Polymyositis, like dermatomyositis, strikes females with greater frequency than males.

Polymyositis is an inflammatory myopathy mediated by cytotoxic T cells with an as yet unknown autoantigen, while dermatomyositis is a humorally mediated angiopathy resulting in myositis and a typical dermatitis.

The cause of polymyositis is unknown and may involve viruses and autoimmune factors. Cancer may trigger polymyositis and dermatomyositis, possibly through an immune reaction against cancer that also attacks a component of muscles.

Every year between 2.18 and 7.7 people per million receive a diagnosis of PM or DM. Around 3.2 children per million per year are diagnosed with DM (termed juvenile dermatomyositis), with an average age of onset of seven years. Diagnosis of adult DM commonly occurs between 30 and 50 years of age. PM is an adult disease, usually emerging after the age of twenty. PM and DM are more common in females, more common in Caucasians, and least common in Asians. At any given time, about 35.5 people per million have IBM; it emerges after the age of 30 (usually after 50), and may be more common in males.

Of the children diagnosed with and treated for JDM, about half will recover completely. Close to 30 percent will have weakness after the disease resolves. Most children will go into remission and have their medications eliminated within two years, while others may take longer to respond or have more severe symptoms that take longer to clear up.

A common lasting effect of JDM is childhood arthritis.

The underlying cause of JDM is unknown. It most likely has a genetic component, as other autoimmune disease tend to run in the families of patients. The disease is usually triggered by a condition that causes immune system activity that does not stop as it should, but the trigger is almost certainly not the cause in most cases. Common triggers include immunizations, infections, injuries, and sunburn.

The cause is unknown, but it may result from an initial viral infection or cancer, either of which could raise an autoimmune response.

Between 7 and 30% of dermatomyositis arise from cancer, probably as an autoimmune response. The most common associated cancers are ovarian cancer, breast cancer, and lung cancer. 18 to 25% of people with amyopathic DM also have cancer.

Some cases are inherited, and HLA subtypes HLA-DR3, HLA-DR52, and HLA-DR6 seem to create a disposition to dermatomyositis.

The cause of IBM is unknown. IBM likely results from the interaction of a number of genetic and environmental factors.

There are two major theories about how sIBM is caused. One hypothesis suggests that the inflammation-immune reaction, caused by an unknown trigger – likely an undiscovered virus or an autoimmune disorder– is the primary cause of sIBM and that the degeneration of muscle fibers and protein abnormalities are secondary features. Despite the arguments "in favor of an adaptive immune response in sIBM, a purely autoimmune hypothesis for sIBM is untenable because of the disease's resistance to most immunotherapy."

The second school of thought advocates the theory that sIBM is a degenerative disorder related to aging of the muscle fibers and that abnormal, potentially pathogenic protein accumulations in myofibrils play a key causative role in sIBM (apparently before the immune system comes into play). This hypothesis emphasizes the abnormal intracellular accumulation of many proteins, protein aggregation and misfolding, proteosome inhibition, and endoplasmic reticulum (ER) stress.

One review discusses the "limitations in the beta-amyloid-mediated theory of IBM myofiber injury."

Dalakas (2006) suggested that a chain of events causes IBM—some sort of virus, likely a retrovirus, triggers the cloning of T cells. These T cells appear to be driven by specific antigens to invade muscle fibers. In people with sIBM, the muscle cells display “flags” telling the immune system that they are infected or damaged (the muscles ubiquitously express MHC class I antigens) and this immune process leads to the death of muscle cells. The chronic stimulation of these antigens also causes stress inside the muscle cell in the endoplasmic reticulum (ER) and this ER stress may be enough to cause a self-sustaining T cell response (even after a virus has dissipated). In addition, this ER stress may cause the misfolding of protein. The ER is in charge of processing and folding molecules carrying antigens. In IBM, muscle fibers are overloaded with these major histocompatibility complex (MHC) molecules that carry the antigen protein pieces, leading to more ER stress and more protein misfolding.

