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Knee Problems: Articular Cartilage Damage |
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What is Articular Cartilage?Articular cartilage is a highly organized avascular tissue composed of chondrocytes embedded within an extracellular matrix of collagens, proteoglycans and noncollagenous proteins. Its primary function is to enable the smooth articulation of joint surfaces, and to cushion compressive, tensile and shearing forces. Hyaline cartilage has one of the lowest coefficients of friction known for any surface to surface contact.
Why is articular cartilage repair necessary?Cartilage is frequently injured, often as a result of sports related trauma, but due to its avascular nature, articular cartilage has very limited capacity for repair. Partial-thickness defects in the articular cartilage do not heal spontaneously. Injuries of the articular cartilage that do not penetrate the subchondral bone do not heal and usually progress to the degeneration of the articular surface. Injuries that penetrate the subchondral bone undergo repair through the formation of fibrocartilage.
Although fibrocartilage fills and covers the defect, this is the wrong tissue from the biomechanical standpoint. The fibrocartilage is made to resist tension forces, while the hyaline cartilage is made to resist compression forces, to enable smooth articulation, and to withstand long-term variable cyclic load and shearing forces. Focal articular cartilage defects, often found in young adults, have been increasingly recognized as a cause of pain and functional problems. There is more and more clinical evidence that full thickness articular cartilage defects continue to progress and deteriorate, although at a slow rate. Early diagnosis and treatment of these patients is recommended prior to the development of more advanced osteoarthritis. In selecting methods of restoring the damaged articular surface, it is important to distinguish articular cartilage repair from articular cartilage regeneration. Repair refers to the healing of injured tissues or replacement of lost tissues by cell proliferation and synthesis of new extracellular matrix. Unfortunately, repaired articular cartilage generally fails to replicate the structure, composition, and function of normal articular cartilage. Regeneration in this context refers to the formation of an entirely new articulating surface that essentially duplicates the original articular cartilage. Therefore, the best we can do at present is to repair the chondral defect.
Articular cartilage repair and reconstructive procedures:Historically there have been many attempts to develop clinically useful procedures to repair damaged articular cartilage. However, most cartilage repair techniques have not proved entirely successful yet. At present, the treatment options are still limited and the long-term outcome is still uncertain. The principal goals for surgical management of the symptomatic chondral and osteochondral defects are to reduce symptoms, improve joint congruence by restoring the joint surface with the best possible tissue, and to prevent additional cartilage deterioration. Although the need for surgical management is based on the patient's history, physical examination, and imaging studies, only knee arthroscopy will provide definitive information regarding the lesion's characteristics (ie, location, size and depth) and associated injuries (menisci and cruciate ligaments). Based upon their anticipated outcome, it is helpful to define treatment options as being palliative, reparative, or restorative. First-line treatment for smaller injuries in lower-demand patients with limited symptoms can be treated effectively with palliative procedures such as Debridement and lavage. Relief, however, may be incomplete and short-lived. Mid-sized lesions in patients with moderate symptoms can be treated with a reparative procedure using a marrow-stimulating technique (Microfracture) in an effort to promote a fibrocartilage healing response. Results in larger lesions in higher-demand patients, however, are generally less favorable and shorter-lived, independent of any prior treatments rendered. Larger defects, especially in higher-demand patients with significant symptoms who have failed less aggressive primary treatment options, are most effectively treated with a restorative treatment option such as Osteochondral Autologous Graft Transplantation (OATS) and Autologous Chondrocyte Implantation (ACI). See also: Debridement and lavageLavage (arthroscopic washout) is one of the most basic of traditional arthroscopic techniques. Dr Robert Jackson, the pioneer of arthroscopy in North America, observed that in the course of performing diagnostic arthroscopies patients with intra-articular knee problems had significant pain relief following joint lavage. Exactly how arthroscopic lavage and debridement may help the early symptoms of osteoarthritis is still not entirely clear. Joint lavage removes loose intra-articular tissue debris and inflammatory mediators known to be generated by the synovial lining. In early stages, removing these degradative enzymes from the joint may allow chondrocyes to increase their biosynthetic activity. Another mechanism by which lavage may relieve the symptoms and increase the resiliency and stiffness of articular cartilage is through changing the ionic environment within the synovial fluid. Lavage may provide some patients with advanced degenerative disease of the knee, which may last as long as 3 years. However, the lavage provides only short-term symptomatic relief without correction of underlying pathology. If predisposing malalignment is not corrected, the beneficial effects seem to be minimised. The outcome of this simple procedure is generally insufficient for the active population, and benefits are short-lived. MicrofractureThis technique was developed and popularised by Dr Richard Stedman, from Vail, Colorado, USA. The treatment involves a disruption of subchondral bone in an attempt to induce bleeding (fibrin clot formation) and to initiate primitive stem cell migration from the bone marrow into the cartilage defect site.
