Arthritis Drugs

Arthritis Drugs

Inflammation and pain in the joints (arthritis) can be caused by many things, but the following are the main types of arthritis diagnoses:

  • Osteoarthritis (OA): This is known as “degenerative joint disease” and involves the wear-and-tear process of aging and joint use. This affliction constitutes 80% of arthritis diagnoses.
  • Rheumatoid arthritis (RA): This an autoimmune disease in which one’s own immune system attacks the joints. This is 10% of arthritis diagnoses.
  • The remaining 10% of arthritis diagnoses are the remaining types of arthritis, including psoriatic arthritis.

What happens in arthritis?

Generally, arthritis means inflammation, and inflammation over the long-term can be damaging and result in joint destruction. Pain can cause inflammation.
In osteoarthritis, which is age- and use-related wear-and-tear, there is osteophytosis, or the production of osteophyte. Osteophytes are commonly called bone spurs, which are bone projections that form along joint margins from chronic inflammation and progress to cause nerve compression and neurological pain. Osteoarthritis causes the deterioration of the cushioning cartilage and ultimately the destruction of the anatomy and function of a joint. It can be localized or affect more than one joint, but it most commonly involves the distal fingers, neck, lower back, knees, and ankles. Osteoarthritis is also characterized by hardened tissue over some of its sites, which is known as Heberden’s and Bouchard’s nodes.
Rheumatoid arthritis is typically polyarthritic (not localized like OA); symmetrical; and involves joint space narrowing, the stretching of tendons and ligaments, and the erosion of cartilage and bone. It is more peripheral in the areas that it commonly affects, as the hands, knees, ankles, and elbows are particularly susceptible to developing rheumatoid arthritis.

How is osteoarthritis treated?

Holistic approach:
Since OA is a wear-and-tear degeneration of the joint cartilage and other aspects of bone juxtaposition, treatment should be tailored to the patient holistically. Aggravating factors, such as obesity, lack of exercise, smoking, and repetitive motion injury, should be targeted first. Education is important.


    • Topical NSAIDs, typically of the diclofenac (Voltaren) formulation.
    • Oral NDAIDs:
  • Ibuprofen (Advil, Motrin)
  • Meloxicam (Mobic)
  • Diclofenac (Voltaren)
  • Ketorolac (Toradol)

COX-2 Inhibitors:
COX-2 enzymes regulate inflammation, and the drugs that inhibit them will decrease inflammation. COX-1 helps protect the intestinal tract, so there can be some crossover that can aggravate gastrointestinal problems.

  • Celecoxib (Celebrex)
  • Rofecoxib (Vioxx)
  • Valdecoxib (Bextra)

Steroid anti-inflammatories:

  • Prednisone (Deltasone)
  • Prednisolone (Omnipred)
    • Topical duloxetine (Cymbalta) can be used when NSAIDs are contraindicated, such as with gastritis or clotting problems.
    • Topical capsaicin: This is a derivative of chili pepper that overwhelms the pain mechanism. It may cause a burning sensation as a side effect.

Injection with steroids:
This treatment approach is only temporary, as it lasts about a month or so, so its routine use is discouraged.

This treatment approach is discouraged due to abuse and addiction potential.

When there is joint destruction to the point of debilitation, joint replacement is beneficial if all other remedies have proven ineffective.

How is rheumatoid arthritis treated?

Care by a specialist in RA, such as a rheumatologist, gives better treatment outcomes for rheumatoid arthritis since therapy is aimed at altering the immune system.

Education, rest and exercise, physical therapy, dietary counseling, and immunizations decrease the risk of infection that accompany immunosuppressive therapies.


Since drug treatment for RA targets the immune system, all patients should be screened for infectious diseases, such as hepatitis, TB, etc. As with OA, appropriate treatments are holistic approaches; steroid anti-inflammatories; non-steroid anti-inflammatories (NSAIDs); COX-2 inhibitors; and, if indicated, surgery.

The goal of treatment, however, is to alter the immune system’s attack with disease modifying antirheumatic drugs (DMARDs).
DMARDs come in the following forms:

  • Non-biologic immune-system suppressants:

    These interfere with combinations of critical pathways in the inflammatory cascade. These suppressants are Category X substances, so using these on pregnant women is ruled out. The following are non-biologic immune-system suppressants:
    • Methotrexate (Trexall): This an antimetabolite and is the cornerstone of RA therapy.
    • Hydroxychloroquine (Plaquenil): This is an antimalarial drug and may be added.
    • Sulfasalazine (Azulfidine) may be added to methotrexate and hydroxychloroquine, resulting in a treatment approach termed the “triple therapy.”
    • Leflunomide (Arava): This is used as a single agent.
    • Azathioprine (Imuran)
  • Biologic immune-system suppressants:
    These are suppressants that are derived from molecular biologic techniques and target specific steps in the inflammatory process, namely, interfering with agents of inflammation, such as B-cells, T-cells, TNF, and the cytokines. As the mysteries of the immune system are deciphered and science progresses, precision strikes at individual inflammatory actions will be possible in the near future.

Biologic suppressants work faster than the non-biologic ones, but these must be given by injection, except for the new subcategory known as a JAK inhibitor, which can be taken by mouth. The biologics include the following:

    • Anti-TNF, including etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira);
    • T-cell interference, including abatacept (Orencia);
    • JAK inhibitor, including tofacitinib (Xeljanz).
  • Surgery:
    When there is joint destruction to the point of debilitation, or if there is pending tendon rupture, surgery may be necessary, and it is important to know when to commit to it, as waiting too long may allow a window of opportunity for this treatment approach to close.

Osteoarthritis and rheumatoid arthritis, which together make up 90% of all arthritic diagnoses, differ from each other by their causes: age and wear-and-tear for OA and auto-immune attack of the joints for RA. The aging process involves many other developments besides osteoarthritis, but OA is a near-certainty if one lives long enough. On the other hand, rheumatoid arthritis can develop in anyone at any time. For the most part, treatment of both OA and RA are the same when attempting to control symptoms. Since RA is an abnormality of the immune system, however, the drug class of immune-suppressants is added to the treatment regimen to try to control the disease.
It is possible, especially in older people with OA, to have both RA and OA. Discretionary treatment to cover both can be tricky, but today’s rheumatologist is best equipped to manage this task.