Because Cherubism changes and improves over time the treatment should be individually determined. Generally moderate cases are watched until they subside or progress into the more severe range. Severe cases may require surgery to eliminate bulk cysts and fibrous growth of the maxilla and mandible. Surgical bone grafting of the cranial facial bones may be successful on some patients. Surgery is preferred for patients ages 5 to 15. Special consideration should be taken when operating on the face to avoid the marginal mandibular branch of the facial nerve as well as the zygomatic branch of the facial nerve. Unintentional damage to these nerves can decrease muscle strength in the face and mandible region. Orthodontic treatment is generally required to avoid permanent dental problems arising from malocclusive bite, misplaced, and unerupted permanent teeth. Orthodontic treatment may be used to erupt permanent teeth that have been unable to descend due to lesions and cysts being in their path of eruption. Patients with orbital issues of diplopia, eye proptosis, and visual loss will require ophthalmologic treatment.

Curettage is performed on some patients, and is sufficient for inactive lesions. The recurrence rate with curettage is significant in active lesions, and marginal resection has been advised. Liquid nitrogen, phenol, methyl methacrylate are considered for use to kill cells at margins of resected cyst.

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.

There is no cure or approved treatment for FOP. Attempts to surgically remove the bone result in explosive bone growth. While under anesthesia, people with FOP may encounter difficulties with intubation, restrictive pulmonary disease, and changes in the electrical conduction system of the heart. Activities that increase the risk of falling or soft tissue injury should be avoided, as even minor trauma may provoke heterotopic bone formation.

The only effective line of treatment for malignant infantile osteopetrosis is hematopoietic stem cell transplantation. It has been shown to provide long-term disease-free periods for a significant percentage of those treated; can impact both hematologic and skeletal abnormalities; and has been used successfully to reverse the associated skeletal abnormalities.

Radiographs of at least one case with malignant infantile osteopetrosis have demonstrated bone remodeling and recanalization of medullar canals following hematopoietic stem cell transplantation. This favorable radiographic response could be expected within one year following the procedure - nevertheless, primary graft failure can prove fatal.

Around 5 years of age, surgical correction may be necessary to prevent any worsening of the deformity. If the mother has dysplasia, caesarian delivery may be necessary. Craniofacial surgery may be necessary to correct skull defects. Coxa vara is treated by corrective femoral osteotomies. If there is brachial plexus irritation with pain and numbness, excision of the clavicular fragments can be performed to decompress it. In case of open fontanelle, appropriate headgear may be advised by the orthopedist for protection from injury.

The disorder is progressive, with the ultimate severity of symptoms often depending on age of onset. In severe cases amputation has been performed when conservative measures such as physical therapy and regional anesthetics have been ineffective.

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.

Symptomatic individuals should be seen by an orthopedist to assess the possibility of treatment (physiotherapy for muscular strengthening, cautious use of analgesic medications such as nonsteroidal anti-inflammatory drugs). Although there is no cure, surgery is sometimes used to relieve symptoms. Surgery may be necessary to treat malformation of the hip (osteotomy of the pelvis or the collum femoris) and, in some cases, malformation (e.g., genu varum or genu valgum). In some cases, total hip replacement may be necessary. However, surgery is not always necessary or appropriate.

Sports involving joint overload are to be avoided, while swimming or cycling are strongly suggested. Cycling has to be avoided in people having ligamentous laxity.

Weight control is suggested.

The use of crutches, other deambulatory aids or wheelchair is useful to prevent hip pain. Pain in the hand while writing can be avoided using a pen with wide grip.

Several studies have reported that life expectancy appears to be normal for people with CCD.

Clinical trials of isotretinoin, etidronate with oral corticosteroids, and perhexiline maleate have failed to demonstrate effectiveness, though the variable course of the disease and small prevalence induces uncertainty.

A handful of pharmaceutical companies focused on rare disease are currently in varying stages of investigation into different therapeutic approaches for FOP.

In August 2015, U.S. Food and Drug Administration (FDA) Office of Orphan Products Development granted La Jolla Pharmaceuticals orphan drug designation for two novel compounds for FOP. The compounds are small-molecule kinase inhibitors designed to selectively block ACVR1 (ALK2).

