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.

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.

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.

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.

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 .

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.

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.

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.

Individuals affected by RS3PE typically have repeated episodes of inflammation of the lining of their synovial joints and swelling of the end portion of the limbs. The arms and hands are more commonly affected than the legs and feet. Both sides are usually involved though RS3PE can affect only one side in certain cases.

Several gene mutations have been identified in patients with camptocormia. These include the RYR1 gene in axial myopathy, the DMPK gene in myotonic dystrophy, and genes related to dysferlinopathy and Parkinson’s disease. These genes could serve as targets for gene therapy to treat the condition in the years to come.

A multitude of neurological disorders cause BSS, including motor neuron disease, CNS disorders, and early amyotrophic lateral sclerosis. Usually, the bent spine is caused by dysfunctioning extensor spinal muscles with a neurological cause.

Neurological origin BSS may also result from damage to the basal ganglia nuclei that are a part of the cerebral cortex, which play a major role in bodily positioning. Damage to this part of the brain can inhibit proper flexion and extension in the muscles necessary for maintaining an upright position. Additionally, the neurotransmitter dopamine plays a key role in the operation of basal ganglia. An abnormally low dopamine concentration, such as that associated with Parkinson’s disease, causes dysfunction in the basal ganglia and the associated muscle groups, leading to BSS. Studies have estimated the prevalence of BSS in people affected by Parkinson's to be between 3% and 18%.

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.

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

It is a common feature of Hemophilia.

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.

The Roussy–Lévy syndrome is not a fatal disease and life expectancy is normal. However, due to progressive muscle wasting patients may need supportive orthopaedic equipment or wheelchair assistance.

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 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.

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 name is derived from the ancient Greek words "kamptos" ("bent") and "daktylos" ("finger").

Camptodactyly is a medical condition that causes one or more fingers to be permanently bent. It involves fixed flexion deformity of the proximal interphalangeal joints. The fifth finger is always affected.

Camptodactyly can be caused by a genetic disorder. In that case, it is an autosomal dominant trait that is known for its incomplete genetic expressivity. This means that when a person has the genes for it, the condition may appear in both hands, one, or neither. A linkage scan proposed that the chromosomal locus of camptodactyly was 3q11.2-q13.12.

Roussy–Lévy syndrome, also known as Roussy–Lévy hereditary areflexic dystasia, is a rare genetic disorder of humans that results in progressive muscle wasting. It is caused by mutations in the genes that code for proteins necessary for the functioning of the myelin sheath of the neurons, affecting the conductance of nerve signals and resulting in loss of muscles' ability to move.

The condition affects people from infants through adults and is inherited in an autosomal dominant manner. Currently, no cure is known for the disorder.

Winchester syndrome is believed to be inherited through autosomal recessive inheritance. For recessive genetic disorders, individuals inherit the mutated gene for the same trait from both parents. It believed that this disease is caused by a nonlysosomal connective-tissue disturbance. The protein inactivation mutation is found on the matrix metalloproteinase 2 gene (MMP2). MM2 is responsible for bone remodeling. Bone remodeling is the process in which old bone is destroyed so that new bone can be created to replace it. This mutation causes a multicentric osteolysis and arthritis syndrome. It is hypothesized that the loss of an upstream MMP-2 protein activator MT1-MMP, results in decreased MMP-2 activity without affecting "MMP2". The inactivating homoallelic mutation of "MT1-MMP" can be seen at the surface of fibroblasts. It was determined that fibroblasts lacking MT1-MMP lack the ability to degrade type I collagen which leads to anomalous function.