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

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

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 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.

Risk factors for developing shin splints include:

- Excessive pronation at subtalar joint

- Excessively tight calf muscles (which can cause excessive pronation)

- Engaging the medial shin muscle in excessive amounts of eccentric muscle activity

- Undertaking high-impact exercises on hard, noncompliant surfaces (ex: running on asphalt or concrete)

- Smoking and low fitness level

While medial tibial stress syndrome is the most common form of shin splints, compartment syndrome and stress fractures are also common forms of shin splints. Females are 1.5 to 3.5 times more likely to progress to stress fractures from shin splints. This is due in part to females having a higher incidence of diminished bone density and osteoporosis.

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.

Because wear on the hip joint traces to the structures that support it (the posture of the legs, and ultimately, the feet), proper fitting shoes with adequate support are important to preventing GTPS. For someone who has flat feet, wearing proper orthotic inserts and replacing them as often as recommended are also important preventive measures.

Strength in the core and legs is also important to posture, so physical training also helps to prevent GTPS. But it is equally important to avoid exercises that damage the hip.

The cause of de Quervain's disease is not established. Evidence regarding a possible relation with occupational risk factors is debated. A systematic review of potential risk factors discussed in the literature did not find any evidence of a causal relationship with occupational factors. However, researchers in France found personal and work-related factors were associated with de Quervain's disease in the working population; wrist bending and movements associated with the twisting or driving of screws were the most significant of the work-related factors. Proponents of the view that De Quervain syndrome is a repetitive strain injury consider postures where the thumb is held in abduction and extension to be predisposing factors. Workers who perform rapid repetitive activities involving pinching, grasping, pulling or pushing have been considered at increased risk. Specific activities that have been postulated as potential risk factors include intensive computer mouse use, trackball use, and typing, as well as some pastimes, including bowling, golf, fly-fishing, piano-playing, sewing, and knitting.

Women are affected more often than men. The syndrome commonly occurs during and after pregnancy. Contributory factors may include hormonal changes, fluid retention and—more debatably—lifting.

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.

Rate in the United States have been estimated to occur among an at-risk population of 1,774,210,081 people each year. Incidence rates published in the American Journal of Sports Medicine for ages 10–17 were found to be about 29 per 100,000 persons per year, while the adult population average for this type of injury ranged between 5.8 and 7.0 per 100,000 persons per year. The highest rates of patellar dislocation were found in the youngest age groups, while the rates declined with increasing ages. Females are more susceptible to patellar dislocation. Race is a significant factor for this injury, where Hispanics, African-Americans and Caucasians had slightly higher rates of patellar dislocation due to the types of athletic activity involved in: basketball (18.2%), soccer (6.9%), and football (6.9%), according to Brian Waterman.

Lateral Patellar dislocation is common among the child population. Some studies suggest that the annual patellar dislocation rate in children is 43/100,000. The treatment of the skeletally immature is controversial due to the fact that they are so young and are still growing. Surgery is recommended by some experts in order to repair the medial structures early, while others recommend treating it non operatively with physical therapy. If re-dislocation occurs then reconstruction of the medial patellofemoral ligament (MPFL) is the recommended surgical option.

While the exact cause is unknown, shin splints can be attributed to the overloading of the lower leg due to biomechanical irregularities resulting in an increase in stress exerted on the tibia. A sudden increase in intensity or frequency in activity level fatigues muscles too quickly to properly help absorb shock, forcing the tibia to absorb most of that shock. This stress is associated with the onset of shin splints. Muscle imbalance, including weak core muscles, inflexibility and tightness of lower leg muscles, including the gastrocnemius, soleus, and plantar muscles (commonly the flexor digitorum longus) can increase the possibility of shin splints. The pain associated with shin splints is caused from a disruption of Sharpey's fibres that connect the medial soleus fascia through the periosteum of the tibia where it inserts into the bone. With repetitive stress, the impact forces eccentrically fatigue the soleus and create repeated tibial bending or bowing, contributing to shin splints. The impact is made worse by running uphill, downhill, on uneven terrain, or on hard surfaces. Improper footwear, including worn-out shoes, can also contribute to shin splints.

