[cite]Posted By: Henry Irving[/cite]On Rowett the Club knew he has a problem hence only every playing a small fraction of the reported fee. The rest was based on appearances.
Again, a calculated risk was taken with Rowett and it didn't come off but we had already hedged our bets on the fee paid.
Off topic, but wasn't it the same for Jeffers as well? Seem to remember something about us only paying £500k for him, not the full £2.5m.
[cite]Posted By: Henry Irving[/cite]On Rowett the Club knew he has a problem hence only every playing a small fraction of the reported fee. The rest was based on appearances.
Again, a calculated risk was taken with Rowett and it didn't come off but we had already hedged our bets on the fee paid.
Off topic, but wasn't it the same for Jeffers as well? Seem to remember something about us only paying £500k for him, not the full £2.5m.
A chondral defect is a defect in the articular (hyaline) cartilage at the end of the bones. The defect is often on the femoral condyle (the rounded end of the thigh bone) and can result from an injury where there is a direct blow to the bent knee. Sometimes the damage involves bone loss resulting in osteochondral defects. The ACTIVE trial includes patients with isolated chondral or osteochondral defects. Candidates for the trial tend to be relatively young and must not have advanced osteoarthritis.
What does articular cartilage do?
Articular cartilage is a tough, smooth, elastic tissue which covers the ends of bones that form joints. It enables the bones to move smoothly over one another and acts as a shock absorber, cushioning the bone from forces of more than five times the body's weight. Damaged articular cartilage in knees can cause the joint to be painful, swollen and difficult to move.
Why doesn't it mend itself?
Cartilage is not like skin, it doesn't have the ability to repair itself properly. Instead, the damage tends to spread, allowing the bones to rub directly against each other. Any repair tissue that does form is not like normal hyaline cartilage and it doesn't work very well.
What is the best treatment?
Many patients appear to do well from an arthroscopic washout and debridement where any loose bodies of cartilage are removed and the defect is tidied back to healthy cartilage. However, when this treatment fails to relieve symptoms it is unclear what the best treatment is. ACTIVE is being run to help identify the best treatment. Only patients for whom previous treatment has failed are included in the ACTIVE trial.
What treatments are included in the ACTIVE trial?
All ACTIVE patients have a surgical treatment which is either a cell grafting treatment (autologous chondrocyte implantation (ACI) or matrix-assisted ACI (MACI)) or a non-ACI alternative. The surgeon will only recruit patients into the trial if he is undecided about whether ACI/MACI or an alternative might be the most appropriate treatment. There are several alternative, existing treatments available (described below) and the surgeon decides which one would be most appropriate for the patient. Within 3 months before surgery the patient is randomly allocated to have either ACI/MACI or the pre-selected alternative.
Non-ACI treatments
Debridement
Debridement is a rather broad term, but for ACTIVE it involves the removal of all "unstable" cartilage from the edge and base of the defect which is then washed or sucked away. Debridement is done arthroscopically which means it is done using keyhole surgery where a thin 'scope' is pushed into the joint (arthro=joint) to view the cartilage structure.
Abrasion/drilling
Abrasion/drilling involves arthroscopic debridement but in addition the base of the defect is debrided until small bleeding points are seen. The philosophy is that primitive blood cells are recruited from the underlying bone and these reform into joint cartilage cells and cover the damaged area with a new articular surface.
Microfracture
Microfracture is a modification of the drilling technique. Debridement is carried out to form a stable perpendicular edge of healthy cartilage. An arthroscopic awl is then used to make multiple holes in the defect, 3-4 mm apart. Blood from the defect is washed away until a clot forms. This "super clot" is believed to be the optimal environment for tissue to regenerate within the lesion.
Mosaicplasty
Mosaicplasty (also known as Osteochondral Cylinder Transplantation) involves filling the defect with osteochondral plugs to form a "mosaic". The plugs are usually taken from relatively non-weight bearing areas on the peripheries of both femoral condyles. The technique is usually done as an open procedure since care is needed to match the plugs with the size and shape of the defect to produce a smooth surface with the plugs fitting closely together. The main advantage of mosaicplasty is that the defect is filled with mature hyaline cartilage straight away. To avoid symptoms occuring from the donor site, this technique is only used for small defects.
