Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen, followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding. Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk reduction in gastrointestinal ulcers and bleeding complications compared to traditional NSAIDs, but carry an increased rate of cardiovascular events such as myocardial infarction (MI) or heart attack, and stroke. Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys.

These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. These immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

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 people and improved outcomes overall.

The following drugs are considered as DMARDs: methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, TNF-alpha inhibitors (certolizumab, infliximab and etanercept), 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.

A 2015 Cochrane review found rituximab with methotrexate to be effective in improving symptoms compared to methotrexate alone. Rituximab works by depicting levels of B-cells (immune cell that is involved in inflammation). People taking rituximab had improved pain, function, reduced disease activity and reduced joint damage based on x-ray images. After 6 months, 21% more people had improvement in their symptoms using rituximab and methotrexate.

Biological agents 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. Biological DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha (TNFα) blockers such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, and tocilizumab T cell co-stimulation blocker such as abatacept. They are often used in combination with either methotrexate or leflunomide. Abatacept should not be used at the same time as other biologics. 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 people 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.

Glucocorticoids can be used in the short term and at the lowest dose possible for flare-ups and while waiting for slow-onset drugs to take effect.

Non-NSAID drugs to relieve pain, like paracetamol may be used to help relieve the pain symptoms; they do not change the underlying disease.

NSAIDs reduce both pain and stiffness in those with RA but do not affect the underlying disease and appear to have no effect on people's long term disease course and thus are no longer first line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular, or kidney 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.

There are several types of medications that are used for the treatment of arthritis. Treatment typically begins with medications that have the fewest side effects with further medications being added if insufficiently effective.

Depending on the type of arthritis, the medications that are given may be different. For example, the first-line treatment for osteoarthritis is acetaminophen (paracetamol) while for inflammatory arthritis it involves non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen. Opioids and NSAIDs are less well tolerated.

Rheumatoid arthritis (RA) is autoimmune so, in addition to pain medications and anti-inflammatory drugs, is treated with another category of drug called disease-modifying antirheumatic drugs (DMARDs), which act on the immune system to slow down the progression of RA. An example of this type of drug is methotrexate.

The main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate antibiotics if still present. Otherwise, treatment is symptomatic for each problem. Nonspecific urethritis may be treated with a short course of tetracycline. Analgesics, particularly NSAIDs, are used. Steroids, sulfasalazine and immunosuppressants may be needed for patients with severe reactive symptoms that do not respond to any other treatment. Local corticosteroids are useful in the case of iritis.

The major types of medications used to treat ankylosing spondylitis are pain-relievers and drugs aimed at stopping or slowing the progression of the disease. All of these have potentially serious side effects. Pain-relieving drugs come in two major classes:

- The mainstay of therapy in all seronegative spondyloarthropathies are anti-inflammatory drugs, which include NSAIDs such as ibuprofen, phenylbutazone, diclofenac, indomethacin, naproxen and COX-2 inhibitors, which reduce inflammation and pain. Indomethacin is a drug of choice. 2012 research showed that those with AS and elevated levels of acute phase reactants seem to benefit most from continuous treatment with NSAIDs.

- Opioid painkillers

Medications used to treat the progression of the disease include the following:

- Disease-modifying antirheumatic drugs (DMARDs) such as sulfasalazine can be used in people with peripheral arthritis. For axial involvement, evidence does not support sulfasalazine. Other DMARDS, such as methotrexate, did not have enough evidence to prove their effect. Generally, systemic corticosteroids were not used due to lack of evidence. Local injection with corticosteroid can be used for certain people with peripheral arthritis.

- Tumor necrosis factor-alpha (TNFα) blockers (antagonists), such as the biologics etanercept, infliximab, golimumab and adalimumab, have shown good short-term effectiveness in the form of profound and sustained reduction in all clinical and laboratory measures of disease activity. Trials are ongoing to determine their long-term effectiveness and safety. The major drawback is the cost. An alternative may be the newer, orally-administered non-biologic apremilast, which inhibits TNF-α secretion, but a recent study did not find the drug useful for ankylosing spondylitis.

- Anti-interleukin-6 inhibitors such as tocilizumab, currently approved for the treatment of rheumatoid arthritis, and rituximab, a monoclonal antibody against CD20, are also undergoing trials.

- Interleukin-17A inhibitor secukinumab is an option for the treatment of active ankylosing spondylitis that has responded inadequately to (TNFα) blockers.

