All of us Vs Keratoconus

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Post Info TOPIC: Some thoughts


Status: Offline
Posts: 437
Date: Tue Oct 10 11:11 AM, 2006
RE: Some thoughts

Thanks Action444!

That's almost complete the picture.

I think we can conclude as follows. We start with the fact that our KC corneas are weaker than the average due to pure randomness. Due to pure randomness we have less cross-links than normal or the anchoring force of the collagen lamelae in limbus is less than normal. Therefore our corneas are less rigid. Therefore the pressure of the displaced ECM upon keratocytes is bigger than in the average cornea. Under the same curcomstenses (eye blinking, rubbing, temperature, whatever...) a KC cornea is less protective than the average one. So keratocytes in KC cornea are put under more pressure and systematically generate enzymes due to a self-defence mechanism. Enzymes destroy some elements of the ECM, namely cross-links, which only amplifies the further diplacement, etc. It can be a very fast phenomenon. All depends on many details that are distributed randomly around the norm. Anyway, if let it go it can may stop naturally due to age (keratocytes become less responsive and cross-links appear naturally). Say in 70% of the cases it stops somewhere on the stage 3-4, having mutilated the vision. In 30% it goes to transplant. Well, it went in the past, in pre x_linking era. Now, if we do x_linking, cornea is stabilised due to induced cross-links, no more displacement, keratocytes are left in peace, no advers enzymes generation. Which, by the way, rulls out (gives a basis to regect) the inflamation hypothesis of the KC. I think it's the way out of the cage...

-- Edited by Yarsky at 11:17, 2006-10-10

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