Episode 146: RA vs OA - a podcast by Rio Bravo Family Medicine Residency Program

Episode 146: RA vs OA    

Future Dr. Magurany explains how to differentiate rheumatoid arthritis from osteoarthritis.  

Written by Thomas Magurany, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.

 

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

1. Etiology:

 

Rheumatoid Arthritis (RA):

 

RA is an autoimmune disease wherein the immune system mistakenly attacks healthy tissues, particularly the synovial joints, usually between the ages of 30-50. Genetic predisposition, environmental factors such as smoking or infections, hormonal imbalances, and lower socioeconomic status have been associated with an increased risk of developing RA(1).

Osteoarthritis (OA):

 

OA primarily arises due to mechanical stress on the joints over time. Factors contributing to OA include age, obesity, joint injury or trauma, repetitive joint use or overuse, genetic abnormalities in collagen structure, and metabolic disorders affecting cartilage metabolism (2).

The greatest risk factor for the development of OA is age with most patients presenting after 45 years of age. The greatest modifiable risk factor for OA is weight. People with a BMI >30 were found to have a 6.8 times greater risk of developing OA. (3) 

Primary

 OA is the most common and is diagnosed in the presence of associated risk factors such as: older age, female gender, obesity, anatomical factors, muscle weakness, and joint injury (occupation/sports activities) in the absence of trauma or disease. 

Secondary

 OA occurs alongside a pre-existing joint deformity including trauma or injury, congenital joint disorders, inflammatory arthritis, avascular necrosis, infectious arthritis, Paget disease, osteopetrosis, osteochondritis dissecans, metabolic disorders (hemochromatosis, Wilson’s disease), Ehlers-Danlos syndrome, or Marfan syndrome.

2. Pathogenesis:

Rheumatoid Arthritis (RA):

In some patients, RA is triggered by some sort of environmental factor in a genetically predisposed person. The best example is tobacco use in a patient with HLA-DRB1. The immune response in RA starts at sites distant from the synovial joints, such as the lung, gums, and GI tract. In these tissues, modified proteins are produced by biochemical reactions such as citrullination. (4)
In RA, an abnormal immune response leads to chronic inflammation within the synovium lining the joints. The inflammatory cytokines released cause synovitis and lead to the destruction of articular cartilage and bone erosion through pannus formation. Immune cells infiltrate the synovium causing further damage. (4) In summary: formation of antibodies to citrullinated proteins, these antibodies begin attacking wrong tissues.

Osteoarthritis (OA):
The primary pathological feature of OA is the degeneration of articular cartilage that cushions the joints causing surface irregularity, and focal erosions. These changes progress down the bone and eventually involve the entire joint surface. Mechanical stress triggers chondrocyte dysfunction, leading to an imbalance between cartilage synthesis and degradation that cause cartilage outgrowths that ossify and form osteophytes. This results in the release of enzymes that degrade the extracellular matrix, leading to progressive cartilage loss. As more of the collagen matrix is damaged, chondrocytes undergo apoptosis. Improperly mineralized collagen causes subchondral bone thickening; in advanced disease, bone cysts infrequently occur (5). In summary: Osteophytes formation and cartilage loss.

3. Clinical Presentation:
Rheumatoid Arthritis (RA):

The most common and predominant symptoms include joint pain and swelling, usually starting insidiously over a period of weeks to months. 
RA typically affects multiple joints symmetrically, commonly involving small joints of the hands, wrists, feet and progresses to involve proximal joints if left untreated. Morning stiffness lasting more than an hour is a characteristic feature. The affected joint will be painful if pressure is applied to the joint or on movement with or without joint swelling. Synovial thickening with a "boggy" feel on palpation will be noted. The classical physical findings of ulnar deviation, metacarpophalangeal joint subluxation, swan neck deformity, Boutonniere deformity, and the "bowstring" sign (prominent and tight tendons on the dorsum of the hand) are seen in advanced chronic disease. (4) Around ¼ of patients with RA may present with rheumatoid noduleswhich are well demarcated, flesh-colored subcutaneous lumps. They are usually described as being doughy or firm and are not typically tender unless they are inflamed. They are usually found on areas susceptible to repeated trauma or pressure and include the elbows, fingers and forearms. 

Osteoarthritis (OA):

OA primarily affects weight-bearing joints such as knees, hips, spine, and hands. Symptoms include joint pain aggravated by activity and relieved with rest, morning stiffness lasting less than 30 minutes, joint swelling due to secondary inflammation, and occasionally the formation of bony outgrowths called osteophytes (6). Tenderness may be present at joint lines, and there may be pain upon passive motion. Classic physical exam findings in hand OA include Heberden’s nodes (posterolateral swellings of DIP joints), Bouchard’s nodes (posterolateral swellings of PIP joints), and “squaring” at the base of the thumb (first Carpal-Metarcapal or CMC joints), bony enlargement, 

crepitus, effusions

 (non-inflammatory), and a limited range of motion. Patients may also experience bony swelling, joint deformity, and instability (patients complain that the joint is “giving way” or “buckling,” a sign of muscle weakness). (5)

4. Lab findings:

Rheumatoid Arthritis: 

Laboratory testing often reveals anemia of chronic disease (increased ferritin, decreased iron and TIBC) and thrombocytosis. Neutropenia may be present if Felty syndrome is present. RF is present in 80-90% of patients with a sensitivity of 69%. In patients who are asymptomatic or those that have arthralgias, a positive RF and especially CCP predicts the onset of clinical RA. Patients with RA with RF, ACPA, or both are designated as having seropositive RA. About 10% of RA patients are seronegative. ESR and levels of CRP are usually elevated in patients with active disease and can be used to assess disease activity. The synovial fluid in RA will also reveal low C3 and C4 levels despite elevated serum levels.(4) Some non-specific inflammatory markers such as ESR, CRP can help you guide your diagnosis of RA.

