effi-science/e-sciences

Osteoarthritis, pain and anti-inflammatories

Anti-inflammatory drugs are often used to treat osteoarthritis to ease the pain. They offer quick relief but are not effective against the underlying problem, they carry the risk of side effects and they quickly become very expensive.

What can be expected from taking 1500 mg/d of Glucosamine Sulphate?

Glucosamine as in Cartilamine 1500 really gets to the root of the problem by slowing down the cartilage degradation mechanism through several mechanisms of action AND by decreasing the inflammatory cascade. It is much cheaper than an anti-inflammatory or painkiller (more information on the mechanism of action later/other page/change the page "treatments")

Moreover, unlike anti-inflammatory drugs, which can cause serious side effects, it does not.

Now we will look at the mechanism of inflammation to better understand how anti-inflammatory drugs work and where they fit in osteoarthritis.

Pain and inflammation

Below is a drawing to give an overview of the inflammatory process.

- It all starts with an event such as a burn, a virus infection or an internal lesion (e.g. cartilage), which triggers the inflammatory reaction.

- The inflammatory reaction will set in motion a whole cascade of inflammatory mediators, which will link together to allow the body to react. Some of these inflammatory mediators are called cytokines.

- The cytokines will then activate certain enzymes. The cytokine IL-1B (interleukin-1B) is very important in the process of osteoarthritis, as well as in the pain process in general. It will activate COX-2 enzymes. Other important cytokines are TNF-α and IL-6, which also have an action on COX-2

- COX-2 enzymes play an important role in pain and will produce prostaglandins, which they will then release into the extra-cellular environment and the blood. Prostaglandins are a type of molecule that have a wide range of physiological functions (their name comes from the fact that they were first discovered in the human body in the prostate).

- The release of prostaglandins triggers pain and other physiological effects that reinforce the sensation of pain (redness, swelling, etc.)

- Pain is communicated to the brain by the nerves, which perceive prostaglandins or other pain mediators, or directly perceive burning, shock etc.

Let's take a closer look at these COX enzymes:

There are two types of enzymes, COX-1 and COX-2. COX-1 is always active, COX-2 will be activated by inflammatory mediators.

The prostaglandins produced by COX-1 are necessary for the proper functioning of the body. For example, there are prostaglandins that have a protective effect on the stomach, and others that allow the kidneys to function properly. In the end, their effects are therefore productive and necessary.

COX-2 enzymes, on the other hand, are activated by inflammatory mediators. The prostaglandins produced by COX-2 will trigger pain signals.

To combat this, the pharmaceutical industry has developed products that block COX: anti-inflammatory drugs or NSAIDs (= non-steroidal anti-inflammatory drugs, a type of anti-inflammatory drug).

Unfortunately, anti-inflammatory drugs will block COX without differentiating between COX-1 or COX-2 enzymes.

If on the one hand the blocking of COX-2 which allows the anti-pain and anti-inflammatory effects, it should be noted that blocking COX-1 amounts to depriving the body of the beneficial effects of the prostaglandins produced by COX-1. This is where the sometimes serious side effects, such as gastric bleeding, come from.

Painkillers and anti-inflammatories

The painkillers and anti-inflammatories that are most often used for osteoarthritis are

A. NSAIDs or non-steroidal anti-inflammatory drugs (over the counter or prescription, list here)

B. Paracetamol

C. Anti-COX2

A. NSAIDs

Exemple : ibuprofène ou acide acétylsalicylique. L’ibuprofène est un des AINS les plus connus et l’acide acétylsalicylique est un des plus anciens. Le nom complet d’AINS est “anti-inflammatoire non-stéroïdien”, un type d’anti-inflammatoire. Ils agissent en bloquant à la fois les enzymes COX-1 et COX-2. Comme vu ci-dessus, en bloquant les COX-2 on diminue la douleur, par contre bloquer les COX-1 va produire les effets secondaires typiques des anti-inflammatoires, comme les ulcères, saignements gastriques, les problèmes de perfusion du rein et l’hypertension (voir schéma ci-dessus). Il n’y pas d’effet sur le reste de la cascade inflammatoire Pour obtenir un effet anti-inflammatoire dans le cadre de l’arthrose suffisant, il faut prendre minimum 1200 mg d’ibuprofène / jour (soit 3 x 400 mg) et 3 g d’acide acétylsalicylique (3 x 1 gramme / jour)

B. Paracetamol

Paracetamol is a purely pain-relieving drug. For a long time its mechanism of action was not clear. It seems that it acts on COX but at the level of the brain, which explains why it does not cause the same side effects as ibuprofen. On the other hand, it is hepatotoxic in too large doses. The risk exists from more than 4 g/day, but the recommended dose for osteoarthritis is 3 grams (1 gram 3 x / day).

C. Anti-COX2

Exemple : celecoxib Pour essayer de remédier aux problèmes d’effets secondaires des médicaments ont été mis au point pour ne bloquer que les enzymes COX-2, sans toucher les COX-1. (Tel que le rofecoxib, celecoxib etc.) Malheureusement ces médicaments sont associés à des risques cardiovasculaires accru et certains ont été retirés du marché suite à des effets secondaires trop importants.

Why are anti-inflammatory drugs not enough for osteoarthritis?

Osteoarthritis is not only a process of inflammation, it is also a cartilage disease. Only glucosamine combines an effect on inflammation and cartilage.

The following are examples of cartilage arthritis problems:

wear and tear of the cartilage due to age, sport, overweight
too much cartilage degradation
not enough cartilage renewal

The anti-inflammatory drug will relieve pain and if taken in sufficient quantities can stop flare-ups.

However, it causes side effects, which glucosamine does not.

Glucosamine is THE solution, because it acts on COX-2 and other elements of the inflammatory cascade, but it also acts on the structure of the cartilage!

We therefore have a double effect: effect on the inflammatory cascade + effect on the cartilage, to finally really combat pain in the long term.