Diagnosis is simple; usually a doctor can diagnose shoulder arthritis by symptoms, but they may ask for an x-ray or MRI for confirmation.

X-rays may help visualize bone spurs, acromial anatomy and arthritis. Further, calcification in the subacromial space and rotator cuff may be revealed. Osteoarthritis of the acromioclavicular (AC) joint may co-exist and is usually demonstrated on radiographs.

MRI imagining can reveal fluid accumulation in the bursa and assess adjacent structures. In chronic cases caused by impingement tendinosis and tears in the rotator cuff may be revealed. At US, an abnormal bursa may show (1) fluid distension, (2) synovial proliferation, and/or (3) thickening of the bursal walls. In any case, the magnitude of pathological findings does not correlate with the magnitude of the symptoms.

Treatment of shoulder arthritis is usually aimed at reducing pain; there is no way to replace lost cartilage except through surgery. Pain medicines available over-the-counter can be prescribed by the doctor, but another form of treatment is cryotherapy, which is the use of cold compression. Some vitamin supplements have been found to prevent further deterioration; glucosamine sulfate is an effective preserver of cartilage. Another way to prevent the further loss of cartilage would be to maintain motion in the shoulder, because once it is lost, it's difficult to regain. Steps to reduce extreme pain in cases of bad shoulder arthritis can involve the doctor giving injections directly into the shoulder, or even shoulder surgery.

For patients with severe shoulder arthritis that does not respond to non-operative treatment, shoulder surgery can be very helpful. Depending on the condition of the shoulder and the specific expectations of the patient, surgical options include total shoulder joint replacement arthroplasty , ‘ream and run’ (humeral hemiarthroplasty with non prosthetic glenoid arthroplasty , and reverse (Delta) total shoulder joint replacement arthroplasty .

In patients with bursitis who have rheumatoid arthritis, short term improvements are not taken as a sign of resolution and may require long term treatment to ensure recurrence is minimized. Joint contracture of the shoulder has also been found to be at a higher incidence in type two diabetics, which may lead to frozen shoulder (Donatelli, 2004).

Imaging features of adhesive capsulitis are seen on non-contrast MRI, though MR arthrography and invasive arthroscopy are more accurate in diagnosis. Ultrasound and MRI can help in diagnosis by assessing the coracohumeral ligament, with a width of greater than 3 mm being 60% sensitive and 95% specific for the diagnosis. The condition can also be associated with edema or fluid at the rotator interval, a space in the shoulder joint normally containing fat between the supraspinatus and subscapularis tendons, medial to the rotator cuff. Shoulders with adhesive capsulitis also characteristically fibrose and thicken at the axillary pouch and rotator interval, best seen as dark signal on T1 sequences with edema and inflammation on T2 sequences. A finding on ultrasound associated with adhesive capsulitis is hypoechoic material surrounding the long head of the biceps tendon at the rotator interval, reflecting fibrosis. In the painful stage, such hypoechoic material may demonstrate increased vascularity with Doppler ultrasound.

Magnetic resonance imaging (MRI) and ultrasound are comparable in efficacy and helpful in diagnosis although both have a false positive rate of 15 - 20%. MRI can reliably detect most full-thickness tears although very small pinpoint tears may be missed. In such situations, an MRI combined with an injection of contrast material, an MR-arthrogram, may help to confirm the diagnosis. It should be realized that a normal MRI cannot fully rule out a small tear (a false negative) while partial-thickness tears are not as reliably detected. While MRI is sensitive in identifying tendon degeneration (tendinopathy), it may not reliably distinguish between a degenerative tendon and a partially torn tendon. Again, magnetic resonance arthrography can improve the differentiation. An overall sensitivity of 91% (9% false negative rate) has been reported indicating that magnetic resonance arthrography is reliable in the detection of partial-thickness rotator cuff tears. However, its routine use is not advised, since it involves entering the joint with a needle with potential risk of infection. Consequently, the test is reserved for cases in which the diagnosis remains unclear.

The calcific deposits are visible on X-ray as discrete lumps or cloudy areas. The deposits look cloudy on X-ray if they are in the process of reabsorption, and this is also when they cause the most pain. The deposits are crystalline when in their resting phase and like toothpaste in the reabsorptive phase. However, poor correlation exists between the appearance of a calcific deposit on plain X-rays and its consistency on needling. Ultrasound is also useful to depict calcific deposits and closely correlates with the stage of disease.

Once PVNS is confirmed by biopsy of the synovium of an affected joint, a synovectomy of the affected area is the most common treatment. Bone lesions caused by the disorder are removed and bone grafting is performed as needed. Because diffuse PVNS has a relatively high rate of recurrence, radiation therapy may be considered as a treatment option. In some cases, a total joint replacement is needed to relieve symptoms when PVNS causes significant joint destruction.

