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Osteo Vs. Rheumatoid Arthritis

joint pain

All about Osteoarthritis and Rheumatoid Arthritis

A brief discussion by Jonathan Krant, MD, GHLF and CreakyJoints Chief Medical Director

Dr. Krant is a board-certified rheumatologist with 20 years clinical experience running an academic service.

Dr. Krant



Osteoarthritis

Osteoarthritis (OA, DJD) is a broadly-defined condition brought about by loss of articular cartilage and degradation of underlying bone. Typically non-inflammatory, OA is derived from the Greek ‘osteo’ (bone) and ‘itis’ (inflammation) – some feel that osteoarthrosis is a more accurate characterization of the disease state.

osteoarthritis

There is ‘nodal’ OA (typically Heberden’s and Bouchard’s nodes of the small joints of the hands), as well as less common ‘erosive’ OA, commonly thought to be inflammatory in nature. Risk factors for primary OA include genetics (with increased incidence among twin offspring of affected parents), mechanical stress (including misalignment), loss of cartilage and neurogenic causes of disease. Secondary OA is frequently seen in the context of rheumatoid arthritis, gout, diabetes, hypothyroidism and infection, amongst other causes.

Articular cartilage consists of a sponge-like material called proteoglycan, which both absorbs fluid and expels it under compressive force. Alterations in the biology of proteoglycan results in both higher fluid content and decreased compressibility. As the ability to resist load-bearing decreases, the impact of stress on underlying (subchondral) bone increases, with eventual cystic degeneration and spur formation.

This inevitable process of cartilage failure, joint space narrowing and bony erosion leads to pain with ambulation (especially involving the hips, knees and lumbar spine) and significant disability. The known clinical correlates of exercise intolerance, weight gain, immobility and mood alteration are well known to 27 million Americans (or more) whose OA accounts for 25% of physician visits and 50% of prescription NSAID use.

 

There is unequivocal evidence supporting the combination of weight loss, exercise, analgesic use (oral, injectable and topical) as well as assist devices (orthotics, canes) for patients with OA. Joint injection with ‘viscoelastic’ hyaluronic acid derivatives provides temporary benefit for some, while oral NSAID use (ibuprofen, Naprosyn and the like) are beneficial, yet not without significant risk for GI bleeding and impaired kidney function when taken continuously for 6 weeks or longer. Tylenol may confer less risk of adverse events, and has good analgesic properties when taken in full therapeutic doses.

Topical NSAIDs (diclofenac drops or gel rubbed into the joint capsule for example) has proven benefit, and there is limited clinical trial-based evidence supporting specific dietary supplements for OA disease management.

One of the great mysteries for physicians managing patients with OA is the apparent discrepancy between advanced radiographic appearance of disease and its clinical features. Despite virtual ‘bone on bone’ anatomy, some patients continue to run, bike, hike and compete in racquet sports while others, with less radiographically-apparent disease burden, are dramatically more affected. Comorbid conditions, drug tolerance (especially with the opioid analgesics), reluctance to embrace behavioral change and other management issues make OA a challenging condition, for both patient and physician.

Rheumatoid Arthritis

Rheumatoid Arthritis (RA) is the prototypic autoimmune disease, characterized by the five cardinal signs of inflammation (warmth, redness, swelling, tenderness and diminished function).

Although joints and organ systems are frequently affected, the fatigue, episodic fever and malaise which accompany early disease are crippling features with significant impact on patients with newly-diagnosed RA. Usually occurring in people ranging in age from their mid-twenties to mid-fifties (with a female predominance of 2:1), RA occurs in 1-2% of the world’s population with occasional variations in prevalence.

This brief discussion will address the genetics of disease susceptibility, clinical features and therapeutic options for patients with RA, including the controversial areas of disease recognition and strategies utilized to treat disease with variations in clinical activity. Controversies surrounding access and distribution are also discussed.

RA is thought to result from a combination of genetic-specified risk factors and environmental exposures which place individuals at risk. The HLA-DR4 locus is an established genetic susceptibility marker, with IgM rheumatoid factor (RF) a commonly-encountered plasma biomarker of disease. The interleukins, especially IL-1 and IL-6 are known cytokines produced by activated cells implicated in disease activity, and the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count and fibrinogen are non-specific markers of inflammation, often tracked in patients both before and after therapeutic intervention as surrogate markers of clinical response. A variety of infections have been implicated as possible precipitants of disease in genetically-susceptible individuals, including viral and mycoplasma upper respiratory infections. Patients with early disease may report the explosive onset of joint swelling plus fever, fatigue and generalized malaise. By contrast, some patients with RA never develop such ‘full-blown’ features and present with rather indolent symptoms (aching, tenderness, soreness) which tend to persist at a low-level of disease activity.