A self-sustaining T cell response would make sIBM a type of autoimmune disorder. When studied carefully, it has not been impossible to detect an ongoing viral infection in the muscles. One theory is that a chronic viral infection might be the initial triggering factor setting IBM in motion. There have been a handful of IBM cases—approximately 15—that have shown clear evidence of a virus called HTLV-1. The HTLV-1 virus can cause leukemia, but in most cases lies dormant and most people end up being lifelong carriers of the virus. One review says that the best evidence points towards a connection with some type of retrovirus and that a retroviral infection combined with immune recognition of the retrovirus is enough to trigger the inflammation process.

- amyloid protein

- The hypothesis that beta amyloid protein is key to IBM has been supported in a mouse model using an Aβ vaccine that was found to be effective against inclusion body myositis in mouse models. Although this vaccine is likely not safe for human use, it still shows that attacking Aβ has efficacy in mice against IBM.

- Following up on earlier leads, the Greenberg group report finding that the protein TDP-43 is a very prominent and highly sensitive and specific feature of IBM. This protein is normally found within the nucleus but in IBM is found in the cytoplasm of the cell. This important advance should help develop a new screening technique for IBM and may provide clues in terms of a therapeutic approach

sIBM is not inherited and is not passed on to the children of IBM patients. There are genetic features that do not directly cause IBM but that appear to predispose a person to getting IBM — having this particular combination of genes increases one's susceptibility to getting IBM. Some 67% of IBM patients have a particular combination of human leukocyte antigen genes in a section of the 8.1 ancestral haplotype in the center of the MHC class II region. sIBM is not passed on from generation to generation, although the susceptibility region of genes may be.

There are also several rare forms of hereditary inclusion body myopathy that are linked to specific genetic defects and that are passed on from generation to generation. Since these forms do not show features of muscle inflammation, they are classified as myopathies rather than forms of myositis. Because they do not display inflammation as a primary symptom, they may in fact be similar, but different diseases to sporadic inclusion body myositis. There are several different types, each inherited in different ways. See hereditary inclusion body myopathy.

A 2007 review concluded there is no indication that the genes responsible for the familial or hereditary conditions are involved in sIBM.

Dermatomyositis (DM) is a long term inflammatory disorder which affects muscles. Symptoms generally a skin rash and worsening muscle weakness over time. Symptoms may occur suddenly or develop over months. Other symptoms may include weight loss, fever, lung inflammation, or light sensitivity. Complications may include calcium deposits in muscles or skin.

The cause is unknown. Theories include that it is an autoimmune disease or a result of a viral infection. It is a type of inflammatory myopathy. Diagnosis is typically based on some combination of symptoms, blood tests, electromyography, and muscle biopsies.

While there is no cure for the condition, treatments generally improve symptoms. Treatments may include medication, physical therapy, exercise, heat therapy, orthotics, and assistive devices, and rest. Medications in the corticosteroids family are typically used with other agents like methotrexate or azathioprine recommended if steroids are not working well. Intravenous immunoglobulin may also improve outcomes. Most people improve with treatment and in some the condition resolves completely.

About 1 per 100,000 people per year are newly affected. The condition usually occurs in those in their 40s and 50s with women being affected more often than men. People of any age, however, may be affected. The condition was first described in the 1800s.

Despite its very similar clinical presentation to PM, IBM does not respond to the drugs that effectively treat PM, and there is no proven effective therapy for IBM. Alemtuzumab is being studied but as of May 2013 it had not demonstrated clinical effectiveness in IBM. Dysphagia (difficulty swallowing) may be improved by intravenous immunoglobulin, though more trials are needed. Non-fatiguing, systematic strength-building exercise has demonstrated benefit. Occupational and rehabilitation therapists can offer good advice on walking without falling and performing fine motor tasks, and can provide appropriate canes, braces and wheelchairs. Speech pathologists can provide advice on preventing choking episodes and reducing the anxiety of an immanent aspiration for both patients and carers.

