Having more than one risk factor greatly increases risk of septic arthritis.

Most cases of septic arthritis involve only one organism; however, polymicrobial infections can occur, especially after large open injuries to the joint.

- Staphyloccoci

- Staphylococcus aureus - the most common cause in most age groups. Can be caused by skin infection, previously damaged joint, prosthetic joint, or intravenous drug use.

- coagulase-negative staphylococci - usually due to prosthetic joint

- Streptococci - the second most common cause

- Streptococcus pyogenes - a common cause in children under 5

- Streptococcus pneumoniae

- Group B streptococci - a common cause in infants

- Haemophilus influenzae

- Neisseria gonorrhoeae - the most common cause of septic arthritis in young, sexually active adults. Multiple macules or vesicles seen over the trunk are a pathognomonic feature.

- Neisseria meningitidis

- Escherichia coli - in the elderly, IV drug users and the seriously ill

- Pseudomonas aeruginosa - IV drug users or penetrating trauma through the shoe

- M. tuberculosis, Salmonella spp. and Brucella spp. - cause septic spinal arthritis

- Eikenella corrodens - human bites

- Pasteurella multocida, bartonella henselae - animal bites or scratches

- Fungal species - immunocompromised state

- Borrelia burgodorferi - ticks, causes lyme disease

The disease is classified as either gonococcal urethritis, caused by "Neisseria gonorrhoeae", or non-gonococcal urethritis (NGU), most commonly caused by "Chlamydia trachomatis". NGU, sometimes called nonspecific urethritis (NSU), has both infectious and noninfectious causes.

Urethritis is part of triad of Reiter's Syndrome.

Other causes include:

- Adenoviridae

- Uropathogenic "Escherichia coli" (UPEC)

- Herpes simplex

- Cytomegalovirus

- "Mycoplasma genitalium"

- Reactive arthritis

- "Trichomonas vaginalis"

- "Ureaplasma urealyticum"

- "Methicillin-resistant Staphylococcus aureus"

- "Group B streptococcus"

The disease incidence varies widely depending on the geographical location. The most extensive epidemiological survey on this subject has been carried out by Dharmasena et al. who analysed the number of neonates who developed neonatal conjunctivitis in England from 2000 to 2011. In addition to the incidence of this sight threatening infection they also investigated the time trends of the disease. According to them the incidence of Neonatal conjunctivitis (Ophthalmia Neonatorum) in England was 257 (95% confidence interval: 245 to 269) per 100,000 in 2011.

There are many causes of NGU. This is in part due to the large variety of organisms living in the urinary tract. "Ureaplasma urealyticum" and "Mycoplasma genitalium" are some of the culprits.

NGU is also associated with Reiter's syndrome,in which triad of Arthritis,Conjunctivitis & Urethritis is there.

The most common bacterial cause of NGU is "Chlamydia trachomatis", but it can also be caused by "Ureaplasma urealyticum", "Haemophilus vaginalis", "Mycoplasma genitalium", Mycoplasma hominis, Gardnerella vaginalis, Acinetobacter lwoffi, Ac.calcoclaceticus and "E.coli".

Chemical irritants such as silver nitrate can cause chemical conjunctivitis, usually lasting 2–4 days. Thus, prophylaxis with a 1% silver nitrate solution is no longer in common use. In most countries neomycin and chloramphenicol eye drops are used instead. However, it is possible for newborns to suffer from neonatal conjunctivitis due to reactions with chemicals in these common eye drops. Additionally, a blocked tear duct may be another non-infectious cause of neonatal conjunctivitis.

Synovitis symptoms can be treated with anti-inflammatory drugs such as NSAIDs. An injection of steroids may be done, directly into the affected joint. Specific treatment depends on the underlying cause of the synovitis.

Urethritis is inflammation of the urethra. The most common symptom is painful or difficult urination. It is usually caused by infection with bacteria. The bacterial infection is often sexually transmitted, but not in every instance. Urethritis can be idiopathic.

Gonococcemia (also known as "Arthritis–dermatosis syndrome" and "Disseminated gonococcal infection") is a condition characterized by a hemorrhagic vesiculopustular eruption, bouts of fever, and arthralgia or actual arthritis of one or several joints.

It's characterized by a triad of symptoms: migratory polyarthritis, tenosynovitis, and dermatitis (pustular skin lesions).

