What is Rheumatoid Arthritis? Causes Symptoms

What is Rheumatoid Arthritis? Causes Symptoms

What is Rheumatoid Arthritis (RA) is a long-term autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Pain and stiffness often worsen following rest. Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body. The disease may also affect other parts of the body. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart. Fever and low energy may also be present. Often, symptoms come on gradually over weeks to months.

Rheumatoid arthritis (RA) is an inflammatory rheumatic disease with progressive course affecting articular and extra-articular structures resulting in pain, disability and mortality [. Persistent inflammation leads to erosive joint damage and functional impairment in the vast majority of patients [. The onset of disease is not similar in all patients but varies in regard to type, number, and the pattern of joint involvement. The course of disease may be also different according to the presence or absence of several variables including genetic background, the frequency of swollen joints, autoantibody in the serum and the severity of inflammatory process [.


Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease of unclear etiology that is manifested in by a progressive and destructive polyarthritis in association with serological evidence of autoreactivity. Its diagnosis is based on the classification criteria that involve four parameters: joint involvement, serology (rheumatoid factor and anti-cyclic citrullinated peptide–anti-CCP), levels of acute phase reactants and the duration of the symptoms Aletaha, et al. [1]. This classification simplifies the categorization of the patients with early RA; however, the diagnosis requires highly trained specialists who are able to differentiate early symptoms of RA from other pathologies.

What is Rheumatoid Arthritis

Rheumatoid arthritis is a long-term condition that causes pain, swelling and stiffness in the joints. The symptoms usually affect the hands, feet and wrist.

Causes of Rheumatoid Arthritis

Oral mucosa and RA-related autoimmunity

In recent years, the oral mucosa, specifically the gingiva and periodontal regions, has been studied as a potential site for the origins of RA. In classifiable RA, there is an increased prevalence and severity of periodontitis that has been associated with systemic RA-related autoantibodies [], and in subjects without classified RA, severe periodontitis has also been associated with RA-related autoantibodies []. In addition, Porphyromonas gingivalis (P. ging), a microbe commonly involved in periodontitis, is uniquely found to express a peptidylarginine deiminase (PAD) enzyme capable of citrullinating human peptides/proteins []. Furthermore, in subjects without classified RA, Mikuls and colleagues identified an association between elevations of antibodies to P. ging and serum RA-related autoantibodies [], and inflamed gingival tissue has been shown to express increased levels of PAD and citrullinated proteins []. Of interest, Harvey and colleagues also identified the presence of local anti-CCP antibodies in gingival crevicular fluid associated with gingivitis. However, despite these intriguing associations, a recent study by Scher and colleagues found that P. ging was associated with the severity of periodontitis but not specifically associated with new-onset RA[]. Rather, they found that Prevotella and Leptotrichia were expanded in new-onset RA, and Anaeroglobus geminatus was associated with RA-related autoantibody positivity.

The lung and RA-related autoimmunity

Another mucosal surface that is a potential originating site of autoimmunity in RA is the lung. This possibility is supported by established data that demonstrate increased RA risk is associated with inhaled exposures such as cigarette smoke [], and a high prevalence of lung disease including airways inflammation has been identified in established RA[]. Furthermore, Demoruelle and colleagues recently identified a higher prevalence of inflammatory airways disease by computed tomographic imaging in arthritis-free subjects (by joint examination and in a subset of subjects, by MRI) with serum RA-related autoantibodies compared to autoantibody negative matched controls []. Importantly, this finding was independent of prior or current cigarette smoking. Additionally, Fischer and colleagues found 80% of anti-CCP positive subjects with chronic lung disease and no joint symptoms had imaging evidence of airways inflammation []; furthermore, in a subset of these subjects that had a lung biopsy, 96% demonstrated histologic evidence of lung inflammation. Importantly, in these 2 studies, 5 subjects developed synovitis classifiable as RA during longitudinal follow-up, and all 5 had evidence of lung inflammation preceding the development of clinically apparent arthritis.

The gut and RA-related autoimmunity

To date, much of the data investigating the gastrointestinal mucosa in RA has focused on the gut microbiome. The gut microbiome is known to influence the development of the innate and adaptive immune system, and may therefore also play a role in the development of autoimmunity []. In murine studies, specific alterations of gut bacteria can enhance or attenuate susceptibility to experimentally-induced arthritis [. In humans, studies have identified differences in the gut microbiota, specifically differences in relative abundance of various microbes, in patients with classifiable RA compared to controls []. However, these studies have been unable to distinguish whether differences in gut microbial communities are a cause of inflammation in RA, the result of an underlying inflammatory environment that selects for sthe urvival of certain microbes, or whether the therapies used in RA are responsible for altering the gut microbial composition. Additional study of subjects prior to onset of joint inflammation will be informative to understand the relationship between the gastrointestinal microbiome and the development RA.

Pathophysiology of Rheumatoid Arthritis

What is Rheumatoid Arthritis

Prominent immunologic abnormalities include immune complexes produced by synovial lining cells and in inflamed blood vessels. Plasma cells produce antibodies (eg, rheumatoid factor [RF], anticyclic citrullinated peptide antibody [anti-CCP]) that contribute to these complexes, but destructive arthritis can occur in their absence. Macrophages also migrate to diseased synovium in early disease; increased macrophage-derived lining cells are prominent along with vessel inflammation. Lymphocytes that infiltrate the synovial tissue are primarily CD4+ T cells. Macrophages and lymphocytes produce pro-inflammatory cytokines and chemokines (eg, TNF-α, granulocyte-macrophage colony-stimulating factor [GM-CSF], various ILs, interferon-γ) in the synovium. Release of inflammatory mediators probably contributes to the systemic and joint manifestations of RA.

What is Rheumatoid Arthritis

In chronically affected joints, the normally thin synovium proliferates, thickens, and develops many villous folds. The synovial lining cells produce various materials, including collagenase and stromelysin, which contribute to cartilage destruction, and IL-1 and TNF-α, which stimulate cartilage destruction, osteoclast-mediated bone absorption, synovial inflammation, and prostaglandins (which potentiate inflammation). Fibrin deposition, fibrosis, and necrosis are also present. Hyperplastic synovial tissue (pannus) releases these inflammatory mediators, which erode cartilage, subchondral

Rheumatoid arthritis statistics

  • The Center for Disease Control and Prevention (CDC) estimates that 1.5 million US adults suffer from rheumatoid arthritis.
  • According to The National Health Service (NHS), UK, about 350,000 British people are affected by rheumatoid arthritis.
  • According to the National Rheumatoid Arthritis Society (UK) rheumatoid arthritis affects 0.8% of the UK population.
  • According to The Mayo Clinic, USA, the disease is two to three times more common in women than in men.
  • Although people of any age may be affected, rheumatoid arthritis is much more common after the age of 40. According to the National Rheumatoid Arthritis Society (UK), approximately 12,000 children under 16 years of age have a juvenile form of the disease.

According to the John Hopkins Arthritis Center, USA

  • Approximately 1% to 2% of the world’s population is affected by the disease.
  • Prevalence increases with age, approaching 5% in women over 55 years of age.
  • Annual average incidence is 70 in every 100,000 in the USA.
  • It is 4 times more common in smokers than non-smokers.

Rheumatoid arthritis is much more common that MS (multiple sclerosis) or leukemia. However, awareness of the disease’s effects and severity are more restricted to patients, their caregivers and their relatives because it is not well publicized.

Classification Criteria

What is Rheumatoid Arthritis

In 2010 the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria were introduced. The new criterion is not a diagnostic criterion but a classification criterion to identify disease with a high likelihood of developing a chronic form. However, a score of 6 or greater unequivocally classifies a person with a diagnosis of rheumatoid arthritis.

These new classification criteria overruled the “old” ACR criteria of 1987 and are adapted for early RA diagnosis. The “new” classification criteria, jointly published by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) establish a point value between 0 and 10. Four areas are covered in the diagnosis:

Joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal joints, the interphalangeal joint of the thumb, second through fifth metatarsophalangeal joint and wrist as small joints, and shoulders, elbows, hip joints, knees, and ankles as large joints:

  • Involvement of 1 large joint gives 0 points
  • Involvement of 2–10 large joints gives 1 point
  • Involvement of 1–3 small joints (with or without involvement of large joints) gives 2 points
  • Involvement of 4–10 small joints (with or without involvement of large joints) gives 3 points
  • Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points

Serological parameters – including the rheumatoid factor as well as ACPA – “ACPA” stands for “anti-citrullinated protein antibody”:

  • Negative RF and negative ACPA gives 0 points
  • Low-positive RF or low-positive ACPA gives 2 points
  • High-positive RF or high-positive ACPA gives 3 points
  • acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated CRP value (c-reactive protein)
  • duration of arthritis: 1 point for symptoms lasting six weeks or longer

Risk Factors

  • The etiology, or cause, of RA is unknown. Many cases are believed to result from an interaction between genetic factors and environmental exposures.
  • Age and sex: The incidence of RA is typically two to three times higher in women than men. The onset of RA, in both women and men, is highest among those in their sixties.
  • Genetics: There is longstanding evidence that specific HLA class II genotypes are associated with increased risk of developing RA. Most attention has been given to the DR4 and DRB1 molecules of the major histocompatability complex HLA class II genes. The strongest associations have been found between RA and the DRB1*0401 and DRB1*0404 alleles. Other recent investigations indicate that of the more than 30 genes studied, the strongest candidate gene is PTPN22, a gene that has been linked to several autoimmune conditions.

Modifiable: Several modifiable risk factors for RA have been studied including reproductive hormonal exposures, tobacco use, dietary factors, and microbial exposures.

Smoking: Among the modifiable risk factors, smoking is the strongest and most consistent modifiable risk factor for RA. A history of smoking is associated with a modest to moderate (1.3 to 2.4 times) increased risk of RA onset. This relationship between smoking and RA is strongest among people who are ACPA-positive (anti-citrullinated protein/peptide antibodies), a marker of auto-immune activities

Reproductive and Breastfeeding History: Hormones related to reproduction have been studied extensively as potential risk factors for RA.

