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Arthritis
photograph of elderly hand depicting advanced rheumatoid arthritis
A hand affected by rheumatoid arthritis, an autoimmune form of arthritis
Pronunciation
SpecialtyRheumatology
SymptomsJoint pain, stiffness, redness, swelling, decreased range of motion[2][3]
ComplicationsAmplified musculoskeletal pain syndrome[4]
Types> 100, most common (osteoarthritis, rheumatoid arthritis)[3][5]
Risk factorsFamily history, age, sex trait, previous joint injury, obesity.[6]
TreatmentResting, applying ice or heat, weight loss, exercise, joint replacement[5]
MedicationIbuprofen, paracetamol (acetaminophen)[7]

Arthritis is a general medical term used to describe a disorder in which the smooth cartilagenous layer that lines a joint is lost, resulting in bone grinding on bone during joint movement.[2] Symptoms generally include joint pain and stiffness.[2] Other symptoms may include redness, warmth, swelling, and decreased range of motion of the affected joints.[2][3] In certain types of arthritis, other organs such as the skin are also affected.[5] Onset can be gradual or sudden.[3]

There are several types of arthritis.[2][8][9] The most common forms are osteoarthritis (most commonly seen in weightbearing joints) and rheumatoid arthritis.[2] Osteoarthritis usually occurs as a person ages and often affects the hips, knees, shoulders, and fingers.[5] Rheumatoid arthritis is an autoimmune disorder that often affects the hands and feet.[5] Other types of arthritis include gout, lupus, and septic arthritis.[3][5] These are inflammatory based types of rheumatic disease.[2]

Early treatment for arthritis commonly includes resting the affected joint and conservative measures such as heating or icing.[5] Weight loss and exercise may also be useful to reduce the force across a weightbearing joint.[5] Medication intervention for symptoms depends on the form of arthritis.[5] These may include anti-inflammatory medications such as ibuprofen and paracetamol (acetaminophen). With severe cases of arthritis, joint replacement surgery may be necessary.[5]

Osteoarthritis is the most common form of arthritis affecting more than 3.8% of people, while rheumatoid arthritis is the second most common affecting about 0.24% of people.[10] In Australia about 15% of people are affected by arthritis,[11] while in the United States more than 20% have a type of arthritis.[3] Overall arthritis becomes more common with age.[2] Arthritis is a common reason people are unable to carry out their work and can result in decreased ability to complete activities of daily living.[2][3] The term arthritis is derived from arthr- (meaning 'joint') and -itis (meaning 'inflammation').[12][13]

Classification

[edit]

There are several diseases where joint pain is the most prominent symptom. Generally when a person has "arthritis" it means that they have one of the following diseases:

Joint pain can also be a symptom of other diseases. In this case, the person may not have arthritis and instead have one of the following diseases:

An undifferentiated arthritis is an arthritis that does not fit into well-known clinical disease categories, possibly being an early stage of a definite rheumatic disease.[43]

Signs and symptoms

[edit]
Extra-articular features of joint disease[44]
Cutaneous nodules
Cutaneous vasculitis lesions
Lymphadenopathy
Oedema
Ocular inflammation
Urethritis
Tenosynovitis (tendon sheath effusions)
Bursitis (swollen bursa)
Diarrhea
Orogenital ulceration

Pain in varying severity is a common symptom in most types of arthritis.[45][46] Other symptoms include swelling, joint stiffness, redness, and aching around the joint(s).[2] Arthritic disorders like lupus and rheumatoid arthritis can affect other organs in the body, leading to a variety of symptoms including:[3]

Causes

[edit]

Several factors contribute to the development of arthritis, differing on the type of arthritis.[2][6]

Osteoarthritis occurs from damage to joint cartilage from prior injury or long-term wear-and-tear, resulting in bone-to-bone contact and grinding.[6] The resulting arthritis can occur over years, or be worsened by further injury or infection.[6] If joint cartilage is severely damaged, inflammation and swelling may add to the extent and pain of osteoarthritis.[6]

In rheumatoid arthritis, the immune system itself, which normally serves to protect against infection and diseases, attacks the lining of the joint capsule, causing inflammation and swelling.[6][47]

Gout is a form of arthritis caused by excessive uric acid production, resulting in urate crystals depositing in joints, particularly in extremities, such as toes.[48][49] Urate levels in the blood may increase from consuming purine-rich foods or from body factors affecting urate clearance from the blood, a topic remaining under study.[48]

Arthritis types may also include ankylosing spondylitis, juvenile idiopathic arthritis, psoriatic arthritis, and reactive arthritis, among others.[2][6]

Risk factors

[edit]

There are common risk factors that increase a person's chance of developing arthritis later in adulthood. Some of these are modifiable while others are not.[2][3]

Some common risk factors that can increase the chances of developing osteoarthritis include obesity, prior injury to the joint, type of joint, and muscle strength.[50][51]

The risk factors with the strongest association for developing inflammatory arthritis (such as rheumatoid arthritis and lupus arthritis) are the female sex, a family history, age, obesity, joint damage from a previous injury, and exposure to tobacco smoke.[6][52][53]

Smoking has been linked to an increased susceptibility of developing arthritis, particularly rheumatoid arthritis.[54]

Diagnosis

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Synovial fluid examination[55][56]
Type WBC (per mm3) % neutrophils Viscosity Appearance
Normal <200 0 High Transparent
Osteoarthritis <5000 <25 High Clear yellow
Trauma <10,000 <50 Variable Bloody
Inflammatory 2,000–50,000 50–80 Low Cloudy yellow
Septic arthritis >50,000 >75 Low Cloudy yellow
Gonorrhea ~10,000 60 Low Cloudy yellow
Tuberculosis ~20,000 70 Low Cloudy yellow
Inflammatory: Arthritis, gout, rheumatoid arthritis, rheumatic fever
Osteoarthritis in the left hand index finger of a 63-year-old woman

Diagnosis is made by clinical examination from an appropriate health professional, and may be supported by tests such as radiologic imaging and blood tests, depending on the type of suspected arthritis.[57] Pain patterns may vary depending on the type of arthritis and the location. Rheumatoid arthritis is generally worse in the morning and associated with stiffness lasting over 30 minutes.[58] On the other hand, with osteoarthritis, the pain tends to initially be related to activity and then becomes more constant over time.[59]

Important features to look out for include the following:

  • Rate of onset of symptoms
  • Pattern of joint involvement
  • Symmetry of symptoms
  • Early morning stiffness
  • Associated tenderness around the joint
  • Locking of joint with inactivity
  • Aggravating and relieving factors, and/or
  • Presence of systemic symptoms

Physical examination may include observing the affected joints, evaluating gait, and examining the skin for findings that could be related to rheumatological disease or pulmonary inflammation. Physical examination may confirm the diagnosis or may indicate systemic disease. Chest radiographs are often used to follow progression or help assess severity.[60]

Screening blood tests for suspected arthritis include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen, and specific antibodies.[60]

Rheumatoid arthritis patients often have elevated erythrocyte sedimentation rate (ESR, also known as sed rate) or C-reactive protein (CRP) levels, which indicates the presence of an inflammatory process in the body.[58] Anti-cyclic citrullinated peptide (anti-CCP) antibodies and rheumatoid factor (RF) are two more common blood tests when assessing for rheumatoid arthritis.[58]

Imaging tests like X-rays are commonly utilized to diagnose and monitor arthritis.[61] Other imaging tests for rheumatoid arthritis that may be considered include computed tomography (CT) scanning, positron emission tomography (PET) scanning, bone scanning, and dual-energy X-ray absorptiometry (DEXA).[61]

Osteoarthritis

[edit]
Main article: Osteoarthritis
Bilateral medial joint space narrowing with osteophytes in varus knees with osteoarthritis

Osteoarthritis (OA) is the most common form of arthritis.[62] It affects humans and other animals like dogs, cats, and horses. It can affect both the larger joints (i.e. knee, hip, shoulder, etc.) and the smaller joints (i.e. fingers, toes, foot, etc.) of the body. Caused by daily wear and tear of the joint, this can speed up its progression. OA results from cartilage breakdown, leading to bones rubbing directly and eroding each other. The symptoms typically begin with minor pain during physical activity, but can eventually progress to be present at rest. The pain can be debilitating and prevent one from doing activities that they would normally do as part of their daily routine. OA typically affects the weight-bearing joints, such as the back, knee and hip due to the mechanical nature of this disease process. Unlike rheumatoid arthritis, OA is more common in the elderly, with increased age being the strongest predictor, likely due to declining chondrocytes ability to maintain cartilage.[63] Over 30 percent of women have some degree of OA by age 65. Diagnosis consists of the primary tools for diagnosing OA are X-rays of the joint. Findings on X-ray that are consistent with OA include those with joint space narrowing (due to cartilage breakdown), bone spurs, sclerosis, and bone cysts.[64]

Rheumatoid arthritis

[edit]
Main article: Rheumatoid arthritis
Bone erosions by rheumatoid arthritis[65]

Rheumatoid arthritis (RA) is a disorder in which the body's own immune system starts to attack body tissues specifically the cartilage at the end of bones known as articular cartilage.[47] The attack is not only directed at the joint but to many other parts of the body. RA often affects joints in the fingers, wrists, knees and elbows, is symmetrical (appears on both sides of the body), and can lead to severe progressive deformity in a matter of years if not adequately treated. RA usually onsets earlier in life than OA and commonly effects people aged 20 and above. In children, the disorder can present with a skin rash, fever, pain, disability, and limitations in daily activities.[47] With earlier diagnosis and appropriate aggressive treatment, many individuals can obtain control of their symptoms leading to a better quality of life compared to those without treatment.[47][66]

One of the main triggers of bone erosion in the joints in rheumatoid arthritis is inflammation of the synovium (lining of the joint capsule), caused in part by the production of pro-inflammatory cytokines and receptor activator of nuclear factor kappa B ligand (RANKL), a cell surface protein present in Th17 cells and osteoblasts.[67] Osteoclast activity can be directly induced by osteoblasts through the RANK/RANKL mechanism.[68]

This is a malar ("butterfly") skin rash that is commonly seen in patients with Lupus.

Lupus

[edit]
Main article: Lupus erythematosus

Lupus is an autoimmune collagen vascular disorder that can be present with severe arthritis. In fact, about 90% of patients with Lupus have musculoskeletal involvement.[69] Symptoms in these patients can often mimic those of rheumatoid arthritis with similar stiffness and pain patterns. Joints in the fingers, wrist, and knee tend to be the most affected.[69] Other features commonly seen in patients with Lupus include a skin rash (pictured on the right), extreme photosensitivity, hair loss, kidney problems, and shortness of breath secondary to scarring that occurs in the lungs.[70]

Gout

[edit]
Main article: Gout
Gout most commonly affects the big toe, leading to swelling, redness, and warmth around that area.

In the early stages of gout, usually only one joint is affected; however over time, many joints can become affected. Gout most commonly occurs in joints located in the big toe, knee, and/or fingers.[49] During a gout flare, the affected joints often become swollen with associated warmth and redness. The resulting pain can be significant and potentially debilitating.[71] When one of these flares occurs, management involves the use of anti-inflammatories, such as NSAIDs, colchicine, or glucocorticoids.[72] In between gout flares, it is recommended that patients take medications that decrease the production of uric acid (i.e. allopurinol, febuxostat) or increase the elimination of uric acid from the body (i.e. probenecid).[72][73]

Gout has been associated with excessive intake of alcohol and food, such as red meat.[49] Thus, it is also recommended that patients with gout adhere to a diet rich in fiber, vegetables, and whole grains, while limiting the intake of alcohol and fatty foods.[49]

There is also an uncommon form of gout that is known as pseudogout, which is caused by the formation of calcium pyrophosphate crystals in the joint.[74] Unlike gout, no targeted treatments are currently available.[74] At this time, management is aimed at decreasing inflammation in order to reduce the intensity and frequency of flares.[74]

Comparison of types

[edit]
Comparison of some major forms of arthritis[75]
Osteoarthritis Rheumatoid arthritis Gouty arthritis
Speed of onset Months-Years Weeks-months[76] Hours for an attack[77]
Main locations Weight-bearing joints (such as knees, hips, vertebral column) and hands Hands (proximal interphalangeal and metacarpophalangeal joint) wrists, ankles, knees and hips Great toe, ankles, knees and elbows
Inflammation May occur, though often mild compared to inflammation in rheumatoid arthritis Yes Yes
Radiologic changes
  • Narrowed joint space
  • Bone erosions
  • "Punched out" bone erosions
Laboratory findings None Anemia, elevated ESR and C-reactive protein (CRP), rheumatoid factor, anti-citrullinated protein antibody Crystal in joints
Other features

Other

[edit]

Infectious arthritis is another severe form of arthritis that is sometimes referred to as septic arthritis. It typically occurs when a patient is ill or has an infection. Common symptoms include the sudden onset of chills, fever, and joint pain. The condition is caused by bacteria that spread through the blood stream from elsewhere in the body. This bacteria can travel to specific joints and start to erode cartilage. Infectious arthritis must be rapidly diagnosed and treated promptly in order to prevent irreversible joint damage.[78] Only about 1% of cases of infectious arthritis are a result of viruses.[79] Within recent years, the virus SARS-CoV-2, which causes Covid-19, has been added to this list.[80] SARS-CoV-2 tends to cause reactive arthritis rather than local septic arthritis.[80]

Psoriasis can develop into psoriatic arthritis.[81] With psoriatic arthritis, most individuals first develop skin symptoms (such as scaly patches and itchiness) and then begin to experience joint related symptoms. They typically experience continuous joint pain, stiffness and swelling like other forms of arthritis. This disease can go into remission, but there is currently no known cure for the disorder.[81] Treatment current revolves around decreasing autoimmune attacks with immune suppressive medications.[81] A small percentage of patients with psoriatic arthritis can develop a severely painful and destructive form of arthritis which destroys the small joints in the hands and sometimes lead to permanent disability and loss of hand function.[81]

Treatment

[edit]

