TNF antagonist therapy

In the article "New Therapeutic Approaches for Spondyloarthritis" we are told the relative effectiveness of three TNF-a antagonist therapies, including infliximab, etanercept, and adalimumab. In the beginning sections of the article we are told that inhibiting TNF will reduce spine inflammation in active AS (ankylosing spondyloarthritis) and inhibit the structural disease progression due to inflammation. In the conclusion paragraphs, we also are reminded that the inhibition of TNF is a successful therapy for decreasing and eliminating spinal inflammation. However, in the middle paragraphs describing the studies using infliximab, etanercept, and adalimumab, the actual "inhibition of TNF" is never mentioned or described. They were introduced as "TNF-a antagonist therapies," but in their descriptions and discussions the mechanism for this inhibition is never touched on. I would be interested to read more about how the TNF is inhibited, such as where in the spine their activity is halted, how fast the therapies occur, how they are performed, etc. Also, throughout the article, it is supported that the inhibition of TNF will decrease deterioration and inflammation, but the author also continues to mention that these therapies did produce compelling argumments regarding structural disease modification. I find this interesting to mention, since all the experiments are studying is the inhibition of TNF, and this would have no affect on structural modification besides the reduction of inflammation. If structural modification, such as the inhibition of the inflammation and degradation in addition to rebuilding lost tissues and bone, was the intent, an additional enzyme or catalyst must be used that will promote the rebuilding. For example, just as TNF was inhibited in the sacrum and iliac crest in these therapies, osteoblast production should be promoted by an activator to in turn promote rebuilding the bone lost to AS. This is a good start to curing and preventing AS, however it is only a start. Now that we have the beginnings of the therapies to stop the disorder, we should begin looking for the second half of therapy which is repair/rebuilding and prevention for future attack.