Treatment in fibrous dysplasia is mainly palliative, and is focused on managing fractures and preventing deformity. There are no medications capable of altering the disease course. Intravenous bisphosphonates may be helpful for treatment of bone pain, but there is no clear evidence that they strengthen bone lesions or prevent fractures. Surgical techniques that are effective in other disorders, such as bone grafting, curettage, and plates and screws, are frequently ineffective in fibrous dysplasia and should be avoided. Intramedullary rods are generally preferred for management of fractures and deformity in the lower extremities. Progressive scoliosis can generally be managed with standard instrumentation and fusion techniques. Surgical management in the craniofacial skeleton is complicated by frequent post-operative FD regrowth, and should focus on correction of functional deformities. Prophylactic optic nerve decompression increases the risk of vision loss and is contraindicated.

Managing endocrinopathies is a critical component of management in FD. All patients with fibrous dysplasia should be evaluated and treated for endocrine diseases associated with McCune–Albright syndrome. In particular untreated growth hormone excess may worsen craniofacial fibrous dysplasia and increase the risk of blindness. Untreated hypophosphatemia increases bone pain and risk of fractures.

Fibrous dysplasia is a disorder where normal bone and marrow is replaced with fibrous tissue, resulting in formation of bone that is weak and prone to expansion. As a result, most complications result from fracture, deformity, functional impairment, and pain. Disease occurs along a broad clinical spectrum ranging from asymptomatic, incidental lesions to severe disabling disease. Disease can affect one bone (monostotic) or multiple (polyostotic), and may occur in isolation or in combination with cafe-au-lait skin macules and hyperfunctioning endocrinopathies, termed McCune-Albright syndrome. More rarely, fibrous dysplasia may be associated with intramuscular myxomas, termed Mazabraud's syndrome. Fibrous dysplasia is very rare, and there is no known cure. Fibrous dysplasia is not a form of cancer.

Recurrence rate of solid form of tumour is lower than classic form.

Polyostotic fibrous dysplasia is a form of fibrous dysplasia affecting more than one bone.

McCune-Albright syndrome includes polyostotic fibrous dysplasia as part of its presentation.

One treatment that has been used is bisphosphonates.

Monostotic fibrous dysplasia (or monostotic osteitis fibrosa) is a form of fibrous dysplasia where only one bone is involved. It comprises a majority of the cases of fibrous dysplasia.

A rare bone disorder characterized by benign bone growths which can cause very painful swellings and bone deformities and makes bone prone to fractures.

It is common in age group of 10–30 years. It is second most common tumor of spine and commonest benign tumor of pelvis in pediatric population. Incidence is slightly more in males than females (1.3:1).

Osteogenesis imperfecta is a rare condition in which bones break easily. There are multiple genetic mutations in different genes for collagen that may result in this condition. It can be treated with some drugs to promote bone growth, by surgically implanting metal rods in long bones to strengthen them, and through physical therapy and medical devices to improve mobility.

Osteofibrous dysplasia is treated with marginal resection with or without bone grafting, depending on the size of the lesion and the extent of bony involvement. However, due to the high rate of recurrence in skeletally immature individuals, this procedure is usually postponed until skeletal maturity.

Osteochondrodysplasia or skeletal dysplasia is a general term for a disorder of the development (dysplasia) of bone ("osteo") and cartilage ("chondro").

Osteochondrodysplasias are rare diseases. About 1 in 5,000 babies are born with some type of skeletal dysplasia.

Some studies suggest a hormonal link. Specifically, the hormone relaxin has been indicated.

A genetic factor is indicated since the trait runs in families and there is an increased occurrence in some ethnic populations (e.g., Native Americans, Lapps / Sami people). A locus has been described on chromosome 13. Beukes familial dysplasia, on the other hand, was found to map to an 11-cM region on chromosome 4q35, with nonpenetrant carriers not affected.

Determining the incidence can be difficult. In addition there is a wide margin in diagnostic results. A German study comparing two methods resulted in twice the usual rate for one method. The condition is eight times more frequent in females than in males.

Native Americans are more likely to have congenital hip dislocation than any of the other races. The risk for Native Americans is about 25-50 in 1000. The overall frequency of developmental dysplasia of the hip is approximately 1 case per 1000 individuals; however, Barlow believed that the incidence of hip instability in newborns can be as high as 1 case for every 60 newborns. Though this rate drops to 1:240 at one week.

Fibrochondrogenesis is quite rare. A 1996 study from Spain determined a national minimal prevalence for the disorder at 8 cases out of 1,158,067 live births.

A United Arab Emirates (UAE) University report, from early 2003, evaluated the results of a 5-year study on the occurrence of a broad range of osteochondrodysplasias. Out of 38,048 newborns in Al Ain, over the course of the study period, fibrochondrogenesis was found to be the most common of the recessive forms of osteochondrodysplasia, with a prevalence ratio of 1.05:10,000 births.

