Two elements are considered: radiology and joint fluid analysis.

Radiology has a large role to play in finding chondrocalcinosis, with radiographs, CT scans, MRIs, US, and nuclear medicine all having a part. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, CPPD can present with similarity to other diseases such as ankylosing spondylitis and gout.

Arthrocentesis, or removing synovial fluid from the affected joint, is performed to test the synovial fluid for the calcium pyrophosphate crystals that are present in CPPD. When stained with H&E stain, calcium pyrophosphate crystals appears deeply blue ("basophilic"). However, CPP crystals are much better known for their rhomboid shape and weak positive birefringence on polarized light microscopy, and this method remains the most reliable method of identifying the crystals under the microscope. However, even this method suffers from poor sensitivity, specificity, and inter-operator agreement.

These two modalities currently define CPPD disease but lack diagnostic accuracy, and are potentially epiphenomenological.

Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain.

For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD. However, if an acute attack is already occurring, higher doses are administered. If nothing else works, hydroxychloroquine or methotrexate may provide relief.

Research into surgical removal of calcifications is underway, however this still remains an experimental procedure.

Diagnosis is made by clinical examination from an appropriate health professional, and may be supported by other tests such as radiology and blood tests, depending on the type of suspected arthritis. All arthritides potentially feature pain. Pain patterns may differ depending on the arthritides and the location. Rheumatoid arthritis is generally worse in the morning and associated with stiffness; in the early stages, patients often have no symptoms after a morning shower. Osteoarthritis, on the other hand, tends to be worse after exercise. In the aged and children, pain might not be the main presenting feature; the aged patient simply moves less, the infantile patient refuses to use the affected limb.

Elements of the history of the disorder guide diagnosis. Important features are speed and time of onset, pattern of joint involvement, symmetry of symptoms, early morning stiffness, tenderness, gelling or locking with inactivity, aggravating and relieving factors, and other systemic symptoms. Physical examination may confirm the diagnosis, or may indicate systemic disease. Radiographs are often used to follow progression or help assess severity.

Blood tests and X-rays of the affected joints often are performed to make the diagnosis. Screening blood tests are indicated if certain arthritides are suspected. These might include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen, and specific antibodies.

Diagnosis of amyloidosis requires tissue biopsy. The biopsy is assessed for evidence of characteristic amyloid deposits. The tissue is treated with various stains. The most useful stain in the diagnosis of amyloid is Congo red, which, combined with polarized light, makes the amyloid proteins appear apple-green on microscopy. Also, thioflavin T stain may be used.

Tissue can come from any involved organ, but in systemic disease the first-line site of the biopsy is subcutaneous abdominal fat, known as a "fat pad biopsy," due to its ease of acquisition versus biopsy of the rectum, salivary gland or internal organs. An abdominal fat biopsy is not completely sensitive, and sometimes, biopsy of an involved organ (such as the kidney) is required to achieve a diagnosis. For example, in AL amyloidosis only 85% of people will have a positive fatpad biopsy using Congo red stain. By comparison, rectal biopsy has sensitivity of 74–94%.

The type of the amyloid protein can be determined in various ways: the detection of abnormal proteins in the bloodstream (on protein electrophoresis or light chain determination); binding of particular antibodies to the amyloid found in the tissue (immunohistochemistry); or extraction of the protein and identification of its individual amino acids. Immunohistochemistry can identify AA amyloidosis the majority of the time, but can miss many cases of AL amyloidosis. Laser microdissection with mass spectrometry is the most reliable method of identifying the different forms of amyloidosis.

AL is the most common form of amyloidosis, and a diagnosis often begins with a search for plasma cell dyscrasia, memory B cells producing aberrant immunoglobulins or portions of immunoglobulins. Immunofixation electrophoresis of urine or serum is positive in 90% of people with AL amyloidosis. Immunofixation electrophoresis is more sensitive than regular electrophoresis but may not be available in all centers. Alternatively immunohistochemical staining of a bone marrow biopsy looking for dominant plasma cells can be sought in people with a high clinical suspicion for AL amyloidosis but negative electrophoresis.

ATTR, or familial transthyretin-associated amyloidosis, is suspected in people with family history of idiopathic neuropathies or heart failure who lack evidence of plasma cell dyscrasias. ATTR can be identified using isoelectric focusing which separates mutated forms of transthyretin. Findings can be corroborated by genetic testing to look for specific known mutations in transthyretin that predispose to amyloidosis.

AA is suspected on clinical grounds in individuals with longstanding infections or inflammatory diseases. AA can be identified by immunohistochemistry staining.

Chondrocalcinosis can be visualized on projectional radiography, CT scan, MRI, US, and nuclear medicine. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis and gout.