  • Oral Contraceptives (OC): Early studies found that women who had taken OCs had a modest to moderate decrease in risk of RA. However, most recent studies have not found a decreased risk. The estrogen concentration of contemporary OCs is typically 80%-90% lower than the first OCs introduced in the 1960s. This may account for the lack of associations in recent studies.
  • Hormone Replacement Therapy (HRT): There is mixed evidence of an association between HRT and RA onset.
  • Live Birth History: Most studies have found that women who have never had a live birth have a slight to moderately increased risk of RA.
  • Breastfeeding: Almost all recent population-based studies have found that RA is less common among women who breastfeed.
  • Menstrual History: At least two studies have observed that women with irregular menses or a truncated menstrual history (e.g., early menopause) have an increased risk of RA. Because women with the polycystic ovarian syndrome (PCOS) have an increased risk of RA, the association with an irregular menstrual history may result from PCOS.
  • Early Life Exposures: Early life exposures may alter the risk of developing RA in adulthood.  For example, one study found that maternal smoking doubled the risk of children developing RA as adults. The relationship between birthweight and later onset of RA is inconsistent: one study found no effect while others have found that both low and high birth weight are risk factors. Lower socio-economic status in childhood has been linked to heightened risk of developing RA.
  • Physical Activity: The only study examining the role of physical activity in the development of RA found a dose-response relationship; that is, the risk of RA declined with increasing levels of leisure time physical activity. However, the risk ratios were not statistically significant.
  • Vitamin D: Two studies examining vitamin D as a risk factor for RA onset found no associations.

 Symptoms of Rheumatoid Arthritis

The joints most commonly affected by rheumatoid arthritis are in the hands, wrists, feet, ankles, knees, shoulders, and elbows. The disease typically causes inflammation symmetrically in the body, meaning the same joints are affected on both sides of the body. Symptoms of rheumatoid arthritis may begin suddenly or gradually.

The typical symptoms of rheumatoid arthritis include the following:

  • Warm, swollen joints: It’s common for the same joints to be swollen on both sides of the body, for instance the fingers of both the right and left hand.
  • Painful joints
  • Stiff joints: After longer periods of rest, and especially in the morning right after you wake up, your joints are stiff. They usually only become more flexible again after an hour or more, or once you have been active for a while.
  • Weakness: Painful, stiff joints often end up not getting as much use, which can cause the muscles to gradually weaken.
  • Exhaustion: Rheumatoid arthritis is an inflammatory disease that affects the entire body. So it often causes tiredness, general physical weakness and occasionally more extreme exhaustion ().
  • Rheumatoid nodules: As the disease progresses, small hard lumps called rheumatoid nodules sometimes develop under the skin. They’re usually not sensitive to pressure or touch.

Rheumatoid arthritis symptoms vary a lot from person to person: It might be that a different joint is affected, or that other symptoms are causing the most trouble.

The following are the most common symptoms of rheumatoid arthritis. However, each individual may experience symptoms differently. Symptoms may include:

  • Inflamed, painful joints
  • Stiff joints
  • Enlarged and/or deformed joints (such as fingers bent toward the little finger and/or swollen wrists)
  • Frozen joints (joints that freeze in one position)
  • Cysts behind the knees that may rupture, causing lower leg swelling and pain
  • Hard nodules (bumps) under the skin near affected joints
  • Low-grade fever
  • Inflamed blood vessels (vasculitis) may occur occasionally, leading to nerve damage and leg sores
  • Inflamed membranes around the lungs (pleurisy), the sac around the heart (pericarditis), or inflammation and scarring of the lungs themselves, that may lead to chest pain, difficulty breathing, and abnormal heart function
  • Swollen lymph nodes
  • Sjögren’s syndrome (dry eyes and mouth)
  • Eye inflammation

If a person has four or more of the following symptoms, he/she may be diagnosed with rheumatoid arthritis:

  • Morning stiffness that lasts longer than one hour for at least six weeks
  • Three or more joints that are inflamed for at least six weeks
  • Presence of arthritis in the hand, wrist, or finger joints for at least six weeks
  • Blood tests that reveal rheumatoid factor
  • X-rays that show characteristic changes in the joints

According to WHo

What is Rheumatoid Arthritis

Symptoms  of Rheumatoid Arthritis 

Rheumatoid arthritis usually develops gradually, but some people experience a sudden onset of symptoms: one day they are perfectly healthy and the next they are dealing with rheumatoid arthritis.

Symptoms commonly associated with rheumatoid arthritis include:

  • Joint pain, joint swelling, joint stiffness, and warmth around the affected joint
  • Morning stiffness that lasts one or more hours
  • Symmetrical pattern of affected joints, meaning the same joint on both sides of the body is affected (e.g., both knees)
  • Small joints of the hands and feet are characteristically involved, although any joint can be affected
  • Rheumatoid nodules (firm lumps under the skin), found on elbows and hands of about one-fifth of people with rheumatoid arthritis
  • Fatigue and noticeable loss of energy
  • Low-grade fever and sometimes flu-like symptoms
  • Loss of appetite, weight loss, anemia associated with chronic diseases, depression
  • Dry eyes and dry mouth associated with a secondary condition Sjogren’s syndrome
  • Joint deformity and instability from damage to cartilage, tendons, ligaments, and bone
  • Limited range of motion in affected joints
  • Flares and remission of disease activity is characteristic of rheumatoid arthritis
  • Rheumatoid arthritis may have systemic effects (i.e., affect the organs of the body)

No two rheumatoid arthritis cases are exactly the same. There is so much variety among the symptoms that some researchers suspect rheumatoid arthritis is not one disease but rather a several diseases with commonalities.

The symptoms of rheumatoid arthritis may resemble other medical conditions or problems, including acute rheumatic fever, Lyme disease, psoriatic arthritis, gout, osteoarthritis, gonococcal arthritis, and ankylosing spondylitis. Always consult your physician for a diagnosis

Rheumatoid Arthritis Diagnosed

Rheumatoid arthritis can be difficult to diagnose in its early stages for several reasons.

Classification Criteria of diagnosis

In 2010 the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria were introduced. The new criterion is not a diagnostic criterion but a classification criterion to identify disease with a high likelihood of developing a chronic form. However, a score of 6 or greater unequivocally classifies a person with a diagnosis of rheumatoid arthritis.

These new classification criteria overruled the “old” ACR criteria of 1987 and are adapted for early RA diagnosis. The “new” classification criteria, jointly published by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) establish a point value between 0 and 10. Four areas are covered in the diagnosis

Joint involvement – designating the metacarpophalangeal joints, proximal interphalangeal joints, the interphalangeal joint of the thumb, second through fifth metatarsophalangeal joint and wrist as small joints, and shoulders, elbows, hip joints, knees, and ankles as large joints:

  • Involvement of 1 large joint gives 0 points
  • Involvement of 2–10 large joints gives 1 point
  • Involvement of 1–3 small joints (with or without the involvement of large joints) gives 2 points
  • Involvement of 4–10 small joints (with or without the involvement of large joints) gives 3 points
  • Involvement of more than 10 joints (with the involvement of at least 1 small joint) gives 5 points

Serological parameters – including the rheumatoid factor as well as ACPA – “ACPA” stands for “anti-citrullinated protein antibody”:

  • Negative RF and negative ACPA gives 0 points
  • Low-positive RF or low-positive ACPA gives 2 points
  • High-positive RF or high-positive ACPA gives 3 points
  • acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated CRP value (c-reactive protein)
  • duration of arthritis: 1 point for symptoms lasting six weeks or longer

The new criteria accommodate to the growing understanding of RA and the improvements in diagnosing RA and disease treatment. In the “new” criteria serology and autoimmune diagnostics carry major weight, as ACPA detection is appropriate to diagnose the disease in an early stage before joints destructions occur. Destruction of the joints viewed in radiological images was a significant point of the ACR criteria from 1987. This criterion no longer is regarded to be relevant, as this is just the type of damage that treatment is meant to avoid.

In clinical practice, the following criteria apply

  • two or more swollen joints
  • morning stiffness lasting more than one hour for at least six weeks
  • the detection of rheumatoid factors or autoantibodies against ACPA such as autoantibodies to mutated citrullinated vimentin can confirm the suspicion of RA. A negative autoantibody result does not exclude a diagnosis of RA.

Differential Diagnosis

Several other medical conditions can resemble RA, and usually, need to be distinguished from it at the time of diagnosis

  • Crystal-induced arthritis (gout, and pseudogout) – usually involves particular joints (knee, MTP1, heels) and can be distinguished with an aspiration of joint fluid if in doubt. Redness, asymmetric distribution of affected joints, pain occurs at night and the starting pain is less than an hour with gout.
  • Steroid induces arthritis-  usually, it can involve multiple joint pain during rest or night time.
  • Osteoarthritis – distinguished with X-rays of the affected joints and blood tests, age (mostly older persons), starting painless than an hour, asymmetric distribution of affected joints and pain worsens when using joint for longer periods.
  • Systemic lupus erythematosus (SLE) – distinguished by specific clinical symptoms and blood tests (antibodies against double-stranded DNA)
  • One of the several types of psoriatic arthritis resembles RA nail changes and skin symptoms distinguish between them
  • Lyme disease – causes erosive arthritis and may closely resemble RA – it may be distinguished by blood test in endemic areas
  • Reactive arthritis (previously Reiter’s disease) – asymmetrically involves heel, sacroiliac joints and large joints of the leg. It is usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica.
  • Axial spondyloarthritis  – (including ankylosing spondylitis) – this involves the spine, although an RA-like symmetrical small-joint polyarthritis may occur in the context of this condition.
  • Hepatitis C – RA-like symmetrical small-joint polyarthritis may occur in the context of this condition. Hepatitis C may also induce Rheumatoid Factor auto-antibodies

Rarer causes that usually behave differently but may cause joint pains

  • Sarcoidosis, amyloidosis, and Whipple’s disease can also resemble RA.
  • Hemochromatosis may cause hand joint arthritis.
  • Acute rheumatic fever can be differentiated from RA by a migratory pattern of joint involvement and evidence of antecedent streptococcal infection. Bacterial arthritis (such as by Streptococcus) is usually asymmetric, while RA usually involves both sides of the body symmetrically.
  • Gonococcal arthritis (another bacterial arthritis) – is also initially migratory and can involve tendons around the wrists and ankles.
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Medical history – The doctor begins by asking the patient to describe the symptoms, and when and how the condition started, as well as how the symptoms have changed over time.

