There is so much more now that we can do for arthritis than we used to be able to. When I started practising over 2 decades ago, we had one approved anti-inflammatory for dogs, that was it. If a dog did not respond to “bute” (phenylbutazone), or got an upset stomach on it, too bad – out of luck. That was one of the most frustrating aspects of my profession: watching these big goofy-grinned dogs, still smiling and thumping their tails, but unable to get up or walk without pain.
Oh, the evolution of arthritis management since then! It gladdens my heart not to have to shrug and give up – we have options now!
Medications: More, and better anti-inflammatories
Arthritis is a vicious cycle. Whatever caused the cartilage to become damaged in the first place – wear and tear, injury, infection, disease, it does not matter – the body responds in the same way: “Oh no, damaged cartilage?!? Must be bacteria!! Better fight back with inflammation!” And so, a whole bunch of inflammatory mediators get dumped into the joint, with the goal of fighting bacteria (whether they are there or not). It so happens that these inflammatory mediators are really rough on the cartilage, causing damage; which causes more inflammation; which causes more damage… get the idea?
So, when we use an anti-inflammatory, it is not just pain control, it is DAMAGE CONTROL. If you can tone down the inflammation in the joint, you can slow down the degradation of that joint.
We have so many more veterinary-approved anti-inflammatories available to us now, and they are so much less likely to have side effects than the old medications.
These drugs are called NSAIDs – that stands for Non-Steroidal Anti-Inflammatory Drugs. That name is to distinguish them from Steroids, or cortisone-type drugs (and while steroids are very good anti-inflammatories, they also have scads of side effects and can promote cartilage degradation in the long run… the rule with Steroids should always be “less is more”).
NSAIDs work by inhibiting an enzyme called Cyclooxygenase (COX), which makes the chemical mediators known as Prostaglandins (PGs). PGs are the chemical signals that cause inflammation to happen, and all the pain, heat and swelling that go with it.
Not all PGs are bad, though. There are many of them that are responsible for regulating certain “housekeeping” functions in the body. These include:
- Maintaining blood flow to your stomach lining – this is why too much of these medications can end up causing stomach ulcers. When the blood supply is messed up, areas of tissue die, and then the stomach acid eats them into big craters.
- Maintaining blood flow to your kidneys – when your blood pressure drops, for example if you get dehydrated, it is a PG that makes sure that blood keeps going through the kidney’s filter systems. If this compensation mechanism gets messed up by an NSAID, then there is nothing to keep the filters working when pressure drops – kidneys can end up damaged.
- How you clot your blood – PGs are a big part of the signalling system used by platelets. Platelets are the “first responders” in stopping bleeding. These flexible little packets of cytoplasm flock to the site of damage and make a “patch” out of their own little bodies. Then they send out signals both to call in more platelets, and to start the biochemical cascade that is the clotting of blood. This is why we take NSAIDs when we do NOT want clots to form: human patients with cardiovascular disease take Daily Low Dose Aspirin therapy to sabotage their platelets on purpose.
So, messing up PG production can mess up these “housekeeping” functions too, producing undesirable side effects.
Now, here is where the “better” part of the new drugs comes in. It turns out that Cyclooxygenase is not just one enzyme… it is at least two. COX-1 is the one that makes the housekeeping PGs. COX-2 makes the pain and inflammation PGs. The new drugs target COX-2, and 90%-plus leave alone the COX-1. Note that I did not say 100% – any NSAID has the chance of side effects by affecting COX-1; however, the chances are a lot less with these drugs than with the old drugs that were non-specific.