There is no known cure for arthritis and rheumatic diseases. Treatment options vary depending on the type of arthritis and include physical therapy, exercise and diet, orthopedic bracing, and oral and topical medications.[2][82] Joint replacement surgery may be required to repair damage, restore function, or relieve pain.[2]

Physical therapy

[edit]

In general, studies have shown that physical exercise of the affected joint can noticeably improve long-term pain relief. Furthermore, exercise of the arthritic joint is encouraged to maintain the health of the particular joint and the overall body of the person.[83]

Individuals with arthritis can benefit from both physical and occupational therapy. In arthritis the joints become stiff and the range of movement can be limited. Physical therapy has been shown to significantly improve function, decrease pain, and delay the need for surgical intervention in advanced cases.[84] Exercise prescribed by a physical therapist has been shown to be more effective than medications in treating osteoarthritis of the knee. Exercise often focuses on improving muscle strength, endurance and flexibility. In some cases, exercises may be designed to train balance. Occupational therapy can provide assistance with activities. Assistive technology is a tool used to aid a person's disability by reducing their physical barriers by improving the use of their damaged body part, typically after an amputation. Assistive technology devices can be customized to the patient or bought commercially.[85]

Medications

[edit]

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.[86]

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 may be less well tolerated.[87] However, topical NSAIDs may have better safety profiles than oral NSAIDs. For more severe cases of osteoarthritis, intra-articular corticosteroid injections may also be considered.[88][89]

The drugs to treat rheumatoid arthritis (RA) range from corticosteroids to monoclonal antibodies given intravenously. Due to the autoimmune nature of RA, treatments may include not only pain medications and anti-inflammatory drugs, but also another category of drugs called disease-modifying antirheumatic drugs (DMARDs). csDMARDs, TNF biologics and tsDMARDs are specific kinds of DMARDs that are recommended for treatment.[90] Treatment with DMARDs is designed to slow down the progression of RA by initiating an adaptive immune response, in part by CD4+ T helper (Th) cells, specifically Th17 cells.[91] Th17 cells are present in higher quantities at the site of bone destruction in joints and produce inflammatory cytokines associated with inflammation, such as interleukin-17 (IL-17).[67]

Surgery

[edit]

A number of surgical interventions have been incorporated in the treatment of arthritis since the 1950s. The primary surgical treatment option of arthritis is joint replacement surgery known as arthroplasty.[92] Common joints that are replaced due to arthritis include the shoulder, hip, and knee.[92] Arthroscopic surgery for osteoarthritis of the knee provides no additional benefit to patients when compared to optimized physical and medical therapy.[93] Joint replacement surgery can last anywhere from 15 to 30 years depending on the patient.[94] Following joint replacement surgery, patients can expect to get back to several physical activities including those such as swimming, tennis, and golf.[95]

Adaptive aids

[edit]

People with hand arthritis can have trouble with simple activities of daily living tasks (ADLs), such as turning a key in a lock or opening jars, as these activities can be cumbersome and painful. There are adaptive aids or assistive devices (ADs) available to help with these tasks,[96] but they are generally more costly than conventional products with the same function. It is now possible to 3-D print adaptive aids, which have been released as open source hardware to reduce patient costs.[97][98] Adaptive aids can significantly help arthritis patients and the vast majority of those with arthritis need and use them.[99]

Alternative medicine

[edit]

Further research is required to determine if transcutaneous electrical nerve stimulation (TENS) for knee osteoarthritis is effective for controlling pain.[100]

Low level laser therapy may be considered for relief of pain and stiffness associated with arthritis.[101] Evidence of benefit is tentative.[102]

Pulsed electromagnetic field therapy (PEMFT) has tentative evidence supporting improved functioning but no evidence of improved pain in osteoarthritis.[103] The FDA has not approved PEMFT for the treatment of arthritis. In Canada, PEMF devices are legally licensed by Health Canada for the treatment of pain associated with arthritic conditions.[104]

Epidemiology

[edit]

Arthritis is predominantly a disease of the elderly, but children can also be affected by the disease.[105] Arthritis is more common in women than men at all ages and affects all races, ethnic groups and cultures. In the United States, a CDC survey based on data from 2013 to 2015 showed 54.4 million (22.7%) adults had self-reported doctor-diagnosed arthritis, and 23.7 million (43.5% of those with arthritis) had arthritis-attributable activity limitation (AAAL). With an aging population, this number is expected to increase. Adults with co-morbid conditions, such as heart disease, diabetes, and obesity, were seen to have a higher than average prevalence of doctor-diagnosed arthritis (49.3%, 47.1%, and 30.6% respectively).[106]

Disability due to musculoskeletal disorders increased by 45% from 1990 to 2010. Of these, osteoarthritis is the fastest increasing major health condition.[107]

Among the many reports on the increased prevalence of musculoskeletal conditions, data from Africa are lacking and underestimated. A systematic review assessed the prevalence of arthritis in Africa and included twenty population-based and seven hospital-based studies.[108] The majority of studies, twelve, were from South Africa. Nine studies were well-conducted, eleven studies were of moderate quality, and seven studies were conducted poorly. The results of the systematic review were as follows:[108]

  • Rheumatoid arthritis: 0.1% in Algeria (urban setting); 0.6% in Democratic Republic of Congo (urban setting); 2.5% and 0.07% in urban and rural settings in South Africa respectively; 0.3% in Egypt (rural setting), 0.4% in Lesotho (rural setting)
  • Osteoarthritis: 55.1% in South Africa (urban setting); ranged from 29.5 to 82.7% in South Africans aged 65 years and older
    • Knee osteoarthritis has the highest prevalence from all types of osteoarthritis, with 33.1% in rural South Africa
  • Ankylosing spondylitis: 0.1% in South Africa (rural setting)
  • Psoriatic arthritis: 4.4% in South Africa (urban setting)
  • Gout: 0.7% in South Africa (urban setting)
  • Juvenile idiopathic arthritis: 0.3% in Egypt (urban setting)

History

[edit]

Evidence of osteoarthritis and potentially inflammatory arthritis has been discovered in dinosaurs.[109][110] The first known traces of human arthritis date back as far as 4500 BC. In early reports, arthritis was frequently referred to as the most common ailment of prehistoric peoples.[111] It was noted in skeletal remains of Native Americans found in Tennessee and parts of what is now Olathe, Kansas. Evidence of arthritis has been found throughout history, from Ötzi, a mummy (c. 3000 BC) found along the border of modern Italy and Austria, to the Egyptian mummies c. 2590 BC.[112]

In 1715, William Musgrave published the second edition of his most important medical work, De arthritide symptomatica, which concerned arthritis and its effects.[113] Augustin Jacob Landré-Beauvais, a 28-year-old resident physician at Salpêtrière Asylum in France was the first person to describe the symptoms of rheumatoid arthritis. Though Landré-Beauvais' classification of rheumatoid arthritis as a relative of gout was inaccurate, his dissertation encouraged others to further study the disease.[114]

John Charnley completed the first hip replacement (total hip arthroplasty) in England to treat arthritis in the 1960s.

Society and culture

[edit]

Arthritis is the most common cause of disability in the United States. More than 20 million individuals with arthritis in the United States have severe limitations in function on a daily basis.[3] Absenteeism and frequent visits to the physician are common in individuals who have arthritis. Arthritis can make it difficult for individuals to be physically active and some become home bound.[115] It is estimated that the total cost of arthritis cases is close to $100 billion of which almost 50% is from lost earnings.

Terminology

[edit]

The term is derived from arthr- (from Ancient Greek: ἄρθρον, romanized: árthron, lit. 'joint') and -itis (from -ῖτις, -îtis, lit. 'pertaining to'), the latter suffix having come to be associated with inflammation.

The word arthritides is the plural form of arthritis, and denotes the collective group of arthritis-like conditions.[116]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Arthritis

View on Grokipedia
from Grokipedia
Arthritis is a broad term encompassing more than 100 medical conditions characterized by , , and in one or more joints, often leading to swelling, redness, and decreased . These conditions affect the joints themselves as well as surrounding tissues and connective structures, with symptoms typically worsening with age and activity. The most common types include , which results from gradual wear-and-tear damage to joint cartilage, and , an autoimmune disorder where the mistakenly attacks the synovial lining of joints, causing chronic . Other notable forms of arthritis include , triggered by the buildup of crystals in the joints, leading to sudden and intense pain episodes often in the big toe; , associated with the skin condition and affecting both joints and skin; and , a rare but serious bacterial of the joint space. Causes vary widely by type: is linked to mechanical stress, aging, , and prior injuries; stems from genetic and environmental factors triggering ; and infectious or metabolic issues underlie conditions like or . Overall, the pathophysiology often involves degradation, , or crystal deposition, resulting in structural joint damage over time. Arthritis is highly prevalent, affecting an estimated 54 million adults in the United States—about 1 in 5— and is projected to increase due to population aging and rising rates. Globally, alone impacts 19-30% of adults over age 45, while affects roughly 1% of the population, with higher rates among women for the latter. It ranks as a leading cause of work and reduced , with risk factors including advancing age, female sex (for certain types), , joint injuries, , and family history. Early symptoms such as persistent , morning stiffness lasting over 30 minutes, and often prompt through physical exams, like X-rays, and blood tests. Although there is no cure for most types of arthritis, strategies emphasize symptom and preserving joint function. Treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and swelling, disease-modifying antirheumatic drugs (DMARDs) for autoimmune forms like , , , and low-impact exercise to strengthen muscles around affected joints. In advanced cases, joint injections or surgical options such as replacement can provide significant , while lifestyle modifications like quitting and protecting joints from injury help prevent progression. Early intervention is crucial to minimize long-term and improve daily functioning.

Types of Arthritis

Osteoarthritis

(OA) is the most common form of arthritis, characterized by the non-inflammatory degeneration of and underlying subchondral . This degenerative process primarily affects the synovial s, leading to structural changes that impair function over time. Unlike inflammatory arthritides, OA involves gradual breakdown of the articular , which normally cushions the ends of , resulting in bone-on-bone contact and secondary alterations in architecture. OA is classified into primary and secondary forms. Primary OA, also known as idiopathic OA, occurs without a clear underlying cause and is often age-related, developing insidiously in joints such as the knees, hips, and spine. Secondary OA arises from identifiable factors, including post-traumatic injuries, metabolic disorders like hemochromatosis, or congenital deformities that alter mechanics. This helps distinguish the , with primary forms more commonly linked to cumulative wear and secondary forms to specific precipitating events. The of OA centers on biomechanical stress that initiates and perpetuates breakdown. Repetitive mechanical loading exceeds the 's reparative capacity, leading to enzymatic degradation of the , loss of proteoglycans, and fibrillation of the surface. This process triggers subchondral , (bone spur) formation as a compensatory response to stabilize the , and low-grade synovial that further exacerbates tissue damage. typically develop at margins, contributing to pain and restricted motion, while synovial changes involve release and mild . Globally, OA affects over 30% of adults aged 65 and older, with clinical evidence indicating a of approximately 33.6% in this demographic. Key risk factors unique to OA include , which increases mechanical load on weight-bearing , and joint overuse from repetitive activities, both of which accelerate wear. These factors highlight the interplay between lifestyle and biomechanical influences in disease progression. Common manifestations include joint pain and morning stiffness lasting less than 30 minutes.

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic systemic characterized by symmetric inflammatory primarily affecting the synovial joints of the hands, wrists, and feet, with potential extra-articular involvement such as rheumatoid nodules or . It differs from by its autoimmune-driven inflammation rather than mechanical joint wear, and from by its classic symmetric small-joint pattern without prominent axial or skin involvement. A hallmark feature is prolonged morning stiffness lasting more than one hour, reflecting active synovial inflammation. RA is classified into seropositive and seronegative forms based on the presence of specific autoantibodies. Seropositive RA, which accounts for the majority of cases, involves (RF) and anti-citrullinated protein antibodies (ACPA), with RF detectable in 60-80% and ACPA in 70-80% of patients; these autoantibodies target modified self-proteins like citrullinated fibrinogen, promoting immune complex formation and . Seronegative RA lacks these markers but still leads to similar joint destruction, often with a more heterogeneous clinical course. The of RA centers on aberrant immune responses leading to production, synovial , and formation. such as ACPA trigger B-cell activation and T-cell infiltration into the synovium, causing of fibroblast-like synoviocytes and accumulation. This results in the formation of an invasive —a hyperplastic synovial tissue mass—that erodes and subchondral through matrix metalloproteinases and activation. storms, particularly involving tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), amplify this process by recruiting inflammatory cells, promoting endothelial activation, and sustaining chronic inflammation. Globally, affects approximately 0.5-1% of the adult population, with a higher in women at a ratio of 2-3:1 compared to men, possibly due to hormonal and genetic factors influencing immune regulation. Systemic symptoms like and low-grade fever may accompany joint involvement, underscoring the disease's multisystem nature.

Psoriatic Arthritis and Spondyloarthropathies

(PsA) is a seronegative spondyloarthropathy defined by chronic inflammatory joint and entheseal disease occurring in individuals with , a T-cell-mediated disorder. Unlike , PsA is typically negative for and antinuclear antibodies, distinguishing it through its association with and predominant involvement of peripheral joints, spine, and entheses. The condition manifests as oligoarticular or polyarticular arthritis, often with and nail changes, and can lead to erosive changes if untreated. The global prevalence of PsA ranges from 0.1% to 0.25% in the general adult population, with higher rates in regions like and compared to and . Among patients with psoriasis, PsA develops in approximately 30%, though estimates vary from 6% to 41% depending on diagnostic criteria and study populations. PsA is classified into distinct clinical patterns based on joint involvement and severity, as originally described by Moll and Wright. The most common is asymmetric , affecting fewer than five , often in the lower extremities, and occurring in about 70% of cases. Distal interphalangeal predominant arthritis involves the at the ends of fingers and toes, frequently linked to nail . Spondylitic PsA features axial involvement with and , resembling . Arthritis mutilans, a rare but severe form, causes profound joint destruction and , particularly in the hands and feet, leading to telescoping digits. PsA belongs to the family of spondyloarthropathies, a group of interrelated inflammatory arthritides that also includes and . It shares clinical overlaps with , such as and , and with , including post-infectious triggers and peripheral patterns. These connections are underscored by common genetic and immunologic features, facilitating unified classification criteria like those from the Assessment of SpondyloArthritis international Society. The of PsA centers on dysregulated immune responses involving the IL-23/IL-17 axis, where IL-23 promotes differentiation of Th17 cells that produce IL-17, driving synovial inflammation, osteoclast activation, and bone erosion. , inflammation at tendon and insertions, is a hallmark distinguishing PsA from other arthritides and contributing to characteristic patterns. Genetic factors, including alleles, are associated particularly with axial forms of PsA, present in 20-50% of such cases, though less prevalent than in . This link highlights shared mechanisms with other spondyloarthropathies, involving and innate immune activation.