  • Physical examination- The doctor will check the patient’s reflexes and general health, including muscle strength. The doctor will also examine bothersome joints and observe the patient’s ability to walk, bend, and carry out activities of daily living. The doctor will also look at the skin for a rash and listen to the chest for signs of inflammation in the lungs.
  • Laboratory tests – A number of lab tests may be useful in confirming a diagnosis of rheumatoid arthritis. Following are some of the more common ones:
  • Rheumatoid factor (RF)- Rheumatoid factor is an antibody that is present eventually in the blood of most people with rheumatoid arthritis. (An antibody is a special protein made by the immune system that normally helps fight foreign substances in the body.) Not all people with rheumatoid arthritis test positive for rheumatoid factor, and some people test positive for rheumatoid factor, yet never develop the disease. Rheumatoid factor also can be positive in some other diseases; however, a positive RF in a person who has symptoms consistent with those of rheumatoid arthritis can be useful in confirming a diagnosis. Furthermore, high levels of rheumatoid factor are associated with more severe rheumatoid arthritis.
  • Anti-CCP antibodies – This blood test detects antibodies to cyclic citrullinated peptide (anti-CCP). This test is positive in most people with rheumatoid arthritis and can even be positive years before rheumatoid arthritis symptoms develop.
  • Others – Other common laboratory tests include a white blood cell count, a blood test for anemia, which is common in rheumatoid arthritis; the erythrocyte sedimentation rate (often called the sed rate), which measures inflammation in the body; and
  • C-reactive protein – another common test for inflammation that is useful both in making a diagnosis and monitoring disease activity and response to anti-inflammatory therapy.
  • Synovial biopsy.
  • CBC,Hb,Widal test ,MT test for tuberculosis
  • IgG, Serum Creatinine
  • Synovial fluid analysis.
  • Erythrocyte Sedimentation Rate An erythrocyte sedimentation rate (ESR or sed rate) measures how fast red blood cells (erythrocytes) fall to the bottom of a fine glass tube that is filled with the patient’s blood. The higher the sed rate the greater the inflammation.
  • C-Reactive Protein High levels of C-reactive protein (CRP) are also indicators of active inflammation. Like the ESR, a high result does not indicate what part of the body is inflamed, or what is causing the inflammation.
  • Anti-CCP Antibody –The presence of antibodies to cyclic citrullinated peptides (CCP) can identify RA years before symptoms develop. In combination with the test for rheumatoid factor, the CCP antibody test is the best predictor of which patients will go on to develop severe RA.
  • Tests for Anemia Anemia is a common complication. Blood tests determine the number of red blood cells (hemoglobin and hematocrit) and iron (soluble transferrin receptor and serum ferritin) in the blood.
  • Joint aspiration – Involves a removal of fluid from the swollen bursa to exclude infection or gout as possible causes
  • Biopsy (of nodules tissue) – A procedure in which tissue samples are removed (with a needle or during surgery) from the body for examination under a microscope; to determine if cancer or other abnormal cells are present
  • X rays X rays are used to determine the degree of joint destruction. They are not useful in the early stages of rheumatoid arthritis before bone damage is evident; however, they may be used to rule out other causes of joint pain. They may also be used later to monitor the progression of the disease.
  • MRI-It can be needed in the critical case to diagnosis the internal structure of joints to ensure where osteophyte form or not, tendon, cartilage, ligament, synovial fluid.

Treatment of Rheumatoid Arthritis 

Non-Pharmacologic Therapies

Non-pharmacologic therapies include treatments other than medications and are the foundation of treatment for all people with rheumatoid arthritis.

  • Rest – When joints are inflamed, the risk of injury of the joint itself and the adjacent soft tissue structures (such as tendons and ligaments) is high. This is why inflamed joints should be rested. However, physical fitness should be maintained as much as possible. At the same time, maintaining a good range of motion in your joints and good fitness overall are important in coping with the systemic features of the disease.
  • Exercise – Pain, and stiffness often prompt people with rheumatoid arthritis to become inactive. However, inactivity can lead to a loss of joint motion, contractions, and a loss of muscle strength. These, in turn, decrease joint stability and further increase fatigue. Regular exercise, especially in a controlled fashion with the help of physical therapists and occupational therapists, can help prevent and reverse these effects. Types of exercises that have been shown to be beneficial include range-of-motion exercises to preserve and restore joint motion, exercises to increase strength and exercises to increase endurance (walking, swimming, and cycling).
  • Physical and Occupational Therapy – Physical and occupational therapy can relieve pain, reduce inflammation, and help preserve joint structure and function for patients with rheumatoid arthritis.

Specific types of therapy are used to address the specific effects of rheumatoid arthritis:

  • The application of heat or cold can relieve pain or stiffness.
  • Use of ultrasound to help reduce inflammation of the sheaths surrounding tendons (tenosynovitis)
  • Passive and active exercises to improve and maintain the range of motion of the joints
  • Rest and splinting to reduce joint pain and improve joint function
  • Finger-splinting and other assistive devices to prevent deformities and improve hand function.
  • Relaxation techniques to relieve secondary muscle spasm

Occupational therapists also focus on helping people with rheumatoid arthritis to be able to continue to actively participate in work and recreational activity with special attention to maintaining good function of the hands and arms.

  • Nutrition and dietary therapy – Weight loss may be recommended for overweight and obese people to reduce stress on inflamed joints. People with rheumatoid arthritis have a higher risk of developing coronary artery disease. High blood cholesterol is one risk factor for coronary disease that can respond to changes in diet. A nutritionist can recommend specific foods to eat or avoid in order to achieve a desirable cholesterol level. Changes in diet have been investigated as treatments for rheumatoid arthritis, but there is no diet that is proven to cure rheumatoid arthritis. No herbal or nutritional supplements, such as cartilage or collagen, can cure rheumatoid arthritis. These treatments can be dangerous and are not usually recommended.
  • Smoking and alcohol – Smoking is a risk factor for rheumatoid arthritis and it has been shown that quitting smoking can improve the condition. People who smoke need to quit completely. Assistance in quitting should be obtained if needed. Moderate alcohol consumption is not harmful to rheumatoid arthritis, although it may increase the risk of liver damage from some drugs such as methotrexate. People should discuss the safety of alcohol use with a doctor because recommendations depend on the medications a person is taking and on their other medical conditions.
  • Measures to reduce bone loss – Inflammatory conditions such as rheumatoid arthritis can cause bone loss, which can lead to osteoporosis. The use of prednisone further increases the risk of bone loss, especially in postmenopausal women. It is important to do a risk assessment and address risk factors that can be changed in order to help prevent bone loss.

Patients may do the following to help minimize the bone loss associated with steroid therapy:

  • Use the lowest possible dose of glucocorticoids for the shortest possible time, when possible, to minimize bone loss.
  • Consume an adequate amount of calcium and vitamin D, either in the diet or by taking supplements.
  • Use medications that can reduce bone loss, including that which is caused by glucocorticoids.
  • Control the disease itself with appropriate medications prescribed by your doctor.


There are many medications available to decrease joint pain, swelling and inflammation and hopefully, prevent or minimize the progression of the disease. The type of drugs that your doctor recommends will depend on how severe your arthritis is and how well you respond to the medications. These medications include:

  • Analgesics – Prescription-strength drugs that relieve pain but not inflammation.
  • Non-steroidal anti-inflammatory drugs (NSAIDs – such as aspirin, ibuprofen or naproxen)Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include aspirin, ibuprofen (Motrin, Advil), and naproxen (Naprosyn, Aleve).
  • COX-2 inhibitors (celecoxib)
  • Antidepressants- A Drugs that block pain messages from your brain and boost the effects of endorphins (your body’s natural painkillers).
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants These medications provide relief from spinal muscle spasms.
  • Neuropathic Agents  Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bones health and healing fracture.
  • Corticosteroid to healing the nerve inflammation and clotted blood in the joints.
  • A dietary supplement to remove the general weakness & improved the health.
  • Disease-modifying anti-rheumatic drugs (DMARDs) – such as hydroxychloroquine, methotrexate, sulfasalazine, and leflunomide, An improvement in symptoms may require four to six weeks of treatment with methotrexate. Improvement may require one to two months of treatment with sulfasalazine and two to three months of treatment with hydroxychloroquine.
  • Biologic agents (such as infliximab, etanercept, adalimumab, certolizumab and golimumab, tocilizumab, rituximab, abatacept, anakinra, tofacitinib) Biologics tend to work rapidly, within two weeks for some medications and within four to six weeks for others. Biologics may be used alone or in combination with other DMARDs. Usually, they are reserved for patients who do not adequately respond to DMARDs, or if adverse prognostic factors are present. Combinations of DMARDs may be more effective than single drugs. For example, hydroxychloroquine, sulfasalazine, and methotrexate together are more effective than methotrexate alone or the other two together.
  • Combining a DMARD with another drug, such as methotrexate plus a TNF-α antagonist or an IL-1 receptor antagonist or a rapidly tapered corticosteroid, may be more effective than using DMARDs alone.