AMIC
Since January 2007 AMIC (Autologous Matrix-Induced Chondrogenesis) has been included as one of the non-ACI treatments available in the trial. This new technique is similar to microfracture but it involves using a collagen membrane patch to stabilise the microfracture clot.
Bone grafting
Since April 2008 patients with osteochondral defects with more than 3 mm of bone loss can be included in ACTIVE. The standard treatment for these defects is bone grafting. Bone grafts may be autologous (the patient's own bone) allogenic (from a donor) or synthetic bone substitute depending on the surgeon's preference. Patients with osteochondral defects randomised to ACI will have bone grafting plus ACI.
Autologous chondrocyte implantation (ACI)
ACI uses the patient's own cells (chondrocytes) which are harvested from healthy articular cartilage, cultivated in a laboratory and implanted over the defect. The cells are held in place either by a periosteal patch which is soft tissue taken from the membrane covering the patient's tibia (shin bone) or by a manufactured collagen membrane patch. ACTIVE patients who are allocated ACI are further randomised to have one of the two types of patches.
In this two-stage procedure surgeons first harvest the cells arthroscopically from a healthy, non-weight bearing area of the knee joint. The chondrocytes are then treated in a laboratory for 3-4 weeks where they will multiple into several million chondrocytes. During the second surgery, the surgeon cleans the defect site, and removes a piece of periosteum (if using the periosteum patch). The patch (either periosteum or manufactured collegen membrane) is stitched and secured over the defect, and the cultured chondrocytes are then injected beneath the patch. There, the chondrocytes should eventually produce a form of cartilage very much like the original hyaline cartilage.
Rehabilitation following ACI is likely to be slower than the other treatments because the cells need time to generate repair tissue. Patients are given a physiotherapy programme to follow and should be prepared to give up driving for 7 weeks and avoid very strenuous activities for several months.
The Robert Jones & Agnes Hunt Orthopaedic Hospital NHS Trust has its own laboratory where cells are prepared for ACI. For more information on ACI please visit the Oscell website.
Matrix-induced ACI
MACI is a variant of ACI which has become an option in the trial (since March 2007) and can be used as an alternative to traditional ACI. With MACI the cells are cultured on collagen membrane in the laboratory before being attached over the defect. MACI does not normally require any stitching to the cartilage and is therefore a quicker procedure.
[cite]Posted By: incorruptible addick[/cite]A month ago we were told: ''He's such an athlete that he's progressed really quickly. Hopefully, it won't take too long.”
I ddn't really believe it, on the boy who cried wolf principle.
But as Oohaah hints at, we do seem to have more of these out-for-a-season-or-two-never-see-them-again injuries than most clubs.
Or is just that one takes more notice of our injuries and every club has its share of Corey Gibbs/Todorov/Kelly Youga type stories?
It would be interesting to hear John Boy, Budgie, Sparrows Lane Lion etc on this topic.
Think west ham have their fair share ... Ashton and dyer are 2 that spring to mind straight away. Although dyer came back against the yids fell over and is out again now
[cite]Posted By: Dazzler21[/cite]What is a chondral defect?
A chondral defect is a defect in the articular (hyaline) cartilage at the end of the bones. The defect is often on the femoral condyle (the rounded end of the thigh bone) and can result from an injury where there is a direct blow to the bent knee. Sometimes the damage involves bone loss resulting in osteochondral defects. The ACTIVE trial includes patients with isolated chondral or osteochondral defects. Candidates for the trial tend to be relatively young and must not have advanced osteoarthritis.
What does articular cartilage do?
Articular cartilage is a tough, smooth, elastic tissue which covers the ends of bones that form joints. It enables the bones to move smoothly over one another and acts as a shock absorber, cushioning the bone from forces of more than five times the body's weight. Damaged articular cartilage in knees can cause the joint to be painful, swollen and difficult to move.
Why doesn't it mend itself?
Cartilage is not like skin, it doesn't have the ability to repair itself properly. Instead, the damage tends to spread, allowing the bones to rub directly against each other. Any repair tissue that does form is not like normal hyaline cartilage and it doesn't work very well.
What is the best treatment?
