There is no known cure. In selected patients orthopaedic surgery may be helpful to try to gain some functionality of severely impaired joints.

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.

Early intervention is considered important. For infants, breathing and feeding difficulties, are monitored. Therapies used are "symptomatic and supportive."

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.

Surgical excision is performed when exostoses lead to growth disturbances or lead to disability. Knee osteotomies are associated with high incidence of peroneal nerve paralysis.

Surgery, physical therapy and pain management are currently the only options available to HME patients, but success varies from patient to patient and many struggle with pain, fatigue and mobility problems throughout their lives.

It is not uncommon for HME patients to undergo numerous surgical procedures throughout their lives to remove painful or deforming exostoses, correct limb length discrepancies or improve range of motion. Usually the treatment can be problematic. The osteochondromas can return in the same places and may be more painful.

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.

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, although curative therapy with bone marrow transplantion is being investigated in clinical trials. It is believed the healthy marrow will provide the sufferer with cells from which osteoclasts will develop. If complications occur in children, patients can be treated with vitamin D. Gamma interferon has also been shown to be effective, and it can be associated to vitamin D. Erythropoetin has been used to treat any associated anemia. Corticosteroids may alleviate both the anemia and stimulate bone resorption. Fractures and osteomyelitis can be treated as usual. Treatment for osteopetrosis depends on the specific symptoms present and the severity in each person. Therefore, treatment options must be evaluated on an individual basis. Nutritional support is important to improve growth and it also enhances responsiveness to other treatment options. A calcium-deficient diet has been beneficial for some affected people.

Treatment is necessary for the infantile form:

- Vitamin D (calcitriol) appears to stimulate dormant osteoclasts, which stimulates bone resorption

- Gamma interferon can have long-term benefits. It improves white blood cell function (leading to fewer infections), decreases bone volume, and increases bone marrow volume.

- Erythropoietin can be used for anemia, and corticosteroids can be used for anemia and to stimulate bone resorption.

Bone marrow transplantation (BMT) improves some cases of severe, infantile osteopetrosis associated with bone marrow failure, and offers the best chance of longer-term survival for individuals with this type.

In pediatric (childhood) osteopetrosis, surgery is sometimes needed because of fractures. Adult osteopetrosis typically does not require treatment, but complications of the condition may require intervention. Surgery may be needed for aesthetic or functional reasons (such as multiple fractures, deformity, and loss of function), or for severe degenerative joint disease.

The long-term-outlook for people with osteopetrosis depends on the subtype and the severity of the condition in each person.The severe infantile forms of osteopetrosis are associated with shortened life expectancy, with most untreated children not surviving past their first decade. seems to have cured some infants with early-onset disease. However, the long-term prognosis after transplantation is unknown. For those with onset in childhood or adolescence, the effect of the condition depends on the specific symptoms (including how fragile the bones are and how much pain is present). Life expectancy in the adult-onset forms is normal.

Oral phosphate, 9, calcitriol, 9; in the event of severe bowing, an osteotomy may be performed to correct the leg shape.

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.

Children who develop severe bowing before the age of 3 may be treated with knee ankle foot orthoses. However, bracing may fail, or bowing may not be detected until the child is older. In some cases, surgery may be performed. Surgery may involve cutting the shin bone (tibia) to realign it, and sometimes lengthen it as well.

Other times, the growth of just the outer half of the tibia can be surgically restricted to allow the child’s natural growth to reverse the bowing process. This second, much smaller surgery is most effective in children with less severe bowing and significant growth remaining.

Return to normal function and cosmetic appearance is expected if the knee can be properly aligned.

Gene-based therapies for patients with HSAN I are not available to date, hence supportive care is the only treatment available for the patients. Ulcero-mutilating complications are the most serious, prominent, and leading diagnostic features in HSAN I. Since the complications mimic foot ulcers caused by diabetic neuropathy, the treatment for foot ulcers and infections can follow the guidelines given for diabetic foot care which starts with early and accurate counseling of patients about risk factors for developing foot ulcerations. Orthopedic care and the use of well fitting shoes without pressure points should also be included. Recently, the treatment of the foot complications has reached an efficient level allowing treatment on an outpatient basis. Early treatment of the foot complications often avoids hospitalization and, in particular, amputations. In sum, the principles of the treatment are removal of pressure to the ulcers, eradication of infection, and specific protective footwear afterwards.

In cases of a minor deviation of the wrist, treatment by splinting and stretching alone may be a sufficient approach in treating the radial deviation in RD. Besides that, the parent can support this treatment by performing passive exercises of the hand. This will help to stretch the wrist and also possibly correct any extension contracture of the elbow. Furthermore, splinting is used as a postoperative measure trying to avoid a relapse of the radial deviation.