Synovitis is the medical term for inflammation of the synovial membrane. This membrane lines joints that possess cavities, known as synovial joints. The condition is usually painful, particularly when the joint is moved. The joint usually swells due to synovial fluid collection.

Synovitis may occur in association with arthritis as well as lupus, gout, and other conditions. Synovitis is more commonly found in rheumatoid arthritis than in other forms of arthritis, and can thus serve as a distinguishing factor, although it is also present in many joints affected with osteoarthritis. Long term occurrence of synovitis can result in degeneration of the joint.

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.

RA reduces lifespan on average from three to twelve years. According to the UK's National Rheumatoid Arthritis Society, Young age at onset, long disease duration, the concurrent presence of other health problems (called co-morbidity), and characteristics of severe RA—such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints—have been shown to associate with higher mortality". Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease, independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor. It is possible that the use of new biologic drug therapies extend the lifespan of people with RA and reduce the risk and progression of atherosclerosis. This is based on cohort and registry studies, and still remains hypothetical. It is still uncertain whether biologics improve vascular function in RA or not. There was an increase in total cholesterol and HDLc levels and no improvement of the atherogenic index.

Intermittent hydrarthrosis is uncommon and its prevalence is not known. (In 1974 more than 200 cases were reported in published literature). It affects men and women equally although some publications suggest the condition is slightly more prevalent in females. Case reports indicate that only white people are affected. First onset of IH is most common between the ages of 20 and 50 years, and in females, onset can often coincide with puberty.

Usually the condition begins spontaneously or following trauma to the joint in otherwise healthy individuals.

PID can cause scarring inside the reproductive system, which can later cause serious complications, including chronic pelvic pain, infertility, ectopic pregnancy (the leading cause of pregnancy-related deaths in adult females), and other complications of pregnancy. Occasionally, the infection can spread to in the peritoneum causing inflammation and the formation of scar tissue on the external surface of the liver (Fitz-Hugh–Curtis syndrome).

Regular testing for sexually transmitted infections is encouraged for prevention. The risk of contracting pelvic inflammatory disease can be reduced by the following:

- Using barrier methods such as condoms; see human sexual behavior for other listings.

- Seeking medical attention if you are experiencing symptoms of PID.

- Using hormonal combined contraceptive pills also helps in reducing the chances of PID by thickening the cervical mucosal plug & hence preventing the ascent of causative organisms from the lower genital tract.

- Seeking medical attention after learning that a current or former sex partner has, or might have had a sexually transmitted infection.

- Getting a STI history from your current partner and strongly encouraging they be tested and treated before intercourse.

- Diligence in avoiding vaginal activity, particularly intercourse, after the end of a pregnancy (delivery, miscarriage, or abortion) or certain gynecological procedures, to ensure that the cervix closes.

- Reducing the number of sexual partners.

- Sexual monogamy.

- Abstinence

There are established epigenetic and environmental risk factors for RA. Smoking is an established risk factor for RA in Caucasian populations, increasing the risk three times compared to non-smokers, particularly in men, heavy smokers, and those who are rheumatoid factor positive. Modest alcohol consumption may be protective.

Silica exposure has been linked to RA.

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.

Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).

The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.

Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.

"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.

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.

PVNS is locally aggressive and can spread to surrounding tissues, causing bone erosion and tissue damage. If not treated early, it can spread to areas outside the joint, and potentially cause permanent loss of range as well as intense pain. The disorder also has, on average, a 45% rate of recurrence.

Dactylitis can occur in seronegative arthropathies, such as psoriatic arthritis and ankylosing spondylitis, and in sickle-cell disease as result of a vasoocclusive crisis with bone infarcts, and in infectious conditions including tuberculosis and leprosy. In reactive arthritis, sausage fingers occur due to synovitis.

In sickle-cell disease it is manifested for the first time between 6-9 month old infants (as their protective fetal hemoglobin, HbF, is replaced with adult hemoglobin and the disease manifests) and is very often the presenting sign of the disorder.

Peripheral arthritis has been reported in 92% of cases of SAPHO as well.

In children, the SAPHO syndrome is most likely to affect the metaphysis of long bones in the legs (tibia, femur, fibula), followed by clavicles and spine.

Villonodular synovitis is a type of synovial swelling.

Types include:

- Pigmented villonodular synovitis (PVNS)

- Giant cell tumor of the tendon sheath (GCTS)

Though they have very different names, they have the same histology, and stain positive for CD68, HAM56, and vimentin.

They are sometimes discussed together.

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.