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.

Hip dysplasia may be caused by a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. Large and giant breeds are most susceptible to hip dysplasia (possibly due to the body mass index (BMI) of the individual animal, though, many other breeds can suffer from it. The Orthopedic Foundation for Animals maintains a list of top 100 breeds affected.

To reduce pain, the animal will typically reduce its movement of that hip. This may be visible as "bunny hopping", where both legs move together, or less dynamic movement (running, jumping), or stiffness. Since the hip cannot move fully, the body compensates by adapting its use of the spine, often causing spinal, stifle (a dog's knee joint), or soft tissue problems to arise.

The causes of hip dysplasia are considered heritable, but new research conclusively suggests that environment also plays a role. To what degree the causality is genetic and what portion environmental is a topic of current debate. Neutering a dog, especially before the dog has reached an age of full developmental maturity, has been proven to almost double the chance he or she will develop hip dysplasia versus intact dogs or dogs that were neutered after reaching adulthood Other environmental influences include overweight condition, injury at a young age, overexertion on the hip joint at a young age, ligament tear at a young age, repetitive motion on forming joint (i.e. jogging with puppy under the age of 1 year). As current studies progress, greater information may help provide procedures to effectively reduce the occurrence of this condition.

The problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling, and can eventually cause severe osteoarthritis.

It is most common in medium-large pure bred dogs, such as Newfoundlands, German Shepherd Dogs, retrievers (such as Labradors, Tollers, or Goldens), rottweilers and Mastiff, but also occurs in some smaller breeds such as spaniels and pugs.

The cause of PFFD is uncertain. Two hypotheses have been advanced. The theory of sclerotome subtraction posits injury to neural crest cells that are the precursors to sensory nerves at the level of L4 and L5. Histologic studies of a fetus with unilateral PFFD have prompted an alternative hypothesis that PFFD is caused by a defect in maturation of chondrocytes (cartilage cells) at the growth plate. In either hypothesis, the agent causing the injury is usually not known. Thalidomide is known to cause PFFD when the mother is exposed to it in the fifth or sixth week of pregnancy, and it is speculated that exposure to other toxins during pregnancy may also be a cause. Other etiologies that have been suggested, but not proven, include anoxia, ischemia, radiation, infection, hormones, and mechanical force. PFFD occurs sporadically, and does not appear to be hereditary.

Hip fractures are seen globally and are a serious concern at the individual and population level. By 2050 it is estimated that there will be 6 million cases of hip fractures worldwide. One study published in 2001 found that in the US alone, 310,000 individuals were hospitalized due to hip fractures, which can account for 30% of Americans who were hospitalized that year. Another study found that in 2011, femur neck fractures were among the most expensive conditions seen in US hospitals, with an aggregated cost of nearly $4.9 billion for 316,000 inpatient hospitalizations. Rates of hip fractures is declining in the United States, possibly due to increased use of bisphosphonates and risk management. Falling, poor vision, weight and height are all seen as risk factors. Falling is one of the most common risk factors for hip fractures. Approximately 90% of hip fractures are attributed to falls from standing height.

Given the high morbidity and mortality associated with hip fractures and the cost to the health system, in England and Wales, the National Hip Fracture Database is a mandatory nationwide audit of care and treatment of all hip fractures.

The majority of hip fractures are the result of a fall, particularly in the elderly. Therefore, identifying why the fall occurred, and implementing treatments or changes, is key to reducing the occurrence of hip fractures. Multiple contributing factors are often identified. These can include environmental factors and medical factors (such as postural hypotension or co-existing disabilities from disease such as Stroke or Parkinson's Disease which cause visual and/or balance impairments). A recent study has identified a high incidence of undiagnosed cervical spondylotic myelopathy (CSM) amongst patients with a hip fracture. This is relatively unrecognised consequent of CSM.

Additionally, there is some evidence to systems designed to offer protection in the case of a fall. Hip protectors, for example appear to decrease the number of hip fractures among the elderly. They; however, are not often used.