  • Methotrexate – is a folate antagonist with immunosuppressive effects at the high dose. It is anti-inflammatory at doses used in RA. It is very effective and has a relatively rapid onset (a clinical benefit often within 3 to 4 wk). Methotrexate should be used with caution, if at all, in patients with hepatic dysfunction or renal failure. Alcohol should be avoided. Supplemental folate, 1 mg PO once/day, reduces the likelihood of adverse effects. CBC, AST, ALT, and albumin and creatinine level should be determined about every 8 wks. When used early in the course of RA, efficacy may equal the biologic agents. Rarely, a liver biopsy is needed if liver function test findings are persistently twice the upper limit of normal or more and the patient needs to continue to use methotrexate. Severe relapses of arthritis can occur after withdrawal of methotrexate. Paradoxically, rheumatoid nodules may enlarge with methotrexate therapy.
  • Hydroxychloroquine – can also control symptoms of mild RA. Funduscopic examination should be done and visual fields should be assessed before and every 12 mo during treatment. The drug should be stopped if no improvement occurs after 9 mo.
  • Leflunomide – interferes with an enzyme involved with pyrimidine metabolism. It is about as effective as methotrexate but is less likely to suppress bone marrow, cause abnormal liver function, or cause pneumonitis. Alopecia and diarrhea are fairly common at the onset of therapy but may resolve with the continuation of therapy.
  • Sulfasalazine – Sulfasalazine (Azulfidine, generic) works best when the disease is confined to the joints. Symptom relief occurs within 1 – 3 months. Side effects are common, particularly stomach and intestinal distress, which usually occur early in the course of treatment. (However, serious gastrointestinal side effects, such as stomach ulcers, occur less frequently with sulfasalazine than with NSAIDs.) A coated-tablet form may help reduce side effects. Other side effects include skin rash and headache. Sulfasalazine increases sensitivity to sunlight. Be sure to wear sunscreen (SPF 15 or higher) while taking this drug. People with intestinal or urinary obstructions or who have allergies to sulfa drugs or salicylates should not take sulfasalazine.
  • Minocycline – Minocycline is a tetracycline antibiotic that is generally reserved for patients with mild RA. It can take 2 – 3 months before symptoms begin to improve and up to a year for full benefit. Side effects include upset stomach, dizziness, and skin rash. Long-term use of minocycline can cause changes in skin color, but this side effect usually disappears once the medication is stopped. Minocycline can cause yeast infections in women. It should not be used by women who are pregnant or planning on becoming pregnant. Minocycline increases sensitivity to sunlight and patients should be sure to wear sunscreen. In rare cases, minocycline can affect the kidneys and liver.
  • Tofacitinib- Tofacitinib is the newest DMARD. Approved in 2012, tofacitinib is the first in a new class of drugs. It works by blocking “Janus kinase” molecules involved in joint inflammation. There is hope that DMARD might be an alternative to biologic DMARDs and a new option for patients with moderate-to-severe RA who have not been helped by methotrexate. Tofacitinib, which is taken as a twice-daily pill, can be used alone or in combination with methotrexate. Tofacitinib may increase the risk of serious infections. Because it is new a drug, long-term side effects are still unknown.
  • Gold- Gold used to be a time-honored DMARD for rheumatoid arthritis but its use has decreased with the development of newer DMARDs and biologic drugs. Gold is usually administered in an injected form because the oral form, auranofin (Ridaura, generic), is much less effective. There are two injectable forms of gold: Gold sodium thiomalate (Myochrysine, generic) and aurothioglucose (Solganal, generic). It can take 3 – 6 months before injections have an effect on RA symptoms. Gold injections can cause a number of side effects including mouth sores and skin rash and in rare cases more serious problems such as kidney damage.
  • Azathioprine Azathioprine suppresses immune system activity. It takes 6 – 8 weeks for early symptom improvement and up to 12 weeks for full benefit. Azathioprine can cause serious problems with the gastrointestinal tract including nausea and vomiting, often accompanied by stomach pain and diarrhea. Azathioprine can also cause problems with liver function and pancreas gland inflammation and can reduce white blood cell count.
  • Cyclosporine – Like azathioprine, cyclosporine (Sandimmune, Neoral, generic) is an immunosuppressant. It is used for people with RA who have not responded to other drugs. It can take a week before symptoms improve and up to 3 months for full benefit. The most serious and common side effects of cyclosporine are high blood pressure and kidney function problems. While kidney function usually improves once the drug is stopped, mild-to-moderate high blood pressure may continue. Swelling of the gums is also common. Patients should practice good dental hygiene, including regular brushing and flossing.
  • Corticosteroids – Systemic corticosteroids decrease inflammation and other symptoms more rapidly and to a greater degree than other drugs. They also seem to slow bone erosion. However, they may not prevent joint destruction, and their clinical benefit often diminishes with time. Furthermore, rebound often follows the withdrawal of corticosteroids in active disease. Because of their long-term adverse effects, some doctors recommend that corticosteroids are given to maintain function only until another DMARD has taken effect Corticosteroids may be used for severe joint or systemic manifestations of RA (eg, vasculitis, pleurisy, pericarditis). Relative contraindications include peptic ulcer disease, hypertension, untreated infections, diabetes mellitus, and glaucoma. The risk of latent TB should be considered before corticosteroid therapy is begun.
  • Intra-articular injections  – of depot corticosteroids may temporarily help control pain and swelling in particularly painful joints. Triamcinolone hexacetonide may suppress inflammation for the longest time. Triamcinolone acetonide and methylprednisolone acetate are also effective. No single joint should be injected with a corticosteroid more than 3 to 4 times a year, as too-frequent injections may accelerate joint destruction (although there are no specific data from humans to support this effect). Because injectable corticosteroid esters are crystalline, local inflammation transiently increases within a few hours in < 2% of patients receiving injections. Although infection occurs in only < 1:40,000 patients, it must be considered if pain occurs > 24 h after injection.
  • Immunomodulatory, cytotoxic, and immunosuppressive drugs – Treatment with azathioprine or cyclosporine (an immunomodulatory drug) provides efficacy similar to DMARDs. However, these drugs are more toxic. Thus, they are used only for patients in whom treatment with DMARDs has failed or to decrease the need for corticosteroids. They are used infrequently unless there are extra-articular complications. For maintenance therapy with azathioprine, the lowest effective dose should be used. Low-dose cyclosporine may be effective alone or when combined with methotrexate. It may be less toxic than azathioprine. Cyclophosphamide is no longer recommended due to its toxicity
  • Rituximab  – is an anti-CD 20 antibody that depletes B cells. It can be used in refractory patients. The response is often delayed but may last 6 mo. The course can be repeated after 6 mo. Mild adverse effects are common, and analgesia, corticosteroids, diphenhydramine, or a combination may need to be given concomitantly. Rituximab is usually restricted to patients who have not improved after using a TNF-α inhibitor and methotrexate. Rituximab therapy has been associated with progressive multifocal leukoencephalopathy, mucocutaneous reactions, delayed leukopenia, and hepatitis B reactivation.
  • Abatacept – a soluble fusion cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) Ig, is indicated for patients with RA with an inadequate response to other DMARDs.
  • Anakinra – is a recombinant IL-1 receptor antagonist. IL-1 is heavily involved in the pathogenesis of RA. Infection and leukopenia can be problems.
  • TNF-α antagonists – (eg, adalimumab, etanercept, golimumab, certolizumab pegol, and infliximab) reduce the progression of erosions and reduce the number of new erosions. Although not all patients respond, many have a prompt, dramatic feeling of well being, sometimes with the first injection. Inflammation is often dramatically reduced. These drugs are often added to methotrexate therapy to increase the effect and possibly prevent the development of drug-neutralizing antibodies.
  • Tocilizumab –  blocks the effect of IL-6 and has clinical efficacy in patients who have responded incompletely to other biologic agents.
  • Tofacitinib is a Janus kinase (JAK) inhibitor that is given orally with or without concomitant methotrexate to patients who do not respond to methotrexate alone or other biologic agents. Although there are some differences among agents, the most serious problem is an infection, particularly with reactivated TB. Patients should be screened for TB with PPD or an interferon-gamma release assay. TNF-α antagonists should probably be stopped before major surgery. Etanercept, infliximab, and adalimumab can and probably should be used with methotrexate. High-dose infliximab should not be used in patients with severe heart failure.

However, the risk of side effects from treatment must be weighed against the benefits on an individual basis.

Common treatments for RA and their targets and toxicities

Abbreviations: CBC: complete blood count, Cr: creatinine, LFTs: liver function tests, PML: progressive multifocal leukoencephalopathy, TB: tuberculosis, TLR: toll-like receptor, TNF: tumor necrosis factor.