Gout and Crystal Arthropathies

is a form of resulting from the deposition of monosodium urate (MSU) crystals in joints and surrounding tissues, triggered by sustained . This arises when serum urate levels exceed the solubility threshold of approximately 6.8 mg/dL, leading to crystal formation primarily in and articular cartilage. The clinical course of gout progresses through distinct phases, beginning with acute gouty arthritis, characterized by sudden, intense inflammation often affecting the first metatarsophalangeal . This is followed by the intercritical period, an asymptomatic interval where persists and further deposition occurs, typically lasting months to years between attacks. If untreated, it advances to chronic tophaceous , marked by the accumulation of tophi—subcutaneous deposits of MSU crystals that can cause , erosion, and . Crystal arthropathies also encompass related conditions such as calcium pyrophosphate deposition disease (CPPD), commonly known as pseudogout, which involves the formation of calcium pyrophosphate (CPP) crystals in joint cartilage and triggers acute inflammatory episodes mimicking gout. Unlike MSU crystals in gout, CPP crystals provoke inflammation through similar innate immune pathways but are associated with distinct metabolic and genetic factors. The unique of gout centers on , which promotes MSU crystal nucleation and deposition, initiating an intense inflammatory cascade. These crystals are phagocytosed by macrophages and , activating the complex, which in turn processes pro-IL-1β into its active form via caspase-1 cleavage, amplifying release and neutrophil recruitment to drive acute flares. This NLRP3-mediated IL-1β production distinguishes gout as an autoinflammatory disorder rather than autoimmune. Globally, gout affects 1-4% of the population, with prevalence in men ranging from 3-6% and rising significantly after age 30 due to age-related declines in urate excretion. The condition's incidence escalates in the presence of , a cluster of cardiovascular risk factors including , , and , which exacerbate through and renal impairment, thereby increasing gout risk by up to twofold in affected individuals.

Septic and Reactive Arthritis

Septic arthritis, also known as infectious or pyogenic arthritis, is characterized by the invasion of pathogens such as bacteria or fungi into the synovial space, leading to acute joint inflammation. This condition typically results from hematogenous spread of microorganisms from a distant site of , direct inoculation during trauma or , or extension from adjacent . Common bacterial culprits include , which accounts for a significant proportion of cases in adults, while in children, species and are more frequent. Fungal and mycobacterial s are rarer but occur in immunocompromised individuals. The pathophysiology of septic arthritis involves direct microbial invasion of the synovium, triggering an intense inflammatory response with influx, synovial proliferation, and rapid degradation. Pathogens like S. aureus produce virulence factors such as toxins and enzymes that exacerbate tissue damage and impair lubrication. This leads to purulent and potential destruction if untreated, with prevalence estimated at 2 to 10 cases per 100,000 person-years in the general , showing a bimodal distribution peaking in young children and older adults. Risk factors include prosthetic joints, , and intravenous drug use, contributing to its relative rarity compared to other arthritides. In contrast, reactive arthritis is a sterile, inflammatory arthropathy that develops 1 to 4 weeks following an extra-articular infection, most commonly in the gastrointestinal or genitourinary tract, without direct joint seeding by the pathogen. Triggering infections include Chlamydia trachomatis for urogenital cases and enteric pathogens like Salmonella, Shigella, Yersinia, or Campylobacter species. It predominantly affects lower limbs in a pauciarticular pattern and is associated with the HLA-B27 genetic marker in up to 80% of cases. The underlying mechanism in involves molecular mimicry, where immune responses to bacterial antigens cross-react with self-antigens in the joints, entheses, and other tissues, perpetuating without viable organisms in the synovium. This post-infectious process results in an incidence of 1 to 30 cases per 100,000 individuals following relevant infections, with higher rates in HLA-B27-positive populations. Recent studies have identified as a potential trigger for , with cases reported in 2023 showing symptom onset 2 to 4 weeks post-infection, often resolving with supportive care but highlighting emerging viral etiologies.

Other Forms

Arthritis associated with systemic lupus erythematosus (SLE) is a common musculoskeletal manifestation, occurring in 80-90% of patients as part of this multisystem that can affect the skin, kidneys, heart, and other organs. Unlike erosive forms seen in , SLE-related arthritis is typically non-erosive, presenting as a symmetrical inflammatory that primarily involves small joints such as the hands, wrists, and knees, often with morning stiffness and mild to moderate pain. The involves the deposition of immune complexes in synovial tissues, which triggers complement activation, infiltration, and subsequent inflammation without leading to joint destruction in most cases. The prevalence of SLE varies globally but is estimated at 20-70 cases per 100,000 individuals, with higher rates among women and certain ethnic groups like . Juvenile idiopathic arthritis (JIA) represents the most common chronic rheumatic disease in children, encompassing a heterogeneous group of subtypes defined by the number of affected joints, age of onset, and serological markers. The oligoarticular subtype, the most prevalent form affecting 50-60% of JIA cases, involves four or fewer joints (typically large ones like knees and ankles) in the first six months and is often associated with (ANA) positivity in up to 70-80% of patients, increasing the risk of anterior . In contrast, the polyarticular subtype affects five or more joints and is divided into (RF)-negative (11-28% of cases) and RF-positive (2-7%) forms, with the latter resembling adult in its potential for more aggressive joint involvement. Pathophysiologically, JIA subtypes like oligoarticular and polyarticular involve dysregulated adaptive immunity, including an imbalance of T helper cells (Th1 and Th17) and elevated cytokines such as IL-17, which promote synovial inflammation and , while ANA positivity in oligoarticular JIA correlates with a more favorable but heightened autoimmune risk. The overall of JIA is 16-150 per 100,000 children, with variations by region and subtype. Other rare forms of arthritis include those linked to sarcoidosis and Whipple's disease, which often mimic more common inflammatory arthropathies but arise from distinct granulomatous or infectious processes. Sarcoid arthropathy, occurring in up to 40% of sarcoidosis patients, manifests in acute or chronic patterns; the acute form, often part of Löfgren's syndrome, presents as symmetrical oligoarthritis primarily affecting ankles and wrists with rapid resolution within weeks, while the chronic variant involves persistent oligo- or polyarthritis in larger joints and is associated with skin or ocular involvement in about 25% of cases. In Whipple's disease, a rare systemic infection caused by Tropheryma whipplei, arthropathy precedes gastrointestinal symptoms in up to 75% of cases and affects 88% of patients as chronic intermittent oligo- or polyarthritis, commonly involving knees, ankles, and wrists, with radiographic erosions in about 18% and occasional axial features like sacroiliitis. These forms highlight the diverse etiologies of arthritis beyond primary rheumatic diseases, emphasizing the need for targeted diagnostic evaluation.

Signs and Symptoms

Joint Symptoms

Joint symptoms are the hallmark manifestations of arthritis, primarily affecting the synovial and leading to significant discomfort and impaired daily activities. These symptoms arise from underlying pathological processes such as , degradation, and synovial changes, which disrupt normal joint mechanics and trigger nociceptive responses. Common to most forms of arthritis, they include , swelling, , reduced , and functional limitations, though their intensity and pattern may vary slightly across types, such as acute flares in or symmetric involvement in . Pain in arthritic joints is predominantly nociceptive, originating from the of peripheral nociceptors due to or mechanical stress on damaged tissues. Inflammatory mediators, such as cytokines, sensitize nociceptors in the synovium and surrounding structures, while mechanical factors like erosion and exacerbate during movement or weight-bearing. This is often described as aching or throbbing, worsening with activity in and potentially constant in inflammatory types, significantly impacting . Swelling and result from synovial proliferation and increased fluid accumulation within the , driven by inflammatory processes that promote and cellular infiltration. In affected , the synovium thickens and produces excess , leading to visible or palpable enlargement, warmth, and tenderness. This contributes to a sensation of fullness and further restricts joint function by increasing intra-articular pressure. Stiffness manifests as a reduced to initiate movement, particularly in the morning or after periods of inactivity, often lasting more than 30 minutes and resolving with gentle activity. This phenomenon, known as gelling, stems from viscous changes in and inflammatory buildup overnight, impairing lubrication and mobility upon waking. In , it typically lasts under an hour, whereas in , it may persist longer due to heightened . Reduced occurs as a consequence of tightening, muscle guarding, and structural deformities, limiting flexion, extension, or rotation. , a or crackling sound and sensation during movement, arises from irregular articular surfaces due to loss and formation. These changes progressively hinder excursion, with often revealing bony enlargements and effusions alongside restricted mobility. Functional limitations from joint symptoms profoundly affect mobility and dexterity, including altered patterns such as limping or reduced walking speed due to lower extremity involvement, and diminished in hand-affected arthritis. and contribute to difficulties in tasks like climbing stairs, buttoning clothes, or carrying objects, leading to broader activity restrictions and dependence in daily living. These impairments are independently associated with decreased physical function and increased risk.

Systemic and Extra-Articular Symptoms

Systemic symptoms in arthritis often stem from the underlying chronic , manifesting as and that significantly impair daily functioning. In (RA), inflammation contributes to persistent exhaustion by affecting energy metabolism and sleep quality, with up to 80% of patients reporting moderate to severe . This is exacerbated in inflammatory rheumatic diseases, where proinflammatory cytokines disrupt pathways, leading to a sense of generalized . During periods of active disease, patients may experience low-grade fever and unintentional due to heightened metabolic demands and appetite suppression from . In , these symptoms occur in conjunction with elevated inflammatory markers, reflecting disease flares that increase production. Similarly, in polymyalgia rheumatica, a related , about one-third of patients develop fever and alongside . Extra-articular manifestations extend beyond joints, involving multiple organ systems and varying by arthritis type. In , rheumatoid nodules—firm, subcutaneous lumps typically on extensor surfaces—affect up to 30% of patients and result from chronic immune complex deposition. Rheumatoid vasculitis, a rarer but serious complication occurring in 1-5% of cases, arises from vessel wall and can lead to ulcers, neuropathy, or organ ischemia, often in patients with longstanding, seropositive disease. In spondyloarthropathies, such as , acute anterior is the most common extra-articular feature, affecting 25-30% of patients and presenting as unilateral eye pain, redness, and due to HLA-B27-associated . Chronic inflammation in arthritis also predisposes patients to , the most frequent hematologic complication in , where proinflammatory cytokines like interleukin-6 suppress and iron utilization, affecting 30-60% of patients with active disease. This anemia correlates with disease severity and contributes to further fatigue. Additionally, the persistent inflammatory milieu in accelerates , elevating risk and fragility fractures by 1.5- to 2-fold compared to the general population, independent of use. The psychological burden of arthritis is substantial, with depression prevalent in 20-30% of patients depending on assessment thresholds, driven by , functional limitations, and inflammatory effects on pathways. This worsens quality of life and disease outcomes, highlighting the need for integrated screening in arthritis management.

Causes and Pathophysiology

Genetic and Molecular Mechanisms

Arthritis encompasses a spectrum of inflammatory joint diseases influenced by genetic predispositions that confer susceptibility across various forms. In (RA), the ()-DR4 allele is a major genetic risk factor, encoding proteins that present autoantigens to T cells, thereby promoting aberrant immune responses. Similarly, in (OA), variants in the growth differentiation factor 5 (GDF5) gene, such as the rs143383 polymorphism, reduce GDF5 expression and impair development, increasing susceptibility to joint degeneration. These genetic elements highlight how inherited variations in immune regulation and skeletal underpin arthritis initiation. At the molecular level, networks drive chronic in arthritis . Pro-inflammatory s like (TNF)-α, interleukin-1 (IL-1), and IL-6 form interconnected signaling cascades that amplify synovial , recruit immune cells, and promote tissue destruction. For instance, TNF-α induces the production of IL-1 and IL-6, creating a feedback loop that sustains damage in RA and other forms. activation further exacerbates this process; the , triggered by cellular damage signals, processes pro-IL-1β into its active form, releasing it to perpetuate in arthritic s. Key pathways such as JAK-STAT signaling mediate these effects, where kinases phosphorylate STAT proteins upon binding, translocating them to the nucleus to upregulate inflammatory genes. Epigenetic modifications, particularly , modulate in autoimmune arthritis without altering the DNA sequence. Hypermethylation of promoter regions in genes like TET2 and hypomethylation in inflammatory loci lead to dysregulated immune cell function and persistent autoimmunity in . The gut also influences arthritis through , where imbalances in microbial communities alter and promote systemic inflammation. Recent 2024 studies indicate that reduced microbial diversity and enrichment of species in the gut precede onset, potentially via metabolite production that activates T-cell responses. In , the PTPN22 variant briefly exemplifies type-specific genetic influences by impairing T-cell regulation.

