Some studies suggest a hormonal link. Specifically, the hormone relaxin has been indicated.

A genetic factor is indicated since the trait runs in families and there is an increased occurrence in some ethnic populations (e.g., Native Americans, Lapps / Sami people). A locus has been described on chromosome 13. Beukes familial dysplasia, on the other hand, was found to map to an 11-cM region on chromosome 4q35, with nonpenetrant carriers not affected.

Hip dysplasia is considered to be a multifactorial condition. That means that several factors are involved in causing the condition to manifest.

The cause of this condition is unknown; however, some factors of congenital hip dislocation are through heredity and racial background. It is also thought that the higher rates in some ethnic groups (such as some Native American groups) is due to the practice swaddling of infants, which is known to be a potential risk factor for developing dysplasia. It also has a low risk in African Americans and southern Chinese.

In general, SCFE is caused by increased force applied across the epiphysis, or a decrease in the resistance within the physis to shearing. No single cause accounts for SCFEs, as several factors play a role in the development of a SCFE, particularly mechanical and endocrine (hormone-related) factors. Mechanical risk factors include obesity, coxa profunda, femoral or acetabular retroversion. Obesity is the most significant risk factor. In 65 percent of cases of SCFE, the person is over the 95th percentile for weight. Common misconception is heredity. Majority of cause is due to being overweight. Endocrine diseases also contribute, such as hypothyroidism, hypopituitarism, and renal osteodystrophy.

Blount's disease occurs in young children and adolescents. The cause is unknown but is thought to be due to the effects of weight on the growth plate. The inner part of the tibia, just below the knee, fails to develop normally, causing angulation of the bone.

Unlike bowlegs, which tend to straighten as the child develops, Blount's disease is progressive and the condition worsens. It can cause severe bowing of the legs and can affect one or both legs.

This condition is more common among children of African ancestry. It is also associated with obesity, short stature, and early walking. There does not appear to be an obvious genetic factor.

SCFE affects approximately 1-10 per 100,000 children. The incidence varies by geographic location, season of the year, and ethnicity. In eastern Japan, the incidence is 0.2 per 100,000 and in the northeastern U.S. it is about 10 per 100,000. Africans and Polynesians have higher rates of SCFE.

SCFEs are most common in adolescents 11–15 years of age, and affects boys more frequently than girls (male 2:1 female). It is strongly linked to obesity, and weight loss may decrease the risk. Other risk factors include: family history, endocrine disorders, radiation / chemotherapy, and mild trauma.

The left hip is more often affected than the right. Over half of cases may have involvement on both sides (bilateral).

Presence at birth is extremely rare and associated with other congenital anomalies such as proximal femoral focal deficiency, fibular hemimelia or anomalies in other part of the body such as cleidocranial dyastosis. The femoral deformity is present in the subtrochantric area where the bone is bent. The cortices are thickened and may be associated with overlying skin dimples. External rotation of the femur with valgus deformity of knee may be noted. This condition does not resolve and requires surgical management. Surgical management includes valgus osteotomy to improve hip biomechanics and length and rotational osteotomy to correct retroversion and lengthening.

Coxa vara is a deformity of the hip, whereby the angle between the head and the shaft of the femur is reduced to less than 120 degrees. This results in the leg being shortened, and the development of a limp. It is commonly caused by injury, such as a fracture. It can also occur when the bone tissue in the neck of the femur is softer than normal, causing it to bend under the weight of the body. This may either be congenital or the result of a bone disorder. The most common cause of coxa vara is either congenital or developmental. Other common causes include metabolic bone diseases (e.g. Paget's disease of bone), post-Perthes deformity, osteomyelitis, and post traumatic (due to improper healing of a fracture between the greater and lesser trochanter). Shepherd's Crook deformity is a severe form of coxa vara where the proximal femur is severely deformed with a reduction in the neck shaft angle beyond 90 degrees. It is most commonly a sequela of osteogenesis imperfecta, Pagets disease, osteomyelitis, tumour and tumour-like conditions (e.g. fibrous dysplasia).

Coxa vara can happen in cleidocranial dysostosis.

Blount's disease is a growth disorder of the tibia (shin bone) that causes the lower leg to angle inward, resembling a bowleg.

It is also known as "tibia vara".

It is named after Walter Putnam Blount (1900–1992), an American pediatric orthopedic surgeon. It has also been known as Mau-Nilsonne Syndrome, after C. Mau and H. Nilsonne, who published early case reports of the condition.

Coxa valga is a deformity of the hip where the angle formed between the head and neck of the femur and its shaft is increased, usually above 135 degrees. It is caused by a slipped epiphysis of the femoral head.

The differential diagnosis includes neuromuscular disorders (i.e. cerebral palsy, spinal dysraphism, poliomyelitis), skeletal dysplasias, and juvenile idiopathic arthritis.

In most cases persisting after childhood, there is little or no effect on the ability to walk. Due to uneven stress and wear on the knees, however, even milder manifestations can see an accelerated onset of arthritis.

Children younger than 6 have the best prognosis, since they have time for the dead bone to revascularize and remodel, with a good chance that the femoral head will recover and remain spherical after resolution of the disease. Children who have been diagnosed with Perthes' disease after the age of 10 are at a very high risk of developing osteoarthritis and coxa magna. When an LCP disease diagnosis occurs after age 8, a better outcome results with surgery rather than nonoperative treatments. Shape of femoral head at the time when Legg-Calve Perthes disease heals is the most important determinant of risk for degenerative arthritis; hence, the shape of femoral head and congruence of hip are most useful outcome measures.

