Specific populations at high risk of primary PFPS include runners, bicyclists, basketball players, young athletes and females.

About 25% of people over the age of 50 experience knee pain from degenerative knee diseases.

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.

In the United States, more than US $3 billion is spent each year on arthroscopic knee surgeries that are known to be ineffective in people with degenerative knee pain.

The following factors may be involved in causing this deformity:

- Inherent laxity of the knee ligaments

- Weakness of biceps femoris muscle

- Instability of the knee joint due to ligaments and joint capsule injuries

- Inappropriate alignment of the tibia and femur

- Malunion of the bones around the knee

- Weakness in the hip extensor muscles

- Gastrocnemius muscle weakness (in standing position)

- Upper motor neuron lesion (for example, hemiplegia as the result of a cerebrovascular accident)

- Lower motor neuron lesion (for example, in post-polio syndrome)

- Deficit in joint proprioception

- Lower limb length discrepancy

- Congenital genu recurvatum

- Cerebral palsy

- Multiple sclerosis

- Muscular dystrophy

- Limited dorsiflexion (plantar flexion contracture)

- Popliteus muscle weakness

- Connective tissue disorders. In these disorders, there are excessive joint mobility (joint hypermobility) problems. These disorders include:

- Marfan syndrome

- Ehlers-Danlos syndrome

- Benign hypermobile joint syndrome

- Osteogenesis imperfecta disease

Isolated and combined posterolateral knee injuries are difficult to accurately diagnose in patients presenting with acute knee injuries. The incidence of isolated posterolateral corner injuries has been reported to be between 13% and 28%. Most PLC injuries accompany an ACL or PCL tear, and can contribute to ACL or PCL reconstruction graft failure if not recognized and treated. A study by LaPrade "et al." in 2007 showed the incidence of posterolateral knee injuries in patients presenting with acute knee injuries and hemarthrosis (blood in the knee joint) was 9.1%.

The most important factors of knee stability include:

- Ligaments of the knee: The knee joint is stabilized by four main ligaments:

- Anterior cruciate ligament (ACL). The ACL has an important role in stabilization of knee extension movement by preventing the knee from hyperextending.

- Posterior cruciate ligament (PCL)

- Medial collateral ligament (MCL)

- Lateral collateral ligament (LCL)

- Joint capsule or articular capsule (especially posterior knee capsule)

- Quadriceps femoris muscle

- Appropriate alignment of the femur and tibia (especially in knee extension position )

The degree of genu valgum can be estimated by the , which is the angle formed by a line drawn from the anterior superior iliac spine through the center of the patella and a line drawn from the center of the patella to the center of the tibial tubercle. In women, the Q angle should be less than 22 degrees with the knee in extension and less than 9 degrees with the knee in 90 degrees of flexion. In men, the Q angle should be less than 18 degrees with the knee in extension and less than 8 degrees with the knee in 90 degrees of flexion. A typical Q angle is 12 degrees for men and 17 degrees for women.

Future research into posterolateral injuries will focus on both the treatment and diagnosis of these types of injuries to improve PLC injury outcomes. Studies are needed to correlate injury patterns and mechanisms with clinical measures of knee instability and laxity.

In most patients with PFPS an examination of their history will highlight a precipitating event that caused the injury. Changes in activity patterns such as excessive increases in running mileage, repetitions such as running up steps and the addition of strength exercises that affect the patellofemoral joint are commonly associated with symptom onset. Excessively worn or poorly fitted footwear may be a contributing factor. To prevent recurrence the causal behaviour should be identified and managed correctly.

The medical cause of PFPS is thought to be increased pressure on the patellofemoral joint. There are several theorized mechanisms relating to how this increased pressure occurs:

- Increased levels of physical activity

- Malalignment of the patella as it moves through the femoral groove

- Quadriceps muscle imbalance

- Tight anatomical structures, e.g. retinaculum or iliotibial band.

