Magnetic resonance imaging (MRI) can be helpful in assessing for a ligamentous injury to the medial side of the knee. Milewski et al. has found that grade I to III classification can be seen on MRI. With a high-quality image (1.5 tesla or 3 tesla magnet) and no previous knowledge of the patient’s history, musculoskeletal radiologists were able to accurately diagnose medial knee injury 87% of the time. MRI can also show associated bone bruises on the lateral side of the knee, which one study shows, happen in almost half of medial knee injuries.

Knee MRIs should be avoided for knee pain without mechanical symptoms or effusion, and upon non-successful results from a functional rehabilitation program.

Anterior-posterior (AP) radiographs are useful for reliably assessing normal anatomical landmarks. Bilateral valgus stress AP images can show a difference in medial joint space gapping. It has been reported that an isolated grade III sMCL tear will show an increase in medial compartment gapping of 1.7 mm at 0° of knee flexion and 3.2 mm at 20° of knee flexion, compared to the contralateral knee. Additionally, a complete medial ligamentous disruption (sMCL, dMCL, and POL) will show increased gapping by 6.5 mm at 0° and 9.8 mm at 20° during valgus stress testing. Pellegrini-Stieda syndrome can also be seen on AP radiographs. This finding is due to calcification of the sMCL (heterotopic ossification) caused by the chronic tear of the ligament.

The diagnosis of patellofemoral pain syndrome is made by ruling out patellar tendinitis, prepatellar bursitis, plica syndrome, Sinding-Larsen and Johansson syndrome, and Osgood–Schlatter disease.

Patients can be observed standing and walking to determine patellar alignment. The Q-angle, lateral hypermobility, and J-sign are commonly used determined to determine patellar maltracking. The patellofemoral glide, tilt, and grind tests (Clarke's sign), when performed, can provide strong evidence for PFPS. Lastly, lateral instability can be assessed via the patellar apprehension test, which is deemed positive when there is pain or discomfort associated with lateral translation of the patella.

Treatment generally includes the following:

- Sometimes pharmacologic therapy for initial disease treatment

- Physical therapy

- Occupational therapy

- Use of appropriate assistive devices such as orthoses

- Surgical treatment

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.

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%.

Knee MRIs should be avoided for knee pain without symptoms or effusion, unless there are non-successful results from a functional rehabilitation program.

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

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 )

Generally, no treatment is required for idiopathic presentation as it is a normal anatomical variant in young children. Treatment is indicated when it persists beyond 3 and a half years old. In the case of unilateral presentation or progressive worsening of the curvature, when caused by rickets, the most important thing is to treat the constitutional disease, at the same time instructing the care-giver never to place the child on its feet. In many cases this is quite sufficient in itself to effect a cure, but matters can be hastened somewhat by applying splints. When the deformity arises in older patients, either from trauma or occupation, the only permanent treatment is surgery, but orthopaedic bracing can provide relief.

Persons with knock knees often have collapsed inner arches of their feet, and their inner ankle bones are generally lower than their outer ankle bones. Adults with uncorrected genu valgum are typically prone to injury and chronic knee problems such as chondromalacia and osteoarthritis. These in turn can cause severe pain and problems in walking.

It is normal for children to have knock knees between the ages of two and five years of age, and almost all of them resolve as the child grows older. If symptoms are prolonged and pronounced or hereditary, doctors often use orthotic shoes or leg braces at night to gently move a child's leg back into position. If the condition persists and worsens later in life, surgery may be required to relieve pain and complications resulting from severe or hereditary genu valgum. Available surgical procedures include adjustments to the lower femur and total knee replacement (TKR).

Weight loss and substitution of high-impact for low-impact exercise can help slow progression of the condition. With every step, the patient's weight places a distortion on the knee toward a knocked knee position, and the effect is increased with increased angle or increased weight. Even in the normal knee position, the femurs function at an angle because they connect to the hip girdle at points much further apart than they connect at the knees.

Physical therapy is generally of benefit to people with knock knees. To correct knock knees, the entire leg must be treated, especially:

1. Activating and developing the arches of the feet,

2. Waking up the outer leg muscles (abductors), and

3. Learning how to move the inner ankle bone inwards towards the outer ankle bone, and upwards towards the knee.

Working with a physical medicine specialist such as a physiatrist, or a physiotherapist may assist a patient learning how to improve outcomes and use the leg muscles properly to support the bone structures. Alternative or complementary treatments may include certain procedures from Iyengar Yoga or the Feldenkrais Method.

Rarely, the bone malformation underlying knock knees can be traced to a lack of nutrition necessary for bone growth, which can cause conditions such as rickets (lack of bone nutrients, especially dietary vitamin D and calcium), or scurvy (lack of vitamin C). The correction of the underlying vitamin deficiency may restore a more normal progression of bone growth.

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.

Measurement and diagnosis of lumbar hyperlordosis can be difficult. Obliteration of vertebral end-plate landmarks by interbody fusion may make the traditional measurement of segmental lumbar lordosis more difficult. Because the L4-L5 and L5-S1 levels are most commonly involved in fusion procedures, or arthrodesis, and contribute to normal lumbar lordosis, it is helpful to identify a reproducible and accurate means of measuring segmental lordosis at these levels.

A visible sign of hyperlordosis is an abnormally large arch of the lower back and the person appears to be puffing out his or her stomach and buttocks. Precise diagnosis is done by looking at a complete medical history, physical examination and other tests of the patient. X-rays are used to measure the lumbar curvature, bone scans are conducted in order to rule out possible fractures and infections, magnetic resonance imaging (MRI) is used to eliminate the possibility of spinal cord or nerve abnormalities, and computed tomography scans (CT scans) are used to get a more detailed image of the bones, muscles and organs of the lumbar region.

