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

In regards to treatment of hypochondroplasia usually takes the form of orthopedic surgery and physical therapy. Genetic counseling is advised for individuals and their families. Specifically in the case of spinal stenosis, one option is laminectomy.

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.

There is no causative / curative therapy. Symptomatic medical treatments are focussing on symptoms caused by orthopaedic, dental or cardiac problems. Regarding perioperative / anesthesiological management, recommendations for medical professionals are published at OrphanAnesthesia.

There is no known cure for Winchester syndrome; however, there are many therapies that can aid in the treatment of symptoms. Such treatments can include medications: anti-inflammatories, muscle relaxants, and antibiotics. Many individuals will require physical therapy to promote movement and use of the limbs affected by the syndrome. Genetic counseling is typically prescribed for families to help aid in the understanding of the disease. There are a few clinical trials available to participate in. The prognosis for patients diagnosed with Winchester syndrome is positive. It has been reported that several affected individuals have lived to middle age; however,the disease is progressive and mobility will become limited towards the end of life. Eventually, the contractures will remain even with medical intervention, such as surgery.

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.

Treatments are usually based on the individuals symptoms that are displayed. The seizures are controlled with anticonvulsant medication. For the behavior problems, the doctors proscribe to a few medications and behavioral modification routines that involve therapists and other types of therapy. Even if mental retardation is severe, it does not seem to shorten the lifespan of the patient or to get worse with age.

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.

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.

Life expectancy for individuals with hypochondroplasia is normal; the maximum height is about 147 cm or 4.8 ft.

Pancreatic exocrine insufficiency may be treated through pancreatic enzyme supplementation, while severe skeletal abnormalities may require surgical intervention. Neutropenia may be treated with granulocyte-colony stimulating factor (GCSF) to boost peripheral neutrophil counts. However, there is ongoing and unresolved concern that this drug could contribute to the development of leukemia. Signs of progressive marrow failure may warrant bone marrow transplantation (BMT). This has been used successfully to treat hematological aspects of disease. However, SDS patients have an elevated occurrence of BMT-related adverse events, including graft-versus-host disease (GVHD) and toxicity relating to the pre-transplant conditioning regimen. In the long run, study of the gene that is mutated in SDS should improve understanding of the molecular basis of disease. This, in turn, may lead to novel therapeutic strategies, including gene therapy and other gene- or protein-based approaches.

Similar to all genetic diseases Aarskog–Scott syndrome cannot be cured, although numerous treatments exist to increase the quality of life.

Surgery may be required to correct some of the anomalies, and orthodontic treatment may be used to correct some of the facial abnormalities. Trials of growth hormone have been effective to treat short stature in this disorder.

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.

There is no treatment at this time to promote bone growth in chondrodystrophy patients. Certain types of growth hormone seem to increase the rate of growth during the first year of life/treatment, but have no substantial effect in adult patients. Only a few surgical centers in the world perform, experimentally, leg and arm lengthening procedures. Most common therapies are found in seeking help from: family physicians, pediatrics, internists, endocrinologists, geneticists, orthopedists and neurologists.

Some people may have some mental slowness, but children with this condition often have good social skills. Some males may have problems with fertility.

There are no cures for FHS. Close monitoring of growth in the first few years is essential, as well as annual general health screening and tests listed below. An FHS diagnosis will affect the individual and those there to support them.

Managing symptoms and features of FHS involves maintaining a close watch on the patient's physical as well as mental health. This would include:

- Sequencing of SRCAP exons 31–34 in all suspected cases

- Complete assessments of auditory and visual systems

- Renal and urinary tract ultrasound

- Orthopedic assessment of hip dysplasia and clavicle abnormalities

- Neurologic assessment if there is a suspicion of seizures

- Dental hygiene to prevent cavities and to monitor for malocclusion

- Evaluation for growth hormone deficiency at baseline, to be repeated if loss of growth velocity occurs

- Monitoring of bone age and pubertal timing in case of precocious puberty

- Psychoeducational assessments corrected for deficiencies in expressive language and sensory issues

- Monitoring of behavioral disturbances and provision of early intervention

- Counseling for families regarding recurrence risk and the offspring of individuals with FHS

Special education programs and vocational training to address developmental disabilities are highly recommended, as well as communication rehabilitation with sign language or alternative means of communication. Behavior management strategies could also include referrals to behavior specialists or psychologists for help. For those concerned, genetic counseling can be sought for issues related to testing of at-risk relatives.

Most reported cases of DEH in the literature have been treated surgically, with excision of the mass, as well as by the correction

of any deformity, while preserving the integrity of the affected joint as much as possible.

Genetic mutations of most forms of dwarfism caused by bone dysplasia cannot be altered yet, so therapeutic interventions are typically aimed at preventing or reducing pain or physical disability, increasing adult height, or mitigating psychosocial stresses and enhancing social adaptation.