Many patients appear to do well from an arthroscopic washout and debridement where any loose bodies of cartilage are removed and the defect is tidied back to healthy cartilage. However, when this treatment fails to relieve symptoms it is unclear what the best treatment is. ACTIVE is being run to help identify the best treatment. Only patients for whom previous treatment has failed are included in the ACTIVE trial.
What treatments are included in the ACTIVE trial?
All ACTIVE patients have a surgical treatment which is either a cell grafting treatment (autologous chondrocyte implantation (ACI) or matrix-assisted ACI (MACI)) or a non-ACI alternative. The surgeon will only recruit patients into the trial if he is undecided about whether ACI/MACI or an alternative might be the most appropriate treatment. There are several alternative, existing treatments available (described below) and the surgeon decides which one would be most appropriate for the patient. Within 3 months before surgery the patient is randomly allocated to have either ACI/MACI or the pre-selected alternative.
Non-ACI treatments
Debridement
Debridement is a rather broad term, but for ACTIVE it involves the removal of all "unstable" cartilage from the edge and base of the defect which is then washed or sucked away. Debridement is done arthroscopically which means it is done using keyhole surgery where a thin 'scope' is pushed into the joint (arthro=joint) to view the cartilage structure.
Abrasion/drilling
Abrasion/drilling involves arthroscopic debridement but in addition the base of the defect is debrided until small bleeding points are seen. The philosophy is that primitive blood cells are recruited from the underlying bone and these reform into joint cartilage cells and cover the damaged area with a new articular surface.
Microfracture
Microfracture is a modification of the drilling technique. Debridement is carried out to form a stable perpendicular edge of healthy cartilage. An arthroscopic awl is then used to make multiple holes in the defect, 3-4 mm apart. Blood from the defect is washed away until a clot forms. This "super clot" is believed to be the optimal environment for tissue to regenerate within the lesion.
Mosaicplasty
Mosaicplasty (also known as Osteochondral Cylinder Transplantation) involves filling the defect with osteochondral plugs to form a "mosaic". The plugs are usually taken from relatively non-weight bearing areas on the peripheries of both femoral condyles. The technique is usually done as an open procedure since care is needed to match the plugs with the size and shape of the defect to produce a smooth surface with the plugs fitting closely together. The main advantage of mosaicplasty is that the defect is filled with mature hyaline cartilage straight away. To avoid symptoms occuring from the donor site, this technique is only used for small defects.
AMIC
Since January 2007 AMIC (Autologous Matrix-Induced Chondrogenesis) has been included as one of the non-ACI treatments available in the trial. This new technique is similar to microfracture but it involves using a collagen membrane patch to stabilise the microfracture clot.
Bone grafting
Since April 2008 patients with osteochondral defects with more than 3 mm of bone loss can be included in ACTIVE. The standard treatment for these defects is bone grafting. Bone grafts may be autologous (the patient's own bone) allogenic (from a donor) or synthetic bone substitute depending on the surgeon's preference. Patients with osteochondral defects randomised to ACI will have bone grafting plus ACI.
Autologous chondrocyte implantation (ACI)
ACI uses the patient's own cells (chondrocytes) which are harvested from healthy articular cartilage, cultivated in a laboratory and implanted over the defect. The cells are held in place either by a periosteal patch which is soft tissue taken from the membrane covering the patient's tibia (shin bone) or by a manufactured collagen membrane patch. ACTIVE patients who are allocated ACI are further randomised to have one of the two types of patches.
In this two-stage procedure surgeons first harvest the cells arthroscopically from a healthy, non-weight bearing area of the knee joint. The chondrocytes are then treated in a laboratory for 3-4 weeks where they will multiple into several million chondrocytes. During the second surgery, the surgeon cleans the defect site, and removes a piece of periosteum (if using the periosteum patch). The patch (either periosteum or manufactured collegen membrane) is stitched and secured over the defect, and the cultured chondrocytes are then injected beneath the patch. There, the chondrocytes should eventually produce a form of cartilage very much like the original hyaline cartilage.
Rehabilitation following ACI is likely to be slower than the other treatments because the cells need time to generate repair tissue. Patients are given a physiotherapy programme to follow and should be prepared to give up driving for 7 weeks and avoid very strenuous activities for several months.
The Robert Jones & Agnes Hunt Orthopaedic Hospital NHS Trust has its own laboratory where cells are prepared for ACI. For more information on ACI please visit the Oscell website.