Conventional DMARDs Target Testing Prior to Starting Medication Toxicities Monitoring
Methotrexate Enhances adenosine release; inhibits polyamines; folic acid antagonist Cr, CBC, LFTs, Hepatitis B and C screening Nausea, Diarrhea, Liver Toxicity, Pneumonitis, Cytopenias, Infections, Lymphoma LFTs, Cr, CBC every 4–8 weeks
Leflunomide Pyrimidine synthesis Cr, CBC, LFTs, Hepatitis B and C screening Nausea, Diarrhea, Liver Toxicity. Pneumonitis(rare), Infections LFTs, Cr, CBC every 4–8 weeks
Hydroxychloroquine TLR signaling; Stabilization of lysosomal membranes Retinal screen Retinal Toxicity, Nausea Yearly ophthalmolog ic exam
Sulfasalazine Enhances adenosine pathways and inhibits arachidonic acid CBC Nausea, Diarrhea, Allergic Reactions, Neutropenia (rare) CBC every 4–8 weeks during first year of treatment
Biologic DMARDs
Anti-TNF drugs TNF-α TB screen, Hepatitis B and C screen, fungal screens (depending on geography) Infusion and injection site reactions, Rash, Infections, Lymphoma None
Rituximab CD-20 Hepatitis B screen, TB screen Infusion reaction (can be severe), PML (rare) None
Abatacept CTLA-4 CD 80/86 interaction TB screen, Hepatitis B and C screen, fungal screens (depending on geography) Possible infusion reaction, Infections None
Anakinra IL-1 receptor antagonist TB screen, CBC Injection site reactions, Neutropenia, Infections Monthly CBC
Tocilizumab IL-6 receptor antagonist Lipid profile, CBC, TB screen, hepatitis B and C screen, fungal screens (depending on geography) Neutropenia, Thrombocytopenia, Elevated total cholesterol and triglycerides, Bowel perforations (rare), Infections Monthly CBC, Cr, cholesterol profile.
DMARDs approved for the treatment of rheumatoid arthritis (cDMARD white, bDMARD olive)
Active substance Dosage The strength of recommendation (S1 guideline []) When? Frequent adverse effects (>1/100; recorded using the treatment monitoring form of the DGRh [http://dgrh.de/therapieueberwachen.html] unless otherwise specified)
Abatacept 10 mg/kg BW/ 4 weeks after induction phase ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Hyperlipidemia, headache, dizziness, drowsiness, bronchitis, coughing, upper airway infections (including tracheitis, nasopharyngitis), rhinitis, abdominal pain, nausea, diarrhea, dyspepsia, skin rash, herpes simplex, urinary tract infection, tiredness, weight loss, hypertension, flushing
Adalimumab 40 mg/2 weeks ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Decreased hemoglobin concentration, hypertension, headache, dizziness, drowsiness, upper airway infections, rhinitis, sinusitis, bronchitis, increased coughing, pneumonia, nausea, diarrhea, sore throat, elevated transaminases, reactions at injection site, skin rash, pruritus, herpes simplex, urinary tract infection, weight loss, influenza syndrome
Anakinra 100 mg/day As alternative to 1st or 2ndbDMARD Reactions at injection site, headache
Antimalarial drugs 4 mg chloroquine/kg or >6.5 mg hydroxychloroquine/kg BW/day As alternative to 2ndcDMARD or in combination with cDMARDs Nausea, lack of appetite, diarrhea
Azathioprine 2–3 mg/kg BW/day As alternative to 2ndcDMARD Nausea, vomiting, diarrhea, leukopenia, anemia, infection, drug fever
Certolizumab 200 mg/ 2 weeks after induction phase ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Urinary tract infection, herpes simplex, upper airway infections, headache, dizziness, skin rash, pruritus, exhaustion, pyrexia, pain and reddening at site of administration (product information 04/2009)
Cyclosporine 2.5–3.5 mg/kg BW/day As alternative to 2ndcDMARD or in combination with cDMARDs Lack of appetite, nausea and occasional vomiting, diarrhea, muscle twitching and cramp may indicate magnesium deficiency, slight trembling of hands, slight increase in body hair, swelling and inflammation of gums, hypertension, tiredness
Etanercept 50 mg/week ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Irritation at injection site, infections
Golimumab 50 mg/month ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Upper airway infections (nasopharyngitis, pharyngitis, laryngitis, rhinitis), bacterial infections (e.g., inflammation of subcutaneous tissue), viral infections (e.g., influenza and herpes), bronchitis, sinusitis, superficial fungal infections, anemia, allergic reactions (bronchospasm, hypersensitivity, urticaria), autoantibody positive, depression, sleeplessness, dizziness, paresthesias, headache, hypertension, obstipation, dyspepsia, gastrointestinal and abdominal pain, nausea, elevated ALT/GPT levels, elevated AST/GOT levels, alopecia, dermatitis, itching, skin rash, fever, asthenia, reaction at injection site (e.g., erythema, urticaria, induration, pain, bruising, itching, irritation und paresthesias), delayed wound healing, thoracic symptoms (product information 11/2012)
Infliximab 3–5 mg/kg BW every 8 weeks after induction phase ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Headache, dizziness, drowsiness, infections of upper and lower respiratory tract (e.g., sinusitis, pneumonia), nausea, diarrhea, elevated transaminases, urticaria, skin rash, pruritus, reactions to infusion
Leflunomide 10–20 mg/day ↑ ↑ As alternative to 1st or 2ndcDMARD or in combination with cDMARDs Diarrhea, nausea, vomiting, abdominal pain, mouth ulcers, elevated liver parameters, leukocytopenia, headache, dizziness, asthenia, hypertension, eczema, hair loss, skin rash, itching, weight loss, mutagenicity, teratogenicity (both in animal experiments)
Methotrexate 10–25 mg/week ↑ ↑ As 1st cDMARD or in combination with cDMARDs and especially bDMARDs Stomatitis, hair loss, nausea, vomiting, elevated transaminases
Parenteral gold 50 mg/ 2 weeks after the initial phase As an alternative to 2ndcDMARD Dermatitis, stomatitis, pruritus, eosinophilia, proteinuria, deposits on cornea/lens if gold dose >1500 mg (harmless), metallic taste
Rituximab Two doses of 1000 mg at a 2-week interval every 6–12 months ↑ ↑ As 2ndbDMARD following inadequate response to 2 cDMARDs Airway infections, reactions to infusion, influenza-like symptoms, infections, transitory hyperuricemia (15%)
Sulfasalazine 2 g/day after initial phase As alternative to 1st or 2ndcDMARD or in combination treatment with cDMARDs Exanthema, pruritus, nausea, abdominal pain, lack of appetite, hyperchromasia, oligospermia, reversible loss of fertility in men, headache, feeling of weakness, tiredness
Tocilizumab 8 mg/kg BW every 28 days ↑ ↑ As 1st or 2ndbDMARD following inadequate response to 2 cDMARDs Skin and subcutaneous infections, pneumonia, oral herpes simplex, herpes zoster, mouth ulcers, gastritis, exanthema, pruritus, headache, dizziness, elevated transaminases, hypertension, leukopenia, neutropenia, conjunctivitis
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Essential Fatty Acids

  • Omega-3 or omega-6 fatty acids – have shown their potential as immunosuppressants and anti-inflammatory agents (). Borage seed oil provides a high amount of omega-6 fatty acid or gamma-linolenic acid (GLA) [. A double-blind trial was conducted on 37 patients with active RA, and they were assigned to consume borage seed oil containing 1.4 g of GLA per day while the placebo group was given cottonseed oil. After 24 weeks of consumption, the group which received GLA had significantly reduced tender and swollen joint scores, whereas the placebo group did not show any change [.
  • Gamma-linolenic acid and omega-3 fatty acid  – alpha-linolenic and stearidonic acid from black currant seed oil (BCSO) have also been investigated for their therapeutic activity. About 10.5 g of BCSO were given to RA patients in double-blind fashion and soybean oil as a placebo for 24 weeks continuously. BCSO treated group, when compared with placebo group came up with significant positive effects in pain relieving and joint tenderness [.
  • Fish oils – provide a high amount of omega-3 fatty acids, and their efficacy to treat RA has been checked in several controlled trials. RA patients were provided with fish oil with 3.6 g of omega-3 fatty acids per day in double-blind fashion, and placebo group was treated with a mixture of fatty acids for 12 weeks, which was very much similar in the amount found in the average diet. The group which received fish oil had reduced morning stiffness, a significant increase in grip strength compared to the placebo group [. Eicosapentaenoic and docosahexaenoic acids are ethyl ester derivatives of omega-3 fatty acids, and their capability to reduce the severity of RA has been assessed. When RA patients consumed these derivatives in an amount of 130 mg/kg body weight/day for 26–30 weeks, a significant decrease in pain, morning stiffness, and tender joints was observed in comparison with the placebo group that received only corn oil [.
  • Synbiotics – are composed of probiotics and prebiotics (the non-digestible food products beneficial for the growth of helpful bacteria in the large intestine and provides health-promoting effects) [. Several reports have confirmed the reduction of oxidative stress in the human body by consumption of synbiotics [. As per FDA, probiotics are “live microorganisms which, when administered in adequate amounts, confer a health benefit on the host” [Bifidobacterium and Lactobacillus are the key strains widely used as probiotics in commercial, pharmaceutical, and nutraceutical products [. Many reports have frequently stated that the population of gut microbes gets altered in a person affected with RA [, and several animal studies have already proved that any alteration in gut microbiota corresponds to the initiation of RA [.


  • Epigallocatechin-3-gallate (EGCG) has proved its therapeutic potential and has been of particular interest among natural products for its use as a nutraceutical [. It is a main phytochemical present in green tea that is obtained from dried leaves of Camellia sinensis and C. assamica of Theacease family [. The protective effects exerted by green tea have been well proved in neurodegenerative disease, inflammatory disease, cardiovascular disease, and several types of cancer [.


Plants with effective health-promoting effects are known as herbs, and these have a long history of being used as medicine to cure several diseases. Synthetic drugs used in arthropathies have been associated with numerous side effects on health, which in return has led the focus toward medicines of botanical origin [.