Osteoarthritis:

Lab findings are not significant. Clinical diagnosis if the following are present: 1) pain worse with activity and better with rest, 2) age more than 45 years, 3) morning stiffness lasting less than 30 minutes, 4) bony joint enlargement, and 5) limitation in range of motion. Blood tests such as CBC, ESR, rheumatoid factor, ANA are usually normal but usually ordered to rule out an inflammatory process. Synovial fluid should show a white blood cell count less than 2,000/microL, predominantly mononuclear cells (non-inflammatory). X-rays of the affected joint can show findings consistent with OA, such as marginal osteophytes, joint space narrowing, subchondral sclerosis, and cysts; however, radiographic findings do not correlate to the severity of the disease and may not be present early in the disease. (5)

5. Treatment Approaches:

Rheumatoid Arthritis (RA):

There is no cure for RA.
The goal of treatment in RA is inducing remission and optimizing quality of life. This is initially done by beginning DMARDs, include methotrexate, hydroxychloroquine, sulfasalazine, and leflunomide. Methotrexate is the initial DMARD of choice. Anti-TNF-alpha inhibitors include etanercept, infliximab, adalimumab, golimumab, and certolizumab may be used if DMARDs fail. NSAIDs are used to control joint pain and inflammation. Corticosteroids may be used as a bridge therapy to DMARDs in a newly diagnosed patient with a very active disease. (7) 

Coronary artery disease has a strong association with RA. RA is an independent risk factor for the development of coronary artery disease (CAD) and accelerates the development of CAD in these patients. Accelerated atherosclerosis is the primary cause of morbidity and mortality. There is increased insulin resistance and diabetes mellitus associated with RA and is thought to be due to chronic inflammation. When treated with specific DMARDs such as hydroxychloroquine, methotrexate, and TNF antagonists, there was a marked improvement in glucose control in these patients. (8) RA is not just a disease of the joints, it is able to affect multiple organ systems.

Osteoarthritis (OA):

OA treatment aims at reducing pain and improving joint function through a combination of non-pharmacological interventions like exercise programs tailored to strengthen muscles around affected joints, weight management strategies, and assistive devices like braces or walking aids if required (9). Medications including analgesics or nonsteroidal anti-inflammatory drugs may be prescribed for pain relief when necessary. Duloxetine has modest activity in relieving pain associated with OA. Intraarticular glucocorticoid joint injections have a variable response but are an option for those wanting to postpone surgical intervention. In severe cases where conservative measures fail, surgical options like joint replacement may be considered (9). Weight loss is a critical intervention in those who have overweight and obesity; each pound of weight loss can decrease the load across the knee 3 to 6-fold. (5) Summary: Medications (NSAIDs, topical, duloxetine), weight loss, PT, intraarticular injections of corticosteroids, and joint replacement.

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Conclusion: Now we conclude episode number 146, “RA vs. OA.” Future Dr. Magurany explained that rheumatoid arthritis is an autoimmune disease that presents with joint pain and inflammation, mostly on hands and small joints, accompanied by morning stiffness longer than 1 hour. The rheumatoid factor and ACPA may be positive in a percentage of patients but not always. The base of treatment is early treatment with disease-modifying antirheumatic drugs to induce remission of the disease. OA affects weight-bearing joints with little to no inflammation, treatment is mainly lifestyle modifications, analgesics, intraarticular injections, and joint replacement.

This week we thank Hector Arreaza and Thomas Magurany. Audio editing by Adrianne Silva.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

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References:

1. Myasoedova E, Crowson CS & Gabriel SE et al. (2010). Is the incidence of rheumatoid arthritis rising?: Results from Olmsted County, Minnesota, 1955-2007. Arthritis and Rheumatism, 62(6), 1576-1582.
2. Goldring MB & Goldring SR. (2007). Osteoarthritis. Journal of Cellular Physiology, 213(3), 626-634.
3. King LK, March L, Anandacoomarasamy A. Obesity & osteoarthritis. Indian J Med Res. 2013;138(2):185-93. PMID: 24056594; PMCID: PMC3788203.
4. Chauhan K, Jandu JS, Brent LH, et al. Rheumatoid Arthritis. [Updated 2023 May 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
5. Sen R, Hurley JA. Osteoarthritis. [Updated 2023 Feb 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
6. Hunter DJ, Bierma-Zeinstra S. & Eckstein F. (2014). OARSI Clinical Trials Recommendations: Design and conduct of clinical trials for primary hip and knee osteoarthritis: An expert consensus initiative of the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) Task Force in collaboration with the Osteoarthritis Research Society International (OARSI). Osteoarthritis Cartilage, 22(7), 363-381.
7. van Everdingen AA, Jacobs JW, Siewertsz Van Reesema DR, Bijlsma JW. Low-dose prednisone therapy for patients with early active rheumatoid arthritis: clinical efficacy, disease-modifying properties, and side effects: a randomized, double-blind, placebo-controlled clinical trial. Ann Intern Med. 2002 Jan 1;136(1):1-12. doi: 10.7326/0003-4819-136-1-200201010-00006. PMID: 11777359.
8. Nicolau J, Lequerré T, Bacquet H, Vittecoq O. Rheumatoid arthritis, insulin resistance, and diabetes. Joint Bone Spine. 2017 Jul;84(4):411-416.
9. Fernandes L, Hagen KB, Bijlsma JWJ et al. (2019). EULAR recommendations for non-pharmacological core management of hip and knee osteoarthritis. Annals of Rheumatic Diseases, 79(6), 715-722.
10. Royalty-free music used for this episode: "Driving the Point." Downloaded on July 29, 2023, from https://www.videvo.net/ 

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