Matrix-induced ACI
MACI is a variant of ACI which has become an option in the trial (since March 2007) and can be used as an alternative to traditional ACI. With MACI the cells are cultured on collagen membrane in the laboratory before being attached over the defect. MACI does not normally require any stitching to the cartilage and is therefore a quicker procedure.
To much imformation there.
Hurty knee, without the details please. I'm eating lunch.
Was looking forward to seeing Youga and Reid on the left them two both going forward would've caused all sorts of problems, maybe defensivley it would've been a bit dodgy.
Sad news, a good hard working player who was looking like a strong defender and attacking force before the injury, good luck in all your new endeavors Kelly
this is crap, really crap. and we can't go through the season with just jackson and fry who arnt out and out left backs. not looking forward to the bristol rovers fixture either as they've now succeeded in crippling our first choice left backs in the last two meetings.....
Youga was getting better. But in the champ his massive positional kamikaze nature would never work. Great to watch last season, when his rambunctious raids seemed to always end with him hitting the bar or post.
Shame he didn't get fit as his athleticism would have always attracted a moron like Pardew or Dowie; mind you Adkins rated him, but his Scunny team were super organised.
Whatever my oppinion I'd never wish this on anyone. Rovers did some awful tackling against us last season, the guy who did Basey in should have been banned for 5-6 games. Whilst Youga's whack seemed 50-50, I can only hope he'll resurrect his career. Just not at Charlton.
Youga was a good attacking wingback but poor defensively. My harsh memory of him is hoofing the ball striaght up in the air in several games, something I never saw Sir Chris do. Good memories are the games against palace where he played great and terrorised them. He would never have got into a Curbs team as he was too inconsistent. I hope the insurance covers our loses a bit. That would be a good question to ask Murray, if not been asked already.
When something like this happens even the most blinkered, I hate spotty parker fan, has to realise why these players have to run to the money cos you never literally know what's round the corner
Limited career span means they have to make as much hay when the sun shines as they can cos their priority has to be to provide for their family imo
Tough setback for Youga. Re: Cory Gibbs, he has been back playing in MLS since he left Charlton. He is one of New England Revolutions best players. And dare I say it, would be one of Charlton's best now if still here. Hopefully Youga can make it back the same way and isn't a permanent career crock.
Massively overated player who had finally found his level at division Three. To see him as any form of loss when he hasn't played for best part of six to eight months for us is almost laughable.
[cite]Posted By: American_Addick[/cite]
Re: Cory Gibbs, he has been back playing in MLS since he left Charlton. He is one of New England Revolutions best players. And dare I say it, would be one of Charlton's best now if still here.
Perhaps we should re-sign him. Sounds like the perfect replacement for Youga!
Looking back on what the OS said at the time, it seems we pretty unlucky to get lumbered with Gibbs, as we beat several other big clubs to his signature.
This from the bio on the OS at the time (so obviously must be true) :
''Able to play at left-back and as a left-sided central defender, Gibbs had plenty of options when it came to choosing his next club, and the Addicks beat off interest from UEFA Cup finalists Middlesbrough, as well as Bolton Wanderers and Premiership new-boys Reading to land their man.''
Plenty of interest, means the agent sent a DVD to everyone and they're just some of the clubs that signed for delivery of DVD. No surprise that like Rommedahl NO European big club went near signing him at that time.
He'd failed at every 'big club' he'd been at. Not one Bundesliga 1 side wanted him after he'd won a meritorious relegation from Bundesliga 1 to the third tier of german football with Pauli. Feyenord wanted rid of him after his first injury with them. They say MLS is champ standard, in multiple games I've rarely seen champ standard some excellent players but few good teams. Fortune is a far superior player and more reliable injury wise. So what point is there even making a fanciful wish Gibbs?
[cite]Posted By: Ketman[/cite]Massively overated player who had finally found his level at division Three. To see him as any form of loss when he hasn't played for best part of six to eight months for us is almost laughable.
