Osteo Vs. Rheumatoid Arthritis

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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.


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.

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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15 Comments

  1. Mary Russell says:

    Would like to know if arthritis causes the arms (above the elbow and below the shoulder) to have severe pain all the time and when reaching you have shooting pain? Am taking Alleve and Meloxicam.

    • Hi Mary, It definitely effects all your joints, whether it from over use, the weather or a flare-up. Talk to your DR & get better meds… pacquinal is a good one & indocine works great for flare-ups. I was allergic to meloxicam. Warm weather helps, as do hot tubs. Good luck & hope you feel better.

    • Mary, I would check out Polymyalgia Rhuematica (PMR) for your symptoms, that is what I have along with Osteoarthritis of shoulders. Read up on it and if it sounds like you go to your doctor for some test.

    • katsra15 says:

      Mary,
      I was diagnosed with RA in July 2015, after being treated for OA for several years. Last fall I experienced sudden extreme pain in the area you are describing. My Dr treated me for inflammation with naproxin (I was already on Plaquinil). I still have pain there, though not as severe. Good luck!

  2. Hampton Wood says:

    you aint seen nothing yet wait till it takes two to get out of bed .

  3. I’m newly diagnosed with RA and want to know what you take for pain relief, particularly during those hellacious flare-ups! Thanks.

    • mondayhm says:

      Sheila, I’ve had RA for a year. I’m on Methotrexate and take Aleve for pain. I try to limit the Aleve, depending on the level of activity I’m required to do on any given day. I take the minimum dose, and always after eating a meal, never on an empty stomach.

  4. ken boren says:

    how good are hot tubs for theraputic help, really need some help

    • Sonya Yoder says:

      I have used a hot tub for pain long before my diagnosis. I have negative serum RA and it took along time tofigure out what was wrong with me. My hot tub was a real lifesaver. I still enjoy getting in it today. Especially when I’m flaring which I am right now. I take a short declining prescription of prednisone when I flare and sit in my hot tub

  5. marystr82hvn says:

    i am newly diagnosed with RA and I bought a hot tub for the relaxing effect but NOW am so glad I have it because when i get in that hot water my pain is gone and i can move like i never had RA…

    • mondayhm says:

      Mary, is your hot tub inside your home? I have RA and have considered a hot tub, but I want to use mine 12 months of the year. I live in Michigan and would need to add on, or put structural supports in the flooring in order to put it inside my home. I believe I would need it throughout the winter and they are brutal in Michigan, so the idea of walking through a slippery patio to get to an out door hot tub in January would not be very inviting to me. Let me know. Shelly

  6. annswam says:

    Sounds like the pain I had from my shoulders. I have had RA for 40 years just recently had to have a shoulder replacement for my replacement I had 30 years ago after falling. Better meds would definitely be an option be sure and let your Dr. know what is going on. There are a lot of choices out there.

  7. pattyduck says:

    is the vinegar cider helpful for osteoarthritis?

  8. PWilson says:

    This is an interesting article, and makes me wonder: in a case where one has secondary OA affecting some of the larger joints, on top of RA, should the patient also consult an orthopedic specialist in addition to the rheumatologist? The OA in at least one joint has gotten to the point of snap-crackle-pop-crunching all the time, and catching/hurting more frequently. I keep it active, but just wonder.

  9. garney57 says:

    I have RA and diabetes. I couldn’t take one of the diabetes drugs Metformin cause I became so sick to my stomach and vomiting that I could bearly get out of bed to go to the bathroom. I called my doctor repeatedly and was told that there were no appts available. After about two months of this with no relief I got up to go to the bathroom and fell breaking my foot. I went to the emergency room and my son had decided I fell because I had taken to much pain medication. This resulted in the ER treating me like a drug addict. I got home and fell again before getting in the house. I was so sick and weak I couldn’t hold myself up. By then my doctor had knee surgery and I still was getting sicker by the day. My A1c went from a 7 to a 9.7 in about 5 months. My blood sugar was between 450 and 575 everyday. I finally got in to see the doctor. The first thing he done after checking my blood sugar was give me a dose of insulin. He tried another diabetes drug but I couldn’t take it either. So I went on 2 different insulin’s a day. So all that left me with a very bad kidney function. He took me off all my RA meds and my Crestor. So I have had nothing but Norco 10’s. I am in pain when I get up till when ever I can finally go to sleep at night. I am currently going to a pain doctor who tells me there is nothing out there that will help me and I have to learn to just live with a little pain. I finally have my A1c down to 7.6 and my kidney function doesn’t show any signs of my diabetes. But the pain is worse now. I have developed horrible pain in my neck arm and hand. I have fought to get to see a doctor for this. After I finally got the referral my EMG was over a year old and he refused to see me with out a current EMG or MRI. Went for the open MRI but I was so claustrophobic I couldn’t get it. My doctor says I need to come in to talk about options. I have an appointment next week. One I have had for 3 months. Is it just me or does every person go thru this just to get a little help. I know I will never be pain-free again. But when it gets to the point you can’t get relief and the pain seems to consume a person and it is always there what can I do? It is like no one listens when I talk. And that includes my family who doesn’t want me on pain meds. Am I crazy and this pain is just me being a baby?

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