It is not always certain why arthritis of the knee develops. Most physicians believe that it is a combination of factors that can include muscle weakness, obesity, heredity, joint injury or stress, constant exposure to the cold, and aging. Cartilage in the knee begins to break down and leaves the bones of the knee rubbing against each other as you walk. Persons who work in a place that applies repetitive stress on the knees are at a high risk of developing this condition. Bone deformities increase the risk for osteoarthritis of the knee since the joints are already malformed and may contain defective cartilage. Having gout, rheumatoid arthritis, Paget's disease of bone or septic arthritis can increase your risk of developing osteoarthritis.

Some physicians and most podiatrist believe that Pes Planus (flat feet) cause increased rates and earlier incidence of knee osteoarthritis. In a study of army recruits with moderate to severe flat feet, the results showed that they had almost double the rate of knee arthritis when compared to recruits with normal arches.

Increased risk of developing knee and hip osteoarthritis was found in those who:

- work with manual handling (e.g. lifting)

- have physically demanding work

- walk at work

- have climbing tasks at work (e.g. climb stairs or ladders)

Increased risk of developing hip osteoarthritis over time was found among those who work in bent or twisted positions.

Increased risk of knee osteoarthritis was found in those who:

- work in a kneeling or squatting position

- experience heavy lifting in combination with a kneeling or squatting posture

- work standing up

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of osteoarthritis is correlated with a history of previous joint injury and with obesity, especially with respect to knees. Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of osteoarthritis as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.

Arthritis mutilans' parent condition psoriatic arthritis leaves people with a mortality risk 60% higher than the general population, with premature death causes mirroring those of the general population, cardiovascular issues being most common. Life expectancy for people with psoriatic arthritis is estimated to be reduced by approximately 3 years.

The exact cause is unknown. Some doctors believe it is caused by abnormal metabolism of fat. Others think it may be caused by repetitive inflammation. Some feel that blood within the joint may cause the inflammatory change. Risk factors for PVNS developing are not yet understood. Very little research has been carried out. However, a common theme in patients is a trauma experienced to the joint prior to the onset of symptoms.

In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.

Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.

An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.

Osteoarthritis is a joint disease that causes the cushion layer between one's bones, or cartilage to wear away. It is also called degenerative joint disease. Symptoms are similar to RA and develop in the same slow manner. They include pain, tenderness in the knee, stiffness when standing or walking, loss of flexibility, and grating sensations that can be heard when the knee joint is used.

Osteoarthritis in the knee begins with the gradual deterioration of cartilage. Without the protective cartilage, the bones begin to rub together, causing pain, loss of mobility, and deformity. It affects approximately 16 million people. The majority of arthritis cases involving the knee are osteoarthritic cases.

In one study, those with stage 2 of the disease were found to have a slightly increased risk of mortality, especially from cancer.

Like many other joints throughout the human body, facets can experience natural degeneration from constant use. Over time, the cartilage within the joints can naturally begin to wear out, allowing it to become thin or disappear entirely which, in turn, allows the conjoining vertebrae to rub directly against one another with little or no lubricant or separation. A result of this rubbing is often swelling, inflammation or other painful symptoms.

Over time, the body will naturally respond to the instability within the spine by developing bone spurs, thickened ligaments or even cysts that can press up against or pinch the sensitive nerve roots exiting the spinal column.

While primarily caused through natural wear and tear, advanced facet syndrome can also occur as a result of injury to the spine, degenerative disease or lifestyle choices. These causes can include:

- An unexpected, traumatic event such as a car accident, significant fall or high impact sports injury.

- Osteoarthritis

- Spondylolisthesis

- Obesity

- Smoking

- Malnutrition

- Lack of physical exercise or daily activity

55% of facet syndrome cases occur in cervical vertebrae, and 31% in lumbar. Facet syndrome can progress to spinal osteoarthritis, which is known as spondylosis. Pathology of the C1-C2 (atlantoaxial) joint, the most mobile of all vertebral segments, accounts for 4% of all spondylosis.

Arthritis mutilans occurs mainly in people who have pre-existing psoriatic arthritis, but can occur, if less often, in advanced rheumatoid arthritis; it can also occur independently. Psoriasis and psoriatic arthritis are interrelated heritable diseases, occurring with greater heritable frequency than rheumatoid arthritis, primary Sjogren's syndrome and thyroid disease. Psoriasis affects 2–3% of the Caucasian population, and psoriatic arthritis affects up to 30% of those. Arthritis mutilans presents in about 5–16% of psoriatic arthritis cases, involves osteolysis of the DIP and PIP joints, and can include bone edema, bone erosions, and new bone growth. Most often psoratic arthitis is seronegative for rheumatoid factor (occurring in only about 13% of cases), and has genetic risk factor overlap with ankylosing spondylitis with HLA-B27, IL-23R77, and IL-1, however, as of 2016, immunopathogenesis is unclear.