In my humbler opinion we were a better team with more attacking fullbacks, and the results at the start of this season vs last kind of bear that out. Particularly when you've got decent wingers (Kelly never really had a proper left sided player in front of him while he was with us), having an athletic full back with pace that gets over half way asks a lot of questions and opens up space for the winger/drags opponents out of the middle. He wasn't the best for us in the Championship, I'd agree, but it was a team on a down and I understand that a lot changed in the background over that season which - more than the change of leagues - might have changed Kelly's form and atttitude. Moot point I guess, because he'll never pull the jersey on again.
Comments
Again, a calculated risk was taken with Rowett and it didn't come off but we had already hedged our bets on the fee paid.
I think so but don't know the numbers
Isn't it about time we got Chris Powell back for the remainder of the season, we've done it twice before
A chondral defect is a defect in the articular (hyaline) cartilage at the end of the bones. The defect is often on the femoral condyle (the rounded end of the thigh bone) and can result from an injury where there is a direct blow to the bent knee. Sometimes the damage involves bone loss resulting in osteochondral defects. The ACTIVE trial includes patients with isolated chondral or osteochondral defects. Candidates for the trial tend to be relatively young and must not have advanced osteoarthritis.
What does articular cartilage do?
Articular cartilage is a tough, smooth, elastic tissue which covers the ends of bones that form joints. It enables the bones to move smoothly over one another and acts as a shock absorber, cushioning the bone from forces of more than five times the body's weight. Damaged articular cartilage in knees can cause the joint to be painful, swollen and difficult to move.
Why doesn't it mend itself?
Cartilage is not like skin, it doesn't have the ability to repair itself properly. Instead, the damage tends to spread, allowing the bones to rub directly against each other. Any repair tissue that does form is not like normal hyaline cartilage and it doesn't work very well.
What is the best treatment?
Many patients appear to do well from an arthroscopic washout and debridement where any loose bodies of cartilage are removed and the defect is tidied back to healthy cartilage. However, when this treatment fails to relieve symptoms it is unclear what the best treatment is. ACTIVE is being run to help identify the best treatment. Only patients for whom previous treatment has failed are included in the ACTIVE trial.
What treatments are included in the ACTIVE trial?
All ACTIVE patients have a surgical treatment which is either a cell grafting treatment (autologous chondrocyte implantation (ACI) or matrix-assisted ACI (MACI)) or a non-ACI alternative. The surgeon will only recruit patients into the trial if he is undecided about whether ACI/MACI or an alternative might be the most appropriate treatment. There are several alternative, existing treatments available (described below) and the surgeon decides which one would be most appropriate for the patient. Within 3 months before surgery the patient is randomly allocated to have either ACI/MACI or the pre-selected alternative.
Non-ACI treatments
Debridement
Debridement is a rather broad term, but for ACTIVE it involves the removal of all "unstable" cartilage from the edge and base of the defect which is then washed or sucked away. Debridement is done arthroscopically which means it is done using keyhole surgery where a thin 'scope' is pushed into the joint (arthro=joint) to view the cartilage structure.
Abrasion/drilling
Abrasion/drilling involves arthroscopic debridement but in addition the base of the defect is debrided until small bleeding points are seen. The philosophy is that primitive blood cells are recruited from the underlying bone and these reform into joint cartilage cells and cover the damaged area with a new articular surface.
Microfracture
Microfracture is a modification of the drilling technique. Debridement is carried out to form a stable perpendicular edge of healthy cartilage. An arthroscopic awl is then used to make multiple holes in the defect, 3-4 mm apart. Blood from the defect is washed away until a clot forms. This "super clot" is believed to be the optimal environment for tissue to regenerate within the lesion.
Mosaicplasty
Mosaicplasty (also known as Osteochondral Cylinder Transplantation) involves filling the defect with osteochondral plugs to form a "mosaic". The plugs are usually taken from relatively non-weight bearing areas on the peripheries of both femoral condyles. The technique is usually done as an open procedure since care is needed to match the plugs with the size and shape of the defect to produce a smooth surface with the plugs fitting closely together. The main advantage of mosaicplasty is that the defect is filled with mature hyaline cartilage straight away. To avoid symptoms occuring from the donor site, this technique is only used for small defects.
AMIC
Since January 2007 AMIC (Autologous Matrix-Induced Chondrogenesis) has been included as one of the non-ACI treatments available in the trial. This new technique is similar to microfracture but it involves using a collagen membrane patch to stabilise the microfracture clot.