There are several diseases where joint pain is primary, and is considered the main feature. Generally when a person has "arthritis" it means that they have one of these diseases, which include:

- Osteoarthritis

- Rheumatoid arthritis

- Gout and pseudo-gout

- Septic arthritis

- Ankylosing spondylitis

- Juvenile idiopathic arthritis

- Still's disease

Joint pain can also be a symptom of other diseases. In this case, the arthritis is considered to be secondary to the main disease; these include:

- Psoriasis (Psoriatic arthritis)

- Reactive arthritis

- Ehlers-Danlos Syndrome

- Haemochromatosis

- Hepatitis

- Lyme disease

- Sjogren's disease

- Hashimoto's thyroiditis

- Celiac disease

- Non-celiac gluten sensitivity

- Inflammatory bowel disease (including Crohn's disease and ulcerative colitis)

- Henoch–Schönlein purpura

- Hyperimmunoglobulinemia D with recurrent fever

- Sarcoidosis

- Whipple's disease

- TNF receptor associated periodic syndrome

- Granulomatosis with polyangiitis (and many other vasculitis syndromes)

- Familial Mediterranean fever

- Systemic lupus erythematosus

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.

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.

Arthritis is the most common cause of disability in the USA. More than 20 million individuals with arthritis have severe limitations in function on a daily basis. Absenteeism and frequent visits to the physician are common in individuals who have arthritis. Arthritis can make it very difficult for individuals to be physically active and some become home bound.

It is estimated that the total cost of arthritis cases is close to $100 billion of which almost 50% is from lost earnings. Each year, arthritis results in nearly 1 million hospitalizations and close to 45 million outpatient visits to health care centers.

Decreased mobility, in combination with the above symptoms, can make it difficult for an individual to remain physically active, contributing to an increased risk of obesity, high cholesterol or vulnerability to heart disease. People with arthritis are also at increased risk of depression, which may be a response to numerous factors, including fear of worsening symptoms.

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

It is not uncommon for drugs to damage muscle fibers. Particular families of drugs are known to induce myopathies on the molecular level, thus altering organelle function such as the mitochondria. Use of multiple drugs from these families in conjunction with one another can increase the risk of developing a myopathy. Many of the drugs associated with inducing myopathies in patients are found in rheumatology practice.

The processes that lead to drug-induced lupus erythematosus are not entirely understood. The exact processes that occur are not known even after 50 years since its discovery, but many studies present theories on the mechanisms of DIL.

A predisposing factor to developing DIL is N-acetylation speed, or the rate at which the body can metabolize the drug. This is greatly decreased in patients with a genetic deficiency of the enzyme N-acetyltransferase. A study showed that 29 of 30 patients with DIL were slow acetylators. In addition, these patients had more hydralazine metabolites in their urine than fast acetylators. These metabolites (byproducts of the interactions between the drug and constituents in the body) of hydralazine are said to have been created when white blood cells have been activated, meaning they are stimulated to produce a respiratory burst. Respiratory burst in white blood cells induces an increased production of free radicals and oxidants such as hydrogen peroxide. These oxidants have been found to react with hydralazine to produce a reactive species that is able to bond to protein. Monocytes, one type of white blood cell, detect the antigen and relay the recognition to T helper cells, creating antinuclear antibodies leading to an immune response. Further studies on the interactions between oxidants and hydralazine are necessary to understand the processes involved in DIL.

Of the drugs that cause DIL, hydralazine has been found to cause a higher incidence. Hydralazine is a medication used to treat high blood pressure. Approximately 5% of the patients who have taken hydralazine over long periods of time and in high doses have shown DIL-like symptoms. Many of the other drugs have a low to very low risk to develop DIL. The following table shows the risk of development of DIL of some of these drugs on a very to high scale.

