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.

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.

The deformities are managed surgically to preserve the function of the limb.

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).

Non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are most used in PDP treatment. These drugs inhibit cyclo-oxygenase activity and thereby prostaglandin synthesis. Since PGE is likely to be involved in periosteal bone formation and acroosteolysis, this is why these drugs can alleviate the polyarthritis associated with PDP. In addition, NSAIDs and corticosteroids decrease formation of inflammatory mediators, reducing inflammation and pain. In case of possible gastropathy, the COX-2 selective NSAID etorixocib is preferred.

Infliximab can reduce pain and arthritis in PDP. It is a monoclonal antibody that blocks the biological action of TNF-α (tumor necrosis factor-alpha). TNF-α is an inflammatory cytokine found in high levels in PDP and it is involved in the production of other inflammatory mediators which increase the expression of RANKL. RANKL is thought to increase bone resorption.

Retinoids are used to improve skin manifestations. Retinoids can act on retinoid nuclear receptors and thus regulate transcription. For example, isotretinoin, the most effective drug to treat acne, improves cosmetic features by inducing apoptosis within human sebaceous glands. As a result of this, the increase of connective tissue and hyperplasia of the sebaceous glands is inhibited. Retinoids also decrease procollagen mRNA in fibroblasts, improving pachyderma.

Like retinoids, colchicines can also improve skin manifestations. It is able to bind to the ends of microtubules to prevent its elongation. Because microtubules are involved in cell division, signal transduction and regulation of gene expression, colchicine can inhibit cell division and inflammatory processes (e.g. action of neutrophils and leukocytes). It is suggested that colchicine inhibit chemotactic activity of leukocytes, which leads to reduction of pachydermia.

Use of botulinum toxin type A (BTX-A) improved leonine facies of patients. BTX-A inhibits release of acetylcholine acting at the neuromuscular junction. Furthermore, it blocks cholinergic transmission to the sweat glands and therefore inhibits sweat secretion. However, the exact mechanism for improving leonine faces is unknown and needs to be further investigated.

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.

While Larsen syndrome can be lethal if untreated, the prognosis is relatively good if individuals are treated with orthopedic surgery, physical therapy, and other procedures used to treat the symptoms linked with Larsen syndrome.

Treatment for Larsen syndrome varies according to the symptoms of the individual. Orthopedic surgery can be performed to correct the serious joint defects associated with Larsen syndrome. Reconstructive surgery can be used to treat the facial abnormalities. Cervical kyphosis can be very dangerous to an individual because it can cause the vertebrae to disturb the spinal cord. Posterior cervical arthrodesis has been performed on patients with cervical kyphosis, and the results have been successful Propranolol has been used to treat some of the cardiac defects associated with Marfan's syndrome, so the drug also has been suggested to treat cardiac defects associated with Larsen syndrome.

CDPX1 activity may be inhibited by warfarin because it is believed that ARSE has enzymatic activity in a vitamin K producing biochemical pathway. Vitamin K is also needed for controlling binding of calcium to bone and other tissues within the body.

The most common method to manage hypoglycemia and diabetes is with an insulin pump. . However in infants and very young children long acting insulins like Glargine and Levemir are preferred to prevent recurrent hypoglycemia . As soon as parent knows Walcott-Rallison syndrome is the source, treatment or therapy plans need to be drawn up along with frequent check ins to make sure kidney and liver functions are around normal and insulin therapy are working. If needed, the patient can undergo thyroxin therapy in order to maintain proper thyroid stimulating hormone levels. This has only been needed in a few cases were hypothyroidism was present in the patient.

Treatment of Gorham's disease is for the most part palliative and limited to symptom management.

Sometimes the bone destruction spontaneously ceases and no treatment is required. But when the disease is progressive, aggressive intervention may be necessary. Duffy and colleagues reported that around 17% of patients with Gorham's disease in the ribs, shoulder, or upper spine experience extension of the disease into the chest, leading to chylothorax with its serious consequences, and that the mortality rate in this group can reach as high as 64% without surgical intervention.

