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.

Synovial chondromatosis (synonyms include synovial osteochondromatosis, primary synovial osteochondromatosis, and synovial chondrometaplasia) is a disease affecting the synovium, a thin flexible membrane around a joint. It is also known as Reichel's syndrome or Reichel-Jones-Henderson syndrome, named after Friedrich Paul Reichel, Hugh Toland Jones and Melvin Starkey Henderson.

Osgood–Schlatter disease generally occurs in boys and girls aged 9–16 coinciding with periods of growth spurts. It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. It has been suggested that difference is related to a greater participation by boys in sports and risk activities than by girls.

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.

OSD occurs from the combined effects of tibial tuberosity immaturity and quadriceps tightness. There is a possibility of migration of the ossicle or fragmentation in Osgood-Schlatter patients. The implications of OSD and the ossification of the tubercle can lead to functional limitations and pain for patients into adulthood.

Of people admitted with OSD, about half were children who were between the ages of 1 and 17. In addition, in 2014, a case study of 261 patients was observed over 12 to 24 months. 237 of these people responded well to sport restriction and non-steroid anti-inflammatory agents, which resulted in recovery to normal athletic activity.

Some researchers suggest that HGF is transmitted as a Mendelian trait since both autosomal dominant and autosomal recessive transmission has been reported since the early 1970s. (SOURCE 1) In more recent scientific literature, there is evidence in which pedigree analyses confirm autosomal dominant, autosomal recessive or even as X-linked inherited cases of the HGF trait.

In 2002, researchers described the SOS1 gene and proved for the first time that a single-nucleotide–insertion mutation of the SOS1 gene on codon 1083 is the preliminary cause of HGF1 in humans. (Source 1) Later on in 2010, there was a case study done on a 16-year-old male with severe gingival overgrowth, almost covering all teeth. Researchers approached this issue with periodontics - a partial gingivectomy and flap surgery. This case study concluded that surgery followed by regular follow-ups is a good way to treat HGF despite the fact that the risks of re-occurrence of the condition remain high.

Even more recently, a study was done in 2013 on a family that showed history of autosomal recessive inheritance of HGF. The study did not dismiss the return of HGF after treatment but did claim that general surgical intervention after scaling and root planning of teeth supplemented with good oral hygiene is good enough to prevent the re-occurrence of HGF. This case study also acknowledged how HGF can be part of a multi-system syndrome associated with disorders such as Zimmermann Laband syndrome (ear, nose, bone, and nail defects with hepatosplenomegaly), Rutherford syndrome (microphthalmia, mental retardation, athetosis, and hypopigmentation), Murray-Puretic Drescher syndrome and Ramon syndrome.

The specific cause of camptodactyly remains unknown, but there are a few deficiencies that lead to the condition. A deficient lumbrical muscle controlling the flexion of the fingers, and abnormalities of the flexor and extensor tendons.

A number of congenital syndromes may also cause camptodactyly:

- Jacobsen syndrome

- Beals Syndrome

- Blau syndrome

- Freeman-Sheldon syndrome

- Cerebrohepatorenal syndrome

- Weaver syndrome

- Christian syndrome 1

- Gordon Syndrome

- Jacobs arthropathy-camptodactyly syndrome

- Lenz microphthalmia syndrome

- Marshall-Smith-Weaver syndrome

- Oculo-dento-digital syndrome

- Tel Hashomer camptodactyly syndrome

- Toriello-Carey syndrome

- Stuve-Wiedemann syndrome

- Loeys-Dietz syndrome

- Fryns syndrome

- Marfan's syndrome

- Carnio-carpo-tarsal dysthropy

HGF1 - Caused by a mutation in the SOS1 gene localized on chromosome 2p21-p22

HGF2 - Caused by a mutation in the SOS1 gene localized on chromosome 5q13-q22

Mutations in the RE1-silencing transcription factor (REST) gene can also cause this syndrome.

- Non genetic

HGF may also be caused by unwanted side effects of pharmacological agents like phenytoin, ciclosporin, and some calcium-channel blockers, meaning HGF is a disease that can be drug-induced. However, there is little next to no research done in this area to support the claim.

- Inflammation

- Hormonal Imbalance

- Neoplasia

- More commonly associated with an autosomal dominant gene inheritance

- Multi-system syndromes: Zimmerman-Laband syndrome, Jones syndrome, Ramon syndrome, Rutherford syndrome, juvenile hyaline fibromatosis, systemic infantile hyalinosis, and mannosidosis

- Some unknown causes

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.

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.