A number of rheumasurgical interventions have been incorporated in the treatment of arthritis since the 1950s. Arthroscopic surgery for osteoarthritis of the knee provides no additional benefit to optimized physical and medical therapy.

JIA is best treated by a multidisciplinary team. The major emphasis of treatment for JIA is to help the child regain normal level of physical and social activities. This is accomplished with the use of physical therapy, pain management strategies, and social support. Another emphasis of treatment is to control inflammation and extra-articular symptoms quickly. Doing so should help to reduce joint damage and other symptoms, which will help reduce levels of permanent damage leading to disability.

Beneficial advances in drug treatment have been made over the last 20 years. Most children are treated with nonsteroidal anti-inflammatory drugs and intra-articular corticosteroid injections. Methotrexate, a disease-modifying antirheumatic drug (DMARD) is a powerful drug which helps suppress joint inflammation in the majority of JIA patients with polyarthritis (though less useful in systemic arthritis). Newer drugs have been developed recently, such as TNF alpha blockers, such as etanercept. No controlled evidence supports the use of alternative remedies such as specific dietary exclusions, homeopathic treatment, or acupuncture. However, an increased consumption of omega-3 fatty acids proved to be beneficial in two small studies.

Celecoxib has been found effective in one study.

Other aspects of managing JIA include physical and occupational therapy. Therapists can recommend the best exercise and also make protective equipment. Moreover, the child may require the use of special supports, ambulatory devices, or splints to help them ambulate and function normally.

Surgery is only used to treat the most severe cases of JIA. In all cases, surgery is used to remove scars and improve joint function.

Home remedies that may help JIA includes getting regular exercises to increase muscle strength and joint flexibility. Swimming is perhaps the best activity for all children with JIA. Stiffness and swelling can also be reduced with application of cold packs, but a warm bath or shower can also improve joint mobility.

In the future, genetic testing may be available allowing earlier detection of JIA. Early detection will help determine the severity of the disease in each child and help identify which therapies will be the most effective and beneficial treatment options.

There is no cure for AS, although treatments and medications can reduce symptoms and pain.

There are no prospective randomized controlled trials studying therapies for relapsing polychondritis. Evidence for efficacy of treatments is based on case reports and series of small groups of patients.

For mild cases limited to joint pain or arthritis, oral nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. Other treatments typically involve medications to suppress the immune system. Corticosteroids are frequently used for more serious disease. Steroid-sparing medications such as azathioprine or methotrexate may be used to minimize steroid doses and limit the side effects of steroids. For severe disease cyclophosphamide is often given in addition to high dose intravenous steroids.

The first line treatment for polymyositis is corticosteroids. Specialized exercise therapy may supplement treatment to enhance quality of life.

In most cases sacroiliitis can be treated without surgery. Often patients will find relief through a combination of rest, heat / ice therapy and anti-inflammatory medication, like ibuprofen. Together these simple treatments help reduce inflammation and allow the body to deliver healing nutrients to the affected SI joints.

For more severe forms of sacroiliitis, sacroiliac joint injections might be recommended to help combat symptoms. If chosen, a physician will inject a numbing agent, usually lidocaine, and a steroid containing powerful anti-inflammatory medication into the joint using fluoroscopic guidance. These steroid injections can be delivered up to three or four times a year and should be accompanied with physical therapy to help rehabilitate the affected joint.

New research shows that identifying what type of JIA a child has can help target treatment and lead to more positive outcomes. Identifying the specific biomarkers related to each type of JIA can help form more personalized treatment plans and decrease remission rates.

Children with JIA are more susceptible to cardiovascular disease, depression, sleep disturbance, anxiety and fatigue than healthy individuals. There is also limited information that suggests that children with JIA are at increased risk for malignancies when being treated with TNF blockers.

Prognosis is more positive when gene testing is undergone to identify what subtype of JIA is present in the child. Standardized treatment protocols are in place specific to each subtype of JIA. Treatment is more successful when targeted to the specific subtype of JIA.

Surgery is often the last resort when dealing with sacroiliitis and is rarely required. However, it may be a viable option for patients who are suffering from severe pain that is unresponsive to nonsurgical treatments and is significantly impacting their quality of life. In these cases, a minimally invasive procedure known as Sacroiliac Joint Fusion can effectively stabilize the joint and increase its load-bearing capacity by fusing it together.

Many individuals have mild symptoms, which recur infrequently, while others may have persistent problems that become debilitating or life-threatening.