Bone grafting
Since April 2008 patients with osteochondral defects with more than 3 mm of bone loss can be included in ACTIVE. The standard treatment for these defects is bone grafting. Bone grafts may be autologous (the patient's own bone) allogenic (from a donor) or synthetic bone substitute depending on the surgeon's preference. Patients with osteochondral defects randomised to ACI will have bone grafting plus ACI.
Autologous chondrocyte implantation (ACI)
ACI uses the patient's own cells (chondrocytes) which are harvested from healthy articular cartilage, cultivated in a laboratory and implanted over the defect. The cells are held in place either by a periosteal patch which is soft tissue taken from the membrane covering the patient's tibia (shin bone) or by a manufactured collagen membrane patch. ACTIVE patients who are allocated ACI are further randomised to have one of the two types of patches.
In this two-stage procedure surgeons first harvest the cells arthroscopically from a healthy, non-weight bearing area of the knee joint. The chondrocytes are then treated in a laboratory for 3-4 weeks where they will multiple into several million chondrocytes. During the second surgery, the surgeon cleans the defect site, and removes a piece of periosteum (if using the periosteum patch). The patch (either periosteum or manufactured collegen membrane) is stitched and secured over the defect, and the cultured chondrocytes are then injected beneath the patch. There, the chondrocytes should eventually produce a form of cartilage very much like the original hyaline cartilage.
Rehabilitation following ACI is likely to be slower than the other treatments because the cells need time to generate repair tissue. Patients are given a physiotherapy programme to follow and should be prepared to give up driving for 7 weeks and avoid very strenuous activities for several months.
The Robert Jones & Agnes Hunt Orthopaedic Hospital NHS Trust has its own laboratory where cells are prepared for ACI. For more information on ACI please visit the Oscell website.
Matrix-induced ACI
MACI is a variant of ACI which has become an option in the trial (since March 2007) and can be used as an alternative to traditional ACI. With MACI the cells are cultured on collagen membrane in the laboratory before being attached over the defect. MACI does not normally require any stitching to the cartilage and is therefore a quicker procedure.
Think west ham have their fair share ... Ashton and dyer are 2 that spring to mind straight away. Although dyer came back against the yids fell over and is out again now
To much imformation there.
Hurty knee, without the details please. I'm eating lunch.
havent we got fry as back up for Lb and 5th choice CB??
I thought fry's looked pretty handy esp for back up when he's played
I agree but surely Jackson is playing to orders ?
I've seen him flying down the wing for Spurs, so believe he is capable.
Shame he didn't get fit as his athleticism would have always attracted a moron like Pardew or Dowie; mind you Adkins rated him, but his Scunny team were super organised.
Whatever my oppinion I'd never wish this on anyone. Rovers did some awful tackling against us last season, the guy who did Basey in should have been banned for 5-6 games. Whilst Youga's whack seemed 50-50, I can only hope he'll resurrect his career. Just not at Charlton.
Wish him well.
Limited career span means they have to make as much hay when the sun shines as they can cos their priority has to be to provide for their family imo
Re: Cory Gibbs, he has been back playing in MLS since he left Charlton. He is one of New England Revolutions best players. And dare I say it, would be one of Charlton's best now if still here.
Hopefully Youga can make it back the same way and isn't a permanent career crock.
Perhaps we should re-sign him. Sounds like the perfect replacement for Youga!
Looking back on what the OS said at the time, it seems we pretty unlucky to get lumbered with Gibbs, as we beat several other big clubs to his signature.
This from the bio on the OS at the time (so obviously must be true) :
''Able to play at left-back and as a left-sided central defender, Gibbs had plenty of options when it came to choosing his next club, and the Addicks beat off interest from UEFA Cup finalists Middlesbrough, as well as Bolton Wanderers and Premiership new-boys Reading to land their man.''
He'd failed at every 'big club' he'd been at. Not one Bundesliga 1 side wanted him after he'd won a meritorious relegation from Bundesliga 1 to the third tier of german football with Pauli. Feyenord wanted rid of him after his first injury with them. They say MLS is champ standard, in multiple games I've rarely seen champ standard some excellent players but few good teams. Fortune is a far superior player and more reliable injury wise. So what point is there even making a fanciful wish Gibbs?