Treatment is frequently by means of removal of the loose bodies and of a partial or full synovectomy (removal of the synovium)

Full synovectomy is a moderately major operation and involves completely exposing the joint and removing the affected tissue. Partial synovectomy is normally done arthroscopically. Synovectomies are normally carried out by shaving the lining of the knee but there are other ways of achieving this by either freezing the synovium or by the use of radiation treatment.

The need for further procedures is greater than 25% although normally the frequency of the required removal of loose bodies is reduced by the previous synovectomy. There have been documented cases of malignant transformation however this is rare.

Whilst the condition can be described as a ‘benign growth’ it seldom affects more than one joint, and does not usually affect surrounding tissue.

Patients usually complain of pain in one joint, which persists for months, or even years, does not ease with exercise, steroid injection or heat treatment, shows nothing on X-ray, but shows a definite restriction of movement.

There are 3 defined stages to this disease:

- early: no loose bodies but active synovial disease;

- transitional: active synovial disease, and loose bodies;

- late: loose bodies but no synovial disease;

In the early stages of the disease it is often confused with tendinitis and/or arthritis. Once it reaches transitional the loose bodies become apparent with X-ray in greater than 70% of cases, with MRI often showing where xray fails. In experienced hands, US is also useful for the diagnosis.

In the disease, the thin flexible membrane of the synovium gradually forms blisters which calcify and enlarge. These nodules eventually break free and float around the joint space becoming larger – these add to the discomfort and stiffness of the joint.

The disease is rare and little known and there is currently no known cure. The affected tissue will show up as a semi-solid mass in a MRI scan, final diagnosis is usually confirmed by taking a biopsy.

Synovial chondromatosis occurs twice as commonly in males as females and usually in their forties. However, online communities for synovial chondromatosis patients have yielded a stark contrast, with equal representation from both genders and members diagnosed as young as late teenage/early 20s.

The disease generally affects only one of the larger weight bearing joints (hip, ankle, knee) – although the elbow, and wrist can also be affected. Rarely involves the temporal mandibular joint.

There are very few ways to test a patient for HGF. Currently, the most common way to diagnose a patient is by means of a physical evaluation. The physician can make a physical evaluation of the patient and send them to a dentist or better yet a specialist like a periodontist to evaluate signs of gingival overgrowth, quality of gingiva, inflammation, mechanical difficulties of the mouth, tooth conditions, and any sort of discomfort.

Aside from obvious physical symptoms seen in a physical evaluation, molecular tests can be run to check if there is a mutation in the SOS1 gene to confirm the diagnosis. If there is indeed a mutation in this gene coupled with the typical physical symptoms, then it is quite probable that a patient suffers from this disease. Also, looking at family history is also becoming more prominent in aiding to diagnose the patient. Otherwise, researchers are working to find new and better ways to test for the presence of HGF.

Because this genetic anomaly is genetically linked, genetic counseling may be the only way to decrease occurrences of Cherubism. The lack of severe symptoms in the parents may be the cause of failure in recognizing the disorder. The optimal time to be tested for mutations is prior to having children. The disorder results from a genetic mutation, and this gene has been found to spontaneously mutate. Therefore, there may be no prevention techniques available.

The chemical imbalance is usually diagnosed when dental abnormalities are found. These abnormalities include premature deciduous teeth and abnormal growth of permanent teeth due to displacement by cysts and lesions. The only definite way to correctly diagnose the condition is by sequence analysis of the SH3BP2 gene. The gene has been found to have missense mutation in exon 9. Initial study of the patient is usually conducted using x-ray and CT scans. Neurofibromatosis may resemble Cherubism and may accompany the condition. Genetic testing is the final diagnosis tool.

Several other illnesses can present with a monoclonal gammopathy, and the monoclonal protein may be the first discovery before a formal diagnosis is made:

X-ray is seldom helpful, but a CT scan and an MRI study may help in diagnosis.

Bone scans are positive early on. Dual energy X-ray absorptiometry is also helpful to rule out comorbid osteoporosis.

Since this condition is generally agreed upon to be hereditary, nothing can be done to prevent HGF. However, in some cases where it can develop as a result of rare multi-system syndromes, such as: Zimmerman-Laband, Jones, Ramon Syndrome, Rutherford Syndrome, Juvenile Hyaline Fibromatosis, Systemic Infantile Hyalinosis, and Mannosidosis, it is best for one to simply monitors the possible progression for HGF with regular dental check-ups.