Environmental and Infectious Triggers

Environmental factors play a significant role in triggering or exacerbating various forms of arthritis, particularly through modifiable exposures that interact with underlying vulnerabilities. is a well-established environmental for (), with current and former smokers exhibiting an increased risk compared to never-smokers. Ever-smokers have approximately 1.7 times higher odds of developing seropositive , and the risk escalates in a dose-dependent manner, reaching up to 2-4 times higher for those with 10-20 pack-years of exposure, especially among individuals positive for anti-citrullinated protein antibodies (ACPA). This association is particularly pronounced in heavy smokers, where 41-50 pack-years correlate with odds ratios exceeding 13, highlighting 's role in promoting production and . Interactions between and certain genetic factors, such as HLA-DRB1 shared alleles, can further amplify this risk. Infectious agents also contribute to arthritis onset, often through direct microbial invasion or post-infectious immune responses. , characterized by chronic inflammation from oral bacteria like , is strongly associated with development and severity, with meta-analyses showing that individuals with periodontitis have significantly higher odds of (pooled odds ratio around 2-3) independent of other confounders. In , distant infections trigger sterile joint inflammation; for instance, post-viral has been documented following , with cases emerging 1-4 weeks after infection in genetically predisposed individuals, as evidenced by a narrative review identifying multiple reports of acute aseptic arthritis post-SARS-CoV-2 exposure. Occupational exposures involving repetitive strain, such as prolonged kneeling, squatting, or heavy lifting, elevate the risk of (OA), particularly in the and , with systematic reviews reporting odds ratios of 1.5-3 for workers in high-physical-demand jobs compared to sedentary occupations. Dietary patterns influence arthritis risk by modulating inflammatory and metabolic pathways. Consumption of purine-rich foods, including red meats, organ meats, and certain seafood, increases serum levels and heightens the likelihood of flares, with acute high-purine intake raising the risk of recurrent attacks by nearly fivefold in susceptible individuals. Conversely, adherence to a —rich in fruits, , , and fish—exerts protective effects against RA, potentially reducing incidence through mechanisms, as supported by cohort studies showing lower RA risk among high adherers. Hormonal fluctuations, particularly variations in women, contribute to arthritis susceptibility; declining levels post-menopause are linked to increased RA risk and disease progression, with postmenopausal women facing up to 35% higher odds compared to premenopausal counterparts due to reduced immunomodulatory effects.

Type-Specific Pathologies

In (OA), the primary pathological process involves the progressive degradation of the articular matrix, predominantly driven by matrix metalloproteinases (MMPs). MMP-13, in particular, acts as a key enzyme that cleaves , the main structural component of , leading to irreversible breakdown and loss of joint integrity. This enzymatic activity is upregulated by proinflammatory cytokines such as interleukin-1β (IL-1β) and tumor factor-α (TNF-α), which are released in response to mechanical stress or , exacerbating matrix degradation and contributing to the formation of osteophytes and subchondral changes. Rheumatoid arthritis (RA), an autoimmune disorder, features distinct synovial pathologies including aberrant and activation that perpetuate chronic and joint destruction. Synovial in RA is fueled by proangiogenic factors like (VEGF) produced by synovial fibroblasts and macrophages, enabling the influx of inflammatory cells and nutrient supply to the hyperplastic synovium, which forms invasive tissue. Concurrently, activation occurs through the receptor activator of nuclear factor kappa-B ligand () pathway, where synovial fibroblasts express to stimulate differentiation, resulting in bone erosion at the joint margins. In gout, the inflammatory response is initiated by the phagocytosis of monosodium urate (MSU) crystals by , triggering a cascade of acute . engulf MSU crystals via receptors such as and NOD-like receptor family pyrin domain containing 3 (), leading to lysosomal destabilization, potassium efflux, and activation of the , which processes pro-IL-1β into its active form to amplify recruitment and perpetuate flares. This process is further intensified by opsonization with immunoglobulins and complement, enhancing phagocytic uptake and oxidative burst in the synovial space. Septic arthritis involves bacterial invasion of the joint space, where pathogens such as form that contribute to persistent and treatment resistance. Biofilm formation begins with bacterial adhesion to synovial surfaces or prosthetic materials, followed by production that encases communities of microbes, shielding them from host immune responses and antibiotics; this leads to chronic inflammation, erosion, and if untreated. In particular, S. aureus in exhibit agglomerate-like structures that impair function and promote recurrent joint damage. Recent research on spondyloarthropathies, including and , has identified shifts in the as a contributing factor to and axial . Studies from 2024 reveal characterized by reduced microbial diversity, enrichment of proinflammatory taxa such as Prevotella and Ruminococcus, and depletion of anti-inflammatory species like Faecalibacterium, which may breach intestinal barriers and trigger IL-23/IL-17 axis activation in distant joints. These alterations correlate with disease activity and suggest a gut-joint axis in .

Risk Factors

Demographic Factors

Arthritis increases significantly with advancing age, with (OA) demonstrating a pronounced peak after age 50, while (RA) exhibits a bimodal distribution often peaking in the 40-60 age range and again in older adulthood. , diagnosed arthritis prevalence rises sequentially from younger adults to 53.9% among those aged 75 and older as of 2022 data. This age-related pattern underscores the cumulative impact of joint wear and immune dysregulation over time, influencing both susceptibility and disease severity across arthritis subtypes. Sex plays a pivotal role in arthritis susceptibility, with notable disparities by subtype. RA affects women approximately three times more frequently than men, with a female-to-male ratio of 2:1 to 3:1 globally, attributed partly to hormonal influences like modulating immune responses. In contrast, is markedly male-dominant, with a global prevalence approximately 3:1 in favor of men, largely due to higher serum uric acid levels in males and postmenopausal shifts in women. Overall, women comprise about 60% of individuals living with OA worldwide, reflecting combined biomechanical and hormonal factors that heighten joint vulnerability post-menopause. Ethnicity influences arthritis prevalence and presentation, with variations observed across populations. Native Americans, including American Indian and Alaska Native groups, experience higher rates of compared to other ethnicities in the United States, potentially linked to genetic predispositions and environmental interactions. For OA, prevalence is generally lower among Asian populations relative to Whites, with recent U.S. data (2022) indicating 13.1% for non-Hispanic Asians versus 24.9% for , though knee OA may show elevated burden in certain Asian subgroups due to body mass and activity patterns. Non-Hispanic Black and Hispanic adults with arthritis report higher severe joint pain (50.9% and 42.0%, respectively) compared to Whites (27.6%), highlighting ethnic disparities in symptom intensity. A 2023 global study estimated that affects about 15% of adults over age 30, making it the predominant form of arthritis, with women accounting for 60% of cases due to longer and sex-specific risks. In low- and middle-income countries, socioeconomic factors exacerbate disparities, as lower income and education levels correlate with reduced access to and treatment, leading to higher unmet needs and poorer outcomes in developing regions. These demographic patterns emphasize the need for tailored strategies to address inequities in arthritis burden.

Lifestyle and Occupational Factors

Obesity significantly elevates the risk of osteoarthritis (OA), particularly in weight-bearing joints like the knees, primarily due to increased mechanical loading on articular cartilage and subchondral bone. Obese individuals have approximately four times the incidence of knee OA compared to non-obese individuals, with each additional 5 kg of body weight conferring approximately a 36% increased risk. This biomechanical stress accelerates cartilage degradation and joint inflammation, independent of systemic metabolic effects. Physical activity levels play a dual role in arthritis risk, where both inactivity and excessive overuse can contribute to pathology. Sedentary behavior exacerbates OA symptoms by promoting stiffness and , particularly after periods of rest, which reduces stability and . Conversely, repetitive high-impact activities, such as those common in athletes, increase the incidence of OA through cumulative mechanical overuse and microtrauma to tissues. For instance, elite runners and other endurance athletes show elevated rates of OA due to prolonged loading, though moderate exercise generally protects against progression. Dietary patterns influence specific arthritis subtypes, notably , which arises from . Consumption of high-purine foods, such as red meats, organ meats, and certain seafood, elevates serum levels, thereby heightening the risk of acute attacks by promoting urate crystal formation in joints. In contrast, omega-3 polyunsaturated fatty acids (PUFAs) from sources like fatty exhibit protective effects against , including reduced flare recurrence and ameliorated (RA) symptoms through anti-inflammatory mechanisms. These dietary interventions, when integrated with overall moderation, can mitigate disease onset and severity. Smoking adversely affects RA progression and management by impairing immune regulation and production. Current smokers with RA experience delayed treatment responses to disease-modifying antirheumatic drugs (DMARDs), with reduced remission rates and persistent higher disease activity compared to non-smokers. This effect stems from and other components that exacerbate and hinder therapeutic efficacy, underscoring the importance of cessation for optimal outcomes. Occupational exposures, particularly to vibrating hand-held tools, contribute to hand OA development through chronic biomechanical stress on small joints. Prolonged , as encountered by workers in industries like or , induces microvascular changes and repetitive microtrauma, increasing the risk of symptomatic hand OA. Such risks are amplified by cumulative exposure duration, highlighting the need for ergonomic interventions to prevent joint degeneration.

Comorbidities and Genetic Predispositions

Arthritis, particularly (RA), is frequently associated with increased (CVD) risk, with patients facing approximately twice the likelihood compared to the general population due to chronic inflammation accelerating . This contributes significantly to morbidity, as CVD accounts for 30-40% of deaths in RA patients. similarly exhibits a bidirectional link with type 2 diabetes mellitus, where individuals with have an elevated risk of developing diabetes, and vice versa, influenced by shared metabolic disruptions like . (OA) clusters with , a condition encompassing , , , and , which heightens OA incidence through systemic inflammation and biomechanical stress on joints. Genetic predispositions play a pivotal role in arthritis susceptibility, with family history conferring a doubled risk for RA development, reflecting heritability estimates of around 60%. This familial aggregation is partly driven by the HLA-DRB1 shared epitope, a sequence motif in the HLA-DRβ chain that enhances susceptibility to severe, seropositive RA by promoting T-cell responses to citrullinated peptides. Recent advancements in 2024 have highlighted polygenic risk scores (PRS) as tools for RA prediction, integrating multiple genetic variants to stratify risk more accurately, particularly in older adults and those with obesity, outperforming single-locus analyses. In rare cases, hereditary hemochromatosis, caused by HFE gene mutations leading to iron overload, manifests as a distinctive arthropathy mimicking inflammatory arthritis, affecting up to 24% of affected individuals with characteristic joint involvement in the metacarpophalangeal joints.

Diagnosis

Clinical History and Examination

The clinical history in suspected arthritis begins with a detailed inquiry into the onset, duration, and pattern of symptoms to guide . Patients typically report , , and swelling, with symptom duration categorized as acute (less than 6 weeks), subacute (6-12 weeks), or chronic (more than 12 weeks). Patterns such as migratory arthritis, where shifts from one to another with resolution in the previously affected site, may suggest conditions like in polyarticular presentations. Morning lasting over 45 minutes often indicates inflammatory processes, contrasting with shorter durations in noninflammatory types. Additional historical elements include aggravating or alleviating factors, such as worsening with activity in degenerative cases or at rest in inflammatory ones, alongside systemic symptoms like . Symmetric involvement of small joints, such as the metacarpophalangeal joints, in the history may point toward rheumatoid arthritis. The physical examination focuses on systematic joint assessment, starting with inspection for deformity, erythema, or asymmetry, followed by palpation to detect tenderness, swelling, effusion, and warmth, which are hallmarks of active inflammation. Range of motion testing reveals limitations due to pain or mechanical blocks, while gait evaluation assesses lower limb involvement and overall mobility, such as antalgic patterns in hip or knee arthritis. Extra-articular examination includes checking for skin changes, nodules, or ocular involvement to contextualize joint findings. Red flags in the history and examination warrant urgent evaluation for serious underlying . These include acute fever with septic presentation, suggesting infectious arthritis, or unexplained and night pain indicating possible malignancy-related . Severe, rapidly progressive symptoms or neurological deficits also signal the need for immediate intervention. Functional assessment during evaluation employs standardized tools like the Health Assessment Questionnaire (HAQ), a self-reported index measuring across , such as dressing and walking, to quantify arthritis impact on . Scores range from 0 (no ) to 3 (severe ), providing a baseline for monitoring progression. In the differential diagnosis, fibromyalgia must be excluded through history and examination, as it features widespread pain for at least 3 months with associated symptoms such as fatigue and sleep disturbances, in the absence of another disorder that would explain the pain; current criteria use a Widespread Pain Index (WPI) of ≥7 and Symptom Severity Scale (SSS) score of ≥5 (or WPI 4–6 and SSS ≥9), without reliance on tender point counts, and lacks joint swelling or inflammatory signs like warmth. The absence of objective joint pathology in fibromyalgia contrasts with the synovial inflammation evident in arthritis.

Laboratory Investigations

Laboratory investigations play a crucial role in confirming the presence of inflammation, identifying specific autoimmune or metabolic markers, and distinguishing between types of arthritis through analysis of blood and synovial fluid. These tests supplement clinical findings by providing objective evidence of underlying processes such as autoimmunity, crystal deposition, or infection. Common tests include assessments of inflammatory markers, autoantibodies, genetic indicators, and fluid analyses, which help guide diagnosis for conditions like rheumatoid arthritis (RA), gout, septic arthritis, systemic lupus erythematosus (SLE), and spondyloarthropathies. Inflammatory markers such as (ESR) and (CRP) are routinely measured to detect active in arthritis. ESR, which quantifies the rate at which red blood cells settle in a tube over one hour, is elevated in conditions involving , including RA and SLE, though it is nonspecific and can also rise due to infections or . CRP, produced by the liver in response to , provides a more sensitive and rapid indicator; levels above 8-10 mg/L suggest significant inflammatory activity in autoimmune arthritides like RA or spondyloarthropathies. Both markers are typically normal in early (OA). Autoantibody tests are essential for diagnosing autoimmune forms of arthritis, particularly . (RF), an targeting the Fc portion of IgG, is present in approximately 70% of patients, though it can also appear in other conditions like SLE or infections, reducing its specificity. Anti-cyclic citrullinated (anti-CCP) antibodies offer higher specificity (around 95%) for and are detected in 60-70% of cases, often preceding clinical symptoms; their combined use with RF improves diagnostic sensitivity to about 85%. For SLE-associated arthritis, (ANA) testing screens for , with positivity in over 95% of SLE cases but also in up to 30% of healthy individuals. Genetic and metabolic tests target specific arthritis subtypes. is associated with spondyloarthropathies such as , present in 80-90% of affected patients, though it occurs in 5-8% of the general population without disease. Serum uric acid levels are evaluated for , where (above 6.8 mg/dL) indicates risk, but diagnosis requires confirmation via analysis. (CBC) often reveals in inflammatory arthritides like RA and leukocytosis (elevated white blood cells) suggestive of . Synovial fluid analysis, obtained through , is critical for crystal-induced or infectious arthritides. In , microscopic examination reveals negatively birefringent monosodium urate crystals, while is confirmed by and culture to identify bacterial pathogens, often accompanied by high white cell counts (>50,000/μL) with predominance. This test differentiates infectious processes from noninfectious and is particularly valuable when blood tests are inconclusive.