Anything compromising the tunnel of the posterior tibial nerve proves significant in the risk of causing TTS. Neuropathy can occur in the lower limb through many modalities, some of which include obesity and inflammation around the joints. By association, this includes risk factors such as RA, compressed shoes, pregnancy, diabetes and thyroid diseases

Though TTS is rare, its cause can be determined in 70% of reported cases. In the workplace TTS is considered a musculoskeletal disorder and accounts for 1.8 million cases a year, which accumulates to about $15–$20 billion a year New studies indicate an occurrence of TTS in sports placing high loads on the ankle joint (3). This can be seen in figure 1. TTS occurs more dominantly in active adults, with a higher pervasiveness among women. Active adults that experience more jumping and landing on the ankle joint are more susceptible (see figure 2). Though athletics and sport are correlations, cases are individualistically assessed because of the oddity.

The condition may result from acute injury to the patella or chronic friction between the patella and a groove in the femur through which it passes during knee flexion. Possible causes include a tight iliotibial band, neuromas, bursitis, overuse, malalignment, core instability, and patellar maltracking.

Pain at the front or inner side of the knee is common in both young adults and those of more advanced years, especially when engaging in soccer, gymnastics, cycling, rowing, tennis, ballet, basketball, horseback riding, volleyball, running, combat sports, figure skating, snowboarding, skateboarding and even swimming. The pain is typically felt after prolonged sitting. Skateboarders most commonly experience this injury in their non-dominant foot due to the constant kicking and twisting required of it. Swimmers acquire it doing the breaststroke, which demands an unusual motion of the knee. People who are involved in an active life style with high impact on the knees are at greatest risk. Proper management of physical activity may help prevent worsening of the condition. Athletes are advised to talk to a physician for further medical diagnosis as symptoms may be similar to more serious problems within the knee. Tests are not necessarily needed for diagnosis, but in some situations it may confirm diagnosis or rule out other causes for pain. Commonly used tests are blood tests, MRI scans, and arthroscopy.

While the term "chondromalacia" sometimes refers to abnormal-appearing cartilage anywhere in the body, it most commonly denotes irritation of the underside of the kneecap (or "patella"). The patella's posterior surface is covered with a layer of smooth cartilage, which the base of the femur normally glides effortlessly against when the knee is bent. However, in some individuals the kneecap tends to rub against one side of the knee joint, irritating the cartilage and causing knee pain.

In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.

Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.

An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.

Chondromalacia patellae (also known as CMP) is inflammation of the underside of the patella and softening of the cartilage.

The cartilage under the kneecap is a natural shock absorber, and overuse, injury, and many other factors can cause increased deterioration and breakdown of the cartilage. The cartilage is no longer smooth and therefore movement and use is painful. While it often affects young individuals engaged in active sports, it also afflicts older adults who overwork their knees.

"Chondromalacia patellae" is sometimes used synonymously with patellofemoral pain syndrome. However, there is general consensus that "patellofemoral pain syndrome" applies only to individuals without cartilage damage.

Like many other joints throughout the human body, facets can experience natural degeneration from constant use. Over time, the cartilage within the joints can naturally begin to wear out, allowing it to become thin or disappear entirely which, in turn, allows the conjoining vertebrae to rub directly against one another with little or no lubricant or separation. A result of this rubbing is often swelling, inflammation or other painful symptoms.

Over time, the body will naturally respond to the instability within the spine by developing bone spurs, thickened ligaments or even cysts that can press up against or pinch the sensitive nerve roots exiting the spinal column.

While primarily caused through natural wear and tear, advanced facet syndrome can also occur as a result of injury to the spine, degenerative disease or lifestyle choices. These causes can include:

- An unexpected, traumatic event such as a car accident, significant fall or high impact sports injury.

- Osteoarthritis

- Spondylolisthesis

- Obesity

- Smoking

- Malnutrition

- Lack of physical exercise or daily activity

55% of facet syndrome cases occur in cervical vertebrae, and 31% in lumbar. Facet syndrome can progress to spinal osteoarthritis, which is known as spondylosis. Pathology of the C1-C2 (atlantoaxial) joint, the most mobile of all vertebral segments, accounts for 4% of all spondylosis.

Hypermobility syndrome is generally considered to comprise hypermobility together with other symptoms, such as myalgia and arthralgia. It is relatively common among children and affects more females than males.

Current thinking suggests four causative factors:

- The shape of the ends of the bones—Some joints normally have a large range of movement, such as the shoulder and hip. Both are ball and socket joints. If a shallow rather than a deep socket is inherited, a relatively large range of movement will be possible. If the socket is particularly shallow, then the joint may dislocate easily.

