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).

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.

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.

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

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.

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

People with Pyle disease are often asymptomatic. Dental anomalies may require orthodontic interventions. Skeletal anomalies may require orthopedic surgery.

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.

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.

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.

There is no known treatment at present, although some investigators have tried to lessen the hypercalcemia with various forms of bisphosphonates.

There is currently no specific treatment available for either of these so-called progeroid syndromes. With this in mind, what is most important when making a differential diagnosis with them is based on the prognosis, which appears to be far better in acrogeria.

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.

Increase bone density

Spool vertebrae

Obtuse angle of mandible

Acroosteolysis

Melorheostosis

Candle dripping sign

Nail patella syndrome

Thanatophoric dwarfism

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.

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.

Spondyloepiphyseal dysplasia congenita (abbreviated to SED more often than SDC) is a rare disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and occasionally problems with vision and hearing. The name of the condition indicates that it affects the bones of the spine (spondylo-) and the ends of bones (epiphyses), and that it is present from birth (congenital). The signs and symptoms of spondyloepiphyseal dysplasia congenita are similar to, but milder than, the related skeletal disorders achondrogenesis type 2 and hypochondrogenesis. Spondyloepiphyseal dysplasia congenita is a subtype of collagenopathy, types II and XI.

Gene based therapy is being studied. In June 2015, BioMarin announced positive results of their Phase 2 study, stating that 10 children experienced a mean increase of 50% in their annualized growth velocity.

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

Though articular cartilage damage is not life-threatening, it does strongly affect the quality of life. Articular cartilage damage is often the cause of severe pain, swellings, strong barriers to mobility and severe restrictions to the patient's activities. Over the last decades, however, surgeons and biotech ventures[who?] have elaborated promising procedures[which?] that contribute to articular cartilage repair. These procedures do not, however, treat osteoarthritis.

Spondyloepimetaphyseal dysplasia, Strudwick type is an inherited disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and problems with vision. The name of the condition indicates that it affects the bones of the spine (spondylo-) and two regions near the ends of bones (epiphyses and metaphyses). This type was named after the first reported patient with the disorder. Spondyloepimetaphyseal dysplasia, Strudwick type is a subtype of collagenopathy, types II and XI.

The signs and symptoms of this condition at birth are very similar to those of spondyloepiphyseal dysplasia congenita, a related skeletal disorder. Beginning in childhood, the two conditions can be distinguished in X-ray images by changes in areas near the ends of bones (metaphyses). These changes are characteristic of spondyloepimetaphyseal dysplasia, Strudwick type.

Pseudoachondroplasia is an inherited disorder of bone growth. It is a genetic autosomal dominant disorder. It is generally not discovered until 2-3 years of age, since growth is normal at first. Pseudoachondroplasia is usually first detected by a drop of linear growth in contrast to peers, a curious, waddling gait or arising lower limb deformities.

Pseudoachondroplasia (also known as PSACH, Pseudoachondroplastic dysplasia, and Pseudoachondroplastic spondyloepiphyseal dysplasia syndrome) is an osteochondrodysplasia that results in mild to severely short stature due to the inhibition of skeletal growth primarily in the limbs. Though similarities in nomenclature may cause confusion, Pseudoachondroplasia should not be confused with achondroplasia, which is a clinically and genetically distinct skeletal dysplasia. Pseudoachondroplasia is caused by a heterozygous mutation in the gene encoding cartilage oligomeric matrix protein COMP. Mutation in the COMP gene can also multiple epiphyseal dysplasia. Despite the radioclinical similarities between pseudoachondroplasia and multiple epiphyseal dysplasia, the latter is less severe.132400

Fibrochondrogenesis is a rare autosomal recessive form of osteochondrodysplasia, causing abnormal fibrous development of cartilage and related tissues.

It is a lethal rhizomelic (malformations which result in short, underdeveloped limbs) form of dwarfism, exhibiting both skeletal dysplasia (malformations of bone) and fibroblastic dysplasia (abnormal development of fibroblasts, specialized cells that make up fibrous connective tissue, which plays a role in the formation of cellular structure and promotes healing of damaged tissues). Death caused by complications of fibrochondrogenesis occurs in infancy.

This is an autosomal recessive osteochondrodysplasia that maps to chromosome 1q21. Deficiency of Cathepsin K, a cysteine protease in osteoclasts, is known to cause this condition. Cathepsin K became a much sought-after drug target in osteoporosis after the cause of pycnodysostosis was discovered. The disease consistently causes short stature. The height of adult males with the disease is less than . Adult females with the syndrome are even shorter.

The disease has been named Toulouse-Lautrec syndrome, after the French artist Henri de Toulouse-Lautrec, who may have had the disease. In 1996, the defective gene responsible for pycnodysostosis was located, offering accurate diagnosis, carrier testing and a more thorough understanding of this disorder.

Many types of dwarfism are currently impossible to prevent because they are genetically caused. Genetic conditions that cause dwarfism may be identified with genetic testing, by screening for the specific variations that result in the condition. However, due to the number of causes of dwarfism, it may be impossible to determine definitively if a child will be born with dwarfism.

Dwarfism resulting from malnutrition or a hormonal abnormality may be treated with an appropriate diet or hormonal therapy. Growth hormone deficiency may be remedied via injections of human growth hormone (HGH) during early life.