X-ray images of the hands and feet are generally performed on patients who have several joints affected. In RA, there may be no changes in the early stages of the disease or the X-ray image may demonstrate juxta-articular osteopenia, soft tissue swelling and loss of joint space. As the disease advances, there may be bony erosions and subluxation. X-rays of other joints may be taken if symptoms of pain or swelling occur in those joints.
Other medical imaging techniques such as magnetic resonance imaging (MRI) and ultrasound are also used in RA.
There have been technical advances in ultrasonography. High-frequency transducers (10 MHz or higher) have improved the spatial resolution of ultrasound images; these images can depict 20% more erosions than conventional radiography. Also, color Doppler and power Doppler ultrasound which show vascular signals of active synovitis depending on the degree of inflammation, are useful in assessing synovial inflammation. This is important, since in the early stages of RA, the synovium is primarily affected and synovitis seems to be the best predictive marker of future joint damage.
When RA is clinically suspected, testing for the presence of rheumatoid factor (RF, a non-specific antibody) and (ACPAs) may be required. A negative RF does not rule out RA; rather, the arthritis is called seronegative. This is the case in about 15% of patients with RA. During the first year of illness, rheumatoid factor is more likely to be negative with some individuals converting to seropositive status over time. RF is also seen in other illnesses, for example Sjögren’s syndrome, hepatitis C, systemic lupus erythematosus, chronic infections and in approximately 10% of the healthy population, therefore the test is not very specific. 
Because of this low specificity, new serological tests have been developed which test for the presence of the anti-citrullinated protein antibodies (ACPAs) or anti-CCP. Like RF, these tests are positive in only a proportion (67%) of all RA cases, but are rarely positive if RA is not present, giving it a specificity of around 95%. As with RF, there is evidence for ACPAs being present in many cases even before onset of clinical disease. 
The most common tests for ACPAs are the anti-CCP (cyclic citrullinated peptide) test and the Anti-MCV assay (antibodies against mutated citrullinatedVimentin). Recently a serological point-of-care test (POCT) for the early detection of RA has been developed. This assay combines the detection of rheumatoid factor and anti-MCV for diagnosis of RA and shows a sensitivity of 72% and specificity of 99. 7%.
Also, several other blood tests are usually done to allow for other causes of arthritis such as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive protein, full blood count, kidney function, liver enzymes and other immunological tests (e. g. , antinuclear antibody/ANA) are all performed at this stage. Elevated ferritin levels can reveal hemochromatosis, a mimic of RA or be a sign of Still’s disease, a seronegative, usually juvenile, variant of 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 RFand negative ACPA gives 0 points
- Low-positive RFor low-positive ACPA gives 2 points
- High-positive RFor 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 carries major weight, as ACPA detection is appropriate to diagnose the disease in an early state, 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 citrullinatedvimentin can confirm the suspicion of RA. A negative autoantibody result does not exclude a diagnosis of RA.
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 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.
- Osteoarthritis – distinguished with X-rays of the affected joints and blood tests, age (mostly older persons), starting pain less than an hour, a-symmetric 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.
- Ankylosing spondylitis – this involves the spine, although a 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. Acterial 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.
There are many tools available for monitoring remission in rheumatoid arthritis. Disease Activity Score of 28 joints (DAS28) is widely used as an indicator of RA disease activity and response to treatment, but is not always a reliable indicator of treatment effect. The joints included in DAS28 are (bilaterally): proximal interphalangeal joints (10 joints), metacarpophalangeal joints (10), wrists (2), elbows (2), shoulders (2) and knees (2). When looking at these joints, both the number of joints with tenderness upon touching (TEN28) and swelling (SW28) are counted. In addition, the erythrocyte sedimentation rate (ESR) is measured. Also, the affected person makes a subjective assessment (SA) of disease activity during the preceding 7 days on a scale between 0 and 100, where 0 is “no activity” and 100 is “highest activity possible”.
There is no known prevention for the condition other than the reduction of risk factors.