  • Sallaki (Boswellia serrata) – is widely recommended as an anti-inflammatory herb as prescribed in Ayurveda [. The phytochemical which acts as a key player is boswellic acid from pentacyclic triterpene family [. Boswellic acid inhibits the expression of lipoxygenase-5 and eventually lowering down leukotriene synthesis and leukotrienes are well known for their role in inflammation [. These have also proved their potency to block NF-κβ activation and brought down the levels of pro-inflammatory cytokines like TNF-α, IL-1, IL-2, IL-4, IL-6, and IFN-γ and also prevented classical complement pathway by restricting the cleavage of C3 to C3b [.
  • Ashwagandha (Withania somnifera) – is one of the plants being described in Ayurveda as a potent anti-inflammatory plant [. It is rich in Withaferin A, a steroidal phytochemical which can prevent proceeding of the NF-κβ signaling pathway [In vitro studies with ashwagandha extract suppressed the release of pro-inflammatory cytokines as TNF-α, IL-12, and IL-1β from synoviocytes of RA patients but it failed to stop synthesis and subsequent release of IL-6 [. Rats with induced arthritis, when treated with powder of Ashwagandha roots, showed less destruction of bone collagen [. Moreover, in a double-blind placebo-controlled study aqueous extract significantly reduced stiffness, disability to move knee and joints, and pain score [.
  • Ginger – has been known for its therapeutic properties due to the presence of pungent phenolics such as shogaols and gingerols [. Turmeric, rich in phenolic curcuminoids, has also proved its beneficial effects against several malignancies [. In a study, a perfect mixture of blended ginger and turmeric were given to the adjuvant-induced arthritic rats. This mixture showed protective effects against extra-articular complications of RA [. In another study conducted by the same group, they found that ginger and turmeric administered at a dose of 200 mg/kg body weight could independently lower down the signs and symptoms of RA in the adjuvant-induced arthritic male Wistar albino rats. The results were significant with a p-value <0.05 as compared to the control group receiving only indomethacin [.
  • Curcumin – has also presented itself as a potent anti-inflammatory spice by blocking the expression of IL-1 and IL-6 in an in vitro study with RA patient-derived fibroblast-like synoviocytes [. Methotrexate is a widely prescribed antirheumatic drug for the treatment of RA but it increases oxidative stress, decreases NO levels, and leads to vascular endothelial dysfunction [. Curcumin and folic acid co-administration were found to lower down methotrexate-induced vascular endothelial dysfunctions in male Wistar rats [.
  • The bark of Cinnamomum zeylanicum (Cinnamon bark) – is widely used in South-East Asian dishes. Rathi et al. treated RA animal models involving male Swiss albino mice and Wistar rats with a polyphenolic fraction of cinnamon barks and found inhibitory effects on the secretion of cytokines IL-2, IL-4, and IFN-γ and reduction in levels of TNF-α [.
  • Kaempferol – an important phytochemical found in grapefruits, can bring down the level of inflammatory cytokine IL-1β, inhibiting the cell signaling pathways like phosphorylation of ERK1/2, p38, and JNK and activation of NF-κβ [. Several enzymes inducing oxidative stress such as MMPs, COX-2, and PGE-2 in RA-derived synoviocytes were lowered down on the administration of kaempferol [. These molecules are reported in the destruction of bone and articular cartilage leading to the pathogenesis of RA [. A mixture of polyphenols composed of epigallocatechin, gallate, catechin, tannic acid, and quercetin when injected at the intra-articular region of a rat model of RA, prevented cartilage destruction while reducing inflammation [.
  • p-Coumaric acid – is largely present in grapes, oranges, apples, tomatoes, spinach, and potatoes. In an in vivo study using a rat model of adjuvant-induced arthritis, p-coumaric acid intake significantly reduced the expression of TNF-α [. Genistein, an important isoflavone present in soybeans maintained a perfect balance between T helper cell, Th1, and Th2, and inhibited IFN-γ and IL-4 production which ultimately brings down the inflammation [. Freshly prepared orange juice has a high content of beta-cryptoxanthin and its intake reduces the risk of RA in humans [. Pineapple stem is a rich source of a proteolytic enzyme called as bromelain. In a study, bromelain was consumed orally by RA patients in dosages of 20 or 40 mg for 3–4 times daily up to 13 months. About 72% of the total patients involved in the study came up with promising results, and there were no side effects detected. In spite of promising results obtained, the significance of the study cannot be explained due to the lack of control groups (.
  • Anthocyanins – have proved themselves as potent antioxidants and are more abundant in black rice, eggplant, and black soybean. These have properties to reduce oxidative stress by increasing superoxide dismutase (SOD) and decreasing serum malondialdehyde (MDA). It has been reported in mouse models of RA that the uptake of anthocyanins can bring down TNF-α levels [, thereby reducing disease activity. Resveratrol from black grapes has been found to exert a protective effect in rat model of RA [. It was reported that resveratrol can lower down specific RA biomarkers such as serum RF, COMP, and MMP-3; immunological biomarkers as IgG and antinuclear antibody; immunomodulatory cytokines (TNF-α) and oxidative stress [. Mangiferin, a polyphenolic compound found in mangoes, used in an in vivo study on RA-induced DBA-1/J male mice reported downregulation of IL-1β, IL-6, and TNF-α, inhibited NF-κβ signaling, and activated extracellular signal-regulated kinase 1/2 (ERK1/2) [. In another study with mangiferin, it was observed that mangiferin prevented joint destruction in RA by inducing proapoptotic effects on human synovium-derived synoviocytes [.
  • Kaempferol – an important phytochemical found in grapefruits, can bring down the level of inflammatory cytokine IL-1β, inhibiting the cell signaling pathways like phosphorylation of ERK1/2, p38, and JNK and activation of NF-κβ [. Several enzymes inducing oxidative stress such as MMPs, COX-2, and PGE-2 in RA-derived synoviocytes were lowered down on the administration of kaempferol [. These molecules are reported in the destruction of bone and articular cartilage leading to the pathogenesis of RA[. A mixture of polyphenols composed of epigallocatechin, gallate, catechin, tannic acid, and quercetin when injected at the intra-articular region of a rat model of RA, prevented cartilage destruction while reducing inflammation [.
  • p-Coumaric acid –  is largely present in grapes, oranges, apples, tomatoes, spinach, and potatoes. In an in vivo study using a rat model of adjuvant-induced arthritis, p-coumaric acid intake significantly reduced the expression of TNF-α [. Genistein, an important isoflavone present in soybeans maintained a perfect balance between T helper cell, Th1,  and Th2, and inhibited IFN-γ and IL-4 production which ultimately brings down the inflammation [. Freshly prepared orange juice has a high content of beta-cryptoxanthin and its intake reduces the risk of RA in humans [. Pineapple stem is a rich source of a proteolytic enzyme called as bromelain. In a study, bromelain was consumed orally by RA patients in dosages of 20 or 40 mg for 3–4 times daily up to 13 months. About 72% of the total patients involved in the study came up with promising results, and there were no side effects detected. In spite of promising results obtained, the significance of the study cannot be explained due to lack of control groups [.

Other strategies to manage rheumatoid arthritis

Other important strategies that can help you manage rheumatoid arthritis include

  • Self-management courses – can help people with rheumatoid arthritis and other chronic (ongoing) conditions to build skills and confidence in becoming more actively involved in your healthcare and in managing rheumatoid arthritis day to day.
  • Aids and equipment – supports such as walking aids and specialized cooking utensils reduce joint strain and can help you to manage pain and fatigue. An occupational therapist can give you advice on aids. You can also phone the Independent Living Centre for advice.
  • Relaxation techniques – muscle relaxation, distraction, guided imagery, and other techniques can help you manage pain and difficult emotions such as anxiety. If exercise is causing sharp pain, stop immediately. If lesser aches and pains continue for more than 2 hours afterward, try a lighter exercise program for a while. Using large joints instead of small ones for ordinary tasks can help relieve pressure, for instance, closing a door with the hip or pushing buttons with the palm of the hand.
  • Exercise – It is important for patients with RA to maintain a balance between rest (which will reduce inflammation) and moderate exercise (which will relieve stiffness and weakness). Studies have suggested that even as little as 3 hours of physical therapy over 6 weeks can help people with RA and that these benefits are sustained. The goal of the exercise is to Maintain a wide range of motion. Increase strength, endurance, and mobility Improve general health, Promote well-being

In general, doctors recommend the following approaches

  • Start with the easiest exercises, stretching and tensing of the joints without movement.
  • Next, attempt mild strength training.
  • The next step is to try aerobic exercises. These include walking, dancing, or swimming, particularly in heated pools. Avoid heavy impact exercises, such as running, downhill skiing, and jumping.
  • Tai chi, which uses graceful slow sweeping movements, is an excellent method for combining stretching and range-of-motion exercises with relaxation techniques. It may be of particular value for elderly patients with RA.