Heberden's nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP) (the joints closest to the end of the fingers and toes). They are a sign of osteoarthritis and are caused by formation of osteophytes (calcific spurs) of the articular (joint) cartilage in response to repeated trauma at the joint.

Heberden's nodes typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways. Bouchard's nodes may also be present; these are similar bony growths in the proximal interphalangeal (PIP) joints (middle joints of the fingers), and are also associated with osteoarthritis.

Heberden's nodes are more common in women than in men, and there seems to be a genetic component involved in predisposition to the condition.

They are named after William Heberden (1710–1801).

Hypermobility syndrome is generally considered to comprise hypermobility together with other symptoms, such as myalgia and arthralgia. It is relatively common among children and affects more females than males.

Current thinking suggests four causative factors:

- The shape of the ends of the bones—Some joints normally have a large range of movement, such as the shoulder and hip. Both are ball and socket joints. If a shallow rather than a deep socket is inherited, a relatively large range of movement will be possible. If the socket is particularly shallow, then the joint may dislocate easily.

- Protein deficiency or hormone problems—Ligaments are made up of several types of protein fibre. These proteins include elastin, which gives elasticity and which may be altered in some people. Female sex hormones alter collagen proteins. Women are generally more supple just before a period and even more so in the latter stages of pregnancy, because of a hormone called relaxin that allows the pelvis to expand so the head of the baby can pass. Joint mobility differs by race, which may reflect differences in collagen protein structure. People from the Indian sub-continent, for example, often have more supple hands than Caucasians.

- Muscle tone—The tone of muscles is controlled by the nervous system, and influences range of movement. Special techniques can change muscle tone and increase flexibility. Yoga, for example, can help to relax muscles and make the joints more supple. Please note that Yoga is not recommended by most medical professionals for people with Joint Hypermobility Syndrome due to likelihood of damage to the joints. Gymnasts and athletes can sometimes acquire hypermobility in some joints through activity.

- Proprioception—Compromised ability to detect exact joint/body position with closed eyes, may lead to overstretching and hypermobile joints.

Hypermobility can also be caused by connective tissue disorders, such as Ehlers-Danlos Syndrome (EDS) and Marfan syndrome. Joint hypermobility is a common symptom for both. EDS has numerous sub-types; most include hypermobility in some degree. When hypermobility is the main symptom, then EDS/hypermobility type is likely. People with EDS-HT suffer frequent joint dislocations and subluxations (partial/incomplete dislocations), with or without trauma, sometimes spontaneously. Commonly, hypermobility is dismissed by medical professionals as nonsignificant.

The cause is unknown but allergic and auto-inflammatory mechanisms have been proposed.

In a 1957 review of IH, Mattingly did not find evidence that the condition is inherited unlike Reimann who, in 1974, describes the condition as “heritable, non-inflammatory, and afebrile”.

More recently, specific association with the Mediterranean fever gene, MEFV, has been proposed. So, with some individuals carrying gene mutations (MEFV and also TRAPS-related genes), the native immune system seems to plays a role in the development of IH, i.e. there is an auto-immune component to the condition.

Once established, periods of remissions and relapse can persist indefinitely.

While IH may remit spontaneously for most people the condition is long-lasting. Treatments as described above can be effective in reducing the frequency and degree of effusions. Deformative changes to joints are not a common feature of this mostly non-inflammatory condition.

Swan neck deformity has many possible causes arising from the DIP, PIP, or even the MCP joints. In all cases, there is a stretching of the volar plate at the PIP joint to allow hyperextension, plus some damage to the attachment of the extensor tendon to the base of the distal phalanx that produces a hyperflexed mallet finger. Duck bill deformity is a similar condition affecting the thumb (which cannot have true swan neck deformity because it does not have enough joints).

Pigmented villonodular synovitis, described distinctly in 1941 by Charles J. Sutro, L. Lichtenstein, and H.L. Jafe, comes in two forms: localized and diffuse. Diffuse PVNS affects the entire synovium and typically occurs in large joints such as the knee or hip. Localized, or nodular, PVNS is less common than the diffuse form and typically occurs in smaller joints such as the hands and feet. Localized PVNS often arises in the form of a large benign tumour on the tendon sheaths of the joint. As the tumor grows in the joint, it damages the surrounding bone and tissues. Localized PVNS is predominantly found in females and is frequently found in the fingers. Although rare, localized PVNS may develop in large joints. In either case, the knee is the most commonly affected joint (80% of cases), followed by the hip, and less commonly the ankles and shoulders. PVNS is generally found more in men than women. 2 cases per million population; incidence of the localized form is 9 cases per million.

Dupuytren’s disease has a high recurrence rate, especially when a person has so called Dupuytren’s diathesis. The term diathesis relates to certain features of Dupuytren's disease and indicates an aggressive course of disease.