Therapeutic strategies are a topic of debate in the rheumatologic community. For patients with explosive disease onset, moderate doses of prednisone or prednisolone are frequently prescribed, along with NSAIDs for an interval of four to six weeks. A lack of response or persistence of clinical features can lead to a DMARD prescription (methotrexate, hydroxychloroquine, azulfadine) in addition to DMARDs, NSAIDs plus/minus steroids. Patients may be treated in this manner for up to 12 weeks prior to consideration of biologic therapy.

Biologics targeting selective elements of the inflammatory pathway, may be added by the 12th week of ongoing disease activity. There are a variety of molecules available for the treating rheumatologist, including both sq and infusion-based regimens of TNF antagonists, IL-1 and IL-6 inhibitors and, if evidence of disease activity persists, selective B-cell inhibitor therapy available via infusion. Oral therapy targeting the janus kinase pathway has recently become available, and the potential benefits of developing targeted, effective therapies to be used in combination with background DMARD (with limited adverse events) has become the holy grail of drug development in this domain.

The downside of parenteral therapy for rheumatoid arthritis (and its cousins, the inflammatory spondyloarthropathies) are legion. Injection site reactions with erythrocyte sedimentation rate (ESR) subcutaneous therapy, low-grade infection, potential drug interactions and malignancy are areas attracting active surveillance by patients and physicians alike. The ideal timing for drug administration, the value of persistence with one agent (as compared with switching within class or to another class of drug) is another area of intense discussion.

Legislative efforts to make drug available for the indigent (these molecules may cost upwards of $30,000 dollars per annum), and changing algorithms among the indemnity plans for access to drug continue to evolve. There are significant barriers to access across continents, based on variations in budget and risk tolerance among health agencies abroad. Finally, the requirements for safe shipping, including maintenance of the cold chain and gentle handling of fragile proteins are also significant impediments to drug distribution.

The most important element in the dialogue involving RA is early disease recognition. Understanding the protean manifestations of disease, both explosive-onset and indolent phenotypes as well as differing approaches to disease management constitute the art and the science of managing RA.


 

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Comments

I was diagnoses with RA in 1975. I almos failed my course in medical laboratory because my own specimen kept coming up positive for the besic screenings. After donating my blood to 25 classmates, we call got the same result.

Fast forward to 1997. No medocation for the OA or RA, until I started having major joint problems. Oh yeah I woke up with the bent hand problem, taking about 30 minutes to become funcrtional. a Knee replacement in 2000, shouder decompression in 1998, tons of cartlidge issues and bone on bone.
Iannly got a rheumatologist who listens to his patients. VIOLA, now a full name, Lupus for part, OA RA and a little fibromylagia. I was a walking alphabet.
Fast Forward to 2013, on Plaquinal, Tramadol, Meloxacam, and a few others.
I am totally functional, but do not ask me abut my dust bunnies (they do not eat much and are very quiet) under the bed..

Speeing forward to 2013, a year I lost totally. I was diagnoses with pneeumonia which was so wrong, taken off most meds. YIKES,and they finally got it right C ( no OH NO- full remission now) The seond plus, besides a large weight loss, is no more pain!!!
My Chemo recipe knocked out all the joint pain big time, I was bending and twisting without fear of pain.

Now no ore Plaquinal since they feel I have no small joint problems, and we handling it so well. DUHH like I am going to feel better not having the meds that made thingss bearable, cut me off!!! At least I still have the pain killers and anti-inflammatories.!

I spoke with my oncology doc and told him that was the big plus, when I went to bend down, I could not get up, I had to wall backwards to the wall and walk my hands up it.

The chemo was massive doses of self-injectible meds.

I decided to do some me time, early retirement, fighting with disability because they declined my initial claim while I was very ill. I appealed and hopefully they will get back to it and re-open it, I sent them the surgiacl report done 2 days after the denial came. I could not respond in a timely manner, and had a good reason to appeal as they did not obtain my medicals until after the denial~~~ the initial problem, not the new one.

What is odd, is I went into the medical billing and appeals field after lab work got boring to me. (too much OSHA involvement). I am known for fighting red tape, but it is harder when it is your own.