- High risk:

- Procainamide (antiarrhythmic)

- Hydralazine (antihypertensive)

Scleromyositis or the PM/Scl overlap syndrome is a complex autoimmune disease (a disease in which the immune system attacks the body). Patients with scleromyositis have symptoms of both systemic scleroderma and either polymyositis or dermatomyositis, and is therefore considered an overlap syndrome. Although it is a rare disease, it is one of the more common overlap syndromes seen in scleroderma patients, together with MCTD and Antisynthetase syndrome. Autoantibodies often found in these patients are the anti-PM/Scl (anti-exosome) antibodies.

The symptoms that are seen most often are typical symptoms of the individual autoimmune diseases and include Raynaud's phenomenon, arthritis, myositis and scleroderma. Treatment of these patients is therefore strongly dependent on the exact symptoms with which a patient reports to a physician and is similar to treatment for the individual autoimmune disease, often involving either immunosuppressive or immunomodulating drugs.

- Clinical characteristics:

- Overlap Syndrome: scleroderma overlap syndrome

- Autoimmune disease

- Scleroderma myositis overlap syndrome

Many dietary factors and aberrations can induce ANIM. Chemical imbalances brought on by abnormal diets may either affect the muscle directly or induce abnormal functionality in upstream pathways.

- Excess Iodine consumption, especially in the form of kelp, can induce Hyperthyroidism. Hyperthyroidism is one of the most common ways to acquire ANIM. A hyperactive thyroid gland produces excessive amounts of hormones T3 and T4 leading to increased metabolism and increased sympathetic nervous system effects. The muscles exhibit a pathology similar to an overdose of epinephrine (commonly known as adrenaline). Patients with hyperthyroidism show weakness of shoulder girdle muscles in particular with this condition often being asymptomatic. More serious weakness of core and limb muscles may present.

- A dietary deficiency of vitamin D is most commonly associated with osteoporosis, but can cause ANIM as well. Vitamin D induced ANIM is most commonly associated with sleep deprivation as it induces tonsillar and adenotonsillar hypertrophy, as well as weakens the airway muscles. These changes induce sleep apnea and sleep disruption. Vitamin D induced ANM can also be associated with daytime impairment through this pathway.

Trauma to any muscle is also a common cause for acute ANIM. This is due to muscular contusions and partial or complete loss of function for affected muscle groups.

In the past, there have been speculations about possible complications after transient synovitis. The current consensus however is that there is no proof of an increased risk of complications after transient synovitis.

One such previously suspected complication was coxa magna, which is an overgrowth of the femoral head and broadening of the femoral neck, accompanied by changes in the acetabulum, which may lead to subluxation of the femur. There was also some controversy about whether continuous high intra-articular pressure in transient synovitis could cause avascular necrosis of the femoral head (Legg-Calvé-Perthes disease), but further studies did not confirm any link between the two conditions.

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.

Treatment consists of rest, non-weightbearing and painkillers when needed. A small study showed that the nonsteroidal anti-inflammatory drug ibuprofen could shorten the disease course (from 4.5 to 2 days) and provide pain control with minimal side effects (mainly gastrointestinal disturbances). If fever occurs or the symptoms persist, other diagnoses need to be considered.

Anti-synthetase syndrome is a autoimmune disease associated with interstitial lung disease, dermatomyositis, and polymyositis.

Antinuclear antibodies are usually positive in drug induced Lupus. Anti-Neutrophil Cytoplasmic antibodies (ANCA) can also be positive in association with certain drugs. Furthermore, Anti-Histone antibodies can also be positive in drug induced lupus.

Anti-Histone antibodies are positive in up to 95% of patients with drug induced lupus. DIThe most common medications associated with drug induced lupus are hydralazine, procainamide, isoniazid, methyldopa, chlorpromazine, quinidine, and minocycline.

While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition.

The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, renal failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, low albumin, and central neurologic failure.

Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is "not" an independent risk for the development of CIP/CIM.