If patients with HSAN I receive appropriate treatment and counseling, the prognosis is good. Early treatment of foot infections may avoid serious complications. Nevertheless, the complications are manageable, thus allowing an acceptable quality of life. The disease progresses slowly and does not influence the life expectancy if signs and symptoms are properly treated.

First options for treatment are conservative, using hot or cold packs, rest and NSAID's at first. If no improvement is made, a splint or brace can be used to keep the deviated arm straight. When none of the conservative treatments work surgical intervention is designated.

Congenital dSMA has a relatively stable disease course, with disability mainly attributed to increased contractures rather than loss of muscle strength. Individuals frequently use crutches, knee, ankle, and/or foot orthoses, or wheelchairs. Orthopaedic surgery can be an option for some patients with severely impaired movement. Physical therapy and occupational therapy can help prevent further contractures from occurring, though they do not reverse the effects of preexisting ones. Some literature suggests the use of electrical stimulation or botulinum toxin to halt the progression of contractures.

Conservative therapies include NSAIDs, pain medication, weight management and exercise restriction. The problems with these therapies is that they do not work well, especially long-term.

Operations that attempt to restore a blood supply to the lunate may be performed.

Depending on the stage the disease is in when it is discovered, varying treatments are applied.

If X-rays show a mostly intact lunate (not having lost a great deal of size, and not having been compressed into a triangular shape), but an MRI shows a lack of blood flow to the bone, then revascularization is normally attempted. Revascularization techniques, usually involving a bone graft taken elsewhere from the body — often held in place by an external fixator for a period of weeks or months — have been successful at stages as late as 3B, although their use at later stages (like most treatments for Kienböck's) is controversial.

One conservative treatment option would be using an Ultrasound Bone Stimulator, which uses low-intensity pulsed ultrasound to increase vascular endothelial growth factor (VEG-F) and increase blood flow to the bone.

Some Kienböck's patients present with an abnormally large difference in length between the radius and the ulna, termed "ulnar variance", which is hypothesized to cause undue pressure on the lunate, contributing to its avascularity. In cases with such a difference, "radial shortening" is commonly performed. In this procedure, the radius (the lateral long bone) is shortened by a given length, usually between 2 and 5 mm, to relieve the pressure on the dying lunate. A titanium plate is inserted to hold the newly shortened bone together.

During Stage 3, the lunate has begun to break apart due to the pressure of the surrounding bones. This causes sharp fragments of bone to float between the joints, causing excruciating pain. At this point, the lunate is ready for removal. The most frequently performed surgery is the "Proximal Row Carpectomy", where the lunate, scaphoid and triquetrum are extracted. This greatly limits the range of motion of the wrist, but pain relief can be achieved for longer than after the other surgeries.

Another surgical option for this stage is a titanium, silicon or pyrocarbon implant that takes place of the lunate, though doctors shy from this due to a tendency of the implant to smooth the edges of the surrounding bones, thus causing painful pinched nerves when the bones slip out of place.

After the lunate is removed, another procedure, "ulnar shortening" can be performed. This relieves pressure on the newly formed wrist joint of the pisiform, hamate and capitate. Depending on the surgeon, the procedure may be performed the same way as the "radial shortening" where a small section is removed, or the entire top of the ulna may be excised.

At Stage 4, the lunate has completely disintegrated and the other bones in the wrist have radiated downward to fill in the void. The hand now has a deformed, crippled appearance. The only procedure that can be done is the "total wrist fusion", where a plate is inserted on the top of the wrist from the radius to the carpals, effectively freezing all flexion and movement in the wrist. Rotation is still possible as it is controlled by the radius and ulna.

This is currently the last and most complete surgical option for Kienböck's sufferers.

Most of the treatments described here are not mutually exclusive — meaning that a single patient may receive many of them in his quest to relieve pain. For instance, some patients have had casting, bone graft, radial shortening, proximal row carpectomy, and wrist fusion, all on the same hand.

More severe types (Bayne type III en IV) of radial dysplasia can be treated with surgical intervention. The main goal of centralization is to increase hand function by positioning the hand over the distal ulna, and stabilizing the wrist in straight position. Splinting or soft-tissue distraction may be used preceding the centralization.

In classic centralization central portions of the carpus are removed to create a notch for placement of the ulna. A different approach is to place the metacarpal of the middle finger in line with the ulna with a fixation pin.

If radial tissues are still too short after soft-tissue stretching, soft tissue release and different approaches for manipulation of the forearm bones may be used to enable the placement of the hand onto the ulna. Possible approaches are shortening of the ulna by resection of a segment, or removing carpal bones. If the ulna is significantly bent, osteotomy may be needed to straighten the ulna. After placing the wrist in the correct position, radial wrist extensors are transferred to the extensor carpi ulnaris tendon, to help stabilize the wrist in straight position. If the thumb or its carpometacarpal joint is absent, centralization can be followed by pollicization. Postoperatively, a long arm plaster splinter has to be worn for at least 6 to 8 weeks. A removable splint is often worn for a long period of time.