Imaging and Diagnostic Criteria

Imaging plays a crucial role in the of arthritis by visualizing structural changes in joints, aiding in the differentiation of various types. Conventional radiography, or , remains the initial imaging modality for assessing (OA) and (RA). In OA, X-rays typically reveal joint space narrowing due to loss, often accompanied by formation and subchondral sclerosis, as evaluated using grading schemes like the Kellgren-Lawrence scale. In RA, X-rays detect marginal bone erosions, particularly in the hands and feet, which represent irreversible joint damage and are visible as early as a few weeks after symptom onset. Advanced imaging techniques such as (MRI) and (US) enhance early detection of , which may precede radiographic changes. MRI provides high-resolution visualization of synovial inflammation, , and erosions, making it superior for identifying preerosive in early RA. Similarly, US detects synovial hypertrophy and power Doppler signals indicative of active with high sensitivity, often outperforming X-rays in early disease stages. Standardized diagnostic criteria incorporate findings to classify specific arthritis types. For , the 2010 ACR/EULAR criteria use a scoring system where patients with at least one involved and a score of 6 or more points (from categories including involvement, serology such as or anti-citrullinated protein antibodies, acute-phase reactants, and symptom duration of 6 weeks or longer) are classified as having definite ; while is not directly scored, erosions on or MRI contribute to confirming persistent disease. In , dual-energy computed (DECT) non-invasively identifies monosodium urate crystal deposits as a hallmark for , offering high specificity even in early or cases. For septic arthritis, prompt MRI is recommended to detect , synovial enhancement, and adjacent , guiding urgent intervention. Recent advancements as of 2025 have integrated (AI) into imaging for OA, enhancing the prediction of disease progression through automated analysis of s and MRI to quantify joint space narrowing and cartilage loss with improved accuracy over traditional methods. For instance, AI models developed in 2025 can predict future knee appearances up to a year ahead, aiding in personalized monitoring and early intervention for OA patients.

Treatment

Non-Pharmacological Interventions

Non-pharmacological interventions play a central role in managing arthritis symptoms by addressing pain, improving joint function, and enhancing without relying on medications. These approaches, including exercise, , physical and occupational therapies, and dietary modifications, are recommended as first-line strategies, particularly for (OA) and (RA), based on evidence from systematic reviews and clinical trials. They focus on reducing mechanical stress on joints, strengthening supporting muscles, and mitigating through lifestyle changes. Exercise, encompassing aerobic activities like walking or and such as resistance exercises, has strong evidence for alleviating arthritis and improving physical function. In patients with OA, aerobic exercise programs demonstrate moderate effects on reduction (standardized mean difference [SMD] 0.52, 95% CI 0.34–0.70) and function (SMD 0.46, 95% CI 0.25–0.67), with benefits sustained over short to medium terms. can significantly reduce OA and improve function compared to controls, as shown in randomized trials involving progressive resistive exercises. For , similar programs enhance muscle strength and reduce without exacerbating disease activity. Overall, regular exercise is associated with reductions of 30-50% in many OA studies, emphasizing low-impact options to avoid joint overload. Weight loss is particularly beneficial for or obese individuals with OA, as even modest reductions decrease joint loading and symptoms. Losing 5% of body weight provides symptomatic relief and improves physical function, while 10% or more yields more substantial benefits, including a fourfold reduction in knee compressive load per step lost. Cohort studies confirm a dose-response relationship, where greater weight loss correlates with lower pain scores on scales like the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). This intervention is most effective when combined with exercise, targeting sustainable lifestyle changes. Physical therapy incorporates techniques like joint protection education and (TENS) to minimize stress and control . For hand and knuckle arthritis, home-based heat therapy using warm compresses, hand soaks in warm water, or paraffin wax baths can loosen stiffness, particularly in the mornings, while cold therapy with ice packs applied for 10-15 minutes post-activity reduces swelling; gentle massage may improve circulation. Joint protection programs for hand arthritis, often delivered by occupational therapists, teach principles such as using larger for tasks, avoiding repetitive grips and tight gripping, and employing proper , leading to reduced (measured via visual analog scale [VAS]) and improved hand function in RA and hand OA patients. TENS provides moderate-certainty evidence for short-term relief in knee OA, lowering intensity during or immediately after application compared to , with no serious adverse events reported in systematic reviews. Occupational therapy focuses on adaptive devices to support daily activities and preserve joint integrity in arthritis patients. Assistive technologies, such as jar openers, padded pens and grips, built-up utensils, reachers, and lever taps, enhance independence and reduce grip demands, improving functional ability in without increasing pain. Randomized trials and reviews indicate these devices facilitate , with benefits like decreased difficulty in tasks (e.g., 40-76% reduction in challenges for administration) and better overall performance in home settings. Anti-inflammatory diets, exemplified by the rich in fruits, vegetables, fish, and , offer benefits for arthritis symptom management. In patients, adherence to this diet significantly reduces (mean difference -14.99 mm on 10 cm VAS, 95% CI -22.87 to -7.11, p=0.0002) and disease activity scores after interventions lasting over three months, though effects on inflammatory markers like are inconsistent. Observational data link higher adherence to lower OA severity and reduced risk. In , non-pharmacological interventions like exercise and diet may support remission maintenance when integrated with standard care.

Conventional Pharmacological Therapies

Conventional pharmacological therapies for arthritis primarily target symptom relief through and effects, while disease-modifying agents aim to slow progression in inflammatory forms such as (RA). These treatments are tailored to the specific type of arthritis, with analgesics and nonsteroidal drugs (NSAIDs) serving as foundational options for (OA) and acute flares across types, while disease-modifying antirheumatic drugs (DMARDs) and corticosteroids play key roles in RA. Conventional DMARDs include (first-line), as well as , , and , which are often used alone or in combination for mild to moderate RA to reduce inflammation and prevent joint damage; evidence from clinical trials supports their efficacy in achieving low disease activity in 30-50% of patients when started early. Biologic DMARDs, such as (TNF) inhibitors (e.g., , ), interleukin-6 inhibitors (e.g., ), and B-cell depleters (e.g., rituximab), are standard for moderate to severe RA unresponsive to conventional DMARDs, demonstrating radiographic halt of progression and remission rates up to 40% in randomized trials. For and , therapies focus on resolving acute inflammation and addressing underlying causes like or infection. Overall, these established, FDA-approved medications form the cornerstone of management, often used in combination to optimize efficacy while minimizing side effects. Analgesics like acetaminophen are commonly recommended as first-line for mild to moderate in OA, providing effective relief without significant anti-inflammatory action. This agent is preferred over NSAIDs in patients with gastrointestinal risks or those requiring long-term use, as it has a favorable safety profile at recommended doses up to 4 grams daily. However, evidence indicates acetaminophen is generally less effective than NSAIDs for reducing OA-related and improving function, making it suitable for initial or adjunctive rather than sole therapy. Topical over-the-counter creams containing counterirritants, such as menthol, capsaicin, or salicylates (e.g., Aspercreme or Bengay), provide localized pain relief in arthritis management by creating sensory distractions through cooling or heating sensations or by reducing pain signal transmission. NSAIDs, such as ibuprofen, are widely used for controlling pain and inflammation during acute flares in both OA and RA, acting by inhibiting cyclooxygenase enzymes to reduce prostaglandin synthesis. Oral formulations like ibuprofen (400-800 mg as needed) or naproxen provide rapid symptomatic relief, with topical versions offering localized benefits for knee OA to limit systemic exposure. Despite their efficacy, NSAIDs carry risks of gastrointestinal ulceration, cardiovascular events, and renal impairment, necessitating gastroprotective agents like inhibitors in at-risk patients. In , methotrexate remains the first-line conventional DMARD, administered weekly at doses starting from 7.5-15 mg to suppress immune-mediated damage and achieve remission in up to 40-50% of early cases. This antagonist inhibits , reducing synovial inflammation and radiographic progression when initiated early. Monitoring for , , and pulmonary effects is essential, with folic acid supplementation mitigating many adverse reactions. Corticosteroids, such as , are employed short-term in RA and other inflammatory arthritides to rapidly alleviate acute and pain, typically at low doses (5-10 mg daily) for bridging until DMARDs take effect. Intra-articular injections, like triamcinolone, provide targeted relief for monoarticular flares with minimal systemic impact. Long-term use is avoided due to risks including , , and infection susceptibility, limiting their role to acute scenarios. For gout, effectively treats and prevents acute flares by disrupting assembly in neutrophils, reducing at low doses (0.6 mg initially, followed by 0.3 mg one hour later). Urate-lowering with , a inhibitor, is standard for chronic management, titrated from 100 mg daily to maintain serum urate below 6 mg/dL and prevent recurrent attacks. Prophylactic is often co-administered during initiation to mitigate mobilization flares. In , intravenous antibiotics such as or are initiated empirically to cover common pathogens like , with de-escalation based on culture results. Treatment duration typically spans 2-6 weeks, often switching to oral agents after initial improvement, alongside surgical drainage to eradicate and preserve joint function.

Surgical and Procedural Treatments

Surgical and procedural treatments for arthritis are typically reserved for cases where conservative measures fail and structural damage has progressed significantly, aiming to alleviate pain, restore function, and prevent further deterioration. These interventions target specific types of arthritis, such as (OA) and (RA), and are performed by orthopedic specialists using techniques that range from minimally invasive procedures to major reconstructions. Success depends on patient factors like age, overall health, and the extent of involvement, with postoperative rehabilitation playing a key role in optimizing outcomes. Joint replacement surgery, also known as , is a cornerstone treatment for end-stage OA in major weight-bearing joints like the and , where loss leads to bone-on-bone contact and severe pain. In total , damaged surfaces are resurfaced with metal and plastic components to mimic natural mechanics, resulting in substantial pain relief and functional improvement in more than 90% of patients. Similarly, total involves removing the arthritic and and implanting prosthetic components, achieving success rates of 90% or higher in long-term pain reduction and mobility restoration. These procedures are indicated when daily activities are severely limited, and in the United States, approximately 2.1 million and joint replacements are performed annually as of 2025. Synovectomy addresses proliferative in , where the becomes inflamed and hypertrophic, eroding and . This procedure involves removal of the inflamed synovium, either through open or , to reduce pain, swelling, and joint destruction while preserving remaining structures. Arthroscopic offers faster recovery and comparable short-term benefits to open techniques in patients, with goals including symptom relief and cartilage protection. Arthroscopy with debridement is employed for early-stage OA, particularly in the knee, to smooth roughened , remove loose fragments, and lavage the , thereby improving symptoms in select patients with mechanical issues. This minimally invasive approach provides sustained relief and functional benefits in symptomatic early degenerative knees, though it is less effective for advanced disease. Joint fusion, or , is utilized for ankle arthritis associated with instability, fusing the and talus to eliminate painful motion and provide stability in end-stage cases unsuitable for replacement. This procedure reliably relieves pain and allows weight-bearing activity by creating a , immobile , though it sacrifices flexibility.

Alternative and Complementary Approaches

Alternative and complementary approaches encompass a range of non-conventional therapies sought by individuals with arthritis to alleviate symptoms such as pain and stiffness, often used alongside standard treatments. These methods, including , dietary supplements, remedies, and mind-body practices, have garnered interest due to their potential low-risk profiles, though supporting their efficacy remains variable and generally modest. Systematic reviews indicate that while some approaches show benefits for (OA) symptoms, results are inconsistent across studies, and they are not considered substitutes for evidence-based medical care. Acupuncture, involving the insertion of thin needles into specific body points, has been investigated for its role in managing arthritis . A Cochrane of randomized controlled trials found that may provide small to moderate reductions in and improvements in physical function for people with OA after about 8 weeks of treatment, particularly when compared to no or sham procedures. However, the review noted that benefits were not always sustained long-term, and effects were less pronounced against sham , suggesting possible contributions. Dietary supplements like and chondroitin, derived from components, are commonly used for OA joint health, as are fish oil supplements providing omega-3 fatty acids for their potential anti-inflammatory effects. Systematic reviews have yielded mixed results for glucosamine and chondroitin: some meta-analyses report modest pain relief and enhanced physical function compared to , especially with glucosamine sulfate formulations over extended periods. Conversely, guidelines from the American College of Rheumatology conditionally recommend against their routine use due to inconsistent evidence from large trials showing no superiority over for knee OA symptoms. Similarly, while fish oil may offer modest relief for OA symptoms, evidence is mixed and it is not strongly recommended. Herbal remedies, particularly turmeric containing , have properties that may benefit arthritis patients. Meta-analyses of randomized trials demonstrate that extracts can reduce pain and in OA, with effects comparable to nonsteroidal drugs in some cases, attributed to inhibition of pro-inflammatory pathways like . Evidence quality is rated moderate, with improvements in function observed, though issues limit efficacy unless enhanced formulations are used. Mind-body practices such as and emphasize gentle movements, breathing, and to enhance overall . Systematic overviews of trials indicate that these interventions can improve physical function and reduce pain in OA, with showing small to moderate effects on knee symptoms and aiding flexibility and balance. A ranked as particularly effective among mind-body exercises for pain relief, followed by , based on patient-reported outcomes. Despite potential benefits, alternative approaches carry risks, including drug interactions and inconsistent product quality due to limited . , dietary supplements like , chondroitin, and herbal extracts are not subject to pre-market approval for safety or efficacy by the , leading to variability in potency and contaminants. Additionally, herbs such as may interact with blood-thinning medications or affect liver enzymes, potentially altering the of arthritis drugs like . Patients should consult healthcare providers to avoid adverse effects.