A search of the medical literature reveals multiple case reports of interventions with varying rates of success as follows:

Cardiothoracic (heart & lung):

- Pleurodesis

- Ligation of thoracic duct

- Pleurperitoneal shunt

- Radiation therapy

- Pleurectomy

- Surgical resection

- Thalidomide

- Interferon alpha-2b

- TPN (total parenteral nutrition)

- Thoracentesis

- Diet rich in medium-chain triglycerides and protein

- Chemotherapy

- Sclerotherapy

- Transplantation

Skeletal:

- Interferon alpha-2b

- Bisphosphonate (e.g. pamidronate)

- Surgical resection

- Radiation therapy

- Sclerotherapy

- Percutaneous bone cement

- Bone graft

- Prosthesis

- Surgical stabilization

- Amputation

To date, there are no known interventions that are consistently effective for Gorham's and all reported interventions are considered experimental treatments, though many are routine for other conditions. Some patients may require a combination of these approaches. Unfortunately, some patients will not respond to any intervention.

Medical management of OFC consists of Vitamin D treatment, generally alfacalcidol or calcitriol, delivered intravenously. Studies have shown that in cases of OFC caused by either end-stage renal disease or primary hyperparathyoidism, this method is successful not only in treating underlying hyperparathyoidism, but also in causing the regression of brown tumors and other symptoms of OFC.

In especially severe cases of OFC, parathyroidectomy, or the full removal of the parathyroid glands, is the chosen route of treatment. Parathyroidectomy has been shown to result in the reversal of bone resorption and the complete regression of brown tumors. In situations where parathyroid carcinoma is present, surgery to remove the tumors has also led to the regression of hyperparathyroidism as well as the symptoms of OFC.

Bone transplants have proven successful in filling the lesions caused by OFC. A report showed that in 8 out of 11 instances where cavities caused by OFC were filled with transplanted bone, the lesion healed and the transplanted bone blended rapidly and seamlessly with the original bone.

Pacman dysplasia (alternatively known as epiphyseal stippling with osteoclastic hyperplasia) is a lethal autosomal recessive skeletal dysplasia. The dysplasia is present during fetal development.

Chondroblastoma has not been known to spontaneously heal and the standard treatment is surgical curettage of the lesion with bone grafting. To prevent recurrence or complications it is important to excise the entire tumor following strict oncologic criteria. However, in skeletally immature patients intraoperative fluoroscopy may be helpful to avoid destruction of the epiphyseal plate. In patients who are near the end of skeletal growth, complete curettage of the growth plate is an option. In addition to curettage, electric or chemical cauterization (via phenol) can be used as well as cryotherapy and wide or marginal resection. Depending on the size of the subsequent defect, autograft or allograft bone grafts are the preferred filling materials. Other options include substituting polymethylmethacrylate (PMMA) or fat implantation in place of the bone graft. The work of Ramappa "et al" suggests that packing with PMMA may be a more optimal choice because the heat of polymerization of the cement is thought to kill any remaining lesion.

Both radiotherapy and chemotherapy are not commonly used. Radiotherapy has been implemented in chondroblastoma cases that are at increased risk of being more aggressive and are suspected of malignant transformation. Furthermore, radiofrequency ablation has been used, but is typically most successful for small chondroblastoma lesions (approximately 1.5 cm). Treatment with radiofrequency ablation is highly dependent on size and location due to the increased risk of larger, weight-bearing lesions being at an increased risk for articular collapse and recurrence.

Overall, the success and method of treatment is highly dependent upon the location and size of the chondroblastoma.

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.