If the patient's disease is treated by means of surgery, it is recommended that the patient undergoes post-surgical therapies for maintenance and periodic monitoring of gums for the sake of the possibility of re-occurrence of HGF.

Blood tests show a high concentration of specific gamma-globulins (monoclonal gammopathy) of the IgM type. It almost always has light chains of the κ-type. A variant in which IgG is raised has been described, which appears to be ten times as rare. The immunoglobulins may show up in the urine as Bence Jones proteins. Signs of inflammation are often present: these include an increased white blood cell count (leukocytosis) and a raised erythrocyte sedimentation rate and C-reactive protein. There can be anemia of chronic disease. Bone abnormalities can be seen on radiological imaging (often increased density or osteosclerosis) or biopsy.

Because it is such a rare condition (as of September 2014, only 281 cases have been reported), it is important to rule out other conditions which can cause periodic fevers, paraproteins or chronic hives. These include (and are not limited to) autoimmune or autoinflammatory disorders such as adult-onset Still's disease, angioedema, hematological disorders such as lymphoma or monoclonal gammopathy of undetermined significance, other causes of hives, cryoglobulinemia, mastocytosis, chronic neonatal onset multisystem inflammatory disease or Muckle–Wells syndrome.

It is however possible to have more than one rare condition as seen by a patient with Schnitzler's syndrome and cold induced urticaria.

A meeting of experts, including Dr Liliane Schnitzler (then retired) took place in Strasbourg in May 2012 and drew up diagnostic criteria known as the "Strasbourg Criteria". These included two obligate criteria (chronic urticarial rash and monoclonal IgM or IgG) and several minor criteria; a definite diagnosis requires the two obligate criteria and two minor criteria if IgM, three if IgG; a probable diagnosis requires the two obligate criteria and one (IgM) or two (IgG) minor criteria.

Most cases of SPB progress to multiple myeloma within 2–4 years of diagnosis, but the overall median survival for SPB is 7–12 years. 30–50% of extramedullary plasmacytoma cases progress to multiple myeloma with a median time of 1.5–2.5 years. 15–45% of SPB and 50–65% of extramedullary plasmacytoma are disease free after 10 years.

The protein electrophoresis test should be repeated annually, and if there is any concern for a rise in the level of monoclonal protein, then prompt referral to a hematologist is required. The hematologist, when first evaluating a case of MGUS, will usually perform a skeletal survey (X-rays of the proximal skeleton), check the blood for hypercalcemia and deterioration in renal function, check the urine for Bence Jones protein and perform a bone marrow biopsy. If none of these tests are abnormal, a patient with MGUS is followed up once every 6 months to a year with a blood test (serum protein electrophoresis). Although patients with MGUS have sometimes been reported to suffer from Small Fiber Neuropathy in monoclonal gammopathy of undetermined significance:a debilitating condition which causes bizarre sensory problems to painful sensory problems. peripheral neuropathy, no treatment is indicated.

This test can see various warning signs that predict if OSD might occur. Ultrasonography can detect if there is any swelling within the tissue as well as cartilage swelling. Ultrasonography's main goal is to identify OSD in the early stage rather than later on. It has unique features such as detection of an increase of swelling within the tibia or the cartilage surrounding the area and can also see if there is any new bone starting to build up around the tibial tuberosity.

Sinding-Larsen and Johansson syndrome, is an analogous condition involving the patellar tendon and the lower margin of the patella bone, instead of the upper margin of the tibia. Sever's disease is an analogous condition affecting the achille's tendon attachment to the heel.

Both blood and the urine can be tested for the light chains, which may form amyloid deposits, causing disease. However, the diagnosis requires a sample of an affected organ.

The life span in patients with Schnitzler syndrome has not been shown to differ much from the general population. Careful follow-up is advised, however. A significant proportion of patients develops a lymphoproliferative disorder as a complication, most commonly Waldenström's macroglobulinemia. This may lead to symptoms of hyperviscosity syndrome. AA amyloidosis has also been reported in people with Schnitzler syndrome.

If a contracture is less than 30 degrees, it may not interfere with normal functioning. The common treatment is splinting and occupational therapy. Surgery is the last option for most cases as the result may not be satisfactory.