There is no cure for RA, but treatments can improve symptoms and slow the progress of the disease. Disease-modifying treatment has the best results when it is started early and aggressively.
The goals of treatment are to minimize symptoms such as pain and swelling, to prevent bone deformity (for example, bone erosions visible in X-rays) and to maintain day-to-day functioning. This can often be achieved using two main classes of medications: analgesics such as NSAIDs and disease-modifying antirheumatic drugs (DMARDs). RA should generally be treated with at least one specific anti-rheumatic medication. The use of benzodiazepines (such as diazepam) to treat the pain is not recommended as it does not appear to help and is associated with risks. Analgesics, other than NSAIDs, offer lesser, but some benefit with respect to pain whilst not causing the same level of gastrointestinal irritation.
Regular exercise is recommended as both safe and useful to maintain muscles strength and overall physical function.  It is uncertain if specific dietary measures have any effect.  Physical activity is beneficial for persons with rheumatoid arthritis complaining of fatigue.  Occupational therapy has a positive role to play in improving functional ability of persons with rheumatoid arthritis.
Disease-modifying antirheumatic drugs (DMARDs) are the primary treatment for RA. They are a diverse collection of drugs grouped by use and convention. They have been found to improve symptoms, decrease joint damage and improve overall functional abilities. DMARDs should be started early in the disease as they result in disease remission in approximately half of the patients and improved outcomes overall. The following drugs are considered as DMARDs: methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, TNF-alpha inhibitors, abatacept and anakinra. Rituximab and tocilizumab are monoclonal antibodies and are also DMARDs.
The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and leflunomide. Sodium aurothiomalate (Gold) and cyclosporin are less commonly used due to more common adverse effects. Agents may be used in combinations.  Methotrexate is the most important and useful DMARD and is usually the first treatment. Adverse effects should be monitored regularly with toxicity including gastrointestinal, hematologic, pulmonary and hepatic. Side effects such as nausea, vomiting or abdominal pain can be reduced by taking folic acid. The most common undesirable effect is that it increases liver enzymes in almost 15% of patients. It is thus recommended that those who consistently demonstrate abnormal levels of liver enzymes or have a history of liver disease or alcohol abuse undergo liver biopsies.
Bioagents should generally only be used if methotrexate and other conventional agents are not effective after a trial of three months. They are associated with a higher rate of serious infections as compared to other DMARDs. These agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha (TNF?) blockers such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab and tocilizumab, T cell costimulation blocker such as abatacept among others. They are often used in combination with either methotrexate or leflunomide. In those who are well controlled on TNF blockers decreasing the dose does not appear to affect overall function. Persons should be screened for latent tuberculosis before starting any TNF blockers therapy to avoid reactivation.
TNF blockers and methotrexate appear to have similar effectiveness when used alone and better results are obtained when used together. TNF blockers appear to have equivalent effectiveness with etanercept appearing to be the safest.  Abatacept appears effective for RA with 20% more patients improving with treatment than without but long term safety studies are yet unavailable. However, there is a lack of evidence to distinguish between the biologics available for RA. Issues with the biologics include their high cost and association with infections including tuberculosis.
NSAIDs reduce both pain and stiffness in those with RA. Generally they appear to have no effect on patients’s long term disease course and thus are no longer first line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular orkidney problems. Use of methotrexate together with NSAIDS is safe, if adequate monitoring is done.
COX-2 inhibitors such as celecoxib and NSAIDs are equally effective. They have a similar gastrointestinal risk as an NSAIDs plus a proton pump inhibitor. In the elderly there is less gastrointestinal intolerance to celecoxib than to NSAIDs alone.  There however is an increased risk of myocardial infarction with COX-2 inhibitors. Anti-ulcer medications are not recommended routinely but only in those high risks of gastrointestinal problems.
Glucocorticoids can be used in the short term for flare-ups while waiting for slow-onset drugs to take effect. Injection of glucocorticoids into individual joints is also effective. While long-term use reduces joint damage it also results in osteoporosis and susceptibility to infections and thus is not recommended.