Due to the rarity of the condition, it's difficult to reliably estimate statistics. However, a 2006 study which followed 7 cases over an average of 8.5 years noted that "In general, cherubism does not have a poor prognosis. It has been noted that the condition does not progress beyond puberty. As the patient grows to adulthood, the jawbone lesions tend to resolve, and a progressively more normal jaw configuration is noted.".

At the Mayo Clinic, MGUS transformed into multiple myeloma or similar lymphoproliferative disorder at the rate of about 1-2% a year, or 17%, 34%, and 39% at 10, 20, and 25 years, respectively, of follow-up—among surviving patients. However, because they were elderly, most patients with MGUS died of something else and did not go on to develop multiple myeloma. When this was taken into account, only 11.2% developed lymphoproliferative disorders.

Kyle studied the prevalence of myeloma in the population as a whole (not clinic patients) in Olmsted County, Minnesota. They found that the prevalence of MGUS was 3.2% in people above 50, with a slight male predominance (4.0% vs. 2.7%). Prevalence increased with age: of people over 70 up to 5.3% had MGUS, while in the over-85 age group the prevalence was 7.5%. In the majority of cases (63.5%), the paraprotein level was <1 g/dl, while only a very small group had levels over 2 g/dl. A study of monoclonal protein levels conducted in Ghana showed a prevalence of MGUS of approximately 5.9% in African men over the age of 50.

In 2009, prospective data demonstrated that all or almost all cases of multiple myeloma are preceded by MGUS. In addition to multiple myeloma, MGUS may also progress to Waldenström's macroglobulinemia, primary amyloidosis, B-cell lymphoma, or chronic lymphocytic leukemia.

Schnitzler syndrome is a rare disease characterised by chronic hives (urticaria) and periodic fever, bone pain and joint pain (sometimes with joint inflammation), weight loss, malaise, fatigue, swollen lymph glands and enlarged spleen and liver.

The urticarial rash is non-itching in more than half of cases, which is unusual for hives. It is most prominent on the trunk, arms and legs, sparing the palms, soles, head and neck. Associated angioedema has been reported in a few patients. A review of 94 cases found a mean age at onset of 51 years, and only four patients developed symptoms before the age of 35. The cause and disease mechanism of Schnitzler syndrome remain largely unknown.

Schnitzler syndrome is considered an autoinflammatory and autoimmune disorder. Chronic hives and a monoclonal gammopathy have been proposed as the major criteria, while the others represent minor criteria.

Respiratory complications are often cause of death in early infancy.

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.

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.

Plasmacytomas are a rare form of cancer. SPB is the most common form of the disease and accounts for 3-5% of all plasma cell malignancies. The median age at diagnosis for all plasmacytomas is 55. Both SPB and extramedullary plasmacytoma are more prevalent in males; with a 2:1 male to female ratio for SPB and a 3:1 ratio for extramedullary plasmacytoma.

The first gene that could cause the syndrome is described recently and is called NF1X (chromosome 19: 19p13.1).

Stress fractures can occur at many sites in the body; "march fracture" simply refers to a stress fracture specifically of the metatarsals, so named because the injury is sometimes sustained by soldiers during sustained periods of marching. Although march fractures can occur to the 5th metatarsal, fractures of this bone are more likely to be trauma-related fractures to the diaphysis, termed Jones fractures. In runners, march fracture occurs most often in the metatarsal neck, while in dancers it occurs in the proximal shaft. In ballet dancers, fracture mostly occurs at the base of the second metatarsal and at Lisfranc joints. This fracture always occurs following a prolonged stress or weight bearing, and the history of direct trauma is very rare. Consideration should always be given to osteoporosis and osteomalacia. Cavus feet are a risk factor for march fracture.

In children, whose bones are still developing, there are risks of either a growth plate injury or a greenstick fracture.

- A greenstick fracture occurs due to mechanical failure on the tension side. That is, since the bone is not so brittle as it would be in an adult, it does not completely fracture, but rather exhibits bowing without complete disruption of the bone's cortex in the surface opposite the applied force.

- Growth plate injuries, as in Salter-Harris fractures, require careful treatment and accurate reduction to make sure that the bone continues to grow normally.

- Plastic deformation of the bone, in which the bone permanently bends, but does not break, also is possible in children. These injuries may require an osteotomy (bone cut) to realign the bone if it is fixed and cannot be realigned by closed methods.

- Certain fractures mainly occur in children, including fracture of the clavicle and supracondylar fracture of the humerus.

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.

Smokers generally have lower bone density than non-smokers, so have a much higher risk of fractures. There also is evidence that smoking delays bone healing.

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.

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.

Erythema marginatum is a type of erythema (redness of the skin or mucous membranes) involving pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months. It is found primarily on extensor surfaces.

An association with bradykinin has been proposed in the case of hereditary angioedema.