Forms of dwarfism associated with the endocrine system may be treated using hormonal therapy. If the cause is prepubescent hyposecretion of growth hormone, supplemental growth hormone may correct the abnormality. If the receptor for growth hormone is itself affected, the condition may prove harder to treat. Hypothyroidism is another possible cause of dwarfism that can be treated through hormonal therapy. Injections of thyroid hormone can mitigate the effects of the condition, but lack of proportion may be permanent.

Pain and disability may be ameliorated by physical therapy, braces or other orthotic devices, or by surgical procedures. The only simple interventions that increase perceived adult height are dress enhancements, such as shoe lifts or hairstyle. Growth hormone is rarely used for shortness caused by bone dysplasias, since the height benefit is typically small (less than ) and the cost high. The most effective means of increasing adult height by several inches is distraction osteogenesis, though availability is limited and the cost is high in terms of money, discomfort, and disruption of life. Most people with dwarfism do not choose this option, and it remains controversial. For other types of dwarfism, surgical treatment is not possible.

To treat the trigonocephaly, expanding the distance between orbits using springs seems to work. It allows enough space for the brain to grow and it creates a normal horizontal axis of the orbits and supraorbital bar. The endoscopic surgery started to become popular since the early 90's, but it has some technical limitations (only strip cranictomy is possible). There have been few attempts to go beyond the limits.

Aesthetic outcomes of metopic surgery have been good. Surgery does not have a perfect outcome because there will most likely be minor irregularities. Sometimes reoperations are needed for the severe cases. Trying to hollow out the temporal, and the hypoterlorism are very hard to correct. The hypotelorism usually stays not corrected and in order to correct the temporal hollowing, a second operation is most likely needed.

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.

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).

Currently there is no cure for these disorders. Medical care is directed at treating systemic conditions and improving the person's quality of life. Physical therapy and daily exercise may delay joint problems and improve the ability to move.

Changes to the diet will not prevent disease progression, but limiting milk, sugar, and dairy products has helped some individuals experiencing excessive mucus.

Surgery to remove tonsils and adenoids may improve breathing among affected individuals with obstructive airway disorders and sleep apnea. Sleep studies can assess airway status and the possible need for nighttime oxygen. Some patients may require surgical insertion of an endotrachial tube to aid breathing. Surgery can also correct hernias, help drain excessive cerebrospinal fluid from the brain, and free nerves and nerve roots compressed by skeletal and other abnormalities. Corneal transplants may improve vision among patients with significant corneal clouding.

Enzyme replacement therapy (ERT) are currently in use or are being tested. Enzyme replacement therapy has proven useful in reducing non-neurological symptoms and pain. Currently BioMarin Pharmaceutical produces enzyme replacement therapies for MPS type I and VI. Aldurazyme is an enzymatic replacement therapy for alpha-L-iduronidase produced by BioMarin for use in Type I MPS. In July 2006, the United States Food and Drug Administration approved a synthetic version of I2S produced by Shire Pharmaceuticals Group, called Elaprase, as a treatment for MPS type II (Hunter syndrome).

Bone marrow transplantation (BMT) and umbilical cord blood transplantation (UCBT) have had limited success in treating the mucopolysaccharidoses. Abnormal physical characteristics, except for those affecting the skeleton and eyes, may be improved, but neurologic outcomes have varied. BMT and UCBT are high-risk procedures and are usually performed only after family members receive extensive evaluation and counseling.

For information on clinical trials visit Clinical Trials Search

Conservative treatment involves the long term use of laxatives and enemas, and has limited success. Dietary changes in order to control the disease are ineffective and high fiber diets often worsen the symptoms in children. As a last resort, surgical treatment (internal sphincter myectomy or colon resection) is used. In extreme cases, the only effective cure is a complete transplant of the affected parts.

The decision to treat is based on a belief that the child will be disabled by being extremely short as an adult, so that the risks of treatment (including sudden death) will outweigh the risks of not treating the symptom of short stature. Although short children commonly report being teased about their height, most adults who are very short are not physically or psychologically disabled by their height. However, there is some evidence to suggest that there is an inverse linear relationship with height and with risk of suicide.

Treatment is expensive and requires many years of injections with human growth hormones. The result depends on the cause, but is typically an increase in final height of about taller than predicted. Thus, treatment takes a child who is expected to be much shorter than a typical adult and produces an adult who is still obviously shorter than average. For example, several years of successful treatment in a girl who is predicted to be as an adult may result in her being instead.

Increasing final height in children with short stature may be beneficial and could enhance health-related quality of life outcomes, barring troublesome side effects and excessive cost of treatments.

It is important that the individual experience independence and self-worth. There are several appliances available to help overcome the disadvantages of small stature, including light-switch extenders and longer pedals in cars to enable effective driving. Several organizations that help Little People interact and get involved, such as the Little People of America.