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.

In dogs, hip dysplasia is an abnormal formation of the hip socket that, in its more severe form, can eventually cause crippling lameness and painful arthritis of the joints. It is a genetic (polygenic) trait that is affected by environmental factors. It is common in many dog breeds, particularly the larger breeds, and is the most common single cause of arthritis of the hips.

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).

Pathologic fractures in children and adolescents can result from a diverse array of disorders namely; metabolic, endocrine, neoplastic, infectious, immunologic, and genetic skeletal dysplasias.

- Osteogenesis imperfecta

- Primary hyperparathyroidism

- Simple bone cyst

- Aneurismal bone cyst

- Disuse osteoporosis

- Chronic osteomyelitis

- Osteogenesis imperfecta

- Rickets

- Renal osteodystrophy

- Malignant infantile osteopetrosis

- juvenile osteoporosis

- juvenile rheumatoid arthritis

In circumstances where other pathologies are excluded (for example, cancer), a pathologic fracture is diagnostic of osteoporosis irrespective of bone mineral density.

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high dose steroids. Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gaucher’s disease, and Caisson disease. The condition may also occur without any clear reason.

Bisphosphonates are associated with osteonecrosis of the mandible. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.

Femoral shaft fractures occur in a bimodal distribution, whereby they are most commonly seen in males age 15-24 (due to high energy trauma) and females aged 75 or older (pathologic fractures due to osteoporosis, low-energy falls).

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.

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.

There are typically four classes (or "types") of PFFD, ranging from class A to class D, as detailed by Aitken.

Accidental or deliberate physical trauma may result in either a fracture, muscle bruising, or a contusion. It is the leading cause of a limp. Deliberate abuse is important to consider.

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.

While genu valgum is often a symptom of genetic disorders it can be caused by poor nutrition. A major contributor to genu valgum is obesity, and far less commonly calcium and vitamin d deficiencies.

These fractures can take at least 4–6 months to heal. Since femoral shaft fractures are associated with violent trauma, there are many adverse outcomes, including fat embolism, acute respiratory distress syndrome (ARDS), multisystem organ failure, and shock associated with severe blood loss. Open fractures can result in infection, osteomyelitis, and sepsis.

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.

FAI has been speculated as a cause of premature hip osteoarthritis and is characterized by abnormal contact between the proximal femur and rim of the acetabulum (hip socket). In most cases, patients present with a deformity in the femoral head, or acetabulum, a poorly positioned femoral-acetabular junction, or any or all of the foregoing. A combination of certain factors may predispose to some form of FAI, predominantly, a marginal developmental hip abnormality together with environmental factors such as activities involving recurrent motion of the legs within a supraphysiologic range.

Three types of FAI are recognized. The first involves an excess of bone along the upper surface of the femoral head, known as a Cam deformity (abbreviation for camshaft which the shape of the femoral head and neck resembles). The second is due to an excess of growth of the upper lip of the acetabular cup and is known as a 'Pincer' deformity. Colloquially, these are referred to as 'Cam' and 'Pincer'. The third is a combination of the two, generally referred to as 'Mixed'. Studies have suggested that 'Cam' deformities are more common in the male, while 'Pincer' deformities are more common in females. However, the most common situation, approximately 70%, is a combination of both. A complicating issue is that some of the radiographic findings of FAI have also been described in asymptomatic subjects. Consequently, the true frequency of femoroacetabular impingement is currently under debate, but the ultimate result is increased friction between the acetabular cup and femoral head which may result in pain and loss or reduction of hip function.

Femoroacetabular Impingement (FAI), or hip impingement syndrome, may affect the hip joint in young and middle-aged adults and occurs when the ball shaped femoral head rubs abnormally or does not permit a normal range of motion in the acetabular socket. Damage can occur to the articular cartilage, or labral cartilage (soft tissue bumper of the socket), or both. Treatment options range from conservative to arthroscopic to open surgery.