Prognosis varies with the type of amyloidosis. Prognosis for untreated AL amyloidosis is poor with median survival of one to two years. More specifically, AL amyloidosis can be classified as stage I, II or III based on cardiac biomarkers like troponin and BNP. Survival diminishes with increasing stage, with estimated survival of 26, 11 and 3.5 months at stages I, II and III, respectively.

Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein.

People with ATTR have better prognosis and may survive for over a decade.

Senile systemic amyloidosis was determined to be the primary cause of death for 70% of people over 110 who have been autopsied.

Based on studies conducted in the United States, the prognosis for individuals with ALECT2 amyloidosis is guarded, particularly because they are elderly and their kidney disease is usually well-advanced at the time of presentation. End-stage renal disease develops in 1 out of 3 patients and has a median renal survival of 62 months. A suggested prognostic tool is to track creatinine levels in ALect2 patients. The attached Figure gives survival plotss for individuals with LECT2 renal amyloidosis and serum creatinine levels less than 2 mg/100 ml versus 2 mg/100 ml or greater than 2 mg/100 ml. The results show that afflicted individuals with lower creatinine levels have a ~four-fold higher survival rate.

When faced with monoarthritis, one of the main decisions to make is whether to perform a "joint aspirate" by inserting a needle into the affected joint and removing some fluid for microscopic analysis. This decision is largely taken on inflammatory markers in blood tests (e.g. CRP), fever and the clinical picture. The main use of aspiration is to detect bacteria and neutrophil granulocytes (in septic arthritis) and crystals (crystal arthropathies).

LECT2 amyloidosis is diagnosed by a kidney biopsy which reveals two key findings: a) histological evidence of Congo red staining material deposited in the interstitial, mesangial, glomerular, and/or vascular areas of the kidney and b) the identification of these deposits as containing mainly ALECT2 as identified by proteomics methodologies. Kidney biopsy shows the presence of LECT2-based amyloid predominantly in the renal cortex interstitium, glomeruli, and arterioles. LECT2 amyloidosis can be distinguished from AL amyloidosis, the most common form of amyloidosis (~85% of total cases), by testing their blood for the presence of high levels of a clonal immunoglobulin light chain. If the patient tests negative for this light chain, positive Congo Red staining of the kidney biopsy strongly suggests LECT2 amyloidosis.

Laboratory testing includes white blood cell count, ESR, and CRP. These values are usually elevated in those with septic arthritis; however, these can be elevated by other infections or inflammatory conditions and are, therefore, nonspecific. Procalcitonin may be more useful than CRP.

Blood cultures can be positive in up to half of patients with septic arthritis.

Imaging such as x-ray, CT,MRI, orultrasoundarenonspecific. They can help determine areas of inflammation but cannot confirm septic arthritis.

When septic arthritis is suspected,x-raysshould generally be taken. This is used to assess for involvement of surrounding structures such as bone and also for comparison purposes when future x-rays are taken.While x-rays may not be helpful early in the diagnosis/treatment, they may show subtle increase in joint space and tissue swelling. Later findings include joint space narrowing due to destruction of the joint.

Ultrasoundcan be done and is effective at detecting joint effusions.

CTandMRI are not required for diagnosis but can be used if diagnosis is unclear or in joints that are hard to examine (ie.sacroiliacorhip joints). They can can help assess for inflammation/infection in or about the joint (ie.osteomyeltis).

There is no known cure for either rheumatoid or osteoarthritis. Treatment options vary depending on the type of arthritis and include physical therapy, lifestyle changes (including exercise and weight control), orthopedic bracing, and medications. Joint replacement surgery may be required in eroding forms of arthritis. Medications can help reduce inflammation in the joint which decreases pain. Moreover, by decreasing inflammation, the joint damage may be slowed.

If the knee is swollen and red and warm to the touch when compared to the other knee, a doctor may be concerned about inflammation due to rheumatoid arthritis or a crystalline arthritis, such as gout or pseudogout, or joint infection. Besides sending the joint fluid to a laboratory for analysis, blood tests may requested to determine a white blood cell count, erythrocyte sedimentation rate, and perhaps the level of C-reactive protein or uric acid. If blood tests reveal Lyme disease antibodies forming, the condition may be attributed to it.

The first clinical manifestation of Paget's disease is usually an elevated alkaline phosphatase in the blood.

Paget's disease may be diagnosed using one or more of the following tests:

- Pagetic bone has a characteristic appearance on X-rays. A skeletal survey is therefore indicated.

- An elevated level of alkaline phosphatase in the blood in combination with normal calcium, phosphate, and aminotransferase levels in an elderly patient are suggestive of Paget's disease.