A common-sense approach to exercise is the best guide

  • Rest – can help you to manage fatigue and is particularly important when your joints are swollen.
  • Nutrition – while there is no specific ‘diet’ for people with rheumatoid arthritis, it is important to have a healthy, balanced diet to maintain general health and, prevent weight gain and other medical problems, such as diabetes and heart disease.
  • Support – a peer support group can provide understanding, advice, support, and information from others in a similar situation. Contact MOVE muscle, bone & joint health for more information.
  • Complementary therapies – such as massage or acupuncture may be helpful. Consult your doctor or rheumatologist before commencing any treatment. Fish oil supplements may also be helpful as they contain a certain type of fat called omega-3. Current research suggests omega-3 fats can help reduce inflammation in rheumatoid arthritis.
  • Omega-3 fatty acids
    There are lots of natural anti-inflammatories, but the best studied by far are omega-3 fatty acids. These heart-healthy, brain-boosting fats are especially prevalent in seafood, especially fatty fish such as salmon, sardines, and tuna. Studies have found that adding omega-3s to the diet can reduce joint pain and morning stiffness in people with RA, says Chaim Putterman, M.D., chief of rheumatology at Montefiore Medical Center and Albert Einstein College of Medicine in New York City. Not a fan of fish? Fish oil capsules can give you the same benefits. But beware: High concentrations of omega-3s can thin the blood, so consult your doctor for the right dose.
  • Gamma linolenic acid
    Gamma linolenic acid (GLA) is another fatty acid with anti-inflammatory properties, says Robert Zurier, M.D., who has studied the effects of GLA in rheumatoid arthritis patients at the University of Massachusetts Medical School. GLA is found mostly in botanical oils—evening primrose, black currant seed and especially borage oil, its richest source. The patients in Dr. Zurier’s studies took three 1,000-milliliter capsules of borage oil every day for six months and reported less joint pain and stiffness than patients who took placebo capsules, and they also reduced their dose of nonsteroidal anti-inflammatory drugs.
  • Joint surgery – may be necessary in some cases if the joint is very painful or there is a risk of losing overall function. Any medication or treatment for arthritis must be discussed with and monitored by your doctor or rheumatologist. They will take into account the condition being treated, any other health issues and identifiable risk factors.
  • Diet – Many patients with RA try dietary approaches, such as fasting, vegan diets, or eliminating specific foods that seem to worsen RA symptoms. There is little scientific evidence to support these approaches but some patients report anecdotally that they are helpful.In recent years, a number of studies have suggested that the omega-3 fatty acids contained in fish oil may have anti-inflammatory properties useful for RA joint pain relief. The best source of fish oil is through increased consumption of fatty fish such as salmon, mackerel, and herring. Fish oil supplements are another option, but they may interact with certain medications. If you are thinking of trying fish oil supplements, talk to your doctor first.
  • Pain with Stress Management – Patients can learn strategies to cope with the stress and frustration of living with chronic pain. Relaxation and stress management techniques such as guided imagery, breathing exercises, hypnosis, or biofeedback can be helpful. Although there is no definitive evidence to support their efficacy, some patients report relief with modalities such as acupuncture, massage, and mineral baths.
  • Assistive Devices – There are many different types of assisted devices that can help make life easier in the home. Kitchen gadgets, such as jar openers, can assist with gripping and grabbing. Door-knob extenders and key turners are helpful for patients who have trouble turning their wrists. Bathrooms can be fitted with shower benches, grip bars, and raised toilet seats. An occupational therapist can advise you on choosing the right kinds of assistive devices.
  • Miscellaneous Supportive Treatments – Various ointments, including Ben Gay and capsaicin (a cream that uses the active ingredient in chili peppers), may help soothe painful joints. Orthotic devices are specialized braces and splints that support and help align joints. Many such devices made from a variety of light materials are available and can be very helpful when worn properly.
Disease-modifying antirheumatic drugs and monitoring in rheumatoid arthritis
Drug Adverse drug reaction Monitoring Action
For all DMARDs Myelosuppression
Routine unless otherwise specified:
FBE, EUC, LFTs at baseline, 2–4 weekly for 3–6 months and every 6–12 weeks thereafter. This regimen is influenced by comorbidities and changes to therapy.
Abnormalities in blood monitoring may lead to dose adjustments, treatment interruption or cessation.
Malignancy Age-related cancer screening programs and self-reported symptoms
Infection Self-reported fever (>38 °C), localising symptoms or unexplained illness. Fever may not always be present due to DMARD-induced alterations in cytokine profile. Maintain a high index of suspicion, particularly for reactivation of latent tuberculosis or hepatitis B infection.
Methotrexate Alopecia Self-reported hair loss Usually reversible after stopping drug
Mouth ulcers Self-reported mouth ulcers
Inspection of oral mucosa
Folic acid supplementation (not on day of methotrexate)
Pneumonitis Symptoms of cough or dyspnoea
Routine respiratory examination
CXR, PFTs and urgent specialist review
Abnormal LFTs
LFTs as per routine for all DMARDs Continue folic acid supplementation.
If AST or ALT <2 x ULN, repeat LFTs in a month. If normalising, continue. If persistent elevation, reduce dose.
If AST or ALT >2 x ULN, interrupt treatment and discuss with rheumatologist.
Sulfasalazine Haemolytic anaemia Symptoms of anaemia Stop treatment and seek specialist advice.
Abnormal LFTs LFTs as per routine for all DMARDs If AST or ALT <2 x ULN, repeat LFTs in a month. If normalising, continue. If persistent elevation, reduce dose.
If AST or ALT >2 x ULN, interrupt treatment and discuss with rheumatologist.
Corticosteroids Adrenal suppression (more likely with courses >3 weeks and prednisolone doses ≥7.5 mg) No specific monitoring required Do not stop abruptly. Consider increasing the dose during intercurrent acute illness.
Diabetes Blood glucose and HbA1c monitoring If continued use is necessary, consider escalation of hypoglycaemic treatment.
Hypertension Blood pressure checks each visit If continued use is necessary, consider antihypertensive drugs.
Osteoporosis (when used at doses of prednisolone ≥7.5 mg for ≥3 months) Bone mineral density assessment at baseline, repeat at 3 months
Self-reported skeletal pain suggesting fracture
If continued use is necessary, strongly consider starting a bisphosphonate.
Vigilance for new or worsened mental
health or sleep disturbance
Cease, or use the lowest possible dose. Seek specialist
advice. Discuss with rheumatologist.
Hydroxychloroquine Photosensitivity Self-reported sensitivity Sun protection strategies
Haemolytic anaemia Symptoms of anaemia Stop treatment and seek specialist advice.
Blue–grey skin discolouration Self-reported skin discolouration and examination of sun-exposed sites Stop treatment immediately and seek specialist advice.
Sun protection strategies
Corneal deposits
Retinal toxicity
Baseline ophthalmological assessment, then repeat at 5 years with annual review thereafter if therapy ongoing. Annual review is recommended from initiation of therapy in high-risk patients (age >70 years, macular disease, renal disease, liver disease, higher than recommended dose).
Self-reported visual disturbance
Stop drug and seek specialist advice.
Leflunomide Alopecia Self-reported hair loss Usually reversible. Reduce dose or stop drug.
Hypertension Blood pressure assessment on each visit Reduce dose and/or add antihypertensive.
Pneumonitis Symptoms of cough or dyspnoea
Routine respiratory examination
CXR, PFTs and seek specialist review.
Peripheral neuropathy Self-reported paraesthesia or weakness Stop drug, consider NCS and EMG if not resolving, seek specialist advice.
Hepatotoxicity LFTs every 2–4 weeks for 3 months, then every 3 months ongoing If AST or ALT <2 x ULN, continue and repeat LFTs in a month.
If AST or ALT 2–3 x ULN, reduce dose and repeat LFTs in 2–4 weeks. Continue if normalising. If persistent elevation, discuss with rheumatologist.
If AST or ALT >3 x ULN, stop drug and repeat LFTs in 2–4 weeks. If elevated, discontinue, consider washout and discuss with rheumatologist.
Note: For any severe reactions to leflunomide consider cholestyramine washout (8 g 3 times a day for 11 days)
Tofacitinib Abnormal LFTs LFT frequency determined by other DMARDs used If AST or ALT 1–2 x ULN, seek specialist advice.
If AST or ALT >2 x ULN, seek urgent advice.
Myelosuppression FBE after 3–4 weeks, then every 3 months Seek specialist advice, stop drug if severe.
Dyslipidaemia Lipid profile 8 weeks after starting and then guided by results Modify lifestyle and diet, consider lipid-lowering therapy.
Reactivated tuberculosis Ideally detected pre-treatment, but may present during treatment as pulmonary or disseminated disease Stop treatment immediately and seek specialist advice.
Herpes zoster Patient-reported rash or pain Start antiviral treatment within 72 hours of rash onset. If recurrent, discuss with rheumatologist.
Abatacept COPD exacerbation Symptoms of COPD exacerbation Treat exacerbation and discuss with rheumatologist.
Hypertension Blood pressure Modify lifestyle, consider antihypertensive.
Injection site reactions Visualisation of injection site Rotation of injection sites, antihistamines, topical cold packs, topical corticosteroids
Anaphylaxis See Australian Prescriberwallchart
Rituximab Infusion reactions Stop or slow the rate of infusion, treat symptoms.
Anaphylaxis See Australian Prescriberwallchart
Myelosuppression FBE before each treatment If severe, delay treatment.
Anakinra Myelosuppression (especially neutropaenia) FBE frequency determined by other DMARDs used. Neutropaenia may be delayed and prolonged. Discontinue and discuss with rheumatologist.
Injection site reactions Visualisation of injection sites Rotation of injection sites, antihistamines, topical cold packs, topical corticosteroids
Infection As per routine monitoring for all DMARDs Arrange follow-up visit, consider antimicrobial, remain vigilant for deterioration and the need for hospitalisation, stop if serious infection.
Anaphylaxis See Australian Prescriberwallchart
TNF inhibitors Injection site reactions Visualisation of injection sites Rotation of injection sites, antihistamines, topical cold packs, topical corticosteroids
Drug-induced lupus Self-reported rash, fever or arthralgia Assess urine for evidence of glomerulonephritis. Assess serum lupus antibody profile and complement levels. Seek urgent advice from rheumatologist.
Demyelinating syndrome Self-reported neurological symptoms Consider MRI, seek specialist advice.
Malignancy Participation in age-appropriate screening programs Stop treatment immediately and seek specialist advice.
Infection As per routine monitoring for all DMARDs Arrange follow-up visit, consider antimicrobial, remain vigilant for deterioration and the need for hospitalisation, stop if serious infection.
Reactivated tuberculosis Ideally detected pre-treatment, but may present during as pulmonary or disseminated disease without fever Stop treatment immediately and seek specialist advice.
Herpes zoster Self-reported rash or pain Start antiviral treatment within 72 hours of rash onset. If recurrent, discuss with rheumatologist.
Tocilizumab Hypertension Blood pressure checks each visit Modify lifestyle modification, consider antihypertensive.
Myelosuppression FBE at baseline, then every 4–8 weeks Interrupt treatment and discuss with rheumatologist.
Dyslipidaemia Lipid profile at baseline. Repeat after 4–8 weeks of treatment, then as per relevant guidelines Modify lifestyle modification, consider lipid-lowering therapy.
Gastrointestinal perforation Self-reported abdominal pain Stop therapy and discuss with rheumatologist.
Infection As per routine monitoring for all DMARDs
Note: CRP is an unreliable marker for infection during tocilizumab therapy due to IL-6 blockade
Minor infection – interrupt treatment until recovered.
Serious infection – stop treatment.
Abnormal LFTs LFTs at baseline and every 4–8 weeks for 6 months, then every 3 months If AST or ALT >1–3 x ULN, reduce dose, or stop until normal.
If AST or ALT >3 x ULN, stop until >1–3 x ULN then reduce dose.
If AST or ALT >5 x ULN, discontinue treatment.
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ALT alanine aminotransferase

AST aspartate aminotransferase

COPD chronic obstructive pulmonary disease

CRP C-reactive protein

CXR chest x-ray

DMARDs disease-modifying antirheumatic drugs

EMG electromyography

EUC electrolytes, urea, creatinine

FBE full blood examination

HbA1c glycated haemoglobin

IL-6 Interleukin-6

LFTs liver function tests

MRI magnetic resonance imaging

NCS nerve conduction study

PFTs pulmonary function tests

TNF tumour necrosis factor

ULN upper limit of normal

Herbal Remedies

1. Massage

This is the first out of the most efficient home remedies for rheumatoid arthritis in the body that I want to reveal in this entire writing.

When being applied properly, massage can help to relieve the pain caused rheumatoid arthritis as it can relax your stiff muscles. Massage will help to boost your blood circulation, which is essential for alleviating the discomfort due to the symptoms of rheumatoid arthritis.

2. Evening Primrose Oil

Evening primrose oil is one kind of plant oil which can help to relieve morning stiffness and pain effectively. This plant oil has the gamma-linolenic acid properties – an essential fatty acid which can help to relieve the intensity of numerous symptoms caused by rheumatoid arthritis.

Take 540 mg to 2.8 g of evening primrose oil in divided doses every day. Remember to consult an expert to get proper dosage because this oil may interfere with some medications.

3. Epsom Salt

Epsom salt is also a great and highly effective natural remedy which can help to soothe the pain and swelling due to rheumatoid arthritis. Epsom salt is an abundant source of magnesium, so it can help to regulate the pH levels in your body effectively as well. In turn, it can help to reduce rheumatoid arthritis, stiffness, and pain in the joints. In addition, it can help to mineralize bone well.

