There is no cure. Maintaining a healthy lifestyle by exercising and avoiding smoking can help prevent fractures. Treatment may include care of broken bones, pain medication, physical therapy, braces or wheelchairs, and surgery. A type of surgery that puts metal rods through long bones may be done to strengthen them.

Bone infections are treated as and when they occur with the appropriate antibiotics and antiseptics.

In 1998, a clinical trial demonstrated the effectiveness of intravenous pamidronate, a bisphosphonate which had previously been used in adults to treat osteoporosis. In severe OI, pamidronate reduced bone pain, prevented new vertebral fractures, reshaped previously fractured vertebral bodies, and reduced the number of long-bone fractures.

Although oral bisphosphonates are more convenient and cheaper, they are not absorbed as well, and intravenous bisphosphonates are generally more effective, although this is under study. Some studies have found oral and intravenous bisphosphonates, such as oral alendronate and intravenous pamidronate, equivalent. In a trial of children with mild OI, oral risedronate increased bone mineral densities, and reduced nonvertebral fractures. However, it did not decrease new vertebral fractures. A Cochrane review in 2016 concluded that though bisphosphonates seem to improve bone mineral density, it is uncertain whether this leads to a reduction in fractures or an improvement in the quality of life of individuals with osteogenesis imperfecta.

Bisphosphonates are less effective for OI in adults.

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).

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.

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.

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.

There is no known cure for achondroplasia even though the cause of the mutation in the growth factor receptor has been found. Although used by those without achondroplasia to aid in growth, human growth hormone does not help people with achondroplasia. However, if desired, the controversial surgery of limb-lengthening will lengthen the legs and arms of someone with achondroplasia.

Usually, the best results appear within the first and second year of therapy. After the second year of growth hormone therapy, beneficial bone growth decreases. Therefore, GH therapy is not a satisfactory long term treatment.

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.

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.

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.

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.

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.

Camurati–Engelmann disease is somewhat treatable. Glucocorticosteroids, which are anti-inflammatory and immunosuppressive agents, are used in some cases. This form of medication helps in bone strength, however can have multiple side effects. In several reports, successful treatment with glucocoricosteroids was described, as certain side effects can benefit a person with CED. This drug helps with pain and fatigue as well as some correction of radiographic abnormalities.

Alternative treatments such as massage, relaxation techniques (meditation, essential oils, spa baths, music therapy, etc.), gentle stretching, and especially heat therapy have been successfully used to an extent in conjunction with pain medications. A majority of CED patients require some form of analgesics, muscle relaxant, and/or sleep inducing medication to manage the pain, specifically if experiencing frequent or severe 'flare-ups' (e.g. during winter).

Treatment for CLSD is largely focused on treating the symptoms of the disorder, because it is still in the early stages of research. Symptomatic treatment is also the only option due to the genetic nature of the disorder. Treatment may include surgeries to correct facial and cranial dysmorphisms or therapy sessions to help alleviate behavioral abnormalities associated with the disorder.

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

Osteochondromas are benign lesions and do not affect life expectancy. Complete excision of osteochondroma is curative and the reoccurrences take place when the removal of tumor is incomplete. Multiple reoccurrences in a well-excised lesion indicate that it may be malignant. The risk of malignant transformation takes place in 1–5% of individuals. If any symptoms of cancerous tumor takes place, then the patient should be evaluated by a bone specialist. No treatment is necessary for Solitary osteochondromas that are asymptomatic. Treatments for solitary osteochondroma are careful observation over time and taking regular x-rays to monitor any changes in the tumor. If the lesion is causing pain with activity, nerve or vessel impingement, or if the bone growth has fully matured and the presence of a large cartilage cap is prominent, then it is advised that the tumor be surgically removed.

Osteochondromas have a low rate of malignancy (<1%) and resection of the tumor is suggested if symptoms such as pain, limitation of movement, or impingement on nerves or vessels occur. Resection of the tumor also takes place when the tumor increases in size and progresses towards malignancy. During surgical resection, the entire lesion along with the cartilaginous cap should be removed to minimize any chances of reoccurrences. Surgical treatment becomes the sole treatment of choice if common complications such as fractures, symptoms of peripheral nerves such as paresthesia, paraplegia, peroneal neuropathy, and upper limb neuropathy take place. A prophylactic resection is suggested if the lesion lies next to a vessel.

Depending on the size and location of the tumor, the time it takes to return to normal daily activities varies between individuals. Limitation on some activities is advised if pain or discomfort persists after surgical excision.

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.

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.

Though the children affected with CLSD will have problems throughout life, the treatment for this disease thus far is symptomatic. However, prognosis is good; at the time of the most recently published articles, identified children were still alive at over 4 years of age.

Mutant proteins still maintain some residual activity, allowing for the release of some collagen, but still form an extremely distended endoplasmic reticulum.

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.

Endodontic intervention can help conserve the existing health of affected permanent teeth. It is difficult to perform an endodontic therapy on teeth that develop abscesses as a resultant of obliteration of the pulp chambers and root canals. An alternative to conventional therapy would be retrograde filling and periapical curettage. However, these therapies are not recommended for teeth with roots that are too short.

Treatment is usually supportive treatment, that is, treatment to reduce any symptoms rather than to cure the condition.

- Enucleation of the odontogenic cysts can help, but new lesions, infections and jaw deformity are usually a result.

- The severity of the basal-cell carcinoma determines the prognosis for most patients. BCCs rarely cause gross disfigurement, disability or death .

- Genetic counseling

The cost of treatment depends on the amount of growth hormone given, which in turn depends on the child's weight and age. One year's worth of drugs normally costs about US $20,000 for a small child and over $50,000 for a teenager. These drugs are normally taken for five or more years.