RS3PE responds excellently to low dose corticosteroids, with sustained and often complete remission. Non-steroidal anti-inflammatory drugs (NSAIDs) have also been used. Hydroxychloroquine has proven effective in some cases.

A vast number of traditional herbal remedies were recommended for "rheumatism". Modern medicine, both conventional and alternative, recognises that the different rheumatic disorders have different causes (and several of them have multiple causes) and require different kinds of treatment.

Nevertheless, initial therapy of the major rheumatological diseases is with analgesics, such as paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs), members of which are ibuprofen and naproxen. Often, stronger analgesics are required.

The ancient Greeks recorded that bee venom had some beneficial effects on some types of rheumatism. Bee and ant stings were known as a folk remedy in the late 19th century, and at least one physician developed a treatment consisting of repeated formic acid injections. Certain Amazonian tribes, including the Zo'é, use fire ant stings as a remedy for aches and pains.

Cod liver oil has also been used as a remedy.

Neem Tree Oil according to East Indian cultures has also been used as a remedy.

Treatment is usually with intravenous antibiotics, analgesia and washout and/or aspiration of the joint. Draining the pus from the joint is important and can be done either by needle (arthrocentesis) or opening the joint surgically (arthrotomy).

Empiric antibiotics for suspected bacteria should be started. This should be based on gram stain of the synovial fluid as well as other clinical findings. General guidelines are as follows:

- Gram positive cocci - vancomycin

- Gram negative cocci - Ceftriaxone

- Gram negative bacilli - Ceftrioxone, cefotaxime, or ceftazidime

- Gram stain negative and immunocompetent - vancomycin

- Gram stain negative and immunocompromised - vancomycin + third generation cephalosphorin

- IV drug use (possible pseudomonas aeruginosa) - ceftazidime +/- an aminoglycoside

Once cultures are available, antibiotics can be changed to target the specific organism.

After a good response to intravenous antibiotics, patients can be switched to oral antibiotics. The duration of oral antibiotics varies, but is generally for 1-4 weeks depending on the offending organism.

In infection of a prosthetic joint, a biofilm is often created on the surface of the prosthesis which is resistant to antibiotics. Surgical debridement is usually indicated in these cases. A replacement prosthesis is usually not inserted at the time of removal to allow antibiotics to clear infection of the region. Patients that cannot have surgery may try long-term antibiotic therapy in order to suppress the infection.

Close follow up with physical exam & labs must be done to make sure patient is no longer feverish, pain has resolved, has improved range of motion, and lab values are normalized.

The pain medication acetaminophen is the first line treatment for osteoarthritis. However, a 2015 review found acetaminophen to only have a small short-term benefit. For mild to moderate symptoms effectiveness is similar to non-steroidal anti-inflammatory drugs (NSAIDs), though for more severe symptoms NSAIDs may be more effective. NSAIDs such as naproxen, while more effective in severe cases, are associated with greater side effects, such as gastrointestinal bleeding. Diclofenac may be the most effective NSAID.

Another class of NSAIDs, COX-2 selective inhibitors (such as celecoxib) are equally effective when compared to nonselective NSAIDs, and have lower rates of adverse gastrointestinal effects, but higher rates of cardiovascular disease such as myocardial infarction. They are also more expensive than non-specific NSAIDs. Benefits and risks vary in individuals and need consideration when making treatment decisions. NSAIDS applied topically are effective for a small number of people.

Failure to achieve desired pain relief in osteoarthritis after 2 weeks should trigger reassessment of dosage and pain medication. Opioids by mouth, including both weak opioids such as tramadol and stronger opioids, are also often prescribed. Their appropriateness is uncertain, and opioids are often recommended only when first line therapies have failed or are contraindicated. This is due to their small benefit and relatively large risk of side effects. Oral steroids are not recommended in the treatment of osteoarthritis.

There are several NSAIDs available for topical use, including diclofenac. A Cochrane review from 2016 concluded that reasonably reliable evidence is available only for use of topical diclofenac and ketoprofen in people aged over 40 years with painful knee arthritis. Transdermal opioid pain medications are not typically recommended in the treatment of osteoarthritis. The use of topical capsaicin to treat osteoarthritis is controversial, as some reviews found benefit while others did not.