  • Add 2 cups of Epsom salt to a bathtub full of warm water.
  • Soak in the bathtub within about half an hour.
  • Apply this method up to 3 times weekly.

In fact, this is also one of the best home remedies for rheumatoid arthritis in the body that people should make use for good!

4. Ginger

In naturopathy and Ayurvedic as well, ginger has been used for people at all ages to deal with inflammatory conditions, including rheumatoid arthritis. Ginger contains a compound named gingerol – a powerful agent with natural anti-inflammatory properties, helping to relieve swelling and pain due to rheumatoid arthritis effectively.

  • You can add ginger to daily food dishes or drink two or three cups of ginger tea every day.
  • Alternatively, you can chew some fresh ginger slices every day.
  • Use ginger oil to rub onto your affected area. Then expose that area to sunlight for five to ten minutes to generate heat and warmth. Apply this tip on a regular basis.

In brief, making use of ginger is one of the most effective home remedies for rheumatoid arthritis pain that people should never look down and should apply for good!

5. Garlic

Thanks to its powerful anti-inflammatory properties, garlic is also advisable for dealing with rheumatoid arthritis. Garlic can help to inhibit the pro-inflammatory substances (also called “cytokines”) production, helping to relieve swelling and pain efficiently and fast.

  • You can take garlic capsules. For correct dosage, remember to consult experts.
  • You can also eat one or two raw garlic cloves every day

6. Apple Cider Vinegar

Apple cider vinegar is considered very useful in helping people relieve several symptoms caused by rheumatoid arthritis. Being rich in minerals, such as phosphorus, potassium, magnesium, and calcium, apple cider vinegar can help to relieve the rheumatoid arthritis pain effectively.

  • You should use some apple cider vinegar to directly apply to the affected area of your body. Then, use warm castor oil to massage your painful area. Finally, use a cotton cloth to wrap that area and use plastic to cover it. Apply this method every day before bedtime for good results as desired.
  • Mix one teaspoon of honey with one tablespoon of raw, unfiltered apple cider vinegar and add them to 1/2 cup of warm water. Consume this solution once every day.

7. Turmeric

Turmeric can help to reduce the risk of joint rheumatoid arthritis by blocking certain cytokines and enzymes causing rheumatoid arthritis.

  • You can add turmeric powder into your daily meals to benefit from this natural ingredient.
  • Alternatively, you can take turmeric in form of capsules by 500 – 1,000 mg three times daily. Remember to consult experts initially.
  • Bring 1 quart of water to a boil. Add 1 tablespoon of turmeric powder and boil it for another 10 minutes. Allow it to cool and drink it once or twice daily.

Note: Do not consume high doses of turmeric because it can act as a blood thinner as well as leading to a stomach upset.

This is actually one of the best home remedies for rheumatoid arthritis pain that I would like to reveal in this entire article and want my readers to make use for good!

8. Fish Oil

Fish oil contains omega-3 fatty acids – DHA and EPA – that have a powerful anti-inflammatory ability and can help to relieve pain as well. In addition, fish oil can help to prevent the risks of heart disease, which rheumatoid arthritis sufferers are usually at high risks.

  • Add cold water fish like salmon and tuna to your daily diet
  • Take up to 2.6 grams of fish oil (containing 30% DHA/EPA at least) 2 times every day.

Note: Before taking fish oil supplements, remember to consult your doctor because the supplements could interfere with some types of medications you are taking.

9. Hot And Cold Compresses

Alternating hot and cold compresses are also a great way to reduce the symptoms caused by rheumatoid arthritis. While a cold compress can dull the pain and relieve rheumatoid arthritis and joint swelling, a hot compress can help to relieve pain by relaxing sore joints and muscles.

  • For the cold compress, use a thin towel to wrap some ice cubes.
  • For the hot compress, use a towel to wrap a hot water bag.
  • Put the hot compress right onto the affected area and let it stay within just three minutes.
  • Remove the hot compress and place the cold compress immediately in its place within just one minute.
  • Repeat these steps for fifteen to twenty minutes 2 – 3 times every day until your pain is relieved.

10. Parsley
In a research conducted by JNR (Journal of Natural Remedies) on rats, it was found that extract made of fresh leaves of parsley had reduced inflammation in their paws. Therefore, using it as a home remedy to relieve you from your arthritis pain can have a positive impact.

11. Carrots
Carrots have an abundance amount of Vitamin C and beta-carotene. Beta-carotene and Vitamin C both have antioxidant properties that kill free radicals which are responsible for arthritis inflammation.

12. Rosemary
Rosemary has a polyphenol called rosmarinic acid which is a potent antioxidant and inflammation reliever.

13. Kale
Kale is a vegetable that is a rich source of anti-oxidants, Vitamin C, Vitamin K, and beta-carotene that can reverse arthritis inflammation.

14. Coriander
According to a medical research conducted by All India Institute of Medical Sciences, the coriander powder has the potential to reduce swelling and inflammation. It can also be digested as green leaves.

15. Olive Oil
Olive oil, especially raw ice-pressed, has many health benefits starting from reducing your blood cholesterol to diabetes and inflammation. It can be used as cooking oil that could not only make your dish tastier but also loads with various health benefits. The anti-inflammatory properties of olive oil relieve you from arthritis joints pain.

16. Green tea
Green tea is a wonder drink that is loaded with antioxidants that have anti-inflammatory properties. Along with relieving you from severe arthritis pain, green tea has many health benefits from lowering your LDL cholesterol to minimizing the risk of bladder cancer.

17.  Pineapple
The stems of pineapples are rich in a protein called bromelain. It acts as a digestive enzyme that relieves from arthritis inflammation.

18. Blueberries
Blueberries are rich in various minerals and they are considered to be the potential sources of antioxidants. However, always go for organically grown berries because they have higher amounts of polyphenols than the non-organically grown. These polyphenols and antioxidants prevent cell damage and reduce inflammation.

Homeopathic Treatment for Rheumatoid Arthritis

The treatment for Rheumatoid Arthritis may vary from cases to the case – some requiring short-term whereas others requiring long-term treatment. The duration of treatment depends on various factors such as the severity, duration, and extent of the illness, the nature of treatment taken for the same and general health of the patient.

Common Homeopathy medicines for Rheumatoid Arthritis are

  • Arnica – Useful for chronic arthritis with a feeling of bruising and soreness. The painful parts feel worse from being moved or touched.
  • Bryonia –  Helpful for stiffness and inflammation with tearing or throbbing pain, made worse by motion. The condition may have developed gradually and is worse in cold dry weather. Discomfort is aggravated by being touched or bumped, or from any movement. Relief can be had from pressure and from rest. The person may want to stay completely still and not be interfered with.
  • Calcarea carbonica- Helpful for deeply aching arthritis involving node formation around the joints. Inflammation and soreness are worse from cold and dampness, and problems may be focused on the knees and hands. Common symptoms are the weakness in the muscles, easy fatigue from exertion, and a feeling of chilliness or sluggishness. The person who benefits from Calcarea is often solid and responsible, but tends to become extremely anxious and overwhelmed when ill or overworked.
  • Aurum metallicum- This remedy is often prescribed for wandering pains in the muscles and joints that are better from motion and warmth, and worse at night. The person may experience deep pain in the limbs when trying to sleep.
  • Causticum – Useful when deformities develop in the joints, in a person with tendon problems, muscle weakness, and contractures. The hands and fingers may be most affected. Stiffness and pain are worse from being cold, and relief may come with warmth. The person often feels best in rainy weather and worse when the days are clear and dry.
  • Calcarea fluorica – Helpful when arthritic pains improve with heat and motion. Joints become enlarged and hard, and nodes or deformities develop. Arthritis after a chronic injury to joints also responds to Calcarea fluorica.
  • Dulcamara – Indicated if arthritis flares up during cold damp weather. The person gets chilled and wet. They are often stout, with a tendency toward back pain, chronic stiffness in the muscles, and allergies.
  • Kali bichromicum – This is useful when arthritic pains alternate with asthma or stomach symptoms. Pains may suddenly come and go, or shift around. Discomfort and inflammation are aggravated by heat and worse when the weather is warm.
  • Kali carbonicum – Arthritis with great stiffness and stitching pains, worse in the early morning hours and worse from cold and dampness, may respond to Kali carbonicum. The joints may be becoming thickened or deformed.
  • Kalmia latiflora – Useful for intense arthritic pain that flares up suddenly. The problems start in higher joints and extend to lower ones. Pain and inflammation may begin in the elbows, spreading down to the wrists and hands. Discomfort is worse from motion and often worse at night.
  • Ledum palustre – Arthritis that starts in lower joints and extends to higher ones are a candidate for this remedy. Pain and inflammation often begin in the toes and spread upward to the ankles and knees. The joints may also make cracking sounds. Ledum is strongly indicated when swelling is significant and relieved by cold applications.
  • Pulsatilla – Applicable when rheumatoid arthritis pain is changeable in quality, or when the flare-ups move from place to place. The symptoms (and the person) feel worse from warmth, and better from fresh air and cold applications. Can benefit people who are emotional and affectionate, sometimes having teary moods.
  • Rhododendron – Strongly indicated if swelling and soreness flare up before a storm, continuing until the weather clears. Cold and dampness aggravate the symptoms. Discomfort is often worse toward early morning, or after staying still too long.
  • Rhus Toxicodendron – Useful for rheumatoid arthritis, with pain and stiffness that is worse in the morning and worse on the first motion, but better from continued movement. Hot baths or showers, and warm applications improve the stiffness and relieve the pain. The condition is worse in cold, wet weather. The person may feel extremely restless, unable to find a comfortable position, and need to keep moving constantly. The continued motion also helps to relieve anxiety.
  • Ruta graveolens  Arthritis with a feeling of great stiffness and lameness, worse from cold and damp and worse from exertion, may be helped by Ruta graveolens. Tendons and capsules of the joints can be deeply affected or damaged. Arthritis may have developed after overuse, from repeated wear and tear.


What is Rheumatoid Arthritis


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