In August 2015, Clementia Pharmaceuticals also began the enrollment of children (ages 6 and above) into its Phase II clinical trial investigating palovarotene for the treatment of FOP. Preclinical studies demonstrated that palovarotene, a retinoic acid receptor gamma agonist, blocked abnormal bone formation in animal models via inhibition of secondary messenger systems in the BMP pathway. Clementia licensed palovarotene from Roche Pharmaceuticals, which previously evaluated the compound in more than 800 individuals including healthy volunteers and patients with chronic obstructive pulmonary disease. Palovarotene received Fast Track designation from the U.S. Food and Drug Administration (FDA) and orphan designations for the treatment of FOP from both the FDA and the European Medicines Agency (EMA).

In September 2015, Regeneron announced new insight into the mechanism of disease involving the activation of the ACVR1 receptor by activin A. In 2016, the company initiated a phase 1 study of its activin antibody, REGN 2477, in healthy volunteers; a phase 2 trial in FOP patients is planned for 2017.

Another potential therapeutic approach involves allele-specific RNA interference that targets mutated mRNA for degradation while preserving normal ACVR1 gene expression.

Further investigation into the mechanisms of heterotopic bone formation in FOP could aid in the development of treatments for other disorders involving extra-skeletal bone formation.

Because kniest dysplasia can affect various body systems, treatments can vary between non-surgical and surgical treatment. Patients will be monitored over time, and treatments will be provided based on the complications that arise.

Like treatment options, the prognosis is dependent on the severity of the symptoms. Despite the various symptoms and limitations, most individuals have normal intelligence and can lead a normal life.

The only treatment for this disorder is surgery to reduce the compression of cranial nerves and spinal cord. However, bone regrowth is common since the surgical procedure can be technically difficult. Genetic counseling is offered to the families of the people with this disorder.

There is currently no cure for pseudoachondroplasia. However, management of the various health problems that result from the disorder includes medications such as analgesics (painkillers) for joint discomfort, osteotomy for lower limb deformities, and the surgical treatment of scoliosis. Prevention of some related health problems includes physical therapy to preserve joint flexibility and regular examinations to detect degenerative joint disease and neurological manifestations (particularly spinal cord compression). Additionally, healthcare providers recommend treatment for psychosocial issues related to short stature and other physical deformities for both affected individuals and their families (OMIM 2008).

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.

Because newborns can breathe only through their nose, the main goal of postnatal treatment is to establish a proper airway. Primary surgical treatment of FND can already be performed at the age of 6 months, but most surgeons wait for the children to reach the age of 6 to 8 years. This decision is made because then the neurocranium and orbits have developed to 90% of their eventual form. Furthermore, the dental placement in the jaw has been finalized around this age.

Treatment usually involves surgical removal of the lesion down to the bone. If there are any adjacent teeth, they are cleaned thoroughly to remove any possible source of irritation. Recurrence is around 16%.

The fibrocartilaginous effects of fibrochondrogenesis on chondrocytes has shown potential as a means to produce therapeutic cellular biomaterials via tissue engineering and manipulation of stem cells, specifically human embryonic stem cells.

Utilization of these cells as curative cartilage replacement materials on the cellular level has shown promise, with beneficial applications including the repair and healing of damaged knee menisci and synovial joints; temporomandibular joints, and vertebra.

Structural nasal deformities are corrected during or shortly after the facial bipartition surgery. In this procedure, bone grafts are used to reconstruct the nasal bridge. However, a second procedure is often needed after the development of the nose has been finalized (at the age of 14 years or even later).

Secondary rhinoplasty is based mainly on a nasal augmentation, since it has been proven better to add tissue to the nose than to remove tissue. This is caused by the minimal capacity of contraction of the nasal skin after surgery.

In rhinoplasty, the use of autografts (tissue from the same person as the surgery is performed on) is preferred. However, this is often made impossible by the relative damage done by previous surgery. In those cases, bone tissue from the skull or the ribs is used. However, this may give rise to serious complications such as fractures, resorption of the bone, or a flattened nasofacial angle.

To prevent these complications, an implant made out of alloplastic material could be considered. Implants take less surgery time, are limitlessly available and may have more favorable characteristics than autografts. However, possible risks are rejection, infection, migration of the implant, or unpredictable changes in the physical appearance in the long term.