While these results represented the most common occurrence within the group studied, they do not dispute the rarity of fibrochondrogenesis. The study also included the high rate of consanguinous marriages as a prevailing factor for these disorders, as well as the extremely low rate of diagnosis-related pregnancy terminations throughout the region.

Osteofibrous dysplasia (also known as ossifying fibroma) is a rare, benign non-neoplastic condition with no known cause. It is considered a fibrovascular defect. Campanacci described this condition in two leg bones, the tibia and fibula, and coined the term. This condition should be differentiated from Nonossifying fibroma and fibrous dysplasia of bone.

As of 2017, approximately 800 cases of FOP have been confirmed worldwide making FOP one of the rarest diseases known. The estimated incidence of FOP is 0.5 cases per million people and affects all races.

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.

Fibrocartilaginous mesenchymoma of bone is (FCMB) is an extremely rare tumor first described in 1984. Fewer than 20 cases have been reported, with patient ages spanning from 9 to 25 years, though a case in a male infant aged 1 year and 7 months has been reported. Quick growth and bulky size are remarkable features of this tumor.

Till date about 18 cases of Spondylocostal dysostosis have been reported in literature.

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.".

Fibrochondrogenesis is a rare autosomal recessive form of osteochondrodysplasia, causing abnormal fibrous development of cartilage and related tissues.

It is a lethal rhizomelic (malformations which result in short, underdeveloped limbs) form of dwarfism, exhibiting both skeletal dysplasia (malformations of bone) and fibroblastic dysplasia (abnormal development of fibroblasts, specialized cells that make up fibrous connective tissue, which plays a role in the formation of cellular structure and promotes healing of damaged tissues). Death caused by complications of fibrochondrogenesis occurs in infancy.

Osteoarthritis, a common symptom associated with Canine Hip Dysplasia in German Shepherds ultimately results in pain and inflammation. The causes are from bone degradation in which the bone is less rigid, cartilage dissipates and structure of joints becomes weak.

Diet can have a major impact for German Shepherds that are exposed to Canine Hip Dysplasia. Incorporating Omega-3 fatty acids such as Docosahexaenoic acid(DHA) and Eicosapentaenoic acid(EPA) into the diet can result in improved symptoms of the disease. Omega 3 fatty acids can help decrease inflammation that occurs from osteoarthritis, as well as improvement in locomotion of dogs who have the disease. EPA and DHA can be supplemented into the diet through fish oils and in return is beneficial for reducing joint inflammation.

Glucosamine and Chondroitin sulfate are Nutraceuticals that can also be added into the diet to help treat osteoarthritis and its quality of life reducing effects. Both nutraceuticals help with improvement of cartilage, joint health and repairing of tissues. This inclusion will allow for a stronger support and reduced negative effects of osteoarthritis. Another nutrient that can help improve the structural support of the body in German Shepherds is Vitamin C. Vitamin C contributes to the building blocks of collagen that can help to strengthen the joints.

Surgery is curative despite possible local relapses. Wide resection of the tumor and resection arthrodesis with an intramedullary nail, vertebrectomy and femoral head allograft replacement of the vertebral body, resection of the iliac wing and hip joint disarticulation have been among the performed procedures.

The close resemblance of FCMB to fibrocartilaginous dysplasia has suggested to some scholars that they might be closely related entities, although the latter features woven bone trabeculae without osteoblastic rimming, which is a quite distinctive aspect. Instead the occurrence of epiphyseal plate-like cartilage is peculiar of the former.

Ischiopatellar dysplasia is often considered a familial condition. Ischiopatellar dysplasia has been identified on region 5.6 cM on chromosome 17q22. Mutations in the TBX4 (T-box protein 4) gene have been found to cause ischiopatellar dysplasia due to the essential role TBX4 plays in lower limb development since TBX4 is a transcription factor.

Spondyloepimetaphyseal dysplasia is a genetic condition affecting the bones.

Types include:

- Spondyloepimetaphyseal dysplasia, Strudwick type

- Spondyloepiphyseal dysplasia congenita

- Spondyloepimetaphyseal dysplasia, Pakistani type

A recent article in 2015 reported a persistent notochord in a fetus at 23 weeks of gestation. The fetus had an abnormal spine, shortened long bones and a left clubfoot. After running postmortem tests and ultrasound, the researchers believed that the fetus suffered from hypochondrogenesis. Hypochondrogenesis is caused when type II collagen is abnormally formed due to a mutation in the COL2A1 gene. Normally, the cartilaginous notochord develops into the bony vertebrae in a human body. The COL2A1 gene results in malformed type II collagen, which is essential in the transition from collagen to bone. This is the first time that researchers found a persistent notochord in a human body due to a COL2A1 mutation.

Fibrodysplasia ossificans progressiva (FOP) is an extremely rare connective tissue disease. The disease is caused by a mutation of the body's repair mechanism, which causes fibrous tissue (including muscle, tendon, and ligament) to be ossified spontaneously or when damaged. In many cases, injuries can cause joints to become permanently frozen in place. Surgical removal of the extra bone growths has been shown to cause the body to "repair" the affected area with even more bone.