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Collagenase induces the degeneration of the articular cartilage by directly digesting collagen from the extracellular matrix of cartilage [ 20], and as a consequence of articular instability due to increased joint laxity [ 22].
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The improvement was accompanied by amelioration of pain and physical dysfunction as a consequence of suppression of articular inflammation and joint destruction.
Post-traumatic arthritis is a frequent consequence of articular fracture.
This incongruence may not be large and may be lessened by mutual deformation of the opposed parts of the surfaces, a consequence of the deformability of articular cartilage.
Alternatively, another explanation for joint morphological -differences is that the position of the first metatarsal – as a consequence of hallux valgus – causes articular metaplasia of the proximal articular joint.
Although there is evidence of micro-damage to subchondral bone, it is not known whether this is a cause or a consequence of MCD, nor is it known whether articular cartilage is modified in the early stages of the disease.
injection of collagenase leads to increased joint laxity [ 22] probably as a consequence of the degradation of collagen from menisci and articular ligaments, suggesting that, in this model, OA develops as a consequence of joint instability [ 18, 40], therefore reproducing an important trait of human OA.
As a consequence of mechanical and biochemical events, imbalance between synthesis and degradation of articular cartilage matrix results in clinical OA.
The susceptibility of articular cartilage to progression towards OA is a consequence of its avascular nature and low capacity for self-repair following injury.
The collagenase model combines the advantage of inducing OA as a consequence of joint instability and degradation of collagen in the articular cartilage, with the methodologically simple i.a.a
articular reduction and fixation; meniscal repair (either as a consequence of injury or surgical approach); MDD reduction and stabilisation.
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