The cause of pain and dysfunction often results from either abnormal forces (e.g. increased pull of the lateral quadriceps retinaculum with acute or chronic lateral PF subluxation/dislocation) or prolonged repetitive compressive or shearing forces (running or jumping) on the PF joint. The result is synovial irritation and inflammation and subchondral bony changes in the distal femur or patella known as "bone bruises". Secondary causes of PF Syndrome are fractures, internal knee derangement, osteoarthritis of the knee and bony tumors in or around the knee.

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.

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.

Medial knee injuries are those to the medial side – the inside of the knee – are the most common. The medial ligament complex of the knee is composed of the superficial medial collateral ligament (sMCL), deep medial collateral ligament (dMCL), and the posterior oblique ligament (POL). These ligaments have also been called the medial collateral ligament (MCL), tibial collateral ligament, mid-third capsular ligament, and oblique fibers of the sMCL, respectively. This complex is the major stabilizer of the medial knee. Injuries to the medial side of the knee are most commonly isolated to these ligaments. A thorough understanding of the anatomy and function of the medial knee structures, along with a detailed history and physical exam, are imperative to diagnosing and treating these injuries.

Jacobson previously described the common problems to medial knee surgery. It was stressed that adequate diagnosis is imperative and all possible injuries should be evaluated and addressed intraoperatively. Damage to the saphenous nerve and its infrapatellar branch is possible during medial knee surgery, potentially causing numbness or pain over the medial knee and leg. As with all surgeries, there is a risk of bleeding, wound problems, deep vein thrombosis, and infection that can complicate the outcome and rehabilitation process. The long term complication of arthrofibrosis and heterotopic ossification (Pellegrini-Stieda syndrome) are problems that are best addressed with early range of motion and following defined rehabilitation protocols. Failure of graft due to intrinsic mechanical forces should be prevented with preoperative alignment assessment (osteotomy treatment) and proper rehabilitation.

Possible causes that lead to the condition of Lumbar hyperlordosis are the following:

- Spines – Natural factors of how spines are formed greatly increase certain individuals' likelihood to experience a strain or sprain in their back or neck. Factors such as having more lumbar vertebrae allowing for too much flexibility, and then in cases of less lumbar the individual not reaching their necessity for flexibility and then pushing their bodies to injury.

- Legs – Another odd body formation is when an individual has a leg shorter than the other, which can be immediate cause for imbalance of hips then putting strain on the posture of the back which an individual has to adjust into vulnerable positions to meet aesthetic appearances. This can lead to permanent damage in the back. Genu recurvatum (sway back knees) is also a factor that forces a dancer to adjust into unstable postures.

- Hips – Common problems in the hips are tight hip flexors, which causes for poor lifting posture, hip flexion contracture, which means the lack of postural awareness, and thoracic hyperkyphosis, which causes the individual to compensate for limited hip turn out (which is essential to dances such as ballet). Weak psoas (short for iliopsoas-muscle that controls the hip flexor) force the dancer to lift from strength of their back instead of from the hip when lifting their leg into arabesque or attitude. This causes great stress and risk of injury, especially because the dancer will have to compensate to obtain the positions required.

- Muscles – One of the greatest contributors is uneven muscles. Because all muscles have a muscle that works in opposition to it, it is imperative that to keep all muscles protected, the opposite muscle is not stronger than the muscle at risk. In the situation of lumbar lordosis, abdominal muscles are weaker than the muscles in the lumbar spine and the hamstring muscles. The muscular imbalance results in pulling down the pelvis in the front of the body, creating the swayback in the spine.

- Growth spurt – Younger dancers are more at risk for development of lumbar hyperlordosis because the lumbar fascia and hamstrings tighten when a child starts to experience a growth spurt into adolescence.

Technical factors

- Improper lifts – When male dancers are performing dance lifts with another dancer they are extremely prone to lift in the incorrect posture, pushing their arms up to lift the other dancer, while letting their core and spine curve which is easy to then hyperlordosis in a dancer's back.