These techniques utilise primitive stem cells, which are capable of differentiating into bone and cartilage under the influence of various biologic and mechanical intraarticular factors. The subchondral bone is penetrated in order to reach a zone of vascularisation, stimulating the formation of a fibrin clot containing pluripotential stem cells. This clot differentiates and remodels, resulting in a fibrocartilaginous repair tissue. Although fibrocartilage often appears to offer the patient significant pain relief, this tissue lacks several key structural components to perform the mechanical functions, as a wear-resistant and as a weight-bearing surface. The fibrocartilage repair tissue does not produce a proper compressive stiffness against applied mechanical load and thus is subjected to an excessive deformation under physiological loading. This in turn causes a mechanical failure of the repaired tissue and eventually leads to a recurrence of degeneration of the repaired cartilage. For more information on Microfracture see Osteochondral Autologous Transplantation (OATS)
This technique was developed simultaneously by Dr L Hangody in Hungary and Mr V Bobic in the UK approximately 10 years ago. Osteochondral autograft transplantation seems to be the only surgical technique that can restore the height and the shape of articulating surface in focal osteochondral defects, with composite autologous material that contains all necessary ingredients: hyaline articular cartilage, intact tidemark and a firm bone carrier. However, like many other orthopaedic procedures that require the use of autologous tissues, osteochondral autograft transfer (or MosaicPlasty) is the "rob Peter to pay Paul" situation. The main problem with this reconstructive technique is the limited availability of autografts, which significantly reduces the choice of treatable defects down to a small focal chondral defect, and a long-term donor morbidity in multiple donor sites. Deep and large, crater-like osteochondral defects are not suitable for osteochondral autograft transplantation, mainly because of the limited availability of autologous osteochondral grafts. Also, it is difficult to reconstruct the subchondral bone and restore the contour of the defect area, and to cover the entire defect area with hyaline articular cartilage. The dead spaces between circular grafts, the lack of integration of donor and recipient hyaline cartilage, different orientation, thickness and mechanical properties of donor and recipient hyaline cartilage are further sources of clinical concern.
V Bobic: The
Utilisation of Osteochondral Autografts For more information on OATS instrumentation/surgical technique please see: For further information please visit this website: The OATS Procedure. John Hopkins University, Baltimore, USA. Autologous Chondrocyte Implantation (ACI)This advanced FDA-approved technology allows cartilage cells, know as chondrocytes, to be harvested from your knee and cultured and multiplied. The fresh chondrocytes are then re-implanted in your knee and cause hyaline-like cartilage to repair the defect in articulating surface.
The ACI restores the articular surface with your own hyaline-like cartilage without compromising the integrity of healthy tissue or the subchondral bone. This technology has demonstrated significant benefits in patients with a femoral focal lesion, in terms of diminished pain and improved function.
Graft hypertrophy is relatively frequent problem and it may require further arthroscopic surgery. The procedure consists of two steps:
For more information on ACI surgery and rehabilitation please see this article: Tom
Minas, MD. and
visit the website: www.cartilagerepaircenter.org
Site last updated on: 20 June 2008
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| Mr Vladimir
Bobic, MD, FRCSEd, Consultant Orthopaedic Knee Surgeon, Chester Knee Clinic at The Grosvenor Nuffield Hospital, Wrexham Road, Chester, CH4 7QP, United Kingdom General Enquiries: 0845 6022500 | Appointments: 01925 215087 Spire Cheshire Hospital, Fir Tree Close, Stretton, Warrington, Cheshire WA4 4LU, United Kingdom General Enquiries: 01925 265000 | Appointments: 01925 215050 © Copyright 2002-2002008. Chester Knee Clinic |