More Complex Explanation of COX-2 Inhibitors
Many, and perhaps most, cells of the body have the cyclo-oxygenase enzyme in them. Given the importance of the pain signal to the survival of the organism, the cyclo-oxygenase pathway leading to prostaglandin E2 most likely evolved very early in the history of life. If this is true, then it probably also has been around long enough to have been incorporated into many other biological processes, and this is exactly what medical research has found. COX is used by the stomach to create the mucous which lines the stomach and prevents it from digesting itself, by platelets in the process of clotting, in the kidney to perform normal function, etc. This explains why, when you take aspirin or Motrin, you bleed more easily(we use this to our advantage in preventing heart attacks and stroke), develop stomach ulcers, etc. This COX enzyme is a normal constituent of the cell and therefore is called a constituitive enzyme.
The COX enzyme that is involved in pain, arthritis, and inflammation in general, is not normally present, but is induced on demand by the cell. This is called an inducible enxyme.
It was discovered that these two COX enzymes are not identical; they are very similar, but not identical. They were therefore given different names: the constituitive enzyme is called COX-1 and the inducible enzyme is called COX-2.
After a lot of work, it was discovered how to block COX-2 but not COX-1. This allows the body to continue with its normal processes (we are not blocking the constituitive enzyme) while decreasing pain and inflammation (we are blocking the inducible enxyme).
There has been some questions about whether or not COX-2 inhibitors will influence fracture healing, since inflammation is a necessary first step in bone healing. You can read more here. There is also question about COX-2 inhibitors and fusion. You can read more here.
This information may help you to decide if you want to spend the money for the COX-2 inhibitors, which cost more than regular NSAID's.
