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.

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.

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.

The worldwide prevalence of inflammatory arthritis is approximately 3%. Rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and undifferentiated spondyloarthritis are the most common subtypes of inflammatory arthritis. The diseases occur most commonly in the 30-40 age group.

Inflammatory arthritis can be disabling to the point where people with the diseases can lose their jobs, which can cause psychological distress. Because it is typically progressive, those who lose their jobs are unlikely to re-enter the workforce after leaving due to their diagnosis. Programs now aim to retain those with inflammatory arthritis by preventing work-related injuries and by making necessary accommodations in the workplace. A 2014 Cochrane review found low-quality evidence that work focused interventions, including counseling, education, advocacy, and occupational medicine consultations, were effective in retaining workers with inflammatory arthritis.

The exact cause of CPPD is unknown, although increased breakdown of adenosine triphosphate (ATP; the molecule used as energy currency in all living things), which results in increased pyrophosphate levels in joints, is thought to be one reason why crystals may develop.

Familial forms are rare. One genetic study found an association between CPPD and a region of chromosome 8q.

The gene ANKH is involved in crystal-related inflammatory reactions and inorganic phosphate transport.

An arthropathy is a disease of a joint. Arthritis is a form of arthropathy that involves inflammation of one or more joints, while the term arthropathy may be used regardless of whether there is inflammation or not.

Spondylarthropathy is any form of arthropathy of the vertebral column.

Arthropathy may also include joint conditions caused by physical trauma to joints, but is traditionally used to describe the following conditions:

- "Reactive arthropathy" (M02-M03) is caused by an infection, but not a direct infection of the synovial space. (See also Reactive arthritis)

- "Enteropathic arthropathy" (M07) is caused by colitis and related conditions.

- "Crystal arthropathy" (also known as "crystal arthritis") (M10-M11) involves the deposition of crystals in the joint.

- In gout, the crystal is uric acid.

- In pseudogout/chondrocalcinosis/calcium pyrophosphate deposition disease, the crystal is calcium pyrophosphate.

- "Diabetic arthropathy" (M14.2, E10-E14) is caused by diabetes.

- "Neuropathic arthropathy" (M14.6) is associated with a loss of .

CPPD affects people of all cultures and ethnic origins, and, in the United States, around 50% of the population over 85 years of age are affected. It may cause considerable pain, but it is never fatal. Women are at a slightly higher risk than men, with an estimated ratio of occurrence of 1.4:1.

The disease mechanism (pathophysiology) of RS3PE remains unknown. One study suggested a possible role for vascular endothelial growth factor. A study using magnetic resonance imaging found that tenosynovitis of the extensors of the hands and feet is the major contributor to edema.

Remitting seronegative symmetrical synovitis with pitting edema (abbreviated RS3PE or sometimes RSPE) is a rare syndrome identified by symmetric polyarthritis, synovitis, acute pitting edema (swelling) of the back of the hands and/or feet, and a negative serum rheumatoid factor. If no underlying disorder can be identified (idiopathic RS3PE), this entity has an excellent prognosis and responds well to treatment.

RS3PE typically involves the joints of the extremities, specifically the metacarpophalangeal and proximal interphalangeal joints, wrists, shoulders, elbows, knees and ankles.

It is more common in older adults, with the mean age between 70 and 80 years in most studies.

It occurs more often in men than in women with a 2:1 ratio.

It is unknown how common this condition is.

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

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

Trochleitis is diagnosed based on three criteria: 1) demonstration of inflammation of superior oblique tendon/ trochlea region, 2) periorbital pain and tenderness to palpation in the area of the sore trochlea, and 3) worsening of pain on attempted vertical eye movement, particularly with adduction of the eye. It is important to identify trochleitis because it is a treatable condition and the patient can benefit much from pain relief. Treatment consists of a single injection of corticosteroids to the affected peritrochlear region. A specific "cocktail" consisting of 0.5 ml of depomedrol (80 mg/ml) and 0.5 ml of 2% lidocaine can be injected into the trochlea; immediate relief due to the effects of the local anesthetic indicates successful placement. However, great care must be taken as the injection is in the region of several arteries, veins and nerves. The needle should not be too small (so as not to penetrate tiny structures), the surgeon should draw back on the syringe (to ensure not have pierced a vessel), the lidocaine should not contain epinephrine (which could cause vasospasm), and the pressure of the injection must always be controlled. Only a limited number of injections can be made as they would otherwise lead to muscle atrophy. Diagnosis can be confirmed by response to this treatment; pain and swelling are expected to disappear in 48–72 hours. Some patients experience recurrence of trochleitis.