In those with calcific tendinitis of the shoulder high energy extracorporeal shock-wave therapy (which uses sound waves) can be useful. It is not useful in other types of tendinitis. This procedure may be known as .

Although a 2011 research article stated that disagreements between hand surgeons and rheumatologists remain regarding the indications, timing and effectiveness of rheumatoid hand surgery, arthritis mutilans may be successfully treated by iliac-bone graft and arthrodesis of the interphalangeal joints and the metacarpophalangeal joint in each finger.

Musculoskeletal ultrasound has been advocated by experienced practitioners, avoiding the radiation of X-ray and the expense of MRI while demonstrating comparable accuracy to MRI for identifying and measuring the size of full-thickness and partial-thickness rotator cuff tears. This modality can also reveal the presence of other conditions that may mimic rotator cuff tear at clinical examination, including tendinosis, calcific tendinitis, subacromial subdeltoid bursitis, greater tuberosity fracture, and adhesive capsulitis. However, MRI provides more information about adjacent structures in the shoulder such as the capsule, glenoid labrum muscles and bone and these factors should be considered in each case when selecting the appropriate study.

Impingement syndrome can usually be diagnosed by history and physical exam. On physical exam, the physician may twist or elevate the patient's arm to test for reproducible pain (Neer sign and Hawkins-Kennedy test). These tests help localize the pathology to the rotator cuff; however, they are not specific for impingement. Neer sign may also be seen with subacromial bursitis.

The physician may inject lidocaine (usually combined with a steroid) into the bursa, and if there is an improved range of motion and decrease in pain, this is considered a positive "Impingement Test". It not only supports the diagnosis for impingement syndrome, but it is also therapeutic.

Plain x-rays of the shoulder can be used to detect some joint pathology and variations in the bones, including acromioclavicular arthritis, variations in the acromion, and calcification. However, x-rays do not allow visualization of soft tissue and thus hold a low diagnostic value. Ultrasonography, arthrography and MRI can be used to detect rotator cuff muscle pathology. MRI is the best imaging test prior to arthroscopic surgery. Due to lack of understanding of the pathoaetiology, and lack of diagnostic accuracy in the assessment process by many physicians, several opinions are recommended before intervention.

The bone edema in arthitis mutilans can be treated with TNF inhibitors in the short term: a 2007 study found that the bone edema associated with psoriatic arthritis (of which arthitis mutilans is a subtype) responded to TNF inhibitors with "dramatic" improvement, but the study was not determinative of whether TNF inhibitors would prevent new bone formation, bone fusion, or osteolysis (bone resorption).

The Schober's test is a useful clinical measure of flexion of the lumbar spine performed during the physical examination.

Variations of the HLA-B gene increase the risk of developing ankylosing spondylitis, although it is not a diagnostic test. Those with the HLA-B27 variant are at a higher risk than the general population of developing the disorder. HLA-B27, demonstrated in a blood test, can occasionally help with diagnosis, but in itself is not diagnostic of AS in a person with back pain. Over 90% of people that have been diagnosed with AS are HLA-B27 positive, although this ratio varies from population to population (about 50% of African Americans with AS possess HLA-B27 in contrast to the figure of 80% among those with AS who are of Mediterranean descent).

As of July 2000, hypermobility was diagnosed using the Brighton criteria. The Brighton criteria do not replace the Beighton score but instead use the previous score in conjunction with other symptoms and criteria. HMS is diagnosed in the presence of either two major criteria, one major and two minor criteria, or four minor criteria. The criteria are:

Diagnosis of tendinitis and bursitis begins with a medical history and physical examination. X rays do not show tendons or the bursae but may be helpful in ruling out bony abnormalities or arthritis. The doctor may remove and test fluid from the inflamed area to rule out infection.

Ultrasound scans are frequently used to confirm a suspected tendinitis or bursitis as well as rule out a tear in the rotator cuff muscles.

Impingement syndrome may be confirmed when injection of a small amount of anesthetic (lidocaine hydrochloride) into the space under the acromion relieves pain.

To prevent the problem, a common recommendation is to keep the shoulder joint fully moving to prevent a frozen shoulder. Often a shoulder will hurt when it begins to freeze. Because pain discourages movement, further development of adhesions that restrict movement will occur unless the joint continues to move full range in all directions (adduction, abduction, flexion, rotation, and extension). Physical therapy and occupational therapy can help with continued movement.

It is important to differentiate between infected and non-infected bursitis. People may have surrounding cellulitis and systemic symptoms include a fever. The bursa should be aspirated to rule out an infectious process.