- Markers of bone turnover in urine "eg". Pyridinoline

- Elevated levels of serum and urinary hydroxyproline are also found.

- Bone scans are useful in determining the extent and activity of the condition. If a bone scan suggests Paget's disease, the affected bone(s) should be X-rayed to confirm the diagnosis.

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 .

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.

In 1980, the American College of Rheumatology agreed on diagnostic criteria for scleroderma.

Diagnosis is by clinical suspicion, presence of autoantibodies (specifically anti-centromere and anti-scl70/anti-topoisomerase antibodies) and occasionally by biopsy. Of the antibodies, 90% have a detectable anti-nuclear antibody. Anti-centromere antibody is more common in the limited form (80-90%) than in the diffuse form (10%), and anti-scl70 is more common in the diffuse form (30-40%) and in African American patients (who are more susceptible to the systemic form).

Other conditions may mimic systemic sclerosis by causing hardening of the skin. Diagnostic hints that another disorder is responsible include the absence of Raynaud's phenomenon, a lack of abnormalities in the skin on the hands, a lack of internal organ involvement, and a normal antinuclear antibodies test result.

Monoarthritis is inflammation ("arthritis") of one joint at a time. It is usually caused by trauma, infection, or crystalline arthritis.

A common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD).

Excessive calcium (due to hypomagnesemia) has a potential relationship with chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis.

Other causes of chondrocalcinosis include:

- Hypercalcaemia, especially when caused by hyperparathyroidism

- Arthritis

- Gout

- Wilson disease

- Hemochromatosis

- Ochronosis

- Hypothyroidism

- Hyperoxalemia

- Acromegaly

- osteoarthritis

Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location i.e. around joints. The accumulations are outside the joint capsule. They are frequently seen in patients undergoing renal dialysis. It is also considered by some to have a hereditary predisposition. The name indicates calcinosis (calcium deposition) which resembles tumor (like a new growth). They are not true neoplasms - they don't have dividing cells. They are just deposition of inorganic calcium with serum exudate.

Children and adolescents (6 to 25 years) are the most commonly affected. The symptom that the accumulations cause is not pain but swelling around joints. They have propensity to enlarge progressively and ulcerate the overlying skin and extrude. They are most common around shoulders, hips and elbows. Laboratory evaluation reveal normal serum calcium levels and hyperphosphatemia. Rarely ALP (alkaline phosphatase - an enzyme active at sites of bone formation) may be elevated. Treatment is normalization of serum phosphate levels and resection of lesion. Surgical removal should be complete and if part of it is left, there is inevitable recurrence. Cutting through the excised calcium deposition reveals semifluid calcium suspension in albumin encapsulated by fibrous tissue.

An X-ray is useful to verify that there is no break or dislocation when there is a history of trauma. May show signs of osteoarthritis.

Although initially diagnosed by a primary care physician, endocrinologists (internal medicine physicians who specialize in hormonal and metabolic disorders), rheumatologists (internal medicine physicians who specialize in joint and muscle disorders), orthopedic surgeons, neurosurgeons, neurologists, oral and maxillofacial surgeons, podiatrists, and otolaryngologists are generally knowledgeable about treating Paget's disease, and may be called upon to evaluate specialized symptoms. It can sometimes difficult to predict whether a person with Paget's disease, who otherwise has no signs or symptoms of the disorder, will develop symptoms or complications (such as a bone fracture) in the future.

The U.S. Preventive Services Task Force (USPSTF) recommend that all women 65 years of age or older be screened by bone densitometry. Additionally they recommend screening women with increased risk factors that puts them at risk equivalent to a 65‑year‑old. There is insufficient evidence to make recommendations about the intervals for repeated screening and the appropriate age to stop screening. In men the harm versus benefit of screening for osteoporosis is unknown. Prescrire states that the need to test for osteoporosis in those who have not had a previous bone fracture is unclear. The International Society for Clinical Densitometry, however, suggest BMD testing for men 70 or older, or those who are indicated for risk equal to that of a 70‑year‑old. A number of tools exist to help determine who is reasonable to test.

There is no diagnostic test for calciphylaxis. The diagnosis is a clinical one. The characteristic lesions are the ischemic skin lesions (usually with areas of skin necrosis). The necrotic skin lesions (i.e. the dying or already dead skin areas) typically appear as violaceous (dark bluish purple) lesions and/or completely black leathery lesions. They can be extensive. The suspected diagnosis can be supported by a skin biopsy. It shows arterial calcification and occlusion in the absence of vasculitis. Sometimes the bone scintigraphy can show increased tracer accumulation in the soft tissues. In certain patients, anti-nuclear antibody may play a role.

After centrifuging, the serum of myoglobinuria is clear, where the serum of hemoglobinuria after centrifuge is pink to red.