- Overuse – Over 45% of anatomical sites of injury in dancers are in the lower back. This can be attributed to the strains of repetitive dance training may lead to minor trauma. If the damaged site is not given time to heal the damage of the injury will increase. Abrupt increases in dance intensity or sudden changes in dance choreography do not allow the body to adapt to the new stresses. New styles of dance, returning to dance, or increasing dance time by a great deal will result in exhaustion of the body.

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

Leri's pleonosteosis is a rare rheumatic condition. It was first described by the French physician Leri in 1921.

Multiple epiphyseal dysplasia (MED) encompasses a spectrum of skeletal disorders, most of which are inherited in an autosomal dominant form. However, there is an autosomal recessive form.

Associated genes include COL9A1, COL9A2, COL9A3, COMP, and MATN3.

Types include:

Fairbank's disease or multiple epiphyseal dysplasia (MED) is a rare genetic disorder (dominant form: 1 in 10,000 births) that affects the growing ends of bones. Long bones normally elongate by expansion of cartilage in the growth plate (epiphyseal plate) near their ends. As it expands outward from the growth plate, the cartilage mineralizes and hardens to become bone (ossification). In MED, this process is defective.

Metaphyseal dysplasia, also known as Pyle's disease, Pyle's syndrome, Pyle-Cohn syndrome, and Bakwin-Krida syndrome is a rare disease in which the outer part of the shafts of long bones is thinner than normal and there is an increased chance of fractures.

Lumbar hyperlordosis is a condition that occurs when the lumbar region (lower back) experiences stress or extra weight and is arched to point of muscle pain or spasms. Lumbar hyperlordosis is a common postural position where the natural curve of the lumbar region of the back is slightly or dramatically accentuated. Commonly known as swayback, it is common in dancers. Imbalances in muscle strength and length are also a cause, such as weak hamstrings, or tight hip flexors (psoas). A major feature of lumbar hyperlordosis is a forward pelvic tilt, resulting in the pelvis resting on top of the thighs.

Other health conditions and disorders can cause hyperlordosis. Achondroplasia (a disorder where bones grow abnormally which can result in short stature as in dwarfism), Spondylolisthesis (a condition in which vertebrae slip forward) and osteoporosis (the most common bone disease in which bone density is lost resulting in bone weakness and increased likelihood of fracture) are some of the most common causes of hyperlordosis. Other causes include obesity, hyperkyphosis (spine curvature disorder in which the thoracic curvature is abnormally rounded), discitits (an inflammation of the intervertebral disc space caused by infection) and benign juvenile lordosis. Other factors may also include those with rare diseases, as is the case with Ehlers Danlos Syndrome (EDS), where hyper-extensive and usually unstable joints (e.g. joints that are problematically much more flexible, frequently to the point of partial or full dislocation) are quite common throughout the body. With such hyper-extensibility, it is also quite common (if not the norm) to find the muscles surrounding the joints to be a major source of compensation when such instability exists.

Excessive lordotic curvature – lumbar hyperlordosis, is also called hollow back, and saddle back (after a similar condition that affects some horses); swayback usually refers to a nearly opposite postural misalignment that can initially look quite similar. Common causes of lumbar hyperlordosis include tight low back muscles, excessive visceral fat, and pregnancy. Rickets, a vitamin D deficiency in children, can cause lumbar lordosis.

The clinical features of this condition include

- Flattened facial features

- Flexion contractures of the interphalangeal joints of hand and foot.

- Limited motion of multiple joints

- Short broad metacarpals, metatarsals and phalanges

Thickening of the skin may occur in a fashion similar to that occurs in scleroderma. The thumbs may be angled in a lateral direction (valgus deformity). The knees may be angled backwards (genu recurvatum). Abnormalities of the upper spinal cord may also occur.

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

Studies have shown that obesity of the mother increases the risk of neural tube disorders such as iniencephaly by 1.7 fold while severe obesity increases the risk by over 3 fold.