Bursae that are not infected can be treated symptomatically with rest, ice, elevation, physiotherapy, anti-inflammatory drugs and pain medication. Since bursitis is caused by increased friction from the adjacent structures, a compression bandage is not suggested because compression would create more friction around the joint. Chronic bursitis can be amenable to bursectomy and aspiration.

Bursae that are infected require further investigation and antibiotic therapy. Steroid therapy may also be considered. In cases when all conservative treatment fails, surgical therapy may be necessary. In a bursectomy the bursa is cut out either endoscopically or with open surgery. The bursa grows back in place after a couple of weeks but without any inflammatory component.

The best diagnosis for a SLAP tear is a clinical exam

followed by an MRI combined with a contrast agent

PVNS is radiologically diagnosed by magnetic resonance imaging (MRI). The disorder is difficult to identify and is often not diagnosed for four years or more after presentation due to nonspecific symptoms or a general paucity of symptoms.

Imaging diagnosis conventionally begins with plain film radiography. Generally, AP radiographs of the shoulder with the arm in internal rotation offer the best yield while axillary views and AP radiographs with external rotation tend to obscure the defect. However, pain and tenderness in the injured joint make appropriate positioning difficult and in a recent study of plain film x-ray for Hill–Sachs lesions, the sensitivity was only about 20%. i.e. the finding was not visible on plain film x-ray about 80% of the time.

By contrast, studies have shown the value of ultrasonography in diagnosing Hill–Sachs lesions. In a population with recurrent dislocation using findings at surgery as the gold standard, a sensitivity of 96% was demonstrated. In a second study of patients with continuing shoulder instability after trauma, and using double contrast CT as a gold standard, a sensitivity of over 95% was demonstrated for ultrasound. It should be borne in mind that in both those studies, patients were having continuing problems after initial injury, and therefore the presence of a Hill–Sachs lesion was more likely. Nevertheless, ultrasonography, which is noninvasive and free from radiation, offers important advantages.

MRI has also been shown to be highly reliable for the diagnosis of Hill-Sachs (and Bankart) lesions. One study used challenging methodology. First of all, it applied to those patients with a single, or first time, dislocation. Such lesions were likely to be smaller and therefore more difficult to detect. Second, two radiologists, who were blinded to the surgical outcome, reviewed the MRI findings, while two orthopedic surgeons, who were blinded to the MRI findings, reviewed videotapes of the arthroscopic procedures. Coefficiency of agreement was then calculated for the MRI and arthroscopic findings and there was total agreement ( kappa = 1.0) for Hill-Sachs and Bankart lesions.

The classic diagnostic technique is with appropriate X-rays and hip scoring tests. These should be done at an appropriate age, and perhaps repeated at adulthood - if done too young they will not show anything. Since the condition is to a large degree inherited, the hip scores of parents should be professionally checked before buying a pup, and the hip scores of dogs should be checked before relying upon them for breeding. Despite the fact that the condition is inherited, it can occasionally arise even to animals with impeccably hip scored parents.

In diagnosing suspected dysplasia, the x-ray to evaluate the internal state of the joints is usually combined with a study of the animal and how it moves, to confirm whether its quality of life is being affected. Evidence of lameness or abnormal hip or spine use, difficulty or reduced movement when running or navigating steps, are all evidence of a problem. Both aspects have to be taken into account since there can be serious pain with little X-ray evidence.

It is also common to X-ray the spine and legs, as well as the hips, where dysplasia is suspected, since soft tissues can be affected by the extra strain of a dysplastic hip, or there may be other undetected factors such as neurological issues (e.g. nerve damage) involved.

There are several standardized systems for categorising dysplasia, set out by respective reputable bodies (Orthopedic Foundation for Animals/OFA, PennHIP, British Veterinary Association/BVA). Some of these tests require manipulation of the hip joint into standard positions, in order to reveal their condition on an X-ray.

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.

The decisions involved in the repair of the Hill–Sachs lesion are complex. First, it is not repaired simply because of its existence, but because of its association with continuing symptoms and instability. This may be of greatest importance in the under-25-year-old and in the athlete involved in throwing activities. The Hill-Sachs role in continuing symptoms, in turn, may be related to its size and large lesions, particularly if involving greater than 20% of the articular surface, may impinge on the glenoid fossa (engage), promoting further episodes of instability or even dislocation. Also, it is a fracture, and associated bony lesions or fractures may coexist in the glenoid, such as the so-called bony Bankart lesion. Consequently, its operative treatment may include some form of bony augmentation, such as the Latarjet or similar procedure. Finally, there is no guarantee that associated non-bony lesions, such as a Bankart lesion, SLAP tear, or biceps tendon injury, may not be present and require intervention.