Emerging and Experimental Therapies

Emerging therapies for arthritis are advancing rapidly, focusing on targeted biologics, regenerative approaches, and to address unmet needs in disease modification and symptom control. These investigational treatments build on foundational disease-modifying antirheumatic drugs by incorporating precision mechanisms, such as inhibition and genetic editing, to achieve deeper remission in conditions like (RA), (PsA), and (OA). Recent approvals and phase 1 trials as of 2025 highlight a shift toward personalized and minimally invasive interventions, with clinical data demonstrating sustained efficacy in refractory cases. In the realm of biologics and (JAK) inhibitors, has gained expanded approval for (GCA) alongside its established use in . The U.S. Food and Drug Administration approved the oral JAK inhibitor (Rinvoq) on April 29, 2025, as the first therapy of its class for adult GCA patients, based on phase 3 trial results showing sustained remission in nearly half of participants compared to alone. For PsA, IL-17 inhibitors continue to evolve, with agents like bimekizumab and sonelokimab demonstrating superior skin and joint outcomes in 2025 studies; for instance, sonelokimab, a nanobody targeting IL-17A and IL-17F, achieved significant reductions in disease activity in phase 2 trials for active PsA. These dual-cytokine blockers offer advantages over earlier IL-17A-only inhibitors like , particularly in patients with inadequate responses to TNF inhibitors. Regenerative strategies, including (MSC) therapy, show promise for OA cartilage repair. Intra-articular MSC injections in 2024 clinical trials led to 50-70% reduction at 12 months, alongside improved function and cartilage preservation, attributed to MSCs' immunomodulatory and chondrogenic effects. Similarly, extracellular vesicles (EVs) derived from stem cells are emerging as a cell-free alternative, with preclinical and early-phase data indicating reduced and enhanced tissue repair in RA and OA models by delivering miRNAs and proteins. In 2025 trials, MSC-EVs slowed OA progression and alleviated symptoms without the risks of whole-cell transplantation. Gene therapy innovations, such as CRISPR-Cas9 editing, target pathogenesis at the cytokine level. RG0401, a CRISPR-based targeting pro-inflammatory genes like TNF-α and IL-6, is planned to enter phase 1 trials in 2026. Precision medicine approaches further personalize care; AI algorithms predict treatment responses and optimize dosing for biologics in , improving remission rates by analyzing patient-specific biomarkers. modulation, via or fecal transplants, restores gut linked to flares, with 2025 studies showing enhanced drug efficacy and reduced inflammation through immune axis regulation. Neuromodulation therapies represent a novel frontier, exemplified by . SetPoint Medical's implantable device received FDA approval on July 31, 2025, for moderate-to-severe unresponsive to standard therapies, activating pathways to achieve clinical remission in up to 60% of trial patients. This non-pharmacologic option reduces reliance on systemic while targeting the cholinergic reflex.

Prognosis and Complications

Disease Progression and Outcomes

The progression of arthritis varies significantly by type, with typically following a slow trajectory involving both mechanical degeneration of articular due to repetitive biomechanical stress and joint overuse, as well as inflammatory processes like , leading to progressive changes in joint morphology, composition, and mechanical properties, often resulting in pain, stiffness, and reduced mobility over years or decades with possible acute inflammatory flares. In contrast, exhibits a more aggressive, erosive pattern if untreated, involving symmetric polyarticular that rapidly causes erosions, breakdown, and irreversible joint destruction within months to years. Untreated RA promotes osteoclast activation and subchondral , exacerbating functional impairment and deformity. Early intervention with disease-modifying antirheumatic drugs (DMARDs) substantially alters RA's trajectory, achieving clinical remission in 20-40% of patients, particularly when initiated within the first year of symptoms. Remission, defined by low disease activity or absence of symptoms, correlates with sustained functional recovery and halted structural damage in these cases, though rates vary by regimen intensity and patient factors like seropositivity. For OA, while no true remission occurs due to its degenerative nature, early non-pharmacological measures can slow mechanical progression and preserve joint function. For other forms, gout prognosis is generally favorable with urate-lowering , preventing recurrent attacks and tophi formation in most patients if adhered to long-term. can progress to joint deformities and spinal without treatment, but early biologic achieves remission in 40-60% and halts radiographic damage. , if promptly treated with antibiotics and drainage, has good outcomes with low mortality (5-10%), though delays lead to permanent joint destruction in up to 50%. Quality of life in arthritis is closely tied to functional status, where the Health Assessment (HAQ) disability index serves as a validated predictor of long-term and mortality. Higher baseline HAQ scores indicate greater limitations in daily activities, such as dressing or walking, and forecast accelerated progression, independent of disease activity measures. In RA cohorts, HAQ improvements with treatment reflect enhanced physical function and reduced healthcare needs, underscoring its role in prognostic assessment. As of 2025, data from observational studies emphasize that prompt DMARD initiation in early significantly reduces radiographic progression compared to delayed therapy, with studies showing milder joint damage over long-term follow-up. This underscores a critical therapeutic window, where intervention within three months of onset minimizes irreversible structural changes and improves decade-long outcomes. Disease activity in RA is routinely monitored using the Disease Activity Score 28 (DAS28), which integrates tender and swollen joint counts, or , and patient global assessment to quantify and guide treatment adjustments. A DAS28 score below 2.6 indicates remission, while values above 5.1 signal high activity requiring escalation; regular scoring enables tight control strategies to optimize progression and remission potential.

Associated Complications

Arthritis, particularly (RA), is associated with an elevated risk of cardiovascular diseases, including (MI). Patients with RA face a 50%-70% higher risk of heart disease compared to the general population, driven by chronic inflammation that accelerates and . This increased vulnerability underscores the need for routine cardiovascular screening in RA management. Osteoporosis represents another significant complication in arthritis patients, often resulting from prolonged immobility due to and , as well as the use of corticosteroids for inflammation control. In RA, generalized loss occurs periarticularly from disuse and systemically from glucocorticoid-induced suppression of formation and increased resorption. Corticosteroids, even at low doses, can lead to rapid vertebral loss in the early months of therapy, compounding risk. Post-surgical infections, particularly prosthetic joint infections following , pose a heightened risk for arthritis patients undergoing replacements. Individuals with experience an increased incidence of these infections, especially in the context of immunosuppressive therapies like corticosteroids, which impair and . The overall risk of revision surgery for infection after total is notably higher in cohorts. Mental health issues, such as anxiety, are prevalent among patients with (JIA), affecting approximately 25% of cases based on reported symptom ranges. Studies indicate anxious symptoms in JIA adolescents and young adults occur at rates from 7% to 36%, often linked to disease chronicity and functional limitations. This can exacerbate overall and . An association exists between RA and increased malignancy risk, particularly lymphoma, with patients showing a 1.5- to 3-fold higher incidence than the general population. This elevated risk is primarily for B-cell non-Hodgkin's lymphomas, influenced by persistent autoimmune inflammation and possibly certain disease-modifying therapies. Joint destruction in arthritis can lead to long-term disability, further amplifying these secondary risks. Complications in other forms include from recurrent due to urate nephropathy, and skin/nail changes or in , which can lead to vision loss if untreated. may cause or as systemic complications.

Epidemiology

Prevalence and Incidence

Arthritis affects an estimated 600 million people worldwide, primarily driven by which impacted 595 million individuals in 2020, making it one of the leading causes of globally. (OA), the most common form, impacts an estimated 595 million individuals as of 2020, representing approximately 7.6% of the world's , with projections indicating continued growth due to aging demographics. As of 2021, the global prevalence of osteoarthritis reached 606 million cases, reflecting ongoing increases. In the United States, arthritis is diagnosed in 67.1 million adults aged 20 years or older, corresponding to a prevalence of 27.9% based on 2025 data from the Centers for Disease Control and Prevention (CDC). This figure is expected to rise to 78.4 million adults by 2040, driven by population aging and increasing longevity. (RA) affects approximately 18 million people globally, with an incidence rate of 13.48 cases per 100,000 population reported in the 2021 Global Burden of Disease (GBD) study. Women account for about 70% of RA cases worldwide, highlighting a notable sex disparity in this subtype. Gout prevalence is increasing globally, with dietary factors such as high-purine intake contributing to a rise estimated at 5-10% in recent years, alongside an overall global case count of 55.2 million in 2020. (JIA), the most common form of arthritis in children, affects an estimated 220,000–300,000 children and adolescents in the United States. , the age-adjusted of diagnosed arthritis among adults rose from 22.8% in 2019 to 23.9% in 2022, reflecting a modest upward trend driven primarily by demographic shifts. The aging population has been identified as the largest contributor to the increasing burden of globally, with cases rising rapidly over the past three decades due to longer life expectancies and . This trend is compounded by rising rates, which exacerbate risk and contribute to higher disease incidence. Additionally, in the post-COVID era, there has been a noted increase in cases linked to infections, with reports documenting elevated incidence of , including reactive forms, from 2023 through 2025. Projections for () indicate a continued rise in incidence through 2025 and beyond to higher levels by 2040, underscoring the need for enhanced preventive measures. At the global level, underdiagnosis remains a significant challenge in low- and middle-income countries, where limited access to diagnostic tools and specialists hinders early identification of conditions like , as highlighted in the World Health Organization's 2023 report. Racial and ethnic disparities in arthritis burden are evident, with non-Hispanic and adults reporting higher rates of severe joint pain (50.9% and 42.0%, respectively) compared to non-Hispanic White adults (27.4%), indicating greater functional limitations despite similar or lower overall prevalence rates. Geographic inequities further compound these issues, as rural residents face substantial access gaps to specialized arthritis care, including fewer in-person visits and diagnostic services compared to urban dwellers, leading to delayed treatment and poorer outcomes.

History

Early Historical Perspectives

Evidence of osteoarthritis has been identified in ancient Egyptian dating back to approximately 3000 BCE, with paleopathological examinations revealing degenerative changes in skeletal remains from this period. These findings, observed through radiographic and direct inspection of mummified tissues, indicate that the condition affected individuals across social strata in early dynastic , often manifesting as joint erosions and . In around 400 BCE, described symptoms resembling and other arthritic conditions, including what he termed "hip gout" or , characterized by severe pain in the attributed to imbalances in bodily humors. He noted the disease's predilection for men over 40 and its association with diet and , distinguishing it from other afflictions while recommending rest, diet modification, and mild purgatives for management. During the medieval period in , treatments for arthritis-like symptoms relied heavily on , employing to restore bodily balance and alleviate perceived excesses causing . remedies were also prevalent, with aching joints treated using infusions or poultices of sweet-smelling plants such as , lavender, sage, and hay, alongside more potent applications of henbane and hemlock for pain relief. Leeches were commonly used for localized in rheumatic conditions, reflecting the era's emphasis on evacuation therapies. In the , English physician , who himself suffered from , provided a detailed clinical description of the disease in his 1683 treatise Tractatus de Podagra et Hydrope, portraying it as the "disease of kings" due to its association with affluent involving rich diets and alcohol. Sydenham emphasized the episodic nature of gouty attacks, particularly in the big toe but extending to other joints, and advocated for colchicum-based remedies alongside lifestyle moderation, solidifying its reputation as an aristocratic malady. In parallel, ancient Indian Ayurvedic traditions, documented in texts like the from around 300 BCE but rooted in practices over 3,000 years old, addressed arthritic symptoms through anti-inflammatory plants to balance vata . Key remedies included (Curcuma longa), valued for its content in reducing joint swelling, and ashwagandha (), used in decoctions to ease pain and stiffness, alongside () resins for their resinous extracts targeting inflammation. These herbal formulations, often combined with dietary adjustments and , formed the cornerstone of pre-modern management in South Asian cultures.

Modern Scientific Developments

In the 19th century, (RA) was first systematically described as a distinct clinical entity, building briefly on earlier observations of chronic joint symptoms. French physician Augustin-Jacob Landré-Beauvais provided the earliest detailed account in his 1800 doctoral thesis, characterizing RA as a progressive, symmetric affecting smaller joints with systemic features like fever and , distinguishing it from or degenerative conditions. This description laid foundational groundwork for later classifications, with British physician Alfred Baring Garrod further refining the concept in 1859 by emphasizing its inflammatory nature and chronic course. Early 20th-century efforts toward standardization culminated in precursors to modern criteria; the American Rheumatism Association (ARA, now the American College of Rheumatology), founded in 1940, began developing diagnostic frameworks, including initial proposals around 1941 that influenced subsequent revisions by focusing on joint involvement, duration, and serological markers. The mid-20th century marked the advent of disease-modifying antirheumatic drugs (DMARDs), revolutionizing management from symptomatic relief to targeted disease control. , initially used in high doses for cancer, emerged as a cornerstone DMARD in the 1980s after low-dose weekly regimens demonstrated efficacy in reducing joint inflammation and slowing radiographic progression in randomized trials; the U.S. (FDA) approved it for in 1988 based on these findings. This approval shifted treatment paradigms, with becoming first-line therapy due to its oral administration, cost-effectiveness, and favorable risk-benefit profile compared to earlier agents like gold salts or antimalarials. The 1990s introduced biologic therapies, specifically tumor necrosis factor (TNF) inhibitors, which targeted key cytokines in RA pathogenesis and achieved unprecedented remission rates. Etanercept, a soluble TNF receptor , was the first approved in 1998 for moderate-to-severe RA, showing rapid symptom improvement and reduced joint damage in phase III trials. Infliximab followed in 1999, a that, when combined with , inhibited radiographic progression more effectively than alone, as evidenced by the ATTRACT trial. These agents, administered via injection or infusion, expanded options for patients unresponsive to conventional DMARDs, with subsequent TNF inhibitors like reinforcing their class's impact on halting erosive disease. Entering the 21st century, (JAK) inhibitors offered the first oral biologics, addressing intracellular signaling pathways downstream of multiple cytokines. , a selective JAK1/3 inhibitor, received FDA approval in November 2012 for patients with inadequate response to , based on phase III trials demonstrating American College of Rheumatology 20% response rates of 59-67% at six months, comparable to TNF inhibitors but with greater convenience. trials in the 2010s explored regenerative approaches, particularly mesenchymal stem cells (MSCs) for and ; for instance, a 2016 phase II trial of allogeneic MSCs in patients showed significant reductions in Disease Activity Score 28 by 20-30% at 12 weeks, with immunomodulatory effects persisting without serious adverse events. Recent milestones include advancements in (AI) for diagnostics in 2024, enhancing early detection and personalization. models, such as those analyzing synovial biopsies, identified RA subtypes with 90% accuracy by classifying patterns, enabling tailored therapies and predicting progression in undifferentiated arthritis cases. In 2025, gene therapies progressed toward clinical viability; a phase I trial at demonstrated safe intra-articular delivery of an interleukin-1 receptor antagonist gene via vectors in knee osteoarthritis, achieving sustained expression and pain reduction for up to 12 months without systemic toxicity. The American College of Rheumatology, evolving from its 1940 founding as the ARA, has driven these developments through guideline updates and trial oversight, standardizing criteria like the 2010 ACR/EULAR classification that incorporates and joint counts for improved sensitivity in early disease.