Treatment for children with Blount's disease is typically braces but surgery may also be necessary, especially for teenagers. The operation consists of removing a piece of tibia, breaking the fibula and straightening out the bone; there is also a choice of elongating the legs. If not treated early enough, the condition worsens quickly.

Diagnosis should be based on the clinical and radiographic findings and a genetic analysis can be assessed.

Since lumbar hyperlordosis is usually caused by habitual poor posture, rather than by an inherent physical defect like scoliosis or hyperkyphosis, it can be reversed. This can be accomplished by stretching the lower back, hip-flexors, hamstring muscles, and strengthening abdominal muscles.Dancers should ensure that they don't strain themselves during dance rehearsals and performances. To help with lifts, the concept of isometric contraction, during which the length of muscle remains the same during contraction, is important for stability and posture.

Lumbar hyperlordosis may be treated by strengthening the hip extensors on the back of the thighs, and by stretching the hip flexors on the front of the thighs.

Only the muscles on the front and on the back of the thighs can rotate the pelvis forward or backward while in a standing position because they can discharge the force on the ground through the legs and feet. Abdominal muscles and erector spinae can't discharge force on an anchor point while standing, unless one is holding his hands somewhere, hence their function will be to flex or extend the torso, not the hip.

Back hyper-extensions on a Roman chair or inflatable ball will strengthen all the posterior chain and will treat hyperlordosis. So too will stiff legged deadlifts and supine hip lifts and any other similar movement strengthening the posterior chain "without involving the hip flexors" in the front of the thighs. Abdominal exercises could be avoided altogether if they stimulate too much the psoas and the other hip flexors.

Controversy regarding the degree to which manipulative therapy can help a patient still exists. If therapeutic measures reduce symptoms, but not the measurable degree of lordotic curvature, this could be viewed as a successful outcome of treatment, though based solely on subjective data. The presence of measurable abnormality does not automatically equate with a level of reported symptoms.

Exact diagnosis remains widely built on precise history taking, with the characteristic clinical and radiographic skeletal features. Genetic diagnosis is based on DNA sequencing. Because plasma COMP levels are significantly reduced in patients with COMP mutations, such as pseudoachondroplasia, measuring plasma COMP levels has become a reliable means of diagnosing this and pathopysiologically similar disorders.

Accurate assessment of plain radiographic findings remains an important contributor to diagnosis of pseudoachondroplasia. It is noteworthy that vertebral radiographic abnormalities tend to resolve over time. Epiphyseal abnormalities tend to run a progressive course. Patients usually suffer early-onset arthritis of hips and knees. Many unique skeletal radiographic abnormalities of patients with pseudoachondroplasia have been reported in the literature.

- Together with rhizomelic limb shortening, the presence of epiphyseal-metaphyseal changes of the long bones is a distinctive radiologic feature of pseudoachondroplasia.

- Hypoplastic capital femoral epiphyses, broad short femoral necks, coxa vara, horizontality of acetabular roof and delayed eruption of secondary ossification center of os pubis and greater trochanter.

- Dysplastic/hypoplastic epiphyses especially of shoulders and around the knees.

- Metaphyseal broadening, irregularity and metaphyseal line of ossification. These abnormalities that are typically encountered in proximal humerus and around the knees are collectively known as “rachitic-like changes”.

- Radiographic lesions of the appendicular skeleton are typically bilateral and symmetric.

- Oval shaped vertebrae with anterior beak originating and platyspondyly demonstrated on lateral radiographs of the spine.

- Normal widening of the interpedicular distances caudally demonstrated on anteroposterior radiographs of the dorsolumbar region. This is an important differentiating feature between pseudoachondroplasia and achondroplasia.

- Odontoid hypoplasia may occur resulting in cervical instability.

Symptomatic individuals should be seen by an orthopedist to assess the possibility of treatment (physiotherapy for muscular strengthening, cautious use of analgesic medications such as nonsteroidal anti-inflammatory drugs). Although there is no cure, surgery is sometimes used to relieve symptoms. Surgery may be necessary to treat malformation of the hip (osteotomy of the pelvis or the collum femoris) and, in some cases, malformation (e.g., genu varum or genu valgum). In some cases, total hip replacement may be necessary. However, surgery is not always necessary or appropriate.

Sports involving joint overload are to be avoided, while swimming or cycling are strongly suggested. Cycling has to be avoided in people having ligamentous laxity.

Weight control is suggested.

The use of crutches, other deambulatory aids or wheelchair is useful to prevent hip pain. Pain in the hand while writing can be avoided using a pen with wide grip.

There are several ways to determine if a child has chondrodystrophy, including parent testing and x-rays. If the fetus is suspected of having chondrodystrophy, the parents can be tested to find out if the fetus in fact does have the disease. It is not until the baby is born that a diagnosis can be declared. The diagnosis is declared with the help of several x-rays and charted bone growth patterns. Once the child is diagnosed the parents have to monitor the children because of several different factors. As the child gets older, hearing, eyesight and motor skills may be defective. Also, breathing (apnea) and weight problems (obesity) may occur. Structurally, scoliosis, bowed legs (genu varum), and arthritis may result.

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.

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.

There is no treatment at this time to promote bone growth in chondrodystrophy patients. Certain types of growth hormone seem to increase the rate of growth during the first year of life/treatment, but have no substantial effect in adult patients. Only a few surgical centers in the world perform, experimentally, leg and arm lengthening procedures. Most common therapies are found in seeking help from: family physicians, pediatrics, internists, endocrinologists, geneticists, orthopedists and neurologists.