Perthes' disease is one of the most common hip disorders in young children, occurring in roughly 5.5 of 100,000 children per year. The lifetime risk of a child developing the disease is about one per 1,200 individuals. Boys are affected about three to five times more often than girls. New cases of Perthes' disease rarely occur after age 14 years (if diagnosed after 14 years of age, then it is usually old disease from early in childhood or avascular necrosis from an alternative cause).

White northern Europeans appear to be affected more frequently than other races, though a paucity of reliable epidemiology exists in the Southern Hemisphere. Children of sufferers of the disease themselves may have a very slightly increased risk, though it is unclear if this is because of a genetic predisposition, or a shared environmental factor. It is most commonly seen in persons aged three to 12 years, with a median of six years of age. The UK incidence rates show an intriguing pattern with low incidence rates in London, and a progressive increase in disease in more northerly areas (maximal in Scotland). Some evidence suggests, at least in developed countries, more socioeconomically deprived communities have a greater risk of disease (a similar trend to diseases such as adult heart disease), though the reason for this remains unknown. One possible explanation that has been considered is tobacco smoke exposure, though this is significantly confounded by the strong socioeconomic gradient common to both smoking and Perthes' disease. Dietary factors of the child, and of the mother during pregnancy, are of interest to the research groups.

If a child is sickly, either with rickets or any other ailment that prevents ossification of the bones, or is improperly fed, the bowed condition may persist. Thus the chief cause of this deformity is rickets. Skeletal problems, infection, and tumors can also affect the growth of the leg, sometimes giving rise to a one-sided bow-leggedness. The remaining causes are occupational, especially among jockeys, and from physical trauma, the condition being very likely to supervene after accidents involving the condyles of the femur.

The cause of snapping hip syndrome is not well understood, and confusion exists within the medical community regarding causation. Athletes appear to be at an enhanced risk for snapping hip syndrome due to repetitive and physically demanding movements.

In athletes such as ballet dancers, gymnasts, horse riders, track and field athletes and soccer players, military training, or any vigorous exerciser, repeated hip flexion leads to injury. In excessive weightlifting or running, the cause is usually attributed to extreme thickening of the tendons in the hip region. Snapping hip syndrome most often occurs in people who are 15 to 40 years old.

Several studies have reported that life expectancy appears to be normal for people with CCD.

Cleidocranial dysostosis (CCD), also called cleidocranial dysplasia, is a birth defect that mostly affects the bones and teeth. The collarbones are typically either poorly developed or absent, which allows the shoulders to be brought close together. The front of the skull often does not close until later, and those affected are often shorter than average. Other symptoms may include a prominent forehead, wide set eyes, abnormal teeth, and a flat nose. Symptoms vary among people; however, intelligence is typically normal.

The condition is either inherited from a person's parents or occurs as a new mutation. It is inherited in an autosomal dominant manner. It is due to a defect in the RUNX2 gene which is involved in bone formation. Diagnosis is suspected based on symptoms and X-rays with confirmation by genetic testing. Other conditions that can produce similar symptoms include mandibuloacral dysplasia, pyknodysostosis, osteogenesis imperfecta, and Hajdu-Cheney syndrome.

Treatment includes supportive measures such as a device to protect the skull and dental care. Surgery may be performed to fix certain bone abnormalities. Life expectancy is generally normal.

It affects about one per million people. Males and females are equally commonly affected. Modern descriptions of the condition date to at least 1896. The term is from "cleido" meaning collarbone, "cranial" meaning head, and "dysostosis" meaning formation of abnormal bone.

Extra-articular snapping hip syndrome is commonly associated with leg length difference (usually the long side is symptomatic), tightness in the iliotibial band (ITB) on the involved side, weakness in hip abductors and external rotators, poor lumbopelvic stability and abnormal foot mechanics (overpronation). Popping occurs when the thickened posterior aspect of the ITB or the anterior gluteus maximus rubs over the greater trochanter as the hip is extended.

Pseudoachondroplasia is inherited in an autosomal dominant manner, though one case of a very rare autosomal recessive form has been documented. The offspring of affected individuals are at 50% risk of inheriting the mutant allele. Prenatal testing by molecular genetic examination is available if the disease-causing mutation has been identified in an affected family member (Hecht et al. 1995).

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

In the past, there have been speculations about possible complications after transient synovitis. The current consensus however is that there is no proof of an increased risk of complications after transient synovitis.

One such previously suspected complication was coxa magna, which is an overgrowth of the femoral head and broadening of the femoral neck, accompanied by changes in the acetabulum, which may lead to subluxation of the femur. There was also some controversy about whether continuous high intra-articular pressure in transient synovitis could cause avascular necrosis of the femoral head (Legg-Calvé-Perthes disease), but further studies did not confirm any link between the two conditions.

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.

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.

Radiographic features include delayed epiphyseal ossification at the hips and knees, platyspondyly with irregular end plates and narrowed joint spaces, diffuse early osteoarthritic changes (in the spine and hands), mild brachydactyly and mild metaphyseal abnormalities which predominantly involve the hips and knees.

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.

This condition 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.

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