Society and Culture

Economic and Social Burden

Arthritis exacts a profound economic toll through direct healthcare expenditures, lost , and indirect societal costs. , the total annual economic burden of arthritis, including medical costs and earnings losses, reached $303.5 billion in 2013 (equivalent to approximately $400 billion in 2025 dollars when adjusted for inflation), accounting for approximately 1% of the nation's . Globally, contributes to substantial societal costs, with systematic reviews indicating annual expenditures varying widely by subtype and region but consistently dominated by medication and indirect productivity losses exceeding hundreds of billions in aggregate across high-burden areas. A key driver of this burden is diminished workforce participation, particularly in the where arthritis leads to 172 million lost workdays annually, underscoring its role as the second-largest contributor to employee and disability expenses. These losses stem from and , where affected individuals report reduced productive time at work—up to 31% for those with pain—compared to unaffected peers. The social dimensions extend to family caregiving, especially in (JIA), where parents bear significant emotional, labor, and financial strain. Caregivers frequently reduce work hours or exit the workforce entirely, with up to 36% reporting reduced hours or job cessation in cases of systemic JIA, compounding household economic vulnerability. Annual out-of-pocket family costs for JIA management range from $1,100 to $44,800, largely from medications, appointments, and travel, positioning JIA as a "family disease" that disrupts parental and . Treatment expenses further intensify the financial pressure, with biologic disease-modifying antirheumatic drugs (DMARDs) for conditions like costing $22,000 to $44,000 per patient annually in the , often placing them in high-cost specialty tiers under plans. These elevated prices, driven by complexity and limited , result in substantial out-of-pocket burdens, averaging over $4,600 yearly even after coverage. Socioeconomic disparities exacerbate this overall burden, as individuals in low groups experience heightened arthritis severity, poorer outcomes, and amplified costs due to barriers in accessing timely care and support resources. The COVID-19 pandemic further widened these gaps by disrupting access to care and increasing indirect costs through delayed treatments.

Awareness and Advocacy

Public awareness campaigns play a crucial role in educating communities about arthritis, with May designated as Arthritis Awareness Month to highlight the condition's impact and promote early intervention. Organized primarily by the Arthritis Foundation, this annual initiative includes events, resources, and media outreach to inform the public about prevention, management, and support options for the diverse forms of arthritis. Key organizations drive these efforts globally. The Arthritis Foundation, established in 1948, leads advocacy, research funding, and education programs in the United States, serving as the primary nonprofit dedicated to combating arthritis through community support and policy influence. In the , Versus Arthritis, launched in 2018 as the nation's largest arthritis charity, focuses on research, helplines, and campaigns to empower patients and reduce the condition's burden. These groups collaborate internationally to amplify messaging and address gaps in public understanding. A persistent stigma surrounds (OA), often misconstrued as an inevitable "" , which discourages younger individuals from seeking timely care and perpetuates myths about its exclusivity to the elderly. initiatives actively combat this by emphasizing OA's occurrence across all ages due to factors like injury and , thereby reducing barriers to and treatment. Advocacy efforts have secured notable policy advancements, particularly since 2023, when the introduction of biosimilars for such as alternatives in the United States enhanced access to affordable biologic therapies, lowering costs and improving equity for patients. These wins, driven by organizations like the Arthritis Foundation, address treatment affordability and help mitigate disparities in care access among underserved populations. In 2025, innovative tools like AI-powered applications are emerging to bolster patient education. The Clara app, developed by The Arthritis Movement, uses artificial intelligence to provide personalized arthritis management guidance, symptom tracking, and educational content tailored to individual needs. Surveys indicate growing adoption of such AI resources, with potential to enhance self-management and reduce educational gaps in arthritis care.

Terminology

Etymology and Definitions

The term "arthritis" originates from the Greek words arthron, meaning "," and itis, denoting "," reflecting its core characteristic as a condition involving . This etymological root traces back to , with the word entering English usage in the mid-, around 1543, as recorded in early translations of medical texts. Historically, the broader of joint-related disorders was encompassed under the term "," which was widely used from the 16th century onward to describe various painful conditions affecting muscles, joints, and connective tissues, prior to more precise distinctions in the early . Arthritis is defined as a group of more than 100 distinct disorders characterized by inflammation of one or more joints, leading to symptoms such as pain, stiffness, swelling, and reduced range of motion. These conditions can affect not only the joints but also surrounding tissues, including muscles, tendons, ligaments, and even skin or organs in systemic forms. The World Health Organization's International Classification of Functioning, Disability and Health (ICF) framework classifies arthritis-related impairments by focusing on body functions and structures, activities, participation, and environmental factors, providing a standardized way to assess functional limitations beyond mere anatomical changes. A prevalent misconception portrays arthritis solely as "wear and tear" on the joints due to aging or overuse, akin to mechanical degeneration; however, this oversimplifies the , as many forms involve active inflammatory, autoimmune, or infectious processes that actively damage joint tissues. For instance, while may involve degenerative elements, inflammatory types like demonstrate immune-mediated destruction unrelated to simple attrition.

Classification and Nomenclature

Arthritis encompasses a diverse group of conditions, and its nomenclature is standardized internationally through the , developed by the . In , inflammatory arthropathies are classified under the block FA20-FA2Z, which includes specific codes for major subtypes such as (FA20), (FA21), (FA22), (FA23), and (FA24). This system facilitates clinical coding, epidemiological tracking, and research by providing a hierarchical structure that distinguishes inflammatory from non-inflammatory forms, with FA2Z reserved for unspecified inflammatory arthropathies. Unlike the preceding ICD-10's M05-M14 block, emphasizes clinical utility and integrates emerging subtypes for more precise diagnostic mapping. Classification of arthritis relies on established criteria from professional societies to ensure consistency in diagnosis and research. For (JIA), the of Associations for Rheumatology (ILAR) provides the primary framework, revised in 2001 and published in 2004, categorizing JIA into seven subtypes—systemic arthritis, , (rheumatoid factor-positive or negative), , enthesitis-related arthritis, undifferentiated arthritis, and other—based on clinical features, age of onset before 16 years, and exclusion of other causes. In adults, the American College of (ACR) and European Alliance of Associations for Rheumatic Diseases (EULAR) jointly developed 2010 classification criteria for , scoring patients on joint involvement, , acute-phase reactants, and symptom duration to achieve a total score of ≥6 out of 10 for . For spondyloarthropathies, the Assessment of SpondyloArthritis international Society (ASAS) criteria, endorsed by EULAR, classify using imaging or status alongside clinical features like inflammatory . Recent refinements, such as the 2022 ASAS-EULAR update to management recommendations, indirectly support by incorporating treat-to-target strategies that highlight evolving diagnostic nuances in these conditions. A key distinction in rheumatoid arthritis nomenclature and classification is between seropositive and seronegative forms, determined by the presence of autoantibodies. Seropositive RA is characterized by positive (RF) or anti-citrullinated protein antibodies (ACPA), which contribute points in the 2010 ACR/EULAR criteria and indicate a more aggressive disease course with higher erosion risk. Seronegative RA lacks these markers, often presenting with similar joint involvement but potentially different extra-articular manifestations and treatment responses, underscoring the serological axis in subclassification. Classification challenges arise from overlap syndromes, where features of multiple arthritides coexist, complicating standardized categorization. Rhupus syndrome, for instance, represents an overlap between and , featuring erosive alongside lupus-specific criteria like or positive antinuclear antibodies, often requiring dual classification under codes for both conditions. Such overlaps, including those in undifferentiated diseases, highlight limitations in rigid frameworks like ILAR or ACR/EULAR, prompting ongoing efforts to refine criteria for better capturing heterogeneous presentations without over-reliance on exclusion rules.