Plasmacytoma is a tumor of plasma cells. The cells are identical to those seen in multiple myeloma, but they form discrete masses of cells in the skeleton (solitary plasmacytoma of bone; SPB) or in soft tissues (extramedullary plasmacytoma; EP). They do not present with systemic disease, which would classify them as another systemic plasma cell disorder.

The International Myeloma Working Group (IMWG) has published criteria for the diagnosis of plasmacytomas. They recognise three distinct entities: SPB, extramedullary plasmacytoma and multiple solitary plasmacytomas (+/- recurrent). The proposed criteria for SPB is the presence of a single bone lesion, normal bone marrow (less than 5% plasma cells), small or no paraprotein, no related organ involvement/damage and a normal skeletal survey (other than the single bone lesion). The criteria for extramedullary plasmacytoma are the same but the tumor is located in soft tissue. No bone lesions should be present. Criteria for multiple solitary plasmacytomas (+/- recurrent) are the same except either multiple solitary bone or soft tissue lesions must be present. They may occur as multiple primary tumors or as a recurrence from a previous plasmacytoma.

For several reasons, a Jones fracture may not unite. The diaphyseal bone (zone II), where the fracture occurs, is an area of potentially poor blood supply, existing in a watershed area between two blood supplies. This may compromise healing. In addition, there are various tendons, including the peroneus brevis and fibularis tertius, and two small muscles attached to the bone. These may pull the fracture apart and prevent healing.

Zones I and III have been associated with relatively guaranteed union and this union has taken place with only limited restriction of activity combined with early immobilization. On the other hand, zone II has been associated with either delayed or non-union and, consequently, it has been generally agreed that fractures in this area should be considered for some form of internal immobilization, such as internal screw fixation.

These zones can be identified anatomically and on x-ray adding to the clinical usefulness of this classification.

It should be emphasized that surgical intervention is not, by itself, a guarantee of cure and has its own complication rate. Other reviews of the literature have concluded that conservative, non-operative, treatment is an acceptable option for the non-athlete.

Median survival for patients diagnosed with AL amyloidosis was 13 months in the early 1990s, but had improved to c. 40 months a decade later.

There are several classification schemes for ankle fractures:

- The Lauge-Hansen classification categorises fractures based on the mechanism of the injury as it relates to the position of the foot and the deforming force (most common type is supination-external rotation)

- The Danis-Weber classification categorises ankle fractures by the level of the fracture of the distal fibula (type A = below the syndesmotic ligament, type B = at its level, type C = above the ligament), with use in assessing injury to the syndesmosis and the interosseous membrane

- The Herscovici classification categorises medial malleolus fractures of the distal tibia based on level.

- The Ruedi-Allgower classification categorizes pilon fractures of the distal tibia.

The first line treatment should be reduction of movements for 6 to 12 weeks. Wooden-soled shoes or a cast should be given for this purpose. In rare cases in which stress fracture occurs with a cavus foot, plantar fascia release may be appropriate.

In athletes or if the pieces of bone are separated by more than 2 mm surgery may be considered. Otherwise surgery is recommended if healing does not occur after 12 weeks of casting.

A bone fracture may be diagnosed based on the history given and the physical examination performed. Radiographic imaging often is performed to confirm the diagnosis. Under certain circumstances, radiographic examination of the nearby joints is indicated in order to exclude dislocations and fracture-dislocations. In situations where projectional radiography alone is insufficient, Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) may be indicated.

In irrigation test, a lacrimal irrigation cannula is passed into the punctum and advanced through the canaliculus to the lacrimal fossa. Clear water or saline is then irrigated through the cannula. If fluid passes into the nose without reflux out of the opposite canaliculus, the system is patent. If no fluid passes but it all comes back through either punctum, nasolacrimal duct obstruction is present.

Camptodactyly is a medical condition that causes one or more fingers to be permanently bent. It involves fixed flexion deformity of the proximal interphalangeal joints. The fifth finger is always affected.

Camptodactyly can be caused by a genetic disorder. In that case, it is an autosomal dominant trait that is known for its incomplete genetic expressivity. This means that when a person has the genes for it, the condition may appear in both hands, one, or neither. A linkage scan proposed that the chromosomal locus of camptodactyly was 3q11.2-q13.12.