Joint injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months. Injections of hyaluronic acid have not produced improvement compared to placebo for knee arthritis, but did increase risk of further pain. In ankle osteoarthritis, evidence is unclear. The effectiveness of injections of platelet-rich plasma is unclear; there are suggestions that such injections improve function but not pain, and are associated with increased risk. A 2015

A 2015 Cochrane review found that intra-articular corticosteroid injections of the knee did not benefit quality of life and had no effect on knee joint space; clinical effects one to six weeks after injection could not be determined clearly due to poor study quality. Another 2015 study reported negative effects of intra-articular corticosteroid injections at higher doses, and a 2017 trial showed reduction in cartilage thickness with intra-articular triamcinolone every 12 weeks for 2 years compared to placebo.

Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain.

For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD. However, if an acute attack is already occurring, higher doses are administered. If nothing else works, hydroxychloroquine or methotrexate may provide relief.

Research into surgical removal of calcifications is underway, however this still remains an experimental procedure.

No treatment has been found to be routinely effective. NSAIDs and COX-2 inhibitors are not generally helpful other than for general pain relief. They do not seem to help reduce effusions or prevent their occurrence. Low-dose colchicine (and some other ‘anti-rheumatic’ therapies e.g. hydroxychloroquine) have been used with some success. (Use of methotrexate and intramuscular gold have not been reported in the literature). More aggressive treatments such as synovectomy, achieved using intra-articular agents (chemical or radioactive) can provide good results, with efficacy reported for at least 1 year.

Reducing acute joint swelling:

Arthrocentesis (or drainage of joint) may be useful to relieve joint swelling and improve range of motion. Local steroid injections can also reduce fluid accumulation short-term, but do not prevent onset of episodes. These treatments provide temporary relief only. Bed rest, ice packs splints and exercise are ineffective.

A single case report of a patient with treatment-refractory IH describes the use of anakinra, an interleukin 1 receptor antagonist. At the first sign of any attack, a single 100 mg dose was given. With this dosing at onset of attacks, each episode of effusion was successfully terminated.

Reducing frequency and severity of IH episodes:

Case reports indicate some success using long-term, low-dose colchicine (e.g. 0.5 mg to 1 mg daily). A recent single case report has shown hydroxychloroquine (300 mg daily) to be effective too.

Small-sized clinical trials have shown positive results with (1) chemical and (2) radioactive synovectomy. (1) Setti et al. treated 53 patients with rifampicin RV (600 mg intra-articular injections weekly for approximately 6 weeks) with good results at 1 year follow-up. (2) Top and Cross used single doses of intra-articular radioactive gold in 18 patients with persistent effusions of mixed causes including 3 with IH. All 3 patients with IH responded well to treatment at one-year follow-up.

The effectiveness of glucosamine is controversial. Reviews have found it to be equal to or slightly better than placebo. A difference may exist between glucosamine sulfate and glucosamine hydrochloride, with glucosamine sulfate showing a benefit and glucosamine hydrochloride not. The evidence for glucosamine sulfate having an effect on osteoarthritis progression is somewhat unclear and if present likely modest. The Osteoarthritis Research Society International recommends that glucosamine be discontinued if no effect is observed after six months and the National Institute for Health and Care Excellence no longer recommends its use. Despite the difficulty in determining the efficacy of glucosamine, it remains a viable treatment option. The European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) recommends glucosamine sulfate and chondroitin sulfate for knee osteoarthritis. Its use as a therapy for osteoarthritis is usually safe.

A 2015 Cochrane review of clinical trials of chondroitin found that most were of low quality, but that there was some evidence of short-term improvement in pain and few side effects; it does not appear to improve or maintain the health of affected joints.

Synovitis symptoms can be treated with anti-inflammatory drugs such as NSAIDs. An injection of steroids may be done, directly into the affected joint. Specific treatment depends on the underlying cause of the synovitis.

Treatment depends on a specific underlying cause. The underlying cause will be treated first and foremost. The treatments may include joint replacement surgery for severely damaged joints, immunosuppressants for immune system dysfunction, antibiotics when an infection is the cause, and discontinuing medication when an allergic reaction is the cause. When treating the primary cause, pain management may still play a role in treatment. The extent of its role varies depending on the specific cause of the arthralgia. Pain management may include stretching exercises, over the counter pain medications, prescription pain medication, or other treatments deemed appropriate for the symptoms.

Capsaicin, a substance found in chili peppers, may relieve joint pain from arthritis and other conditions. Capsaicin blocks the actions of substance P, which helps transmit pain signals, and capsaicin triggers the release of pain-blocking chemicals in the body known as endorphins. Side effects of capsaicin cream include burning or stinging in the area where it is applied. Another topical option is an arthritis cream containing the ingredient, methyl salicylate (Bengay).