- Protein deficiency or hormone problems—Ligaments are made up of several types of protein fibre. These proteins include elastin, which gives elasticity and which may be altered in some people. Female sex hormones alter collagen proteins. Women are generally more supple just before a period and even more so in the latter stages of pregnancy, because of a hormone called relaxin that allows the pelvis to expand so the head of the baby can pass. Joint mobility differs by race, which may reflect differences in collagen protein structure. People from the Indian sub-continent, for example, often have more supple hands than Caucasians.

- Muscle tone—The tone of muscles is controlled by the nervous system, and influences range of movement. Special techniques can change muscle tone and increase flexibility. Yoga, for example, can help to relax muscles and make the joints more supple. Please note that Yoga is not recommended by most medical professionals for people with Joint Hypermobility Syndrome due to likelihood of damage to the joints. Gymnasts and athletes can sometimes acquire hypermobility in some joints through activity.

- Proprioception—Compromised ability to detect exact joint/body position with closed eyes, may lead to overstretching and hypermobile joints.

Hypermobility can also be caused by connective tissue disorders, such as Ehlers-Danlos Syndrome (EDS) and Marfan syndrome. Joint hypermobility is a common symptom for both. EDS has numerous sub-types; most include hypermobility in some degree. When hypermobility is the main symptom, then EDS/hypermobility type is likely. People with EDS-HT suffer frequent joint dislocations and subluxations (partial/incomplete dislocations), with or without trauma, sometimes spontaneously. Commonly, hypermobility is dismissed by medical professionals as nonsignificant.

Shoulder impingement syndrome, also called subacromial impingement, painful arc syndrome, supraspinatus syndrome, swimmer's shoulder, and thrower's shoulder, is a clinical syndrome which occurs when the tendons of the rotator cuff muscles become irritated and inflamed as they pass through the subacromial space, the passage beneath the acromion. This can result in pain, weakness and loss of movement at the shoulder.

Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.

Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.

In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.

Those who have this disease may experience sprained ankles more frequently than other people.

Those with hypermobile joints are more likely to have fibromyalgia, mitral valve prolapse, and anxiety disorders such as panic disorder.

De Quervain syndrome, is a tenosynovitis of the sheath or tunnel that surrounds two tendons that control movement of the thumb.

Greater trochanteric pain syndrome (GTPS), also known as trochanteric bursitis, is inflammation of the trochanteric bursa, a part of the hip.

This bursa is at the top, outer side of the femur, between the insertion of the gluteus medius and gluteus minimus muscles into the greater trochanter of the femur and the femoral shaft. It has the function, in common with other bursae, of working as a shock absorber and as a lubricant for the movement of the muscles adjacent to it.

Occasionally, this bursa can become inflamed and clinically painful and tender. This condition can be a manifestation of an injury (often resulting from a twisting motion or from overuse), but sometimes arises for no obviously definable cause. The symptoms are pain in the hip region on walking, and tenderness over the upper part of the femur, which may result in the inability to lie in comfort on the affected side.

More often the lateral hip pain is caused by disease of the gluteal tendons that secondarily inflames the bursa. This is most common in middle-aged women and is associated with a chronic and debilitating pain which does not respond to conservative treatment. Other causes of trochanteric bursitis include uneven leg length, iliotibial band syndrome, and weakness of the hip abductor muscles.

Greater trochanteric pain syndrome can remain incorrectly diagnosed for years, because it shares the same pattern of pain with many other musculoskeletal conditions. Thus people with this condition may be labeled malingerers, or may undergo many ineffective treatments due to misdiagnosis. It may also coexist with low back pain, arthritis, and obesity.

The most common symptoms in impingement syndrome are pain, weakness and a loss of movement at the affected shoulder. The pain is often worsened by shoulder overhead movement and may occur at night, especially if the patient is lying on the affected shoulder. The onset of the pain may be acute if it is due to an injury or may be insidious if it is due to a gradual process such as an osteoarthritic spur. The pain has been described as dull rather than sharp, and lingers for long periods of a time, making it hard to fall asleep at night. Other symptoms can include a grinding or popping sensation during movement of the shoulder.

The range of motion at the shoulder may be limited by pain. A painful arc of movement may be present during forward elevation of the arm from 60° to 120°. Passive movement at the shoulder will appear painful when a downwards force is applied at the acromion but the pain will ease once the downwards force is removed.