Radial angulation of the hand enables patients with stiff elbows to reach their mouth for feeding; therefore treatment is contraindicated in cases of extension contracture of the elbow. A risk of centralization is that the procedure may cause injury to the ulnar physis, leading to early epiphyseal arrest of the ulna, and thereby resulting in an even shorter forearm. Sestero et al. reported that ulnar growth after centralization reaches from 48% to 58% of normal ulnar length, while ulnar growth in untreated patients reaches 64% of normal ulnar length. Several reviews note that centralization can only partially correct radial deviation of the wrist and that studies with longterm follow-up show relapse of radial deviation.

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.

The elbow is a complex joint, bears 60% of body load, and tolerates problems less well than the hips. As a result, elbow replacement is more complex than hip replacement, rehabilitation can take significantly longer, and some degree of lameness will remain. The surgery is classified as of 2010 as a "salvage" operation - that is, a last resort for an otherwise viable animal. Success rates of around 80 - 85% (approximately 5 in 6) were being discussed by sources in 2005 and again in 2008.

There are also fewer options if the replacement fails, the main option being arthrodesis (surgical fusion of the joint) which results in a pain-free but lame gait. However arthrodesis is itself a complex surgery with a long recovery time, and if arthrodesis is required, additional strain will be borne by other nearby joints, so other leg and shoulder conditions such as osteoarthritis may become more significant.

In 2012, Dr. Kirk Wendelburg, DVM, founder of Animal Specialty Group (ASG) in Los Angeles, collaborated with Swiss veterinary technology company, Kyon, to design an advanced elbow replacement system. This new system maintains the normal range of motion through the sagittal plane, around a normal center of rotation, while allowing normal supination and pronation. The compact design has no mechanical linkages between the elbow compartments, significantly reducing undue stresses which may lead to early failure. Dr. Wendelburg also invented the implantational procedure for the prosthesis. This repeatable, highly advanced procedure also allows the surgeon to make an intraoperative decision on whether a total or partial elbow replacement is needed. For example, a dog with only medial compartment disease may only receive a partial replacement. This intraoperative flexibility is possible due to the modular design of the implant. The system invented by Dr. Wendelburg is the first and only to allow for a, "Biomechanically Anatomical, Nonconstrained, Compartmental (BANC) Elbow Arthroplasty."

"Ulna reduction"

Adults with Madelung’s deformity may suffer from ulnar-sided wrist pain. Madelung's Deformity is usually treated by treating the distal radial deformity. However, if patients have a positive ulnar variance and focal wrist pathology, it’s possible to treat with an isolated ulnar-shortening osteotomy. In these patients the radial deformity is not treated.

The ulna is approached from the subcutaneous border. A plate is attached to the distal end of the ulna, to plan the osteotomy. An oblique segment is removed from the ulna, after which the distal radial-ulnar joint is freed, making sure structures stay attached to the styloid process. After this, the freed distal end is reattached to the proximal ulna with the formerly mentioned plate.

"Total DRUJ replacement"

An alternative treatment for patients with ulnar-sided wristpain is a total replacement of the distal radial-ulnar joint. There are many surgical treatments of the condition, but most of these only improve the alignment and function of the radiocarpal joint. A persistent problem in these treatments has been the stiff DRUJ. However, a prosthesis helps in managing the pain, and might also improve the range of motion of the wrist.

The procedure consists of making a hockey-stick shaped incision along the ulnar border. This incision is made between the fifth and sixth dorsal compartment. Being careful not to harm any essential structures, like the posterior interosseous nerve, the incision is continued between the extensor carpi ulnaris and the extensor digiti quinti, until the ulna is found. The ulnar head is then removed. A guide wire is then inserted in the medullary canal of the ulna, allowing centralization for a cannulated drill bit. A poly-ethylene ball, which will serve as the prosthesis, is then placed over the distal peg. After confirming full range of motion, the skin will be closed.

"Dome Osteotomy"

In case of Madelung's Deformity in conjunction with radial pain, a dome osteotomy may be conducted. For more information about this procedure, please refer to the treatment of Madelung's Deformity in children.

Léri–Weill dyschondrosteosis or LWD is a rare pseudoautosomal dominant genetic disorder which results in dwarfism with short forearms and legs (mesomelic dwarfism) and a bayonet-like deformity of the forearms (Madelung's deformity).

Langer mesomelic dysplasia (LMD) is a rare congenital disorder characterized by an altered bone formation that causes a severe short and disproportionate stature.

Ischiopatellar dysplasia is a rare autosomal dominant disorder characterized by a hypoplasia of the patellae as well as other bone anomalies, especially concerning the pelvis and feet.