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 cure and no standard course of treatment for Coffin–Lowry syndrome. Treatment is symptomatic and supportive, and may include occupational, physical and speech therapy and educational services.

The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating the disease.

The caloric intake of children with SRS must be carefully controlled in order to provide the best opportunity for growth. If the child is unable to tolerate oral feeding, then enteral feeding may be used, such as the percutaneous endoscopic gastrostomy.

In children with limb-length differences or scoliosis, physiotherapy can alleviate the problems caused by these symptoms. In more severe cases, surgery to lengthen limbs may be required. To prevent aggravating posture difficulties children with leg length differences may require a raise in their shoe.

Growth hormone therapy is often prescribed as part of the treatment of SRS. The hormones are given by injection typically daily from the age of 2 years old through teenage years. It may be effective even when the patient does not have a growth hormone deficiency. Growth hormone therapy has been shown to increase the rate of growth in patients and consequently prompts 'catch up' growth. This may enable the child to begin their education at a normal height, improving their self-esteem and interaction with other children. The effect of growth hormone therapy on mature and final height is as yet uncertain. There are some theories suggesting that the therapy also assists with muscular development and managing hypoglycemia.

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.

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

Enzyme replacement therapies are currently in use. BioMarin Pharmaceutical provides therapeutics for mucopolysaccaradosis type I (MPS I), by manufacturing laronidase (Aldurazyme), commercialized by Genzyme. Enzyme replacement therapy has proven useful in reducing non-neurological symptoms and pain.

Bone marrow transplantation (BMT) and umbilical cord blood transplantation (UCBT) can be used as treatments for MPS. Abnormal physical characteristics, except for those affecting the skeleton and eyes, can be improved, and neurologic degeneration can often be halted. BMT and UCBT are high-risk procedures with high rates of morbidity and mortality. No cure for MPS I is known.

Treatment plans will vary depending on the severity of the condition and its evidences in each patient.

Areas that will probably need to be evaluated and assessed include speech, vision, hearing and EEG. Treatment measures may include physical therapy, occupational therapy, Speech therapy, anti-seizure drugs and orthotic devices. Surgery may be needed to assuage spastic motor problems. Various supportive measures such as joint contractures that could prevent complications.

Genetic counseling may also be recommended

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 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.

A cure does not exist for I-Cell disease/Mucolipidosis II disease. Treatment is limited to controlling or reducing the symptoms that are associated with this disorder. Nutritional supplements, particularly iron and vitamin B12, are often recommended for individuals with I-Cell disease. Physical therapy to improve motor delays and speech therapy to improve language acquisition are treatment options. Surgery can remove the thin layer of corneal clouding to temporarily improve the complication. It is possible that bone marrow transplant may be helpful in delaying or correcting the neurological deterioration that occurs with I-Cell disease.. Even though there is no existing treatment, the Yash Gandhi Foundation is a 501(c)(3) non-profit organization focused on funding research for I-Cell disease

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

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.

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.

A great deal of interest exists in treating MPS I with gene therapy. This approach has been taken with retroviral, lentiviral, adeno-associated virus, and even nonviral vectors to deliver the iduronidase gene. Successful treatments of the mouse, dog, and cat models of MPS I have occurred and may pave the way for future human trials.

Administration of GH has no effect on IGF-1 production, therefore treatment is mainly by biosynthetic IGF-1. IGF-1 must be taken before puberty to be effective.

The drug product Increlex (mecasermin), developed by the company Tercica, now Genentech, was approved by the US Food and Drug Administration in August 2005 for replacing IGF-1 in patients who are deficient.

IPLEX (Mecasermin rinfabate) is composed of recombinant human IGF-1 (rhIGF-1) and its binding protein IGFBP-3. It was approved by the U.S. Food and Drug Administration (FDA) in 2005 for treatment of primary IGF-1 deficiency or GH gene deletion. Side effects from IPLEX are hypoglycemia. IPLEX's manufacturing company, Insmed, after selling its protein production facility, can no longer develop proteins, thus can no longer manufacture IPLEX as of a statement released in July 2009.

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.

Cartilage–hair hypoplasia (CHH), also known as McKusick type metaphyseal chondrodysplasia, is a rare genetic disorder. It is a highly pleiotropic disorder that clinically manifests by form of short-limbed dwarfism due to skeletal dysplasia, variable level of immunodeficiency and predisposition to malignancies in some cases. It was first reported in 1965 by McKusick et al. Actor Verne Troyer is affected with this form of dwarfism, as was actor Billy Barty, who was renowned for saying "The name of my condition is Cartilage Hair Syndrome Hypoplasia, but you can just call me Billy."

Sensenbrenner syndrome (OMIM #218330) is a rare (less than 20 cases reported by 2010) multisystem disease first described in 1975. It is inherited in an autosomal recessive fashion, and a number of genes appear to be responsible. Three genes responsible have been identified: intraflagellar transport (IFT)122 (WDR10), IFT43 — a subunit of the IFT complex A machinery of primary cilia, and WDR35 (IFT121: TULP4)

It is also known as Sensenbrenner–Dorst–Owens syndrome, Levin Syndrome I and cranioectodermal dysplasia (CED)

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.

The Seckel syndrome or microcephalic primordial dwarfism (also known as bird-headed dwarfism, Harper's syndrome, Virchow-Seckel dwarfism, and Bird-headed dwarf of Seckel) is an extremely rare congenital nanosomic disorder.

Inheritance is autosomal recessive.

It is characterized by intrauterine growth retardation and postnatal dwarfism with a small head, narrow bird-like face with a beak-like nose, large eyes with down-slanting palpebral fissures , receding mandible and intellectual disability.

A mouse model has been developed. This mouse model is characterized by a severe deficiency of ATR protein. These mice suffer high levels of replicative stress and DNA damage. Adult Seckel mice display accelerated aging. These findings are consistent with the DNA damage theory of aging.

SCARF syndrome is a rare syndrome characterized by skeletal abnormalities, cutis laxa, craniostenosis, ambiguous genitalia, retardation, and facial abnormalities. It shares some features with Lenz-Majewski hyperostotic dwarfism syndrome.

Ellis–van Creveld Syndrome (also called "chondroectodermal dysplasia" or "mesoectodermal dysplasia" but see 'Nomenclature' section below) is a rare genetic disorder of the skeletal dysplasia type.

Stimmler syndrome is a rare autosomal recessive congenital disorder first described by Stimmler et al. in 1970. It is characterized by dwarfism, diabetes, a small head, and high levels of alanine in the urine.

Lenz–Majewski syndrome is a skin condition characterized by hyperostosis, craniodiaphyseal dysplasia, dwarfism, cutis laxa, proximal symphalangism, syndactyly, brachydactyly, mental retardation, enamel hypoplasia, and hypertelorism.

In 2013, whole-exome sequencing showed that a missense mutation resulting in overactive phosphatidylserine synthase 1 was the cause of LMS, making it the first known human disease to be caused by disrupted phosphatidylserine metabolism. The researchers suggested a link between the condition and bone metabolism.