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.

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 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.

Osteogenesis imperfecta is a rare condition in which bones break easily. There are multiple genetic mutations in different genes for collagen that may result in this condition. It can be treated with some drugs to promote bone growth, by surgically implanting metal rods in long bones to strengthen them, and through physical therapy and medical devices to improve mobility.

The term thanatophoric is Greek for "death bearing". Children with this condition are usually stillborn or die shortly after birth from respiratory failure, however a small number of individuals have survived into childhood and a very few beyond. Survivors have difficulty breathing on their own and require respiratory support such as high flow oxygen through a canula or ventilator support via tracheostomy. There may also be evidence of spinal stenosis and seizures.

The oldest known living TD survivor is a 29-year-old female. One male lived to be 26 years old. Another male lived to age 20. TD survivor, Chrisopher Álvarez, 18, is Colombian living in New York. Two children with TD aged 10 and 12, a male and a female, are known in Germany. There is also a 6-year-old male living with TD and two 1-year old males.

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

Fibrochondrogenesis is quite rare. A 1996 study from Spain determined a national minimal prevalence for the disorder at 8 cases out of 1,158,067 live births.

A United Arab Emirates (UAE) University report, from early 2003, evaluated the results of a 5-year study on the occurrence of a broad range of osteochondrodysplasias. Out of 38,048 newborns in Al Ain, over the course of the study period, fibrochondrogenesis was found to be the most common of the recessive forms of osteochondrodysplasia, with a prevalence ratio of 1.05:10,000 births.

While these results represented the most common occurrence within the group studied, they do not dispute the rarity of fibrochondrogenesis. The study also included the high rate of consanguinous marriages as a prevailing factor for these disorders, as well as the extremely low rate of diagnosis-related pregnancy terminations throughout the region.

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.

A recent article in 2015 reported a persistent notochord in a fetus at 23 weeks of gestation. The fetus had an abnormal spine, shortened long bones and a left clubfoot. After running postmortem tests and ultrasound, the researchers believed that the fetus suffered from hypochondrogenesis. Hypochondrogenesis is caused when type II collagen is abnormally formed due to a mutation in the COL2A1 gene. Normally, the cartilaginous notochord develops into the bony vertebrae in a human body. The COL2A1 gene results in malformed type II collagen, which is essential in the transition from collagen to bone. This is the first time that researchers found a persistent notochord in a human body due to a COL2A1 mutation.

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.

Thanatophoric dysplasia (thanatophoric dwarfism) is a severe skeletal disorder characterized by a disproportionately small ribcage, extremely short limbs and folds of extra skin on the arms and legs.

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.

Early journal reports of boomerang dysplasia suggested X-linked recessive inheritance, based on observation and family history. It was later discovered, however, that the disorder is actually caused by a genetic mutation fitting an autosomal dominant genetic profile.

Autosomal dominant inheritance indicates that the defective gene responsible for a disorder is located on an autosome, and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder.

Boomerang dysplasia, although an autosomal dominant disorder, is "not" inherited because those afflicted do not live beyond infancy. They cannot pass the gene to the next generation.

Osteochondrodysplasia or skeletal dysplasia is a general term for a disorder of the development (dysplasia) of bone ("osteo") and cartilage ("chondro").

Osteochondrodysplasias are rare diseases. About 1 in 5,000 babies are born with some type of skeletal dysplasia.

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.

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.

Mesomelia refers to conditions in which the middle parts of limbs are disproportionately short. When applied to skeletal dysplasias, mesomelic dwarfism describes generalised shortening of the forearms and lower legs. This is in contrast to rhizomelic dwarfism in which the upper portions of limbs are short such as in achondroplasia.

Forms of mesomelic dwarfism currently described include:

- Langer mesomelic dysplasia

- Ellis–van Creveld syndrome

- Robinow syndrome

- Léri–Weill dyschondrosteosis

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.

Spondyloepiphyseal dysplasia congenita is one of a spectrum of skeletal disorders caused by mutations in the "COL2A1" gene. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the eyeball (the vitreous). Type II collagen is essential for the normal development of bones and other connective tissues. Mutations in the "COL2A1" gene interfere with the assembly of type II collagen molecules, which prevents bones from developing properly and causes the signs and symptoms of this condition.

Spondyloepiphyseal dysplasia congenita is inherited in an autosomal dominant pattern, which means one copy of the altered gene is sufficient to cause the disorder.

Boomerang dysplasia is a lethal form of osteochondrodysplasia known for a characteristic congenital feature in which bones of the arms and legs are malformed into the shape of a boomerang. Death usually occurs in early infancy due to complications arising from overwhelming systemic bone malformations.

Osteochondrodysplasias are skeletal disorders that cause malformations of both bone and cartilage.

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.

Parastremmatic dwarfism is apparent at birth, with affected infants usually being described as "stiff", or as "twisted dwarfs" when the skeletal deformities and appearance of dwarfism further present themselves. Skeletal deformities usually develop in the sixth to twelfth month of an infant's life. The deformities may be attributed to osteomalacia, a lack of bone mineralization.

Increase bone density

Spool vertebrae

Obtuse angle of mandible

Acroosteolysis

Melorheostosis

Candle dripping sign

Nail patella syndrome

Thanatophoric dwarfism

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.