The cause of trochleitis is often unknown (idiopathic trochleitis), but it has been known to occur in patients with rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, enteropathic arthropathy, and psoriasis. In his study, Tychsen and his group evaluated trochleitis patients with echography and CT scan to demonstrate swelling and inflammation. Imaging studies showed inflammation of superior oblique tendon/ trochlear pulley. It was unclear whether the inflammation involved the trochlea itself, or the tissues surrounding the trochlea.

A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear. According to a study in the Journal of Orthopaedic Surgery and Traumatology the frequency of rotator cuff tears can increase with age. The study shows the participants that were the ages of 70–90 years old had a rate of rotator cuff tears that were 1 to 5. The participants who were 90+ years old the frequency of a rotator cuff tear jumped to 1 to 3. This study shows that with an increase in age there is also an increase in the probability of a rotator cuff tear.

Enteropathic arthropathy or enteropathic arthritis refers to acute or subacute arthritis in association with, or as a reaction to, an enteric (usually colonic) inflammatory condition.

Note that reactive arthritis can also occur secondary to urethral infection. In that case, the term enteropathic arthropathy would not be used.

While people with rotator cuff tears may not have any noticeable symptoms, studies have shown that over time 40% will have enlargement of the tear over a five-year period. Of those whose tears enlarge, 20% have no symptoms while 80% eventually develop symptoms.

There is no irrefutable evidence that rotator cuff surgery benefits patients more than non-surgical management and a percentage of patients never regain full range of motion after surgery.

Epidemiological studies strongly support a relationship between age and cuff tear prevalence. In a recent study the frequency of such tears increased from 13% in the youngest group (aged 50–59 y) to 20% (aged 60–69 y), 31% (aged 70–79 y), and 51% in the oldest group (aged 80–89 y). This high rate of tear prevalence in asymptomatic individuals suggests that rotator cuff tears could be considered a "normal" process of aging rather than a result of an apparent pathological process.

Up to a quarter of all severe ligament or capsular knee injuries leading to a haemarthrosis are associated with cartilage damage that can lead to progressive degenerative arthritis.

Hemarthrosis (or haemarthrosis) is a bleeding into joint spaces.

It is a common feature of Hemophilia.

The exact cause of sarcoidosis is not known. The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is caused through alteration to the immune response after exposure to an environmental, occupational, or infectious agent. Some cases may be caused by treatment with TNF inhibitors like etanercept.

The heritability of sarcoidosis varies according to ethnicity. About 20% of African Americans with sarcoidosis have a family member with the condition, whereas the same figure for European Americans is about 5%. Additionally, in African Americans, who seem to experience more severe and chronic disease, siblings and parents of sarcoidosis cases have about a 2.5-fold increased risk for developing the disease. Investigations of genetic susceptibility yielded many candidate genes, but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is "BTNL2"; several "HLA-DR" risk alleles are also being investigated. In persistent sarcoidosis, the HLA haplotype "HLA-B7-DR15" are either cooperating in disease or another gene between these two loci is associated. In nonpersistent disease, there is a strong genetic association with HLA DR3-DQ2. Cardiac sarcoid has been connected to TNFA variants.

Winchester syndrome is a rare congenital connective tissue disease described in 1969, of which the main characteristics are short stature, marked contractures of joints, opacities in the cornea, coarse facial features, dissolution of the carpal and tarsal bones (in the hands and feet, respectively), and osteoporosis. Winchester syndrome was once considered to be related to a similar condition, multicentric osteolysis, nodulosis, and arthropathy (MONA). However, it was discovered that the two are caused by mutations found in different genes; they are now thought of as two separate disorders. Appearances resemble rheumatoid arthritis. Increased uronic acid is demonstrated in cultured fibroblasts from the skin and to a lesser degree in both parents. Despite initial tests not showing increased mucopolysaccharide excretion, the disease was regarded as a mucopolysaccharidosis. Winchester syndrome is thought to be inherited as an autosomal recessive trait.

The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries the rate of women receiving a diagnosis of Whipple's disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population.

"T. whipplei" appears to be an environmental organism that is commonly present in the gasterointestinal tract but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for "T. whipplei", since the disease is not associated with a substantially increased risk of other infections.

The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s.