If there is a high probability of a fracture resulting from the unicameral bone cyst, then surgical treatment is necessary. Specific methods can be determined by the physician based upon the patient’s age, medical history, tolerance for certain medical procedures or medicine, health, and extremity of the disease. The treatment can involve or incorporate one or more of the following surgical methods, which are performed by a pediatric orthopedic surgeon:

- Curettage:

- Bone Grafting:

- Steroid injection:

If a patient needs to be treated with surgery, a standard surgical procedure would be called for; the patient would be resting in Fowler’s position, a semi-sitting position, under general anesthesia. The exact size, shape, and distance between the acromion to the midpoint of the cyst are measured by a digital radiograph or MRI scan. A small, longitudinal skin incision, about 1 cm long, is made at the center of the cyst. Next, by using a trephine or drill bit, a small aperture is made inside the incision. Fluids contained in the cyst are drained and curved, metal impactors are used to break any septa, or membranes, within the cyst. Curettes are then used to remove the entire cyst from the diaphysis. After the removal of the cystic membrane, a 95% ethanol solution is injected into the cavity to produce a chemical cauterization to burn away any residual active membrane for 30 seconds and then aspirated. Saline solution is then immediately injected into the cavity to wash out any residual ethanol solution and to mitigate any damage to healthy tissue; this irrigation process of ethanol and saline solutions is repeated for another 2 to 3 times. A curved impactor is inserted into the cavity and used to penetrate the boundary between the cyst and bone marrow; the intentional penetrations will allow bone marrow cells to migrate into the cavity to produce a source of osteoinductive cells, cells that induce bony growth. Furthermore, the cavity is completely filled with bone graft substitute, such as calcium sulfate. Finally, one cannulated screw is placed into the aperture.

Spondyloepimetaphyseal dysplasia, Pakistani type is a form of spondyloepimetaphyseal dysplasia involving "PAPSS2" (also known as "ATPSK2"). The condition is rare.

They are benign lesions and malignant degeneration is rare. They are usually treated with curettage which however have a high recurrence rate of 25%. As such if an en-bloc resection is possible this is advisable

Autoimmune polyendocrine syndrome type 1 treatment is based on the symptoms that are presented by the affected individual, additionally there is:

- Hormone replacement

- Systemic antifungal treatment

- Immunosuppressive treatment

Autosomal recessive multiple epiphyseal dysplasia (ARMED), also called epiphyseal dysplasia, multiple, 4 (EDM4), multiple epiphyseal dysplasia with clubfoot or –with bilayered patellae, is an autosomal recessive congenital disorder affecting cartilage and bone development. The disorder has relatively mild signs and symptoms, including joint pain, scoliosis, and malformations of the hands, feet, and knees.

Some affected individuals are born with an inward- and downward-turning foot (a clubfoot). An abnormality of the kneecap called a double-layered patella is also relatively common. Although some people with recessive multiple epiphyseal dysplasia have short stature as adults, most are of normal height. The incidence is unknown as many cases are not diagnosed due to mild symptoms.

Gerodermia osteodysplastica (GO), also called geroderma osteodysplasticum and Walt Disney dwarfism, is a rare autosomal recessive connective tissue disorder included in the spectrum of cutis laxa syndromes.

Usage of the name "Walt Disney dwarfism" is attributed to the first known case of the disorder, documented in a 1950 journal report, in which the authors described five affected members from a Swiss family as having the physical appearance of dwarves from a Walt Disney film.

The terms "geroderma" or "gerodermia" can be used interchangeably with "osteodysplastica" or "osteodysplasticum", with the term "hereditaria" sometimes appearing at the end.

This condition is a skeletal dysplasia characterized by short stature, mild brachydactyly, kyphoscoliosis, abnormal gait, enlarged knee joints, precocious osteoarthropathy, platyspondyly, delayed epiphyseal ossification, mild metaphyseal abnormalities, short stature and short and bowed legs. Intelligence is normal.

Some patients may manifest premature pubarche and hyperandrogenism.

Other features that may form part of the syndrome include precocious costal calcification, small iliac bones, short femoral necks, coxa vara, short halluces and fused vertebral bodies.

Ollier disease is a rare nonhereditary sporadic disorder where intraosseous benign cartilaginous tumors (enchondroma) develop close to growth plate cartilage. Prevalence is estimated at around 1 in 100,000.