The presence of all new Dupuytren’s diathesis factors increases the risk of recurrent Dupuytren’s disease by 71% compared with a baseline risk of 23% in people lacking the factors. In another study the prognostic value of diathesis was evaluated. They concluded that presence of diathesis can predict recurrence and extension. A scoring system was made to evaluate the risk of recurrence and extension evaluating the following values: bilateral hand involvement, little finger surgery, early onset of disease, plantar fibrosis, knuckle pads and radial side involvement.

Minimally invasive therapies may precede higher recurrence rates. Recurrence lacks a consensus definition. Furthermore, different standards and measurements follow from the various definitions.

In reality, both of these mechanisms probably play a role in the development of a Charcot joint.

Sacroiliitis (say-kroe-il-e-I-tus) is a medical condition caused by any inflammation within one, or both, of the sacroiliac joints. Sacroiliitis is a feature of spondyloarthropathies, such as axial spondyloarthritis (including ankylosing spondylitis), psoriatic arthritis, reactive arthritis or arthritis related to inflammatory bowel diseases, including ulcerative colitis or Crohn's disease. It is also the most common presentation of arthritis from brucellosis.

Any condition resulting in decreased peripheral sensation, proprioception, and fine motor control:

- Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics. Related to long-term poor glucose control.

- Alcoholic neuropathy

- Cerebral palsy

- Leprosy

- Syphilis ("tabes dorsalis"), caused by the organism "Treponema pallidum"

- Spinal cord injury

- Myelomeningocele

- Syringomyelia

- Intra-articular steroid injections

- Congenital insensitivity to pain

- Peroneal muscular atrophy

Joint hypermobility syndrome shares symptoms with other conditions such as Marfan syndrome, Ehlers-Danlos Syndrome, and osteogenesis imperfecta. Experts in connective tissue disorders formally agreed that severe forms of Hypermobility Syndrome and mild forms of Ehlers-Danlos Syndrome Hypermobility Type are the same disorder.[""]

Generalized hypermobility is a common feature in all these hereditary connective tissue disorders and many features overlap, but often features are present that enable differentiating these disorders.

The inheritance pattern of Ehlers-Danlos syndrome varies by type. The arthrochalasia, classic, hypermobility and vascular forms usually have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance occurs when one copy of a gene in each cell is sufficient to cause a disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases result from new (sporadic) gene mutations. Such cases can occur in people with no history of the disorder in their family.

The dermatosparaxis and kyphoscoliosis types of EDS and some cases of the classic and hypermobility forms, are inherited in an autosomal recessive pattern. In autosomal recessive inheritance, two copies of the gene in each cell are altered. Most often, both parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.

Clutton's joints is a term describing the finding of symmetrical joint swelling seen in patients with congenital syphilis. It most commonly affects the knees, presenting with synovitis and joint effusions (collections of fluid within the joint capsules) lasting up to a year. It has also been reported affecting the ankles, elbows, wrists and fingers. It is usually painless, although pain in the absence of trauma can occur in a few cases. There is usually no disability associated with the joint swelling, and recovery is usually complete. It occurs between 5 and 20 years of age in both sexes.

The condition was described in 1886 by Henry Hugh Clutton in "The Lancet".

Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.

Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.

In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.

Those who have this disease may experience sprained ankles more frequently than other people.

Jaccoud arthropathy (JA), Jaccoud deformity or Jaccoud's arthopathy is a chronic non-erosive reversible joint disorder that may occur after repeated bouts of arthritis. It is caused by inflammation of the joint capsule and subsequent fibrotic retraction, causing ulnar deviation of the fingers, through metacarpophalangeal joint (MCP) subluxation, primarily of the ring and little-finger. Joints in the feet, knees and shoulders may also get affected. It is commonly associated with systemic lupus erythematosus (SLE), and occurs in roughly 5% of all cases.

When associated with rheumatic fever it is also called chronic post–RF arthropathy.

Originally thought to be associated only with rheumatic fever, it has since been shown to occur also in SLE, Sjögren syndrome, scleroderma, dermatomyositis, psoriatic arthritis, vasculitis, ankylosing spondylitis, mixed connective tissue disease, and pyrophosphate deposition disease. It is distinct from bone erosion which is commonly associated with rheumatic arthritis, and also distinct from mild deforming arthropathy which is associated with SLE. There have also been cases of non-rheumatic JA associated with Lyme disease, HIV-infection and a number of other conditions.

Treatment focuses toward alleviating pain and in maintaining functionality of the affected joints through use of nonsteroidal anti-inflammatory drugs, corticosteroids, antimalarial drugs and physiotherapy. Surgery is also a possibility, with osteotomy or stabilization with Kirschner intramedullary wire. Tendon relocation, however, has been shown to only work in 30% of cases. The condition is named after the French 19th century physician Sigismond Jaccoud.