Osteoarthritis of the knee progresses through stages.
Joint cartilage is a strange material. It is able to withstand repetitive movement over many years, but at the same time it is relatively fragile.
The cells of joint cartilage are not locked together like most tissues, but are suspended alone or with one or two other cells in little bubbles (lacunae) within a background matrix like a soft plastic, but within which is suspended a mesh of tiny fibres.
The matrix gives the joint cartilage its slipperiness; the fibrils its strength.
What you don't see in joint cartilage is blood vessels - the cartilage is dependent for its nutrition on nutrients filtering in from blood vessels in the bone underneath the joint cartilage or from the fluid within the joint space. So if cartilage is damaged it is in a precarious position - the cells are unable to quickly multiply to cover the defect and nutrition can easily become compromised.
In its advanced stages osteoarthritis IS a destructive disorder. But it doesn't start that way. The joint destruction of arthritis follows a set pattern.
Stages of cartilage destruction
EARLY - softening of the joint cartilage (chondromalacia)
During arthroscopy the surgeon is able to feel the softening of the joint surface when he/she presses it with the tip of an instrument (a 'probe'). At this stage the joint surface has not actually broken down but is under stress and boggy with fluid. At a later stage the cartilage is evidently boggy without being probed.
LATER - fissuring of the joint cartilage
Often these fissures or cracks cannot be seen - the surgeon will reveal them when probing with the probe. Although this looks minor, the cartilage surface is now on its way to arthritis.
BEGINNING TO BE SERIOUS - crabmeat appearance of cartilage("fibrillation")
Note that the damage is still confined to the cartilagenous ('gristle') covering of the bone. The bone is still intact. At this stage surgical intervention may still allow the cartialge to heal (albeit poorly) (eg. abrasion arthroplasty (shaving the surface), microfracture (poking holes in the surface to encourage blood vessels).
Now the damaged joint surface breaks into loose and friable fronds, which release enzymes that further aid the joint surface destruction.
SERIOUS - exposure of and damage to underlying bone
Once the destruction has progressed through into the underlying bone the prospect of healing without surgical intervention is nil.