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

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.

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.

Because women may be underdiagnosed, the exact incidence of reactive arthritis is difficult to estimate. A few studies have been completed, though. In Norway between 1988 and 1990, the incidence was 563.3 cases per 100,000 for chlamydia-induced reactive arthritis and 5 cases per 100,000 for that induced by enteric bacteria. In 1978 in Finland, the annual incidence was found to be 5835.7 per 100,000.

Reactive arthritis may be self-limiting, frequently recurring, chronic or progressive. Most patients have severe symptoms lasting a few weeks to six months. 15 to 50 percent of cases involve recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15–30 percent of cases. Repeated attacks over many years are common, and patients sometimes end up with chronic and disabling arthritis, heart disease, amyloid deposits, ankylosing spondylitis, immunoglobulin A nephropathy, cardiac conduction abnormalities, or aortitis with aortic regurgitation. However, most people with reactive arthritis can expect to live normal life spans and maintain a near-normal lifestyle with modest adaptations to protect the involved organs.

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

Treatment for infectious tenosynovitis is more effective the earlier the condition is identified and treated. Factors that worsen patient outcomes include being older than 43, having diabetes mellitus, and a polymicrobial infection.

Tenosynovitis most commonly results from the introduction of bacteria into a sheath through a puncture or laceration wound, though bacteria can also be spread from adjacent tissue or via hematogenous spread. The clinical presentation is therefore as acute infection following trauma. The infection can be mono- or polymicrobial and can vary depending on the nature of the trauma. The most common pathogenic agent is staphylococcus aureus introduced from the skin. Other bacteria linked to infectious tenosynovitis include Pasteurella multocida (associated with animal bites), Eikenella spp. (associated with IV drug use), and Mycobacterium marinum (associated with wounds exposed to fresh or salt water). Additionally, sexually active patients are at risk for hematogenous spread due to Neisseria gonorrhea (see infectious arthritis).

Noninfectious tenosynovitis can arise from overuse or secondary to other systemic inflammatory conditions such as [rheumatoid arthritis] or [reactive arthritis]. If left untreated, the tendons may undergo stenosis, causing conditions such as de Quervain’s and trigger finger.

25% of cases progress to severe destructive arthritis. In the United States and Canada, mortality is estimated at about 4% and in Europe, mortality is estimated at 21.7%.

JIA occurs in both sexes, but like other rheumatological diseases, is more common in females. Symptoms onset is frequently dependent on the subtype of JIA and is from the preschool years to the early teenaged years.

The cause of JIA remains a mystery. However, the disorder is autoimmune — meaning that the body's own immune system starts to attack and destroy cells and tissues (particularly in the joints) for no apparent reason. The immune system is thought to be provoked by changes in the environment, in combination with mutations in many associated genes and/or other causes of differential expression of genes. Experimental studies have shown that certain mutated viruses may be able to trigger JIA. The disease appears to be more common in girls, and the disease is most common in Caucasians.

Associated factors that may worsen or have been linked to rheumatoid arthritis include:

- Genetic predisposition; When one family member has been diagnosed with rheumatoid arthritis or another autoimmune disorder, the chances are higher that other family members or siblings may also develop arthritis.

- Females are more likely to develop rheumatoid arthritis than males at all ages.

- A strong belief is held that psychological stress may worsen the symptoms of rheumatoid arthritis. However, when the emotional stress is under control, the arthritis symptoms do not always disappear, suggesting that the association is not straightforward.

- Though no distinct immune factor has been isolated as a cause of arthritis, some experts believe that the triggering factor may be something like a virus which then disappears from the body after permanent damage is done.

- Because rheumatoid arthritis is more common in women, perhaps sex hormones may play a role in causing or modulating arthritis. Unfortunately, neither sex hormone deficiency nor replacement has been shown to improve or worsen arthritis.

The cause of JIA, as the word "idiopathic" suggests, is unknown and an area of active research. Current understanding of JIA suggests that it arises in a genetically susceptible individual due to environmental factors.

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.

In the US it affects about 250,000-294,000 children and teens making it one of the most common childhood diseases .

Palindromic rheumatism is a disease of unknown cause. It has been suggested that it is an abortive form of rheumatoid arthritis (RA), since anti-cyclic citrullinated peptide antibodies (anti-CCP) and antikeratin antibodies (AKA) are present in a high proportion of patients, as is the case in rheumatoid arthritis. Unlike RA and some other forms of arthritis, palindromic rheumatism affects men and women equally. Palindromic rheumatism is frequently the presentation for Whipple disease which is caused by the infectious agent "Tropheryma whipplei" (formerly "T. whippelii").

Anti-citrullinated protein antibody is frequently associated.

Septic arthritis is due to a bacterial infection to the joint. It requires urgent joint washout in the operating room followed by intravenous antibiotic therapy for large joints. Small joints or children can be treated with repeated aspirations and intravenous antibiotics.

In "gout", the acute inflammatory arthritis is caused by excess uric acid caused by either overproduction or under-excretion. Before the age of menopause, women have a lower incidence than males, but the rates are equal above this age. Gout can cause mono- or polyarthritis, but usually results in monoarthritis first.

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.

Worldwide prevalence of spondyloarthropathy is approximately 1.9%.

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.

Seventy percent of people who develop psoriatic arthritis first show signs of psoriasis on the skin, 15 percent develop skin psoriasis and arthritis at the same time, and 15 percent develop skin psoriasis following the onset of psoriatic arthritis.

Psoriatic arthritis can develop in people who have any level severity of psoriatic skin disease, ranging from mild to very severe.

Psoriatic arthritis tends to appear about 10 years after the first signs of psoriasis. For the majority of people, this is between the ages of 30 and 55, but the disease can also affect children. The onset of psoriatic arthritis symptoms before symptoms of skin psoriasis is more common in children than adults.

More than 80% of patients with psoriatic arthritis will have psoriatic nail lesions characterized by nail pitting, separation of the nail from the underlying nail bed, ridging and cracking, or more extremely, loss of the nail itself (onycholysis).

Enthesitis is observed in 30 to 50% of patients and most commonly involves the plantar fascia and Achilles’ tendon, but it may cause pain around the patella, iliac crest, epicondyles,

and supraspinatus insertions

Men and women are equally affected by this condition. Like psoriasis, psoriatic arthritis is more common among Caucasians than African or Asian people.

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.

Polyarthritis is most often caused by an auto-immune disorder such as rheumatoid arthritis, amyloidosis, psoriatic arthritis, and lupus erythematosus but can also be caused by infection with an alphavirus such as chikungunya virus and Ross River virus. This condition is termed alphavirus polyarthritis syndrome. Sindbis virus, which is endemic in Northern Europe, Africa, the Middle East, and Australia, is the most widely distributed of the alphaviruses causing polyarthritis, though infection is usually mild or asymptomatic.