At the age of skeletal maturity, orthognathic surgery may be needed because of the often hypoplastic maxilla. Skeletal maturity is usually reached around the age of 13 to 16. Orthognathic surgery engages in diagnosing and treating disorders of the face and teeth- and jaw position.

Non-surgical interventions include three elements: weight control, exercise control, and medication. Canine massage may alleviate discomfort and help move lymph and nutrients through the system. Weight control is often "the single most important thing that we can do to help a dog with arthritis", and consequentially "reducing the dog's weight is enough to control all of the symptoms of arthritis in many dogs". Reasonable exercise stimulates cartilage growth and reduces degeneration (though excessive exercise can do harm too), and also regular long walks in early or mild dysplasia can help prevent loss of muscle mass to the hips. Medication can reduce pain and discomfort, and also reduce damaging inflammation.

Non-surgical intervention is usually via a suitable non-steroidal anti-inflammatory drug (NSAID) which doubles as an anti-inflammatory and painkiller. Typical NSAIDs used for hip dysplasia include carprofen and meloxicam (often sold as Rimadyl and Metacam respectively), both used to treat arthritis resulting from dysplasia, although other NSAIDs such as tepoxalin (Zubrin) and prednoleucotropin ("PLT", a combination of cinchophen and prednisolone) are sometimes tried. NSAIDs vary dramatically between species as to effect: a safe NSAID in one species may be unsafe in another. It is important to follow veterinary advice.

A glucosamine-based nutritional supplement may give the body additional raw materials used in joint repair. Glucosamine can take 3–4 weeks to start showing its effects, so the trial period for medication is usually at least 3–5 weeks. In vitro, glucosamine has been shown to have negative effects on cartilage cells.

It is also common to try multiple anti-inflammatories over a further 4–6 week period, if necessary, since an animal will often respond to one type but fail to respond to another. If one anti-inflammatory does not work, a vet will often try one or two other brands for 2–3 weeks each, also in conjunction with ongoing glucosamine, before concluding that the condition does not seem responsive to medication.

Carprofen, and other anti-inflammatories in general, whilst very safe for most animals, can sometimes cause problems for some animals, and (in a few rare cases) sudden death through liver toxicity. This is most commonly discussed with carprofen but may be equally relevant with other anti-inflammatories. As a result, it is often recommended to perform monthly (or at least, twice-annually) blood tests to confirm that the animal is not reacting adversely to the medications. Such side effects are rare but worth being aware of, especially if long-term use is anticipated.

This regimen can usually be maintained for the long term, as long as it is effective in keeping the symptoms of dysplasia at bay.

Some attempts have been made to treat the pain caused by arthritic changes through the use of "laser therapy", in particular "class IV laser therapy". Well-controlled clinical trials are unfortunately lacking, and much of the evidence for these procedures remains anecdotal.

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.

Treatment is supportive.

- The aplastic anemia and immunodeficiency can be treated by bone marrow transplantation.

- Supportive treatment for gastrointestinal complications and infections.

- Genetic counselling.

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.

Mesenchymal stem cells (MSCs) have been used for a number of years to treat osteoarthritis. Their use has mostly been autologous (self); used fresh (in the form of a mixed cell population mainly sourced from adipose tissue), or expanded in number via culture; or allogeneic (non-self). The majority of their action via a paracrine effect, and hence the route of administration has been mostly via intra-articular injection. In vitro, this paracrine effect has been shown to enhance type II collagen expression in OA chondrocytes while decreasing matrix metalloproteinase activity (MMP-3 and MMP-13). In clinical cases, this has been shown via their anti-inflammatory/pain relieving effects. Dogs treated with adipose derived stem cell therapy have had significantly improved scores for lameness and compiled scores for pain and range of motion compared with control dogs. Other randomised studies have shown similar improved results with functional limitation, range of motion, and owner and veterinary investigator visual analogue scale for pain all showing improvement. Beyond this, significant improvements in MSC treated animals as measured by peak vertical force and vertical impulse in force platform have been observed.

Patient-side autologous therapy in the US is subject to change. New guidance issued (FDA#218 Guidance for Industry - Cell-Based Products for Animal Use) will likely require stem cell therapy to be produced via cGMP. Resources required to implement these changes may change the US veterinary stem cell industry more towards a hub and spoke approach or towards allogeneic therapy, and away from patient-side therapy.