Knee 'arthritis' is usually 'osteoarthritis', not the crippling sort of arthritis called 'rheumatoid' arthritis. In the knee it is caused by wear and tear or sometimes an injury. Often it is triggered by a mechanical focus - such as a kneecap which does not track properly - this triggers a sequence of local inflammation and joint surface softening, then local joint surface destruction which is accompanied by release of chemical substances into the injured joint, which then in turn sets off a destructive process in the joint as a whole.
Knee arthritis may become established from a number of causes - but once joint destruction sets the pattern of damage is much the same irrespective of the original cause. So, it doesn't matter what disorder one starts with - insufficient or inappropriate treatment may lead everyone down the same common arthritis pathway!
Note that ostoarthritis of the knee can arise without a mechanical trigger, but our point is that it is very often the end result of long term problems in the knee - a torn meniscus, a maltracking patella, a fracture, or even inappropriate or over-enthusiastic surgery!
When a kneecap tracks badly, the one side of it contacts the femur bone with too much pressure, while the other side contacts it with too little pressure. The kneecap needs a certain amount of contact pressure to 'pump' the nourishment from the joint fluid. When the pressures are wrong the joint cartilage softens and swells (chondromalacia), then blisters or fissures, then the blister or fissure breaks into fibrils, and these later break off and float into the joint. This destructive processs releases enzymes into the joint, and these cause destruction elsewhere in the joint.
At the point of contact of the abnormal plica with the underlying bone, the plica becomes reddened, traumatised and thickened. Catching is aggravated and the underlying joint surface becomes softened and undergoes the same destructive cycle described above, while the damaged plica releases the same destructive enzymes which spreadthe damage elsewhere in the joint.
When the integrity of the meniscal shock-absorber is badly disrupted the joint is unstable in addition to the joint surface being insufficiently buffered from shocks. Also the flap of loose meniscus can twist over and lock the joint, further damaging the surface. The joint cartilage undergoes the same softening/fibrillation cycle, with the enzyme damage spreading the destruction.
When the cruciate is torn, it is usually the result of a significant injury, and meniscus and joint surface are often damaged at the same time. But even when this is not the case the instability of the joint introduces forces which eventually do stress both the meniscus and the joint cartilage, and the softening/fibrillation/enzyme cycle is triggered once more.