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.

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.

A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear. According to a study in the Journal of Orthopaedic Surgery and Traumatology the frequency of rotator cuff tears can increase with age. The study shows the participants that were the ages of 70–90 years old had a rate of rotator cuff tears that were 1 to 5. The participants who were 90+ years old the frequency of a rotator cuff tear jumped to 1 to 3. This study shows that with an increase in age there is also an increase in the probability of a rotator cuff tear.

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).

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.

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.

According to a study in the Journal of Orthopaedics the prevalence of a rotator cuff tear was considerably greater in males than in females within the ages of 50–60 years old, within the ages of 70–80 years old there wasn’t much difference in prevalence. The data of this study showed that the prevalence of a rotator cuff tear in the general population is 22.1% Yamamoto et al. performed a medical examination on 683 people whom live in a mountain village. The purpose of this study was to determine the prevalence of a rotator cuff tear among a population. Yamamoto found that among the mountain village population, rotator cuff tears were present in 20.7% of the village population. In both of these studies we see that the percentages of the prevalence of a rotator cuff tear are very close in number so these numbers show us the prevalence of rotator cuff tears in the general population.

In an autopsy study of rotator cuff tears, the incidence of partial tears was 28%, and of complete rupture 30%. Frequently, tears occurred on both sides and the frequency increased with age. The frequency was also higher in females. Other cadaver studies have noted intratendinous tears to be more frequent (7.2%) than bursal-sided (2.4%) or articular-sided tears (3.6%). However, clinically, articular-sided tears are found to be 2 to 3 times more common than bursal-sided tears and among a population of young athletes, articular-sided tears constituted 91% of all partial-thickness tears.

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.

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).

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.

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.

Other infections that classically lead to a limp include Lyme disease (a bacterial infection spread by a deer tick) and osteomyelitis (an infection of the bone).

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.

OCD is a relatively rare disorder, with an estimated incidence of 15 to 30 cases per 100,000 persons per year. Widuchowski W "et al." found OCD to be the cause of articular cartilage defects in 2% of cases in a study of 25,124 knee arthroscopies. Although rare, OCD is noted as an important cause of joint pain in active adolescents. The juvenile form of the disease occurs in children with open growth plates, usually between the ages 5 and 15 years and occurs more commonly in males than females, with a ratio between 2:1 and 3:1. However, OCD has become more common among adolescent females as they become more active in sports. The adult form, which occurs in those who have reached skeletal maturity, is most commonly found in people 16 to 50 years old.

While OCD may affect any joint, the knee—specifically the medial femoral condyle in 75–85% of knee cases—tends to be the most commonly affected, and constitutes 75% of all cases. The elbow (specifically the capitulum of the humerus) is the second most affected joint with 6% of cases; the talar dome of the ankle represents 4% of cases. Less frequent locations include the patella, vertebrae, the femoral head, and the glenoid of the scapula.

Despite much research, the causes remain unclear but include repetitive physical trauma, ischemia (restriction of blood flow), hereditary and endocrine factors, avascular necrosis (loss of blood flow), rapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and problems of bone formation. Although the name "osteochondritis" implies inflammation, the lack of inflammatory cells in histological examination suggests a non-inflammatory cause. It is thought that repetitive microtrauma, which leads to microfractures and sometimes an interruption of blood supply to the subchondral bone, may cause subsequent localized loss of blood supply or alteration of growth.

Trauma, rather than avascular necrosis, is thought to cause osteochondritis dissecans in juveniles. In adults, trauma is thought to be the main or perhaps the sole cause, and may be endogenous, exogenous or both. The incidence of repetitive strain injury in young athletes is on the rise and accounts for a significant number of visits to primary care; this reinforces the theory that OCD may be associated with increased participation in sports and subsequent trauma. High-impact sports such as gymnastics, soccer, basketball, lacrosse, football, tennis, squash, baseball and weight lifting may put participants at a higher risk of OCD in stressed joints (knees, ankles and elbows).

Recent case reports suggest that some people may be genetically predisposed to OCD. Families with OCD may have mutations in the aggrecan gene. Studies in horses have implicated specific genetic defects.

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.

Dislocation of the hip is a common injury to the hip joint. Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis.

Dislocations may be developmental or due to acute trauma. The emphasis of this article is on acute dislocation. For developmental dislocation, see hip dysplasia.

Acute traumatic hip dislocations are severe injuries. These dislocations typically occur in 16- to 40-year-olds involved in high energy trauma like motor vehicle accidents.

16-40 year-old males are responsible for the majority of hip dislocations. These hip dislocations are typically posterior, and a direct result of motor vehicle traffic collisions.

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.

The literature on the pathophysiology of bursitis describes inflammation as the primary cause of symptoms. Inflammatory bursitis is usually the result of repetitive injury to the bursa.

In the subacromial bursa, this generally occurs due to microtrauma to adjacent structures, particularly the supraspinatus tendon. The inflammatory process causes synovial cells to multiply, increasing collagen formation and fluid production within the bursa and reduction in the outside layer of lubrication (Ishii et al., 1997).

Less frequently observed causes of subacromial bursitis include hemorrhagic conditions, crystal deposition and infection.

Many causes have been proposed in the medical literature for subacromial impingement syndrome. The bursa facilitates the motion of the rotator cuff beneath the arch, any disturbance of the relationship of the subacromial structures can lead to impingement. These factors can be broadly classified as intrinsic such as tendon degeneration, rotator cuff muscle weakness and overuse. Extrinsic factors include bone spurs from the acromion or AC joint, shoulder instability and neurologic problems arising outside of the shoulder.

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.

In 1997 Morrison et al.

published a study that reviewed the cases of 616 patients (636 shoulders) with impingement syndrome (painful arc of motion) to assess the outcome of non-surgical care. An attempt was made to exclude patients who were suspected of having additional shoulder conditions such as, full-thickness tears of the rotator cuff, degenerative arthritis of the acromioclavicular joint, instability of the glenohumeral joint, or adhesive capsulitis. All patients were managed with anti-inflammatory medication and a specific, supervised physical-therapy regimen. The patients were followed up from six months to over six years. They found that 67% (413 patients) of the patients improved, while 28% did not improve and went to surgical treatment. 5% did not improve and declined further treatment.

Of the 413 patients who improved, 74 had a recurrence of symptoms during the observation period and their symptoms responded to rest or after resumption of the exercise program.

The Morrison study shows that the outcome of impingement symptoms varies with patient characteristics. Younger patients ( 20 years or less) and patients between 41 and 60 years of age, fared better than those who were in the 21 to 40 years age group. This may be related to the peak incidence of work, job requirements, sports and hobby related activities, that may place greater demands on the shoulder. However, patients who were older than sixty years of age had the "poorest results". It is known that the rotator cuff and adjacent structures undergo degenerative changes with ageing.

The authors were unable to posit an explanation for the observation of the bimodal distribution of satisfactory results with regard to age. They concluded that it was "unclear why (those) who were twenty-one to forty years old had less satisfactory results". The poorer outcome for patients over 60 years old was thought to be potentially related to "undiagnosed full-thickness tears of the rotator cuff".

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.

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.