In early phases of the disease, an arthroscopic or open synovectomy may be performed. It consists of the removal of the inflamed synovia and prevents a quick destruction of the affected joints. Severely affected joints may require joint replacement surgery such as knee replacement. Postoperatively, physiotherapy is always necessary.
In general, there is not enough evidence to support any complementary health approaches for RA, with safety concerns for some of them. Some mind and body practices and dietary supplements may help patients with symptoms and therefore may be beneficial additions to conventional treatments, but there is not enough evidence to draw conclusions. A systematic review of CAM modalities (excluding fish oil) found that ” The available evidence does not support their current use in the management of RA. “. Studies showing beneficial effects in RA on a wide variety of CAM modalities are often affected by publication bias and are generally not high quality evidence such as randomized controlled trials (RCTs).
The American College of Rheumatology states that no herbal medicines have health claims supported by high quality evidence and thus they do not recommend their use. There is no scientific basis to suggest that herbal supplements advertised as “natural” are safer for use than conventional medications as both are chemicals. Herbal medications, although labeled “natural”, may be toxic or fatal if consumed. Some evidence supports omega-3 fatty acids and gamma-linolenic acid in RA. The benefit from omega-3 appears modest but consistent though the current evidence is not strong enough to determine that supplementation with omega-3 polyunsaturated fatty acids (found in fish oil) is an effective treatment for RA. Gamma-linolenic acid which may reduce pain, tender joint count and stiffness, is generally safe.
The following are under investigation for treatments for RA, based on preliminary promising results (not recommended for clinical use yet): boswellic acid, curcumin, Devil’s claw, Euonymus alatus and thunder god vine (Tripterygiumwilfordii). NCCIH has noted that, “In particular, thunder god vine (Tripterygiumwilfordii) can have serious side effects. ”
Due to the false belief that herbal supplements are always safe, there is sometimes a hesitancy to report their use which may increase the risk of adverse reaction. 
There is conflicting evidence on the role of Erythropoiesis-stimulating agents for treatment of anemia in persons with rheumatoid arthritis.
More than 75% of patients with rheumatoid arthritis have symptoms improve during pregnancy but might have worsening after delivery. Methotrexate and leflunomide are teratogenic (harmful to fetus) and not used in pregnancy. It is recommended women of childbearing age should use contraceptives to avoid pregnancy and to discontinue its use if pregnancy is planned. Low dose of prednisolone, hydroxychloroquine and sulfasalazine are considered safe in pregnant persons with rheumatoid arthritis.
People with RA have an increased risk of infections and mortality and recommended vaccinations can reduce these risks. Influenza vaccine should be received annually.
The pneumococcal vaccine should be administered twice for patients under the age 65 and once for those over 65. Lastly, the live-attenuated zoster vaccine should be administered once after the age 60, but is not recommended in patients on a tumor necrosis factor alpha blocker.
The course of the disease varies greatly. Some patients have mild short-term symptoms, but in most the disease is progressive for life. Around 20%–30% will have subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor prognosis.
Poor prognostic factors include
- Persistent synovitis
- Early erosive disease
- Extra-articular findings (including subcutaneous rheumatoid nodules)
- Positive serum RF findings
- Positive serum anti-CCP autoantibodies
- Carriership of HLA-DR4 “Shared Epitope” alleles
- Family history of RA
- Poor functional status
- Socioeconomic factors
- Elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP])
- Increased clinical severity.
RA reduces lifespan on average from three to twelve years. Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease independent of other risk factors such as diabetes, alcohol abuse and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor. It is possible that the use of new biodrug therapies extend the lifespan of patients with RA and reduce the risk and progression of atherosclerosis. This is based on cohort and registry studies and currently still remains hypothetical. It is still uncertain whether biologics improve vascular function in RA or not. There was increase in total cholesterol and HDLc levels and no improvement of the atherogenic index.