An ascorbic acid molecule carries two extra electrons with which it can can neutralize two free radicals. When it gives up those two electrons, it is mostly finished unless the mitochondria give it back two electrons. Then the ascorbate can be used over and over again. A major problem, however, is that when there is an inflammation in a tissue, the mitochondria there are so damaged as to not be able to rereduce the dehydroascorbate back to ascorbate. Additionally, the damaged mitochondria become a major source of free radicals. A free radical cascade results.
Only massive doses of ascorbate will shut down this free radical cascade. I am actually after the extra electrons carried by the ascorbate, not the ascorbate itself. When the concentration of these electrons is raised over a threshold point in the inflamed tissues, the free radicals are instantly neutralized and the free radical cascade is shut down.
If the concentration of the ascorbate (electrons, reducing redox potential) are driven in high enough concentrations into the inflamed tissues, the inflammation medicated by free radicals, the inflammation will be shut down. Therefore, the degree to which massive doses of ascorbate can cure or ameliorate a condition is proportional to the importance of free radicals in the pathology of that condition.