References

  1. https://www.mayoclinic.org/diseases-conditions/arthritis/symptoms-causes/syc-20350772
  2. https://www.cdc.gov/arthritis/basics/index.html
  3. https://www.ncbi.nlm.nih.gov/books/NBK518992/
  4. https://www.mayoclinic.org/diseases-conditions/arthritis/diagnosis-treatment/drc-20350777
  5. https://www.who.int/news-room/fact-sheets/detail/osteoarthritis
  6. https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/joint-disorders/osteoarthritis-oa
  7. https://www.ncbi.nlm.nih.gov/books/NBK507884/
  8. https://my.clevelandclinic.org/health/diseases/5599-osteoarthritis
  9. https://pmc.ncbi.nlm.nih.gov/articles/PMC3635670/
  10. https://www.mdpi.com/2079-7737/9/8/194
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC7696673/
  12. https://www.sciencedirect.com/science/article/pii/S1063458413007607
  13. https://www.nia.nih.gov/health/osteoarthritis/osteoarthritis
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC3266544/
  15. https://www.hopkinsmedicine.org/health/conditions-and-diseases/arthritis/osteoarthritis
  16. https://www.msdmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/joint-disorders/rheumatoid-arthritis-ra
  17. https://www.nature.com/articles/nrdp20181
  18. https://www.ncbi.nlm.nih.gov/books/NBK441999/
  19. https://www.ncbi.nlm.nih.gov/books/NBK547710/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC11637478/
  21. https://www.arthritis.org/diseases/psoriatic-arthritis
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC5104808/
  23. https://www.openaccessjournals.com/articles/classification-and-categorization-of-psoriatic-arthritis.pdf
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC3302034/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC7871349/
  26. https://academic.oup.com/rheumatology/article/55/2/221/1822163
  27. https://www.ncbi.nlm.nih.gov/books/NBK546606/
  28. https://rheumatology.org/patients/calcium-pyrophosphate-deposition-cppd
  29. https://www.nature.com/articles/s41572-019-0115-y
  30. https://www.ncbi.nlm.nih.gov/books/NBK538176/
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC126863/
  33. https://www.ncbi.nlm.nih.gov/books/NBK499831/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC8091991/
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC10017067/
  36. https://www.ncbi.nlm.nih.gov/books/NBK535405/
  37. https://pmc.ncbi.nlm.nih.gov/articles/PMC9604412/
  38. https://www.ncbi.nlm.nih.gov/books/NBK554605/
  39. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2020.565420/full
  40. https://www.nature.com/articles/s41598-021-91671-9
  41. https://www.arthritis.org/health-wellness/healthy-living/managing-pain/understanding-pain/mechanisms-of-arthritis-pain
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC8278572/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC6157001/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC4254338/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC9050956/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC6504589/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC3496084/
  48. https://www.mayoclinic.org/diseases-conditions/osteoarthritis/symptoms-causes/syc-20351925
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC4039183/
  50. https://www.arthritis.org/getmedia/8164d2b1-e59c-463b-8531-3f96763ff669/Answers-FactSheet-2-22.pdf
  51. https://www.ncbi.nlm.nih.gov/books/NBK482326/
  52. https://pubmed.ncbi.nlm.nih.gov/21272657/
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC2597216/
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC3529154/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC3753584/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC10470972/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC10418999/
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC6827268/
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC6422329/
  60. https://www.arthritis.org/diseases/polymyalgia-rheumatica
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC5642136/
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC3999374/
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC3512172/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC1004740/
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC7687316/
  66. https://pmc.ncbi.nlm.nih.gov/articles/PMC3828510/
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC130004/
  68. https://academic.oup.com/hmg/article/16/18/2226/713753
  69. https://www.mdpi.com/1422-0067/22/20/10922
  70. https://www.sciencedirect.com/science/article/pii/S258900422201820X
  71. https://pmc.ncbi.nlm.nih.gov/articles/PMC6009092/
  72. https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2019.00570/full
  73. https://ard.bmj.com/content/early/2024/10/22/ard-2024-226362
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC3655138/
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC4747051/
  76. https://www.nature.com/articles/s41392-023-01330-w
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC4879881/
  78. https://www.hopkinsarthritis.org/arthritis-info/rheumatoid-arthritis/ra-pathophysiology-2/
  79. https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-020-02244-6
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC10960513/
  81. https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2021.724113/full
  82. https://academic.oup.com/jid/article/211/4/641/2910582
  83. https://onlinelibrary.wiley.com/doi/10.1111/1756-185X.15130
  84. https://journals.lww.com/md-journal/fulltext/2025/03210/trends_and_disparities_in_the_prevalence_of.46.aspx
  85. https://www.cdc.gov/pcd/issues/2025/24_0393.htm
  86. https://www.nature.com/articles/s41598-025-92150-1
  87. https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913%2824%2900117-6/fulltext
  88. https://www.rheumatologyadvisor.com/news/race-ethnic-disparities-seen-in-age-adjusted-prevalence-of-arthritis/
  89. https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/acr.25316
  90. https://www.healthdata.org/news-events/newsroom/news-releases/lancet-new-study-reveals-most-common-form-arthritis
  91. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-017-1624-z
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC10456094/
  93. https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-018-1727-4
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC4238740/
  95. https://pmc.ncbi.nlm.nih.gov/articles/PMC7349942/
  96. https://oaaction.unc.edu/oa-module/oa-signs-and-symptoms/
  97. https://pubmed.ncbi.nlm.nih.gov/16790540/
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC4350574/
  99. https://extension.usu.edu/nutrition/research/treating-arthritis-through-food
  100. https://pmc.ncbi.nlm.nih.gov/articles/PMC6717014/
  101. https://pmc.ncbi.nlm.nih.gov/articles/PMC9281000/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC12129895/
  103. https://pmc.ncbi.nlm.nih.gov/articles/PMC6718206/
  104. https://pmc.ncbi.nlm.nih.gov/articles/PMC7065017/
  105. https://cdr.lib.unc.edu/downloads/wd376697c
  106. https://creakyjoints.org/living-with-arthritis/symptoms/how-family-history-affects-rheumatoid-arthritis-risk-study/
  107. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2024.1421328/full
  108. https://www.nature.com/articles/srep25766
  109. https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-024-17682-z
  110. https://pmc.ncbi.nlm.nih.gov/articles/PMC2921962/
  111. https://pubmed.ncbi.nlm.nih.gov/38282146/
  112. https://pubmed.ncbi.nlm.nih.gov/20954257/
  113. https://www.ncbi.nlm.nih.gov/books/NBK585764/
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC12195327/
  115. https://pubmed.ncbi.nlm.nih.gov/12508408/
  116. https://www.ncbi.nlm.nih.gov/books/NBK540974/
  117. https://www.arthritis.org/health-wellness/about-arthritis/understanding-arthritis/blood-tests-for-arthritis
  118. https://pmc.ncbi.nlm.nih.gov/articles/PMC10894719/
  119. https://pmc.ncbi.nlm.nih.gov/articles/PMC3306456/
  120. https://pmc.ncbi.nlm.nih.gov/articles/PMC4096779/
  121. https://ajronline.org/doi/10.2214/AJR.07.2548
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC5392548/
  123. https://pubmed.ncbi.nlm.nih.gov/20872595/
  124. https://pmc.ncbi.nlm.nih.gov/articles/PMC5355369/
  125. https://acsearch.acr.org/docs/3094201/Narrative/
  126. https://pmc.ncbi.nlm.nih.gov/articles/PMC12015311/
  127. https://www.sciencedaily.com/releases/2025/10/251022023116.htm
  128. https://www.mayoclinic.org/diseases-conditions/arthritis/in-depth/arthritis/art-20046440
  129. https://www.arthritis.org/health-wellness/healthy-living/managing-pain/pain-relief-solutions/natural-relief-for-arthritis-pain
  130. https://www.mayoclinic.org/diseases-conditions/rheumatoid-arthritis/diagnosis-treatment/drc-20353653
  131. https://www.mayoclinic.org/diseases-conditions/gout/diagnosis-treatment/drc-20372903
  132. https://pmc.ncbi.nlm.nih.gov/articles/PMC3891482/
  133. https://www.mayoclinic.org/diseases-conditions/osteoarthritis/diagnosis-treatment/drc-20351930
  134. https://pmc.ncbi.nlm.nih.gov/articles/PMC8275921/
  135. https://pubmed.ncbi.nlm.nih.gov/16437479/
  136. https://www.arthritis.org/drug-guide/medication-topics/topicals
  137. https://www.mayoclinic.org/diseases-conditions/osteoarthritis/in-depth/pain-medications/art-20045899
  138. https://pmc.ncbi.nlm.nih.gov/articles/PMC8586433/
  139. https://pmc.ncbi.nlm.nih.gov/articles/PMC3527878/
  140. https://pmc.ncbi.nlm.nih.gov/articles/PMC6360124/
  141. https://pubmed.ncbi.nlm.nih.gov/28866645/
  142. https://www.ncbi.nlm.nih.gov/books/NBK584390/
  143. https://pmc.ncbi.nlm.nih.gov/articles/PMC10563586/
  144. https://pmc.ncbi.nlm.nih.gov/articles/PMC6366613/
  145. https://pubmed.ncbi.nlm.nih.gov/34913662
  146. https://www.hss.edu/health-library/conditions-and-treatments/synovectomy
  147. https://orthop.washington.edu/patient-care/articles/knee/total-knee-replacement-a-patients-guide.html
  148. https://orthop.washington.edu/patient-care/articles/hip/what-is-hip-replacement-a-review-of-total-hip-arthroplasty.html
  149. https://www.aahks.org/wp-content/uploads/2024/09/2024-Hip-and-Knee.pdf
  150. https://pmc.ncbi.nlm.nih.gov/articles/PMC5586937/
  151. https://pmc.ncbi.nlm.nih.gov/articles/PMC11900960/
  152. https://pmc.ncbi.nlm.nih.gov/articles/PMC9771083/
  153. https://pmc.ncbi.nlm.nih.gov/articles/PMC6289903/
  154. https://pmc.ncbi.nlm.nih.gov/articles/PMC5112338/
  155. https://www.hss.edu/health-library/conditions-and-treatments/list/arthrodesis
  156. https://www.cochrane.org/evidence/CD001977_acupuncture-osteoarthritis
  157. https://pmc.ncbi.nlm.nih.gov/articles/PMC6035477/
  158. https://www.nccih.nih.gov/health/glucosamine-and-chondroitin-for-osteoarthritis-what-you-need-to-know
  159. https://pmc.ncbi.nlm.nih.gov/articles/PMC9413343/
  160. https://pmc.ncbi.nlm.nih.gov/articles/PMC5003001/
  161. https://www.sciencedirect.com/science/article/abs/pii/S1876382020314335
  162. https://pubmed.ncbi.nlm.nih.gov/37115606/
  163. https://www.sciencedirect.com/science/article/pii/S0965229925000639
  164. https://pmc.ncbi.nlm.nih.gov/articles/PMC2957745/
  165. https://www.ncbi.nlm.nih.gov/books/NBK538520/
  166. https://www.nejm.org/doi/abs/10.1056/NEJMoa2413449
  167. https://news.abbvie.com/2025-04-29-RINVOQ-R-upadacitinib-Receives-U-S-FDA-Approval-for-Giant-Cell-Arteritis-GCA
  168. https://www.nature.com/articles/s41591-025-03971-6
  169. https://.ncbi.nlm.nih.gov/41189198/
  170. https://cells4life.com/us/2024/08/new-stem-cell-therapy-could-treat-osteoarthritis-study-finds/
  171. https://pmc.ncbi.nlm.nih.gov/articles/PMC12365376/
  172. https://www.frontiersin.org/journals/bioengineering-and-biotechnology/articles/10.3389/fbioe.2025.1570526/full
  173. https://www.medscape.com/viewarticle/could-gene-therapy-ra-soon-be-ready-take-2025a100032y
  174. https://journals.sagepub.com/doi/10.1177/1759720X251343579
  175. https://www.jci.org/articles/view/195374
  176. https://setpointmedical.com/setpoint-medical-receives-fda-approval-for-novel-neuroimmune-modulation-therapy-for-rheumatoid-arthritis/
  177. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfpma/pma.cfm?id=P240039
  178. https://pmc.ncbi.nlm.nih.gov/articles/PMC6565968/
  179. https://pmc.ncbi.nlm.nih.gov/articles/PMC11987368/
  180. https://pmc.ncbi.nlm.nih.gov/articles/PMC8365438/
  181. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9286571/
  182. https://www.ncbi.nlm.nih.gov/books/NBK538174/
  183. https://pmc.ncbi.nlm.nih.gov/articles/PMC1754988/
  184. https://pmc.ncbi.nlm.nih.gov/articles/PMC6562164/
  185. https://pubmed.ncbi.nlm.nih.gov/28956118/
  186. https://pmc.ncbi.nlm.nih.gov/articles/PMC11879312/
  187. https://pmc.ncbi.nlm.nih.gov/articles/PMC3616381/
  188. https://pubmed.ncbi.nlm.nih.gov/27762189/
  189. https://pmc.ncbi.nlm.nih.gov/articles/PMC1856019/
  190. https://www.sciencedirect.com/science/article/pii/S277263202300034X
  191. https://pmc.ncbi.nlm.nih.gov/articles/PMC9827945/
  192. https://pubmed.ncbi.nlm.nih.gov/9536336/
  193. https://arthritis-research.biomedcentral.com/articles/10.1186/ar2352
  194. https://pmc.ncbi.nlm.nih.gov/articles/PMC3923416/
  195. https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/acr.20036
  196. https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-024-03312-x
  197. https://pmc.ncbi.nlm.nih.gov/articles/PMC6830373/
  198. https://pmc.ncbi.nlm.nih.gov/articles/PMC8413949/
  199. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2020.601618/full
  200. https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(23)00163-7/fulltext
  201. https://www.singlecare.com/blog/news/arthritis-statistics/
  202. https://www.sciencedirect.com/science/article/pii/S1063458425011276
  203. https://odphp.health.gov/healthypeople/about/workgroups/arthritis-workgroup
  204. https://www.who.int/news-room/fact-sheets/detail/rheumatoid-arthritis
  205. https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(24)00117-6/fulltext
  206. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-024-08180-9
  207. https://www.arthritis.org/diseases/juvenile-arthritis
  208. https://www.cdc.gov/mmwr/volumes/72/wr/mm7229a3.htm
  209. https://www.cureus.com/articles/247325-trends-in-arthritis-prevalence-and-associated-chronic-health-indicators-among-adults-insights-from-the-behavioral-risk-factor-surveillance-system-brfss-database.pdf
  210. https://www.sciencedirect.com/science/article/abs/pii/S156899722300143X
  211. https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/acr.25192
  212. https://www.cdc.gov/nchs/data/series/sr_11/sr11_020acc.pdf
  213. https://academic.oup.com/bja/article/99/4/461/305514
  214. https://pubmed.ncbi.nlm.nih.gov/40332982/
  215. https://pmc.ncbi.nlm.nih.gov/articles/PMC3573364/
  216. https://pmc.ncbi.nlm.nih.gov/articles/PMC3757849/
  217. https://hekint.org/2017/10/11/thomas-sydenham/
  218. https://pmc.ncbi.nlm.nih.gov/articles/PMC3226106/
  219. https://pmc.ncbi.nlm.nih.gov/articles/PMC5871155/
  220. https://phcogrev.com/sites/default/files/PharmacognRev-14-28-121.pdf
  221. https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2019.00659/full
  222. https://www.the-rheumatologist.org/article/why-did-rheumatoid-arthritis-begin-in-1800/
  223. https://pmc.ncbi.nlm.nih.gov/articles/PMC3119866/
  224. https://www.the-rheumatologist.org/article/a-brief-history-of-american-rheumatology/
  225. https://pmc.ncbi.nlm.nih.gov/articles/PMC5977479/
  226. https://www.uptodate.com/contents/use-of-methotrexate-in-the-treatment-of-rheumatoid-arthritis/print
  227. https://www.the-rheumatologist.org/article/remembering-etanercept-the-advent-of-the-biologic-era/
  228. https://pubmed.ncbi.nlm.nih.gov/20173395/
  229. https://www.pfizer.com/news/press-release/press-release-detail/multimedia_u_s_food_and_drug_administration_approves_pfizer_s_xeljanz_tofacitinib_citrate_for_adults_with_moderately_to_severely_active_rheumatoid_arthritis_ra_who_have_had_an_inadequate_response_or_intolerance_to
  230. https://www.the-rheumatologist.org/article/mesoblast-cell-treatment-shows-promise-rheumatoid-arthritis/
  231. https://news.weill.cornell.edu/news/2024/08/machine-learning-helps-identify-rheumatoid-arthritis-subtypes
  232. https://www.mayoclinic.org/medical-professionals/physical-medicine-rehabilitation/news/phase-1-clinical-trial-testing-gene-therapy-treatment-for-knee-osteoarthritis/mac-20590271
  233. https://www.cdc.gov/cdi/indicator-definitions/arthritis.html
  234. https://www.arthritis.org/partnership/atwork
  235. https://pmc.ncbi.nlm.nih.gov/articles/PMC8605034/
  236. https://www.valueinhealthjournal.com/article/S1098-3015(17)31255-X/fulltext
  237. https://www.healio.com/news/rheumatology/20211022/total-annual-cost-of-juvenile-idiopathic-arthritis-ranges-from-1100-to-44800
  238. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764813
  239. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1547763/full
  240. https://www.arthritis.org/about-arthritis/arthritis-awareness-month
  241. https://www.arthritis.org/about-us
  242. https://versusarthritis.org/about-arthritis/your-experiences/
  243. https://oaaction.unc.edu/2019/05/myths-about-osteoarthritis/
  244. https://www.nuffieldhealth.com/article/5-myths-about-osteoarthritis
  245. https://www.act4biosimilars.com/latest-insights/biosimilars-rheumatoid-arthritis-US-year-on/
  246. https://www.arthritis.org/advocate
  247. https://www.arthritis.org.au/how-we-can-help/download-clara/
  248. https://jointhealthinsight.jointhealth.org/2025/09/23/arthritis-consumer-experts-national-survey-on-artificial-intelligence-and-arthritis-care-report/
  249. https://www.etymonline.com/word/arthritis
  250. https://www.the-rheumatologist.org/article/how-rheumatism-got-its-name/
  251. https://my.clevelandclinic.org/health/diseases/12061-arthritis
  252. https://www.who.int/standards/classifications/international-classification-of-functioning-disability-and-health
  253. https://icd.who.int/browse11/l-m/en
  254. https://www.jrheum.org/content/31/2/390
  255. https://ard.bmj.com/content/69/9/1580
  256. https://www.sciencedirect.com/science/article/abs/pii/S1568997220301798
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