metabolic stability. Read More...
