It is sometimes possible to correct the problem with surgery, though this has high failure rates for treatment of post-traumatic radioulnar synostosis.

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.

As an acquired condition it has often been linked to traditions of swaddling infants, use of overly restrictive baby seats, carriers and other methods of transporting babies, or use of a cradle board which locks the hip joint in an "adducted" position (pulling the knees together tends to pull the heads of the femur bone out of the sockets or acetabulae) for extended periods. Modern swaddling techniques, such as the 'hip healthy swaddle' have been developed to relieve stress on hip joints caused by traditional swaddling methods.

Further risk factors include breech birth, gender, genetics (family history), and firstborns. In breech position the femoral head tends to get pushed out of the socket. A narrow uterus also facilitates hip joint dislocation during fetal development and birth.

Depending on the severity of the deformities, the treatment may include the amputation of the foot or part of the leg, lengthening of the femur, extension prosthesis, or custom shoe lifts. Amputation usually requires the use of prosthesis. Another alternative is a rotationplasty procedure, also known as Van Ness surgery. In this situation the foot and ankle are surgically removed, then attached to the femur. This creates a functional "knee joint". This allows the patient to be fit with a below knee prosthesis vs a traditional above knee prosthesis.

In less severe cases, the use of an Ilizarov apparatus can be successful in conjunction with hip and knee surgeries (depending on the status of the femoral head/kneecap) to extend the femur length to normal ranges. This method of treatment can be problematic in that the Ilizarov might need to be applied both during early childhood (to keep the femur from being extremely short at the onset of growth) and after puberty (to match leg lengths after growth has ended). The clear benefit of this approach, however, is that no prosthetics are needed and at the conclusion of surgical procedures the patient will not be biologically or anatomically different from a person born without PFFD.

Post-traumatic cases are most likely to develop following surgery for a forearm fracture, this is more common with high-energy injuries where the bones are broken into many pieces (comminuted). It can also develop following soft tissue injury to the forearm where there is haematoma formation.

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.

First options for treatment are conservative, using hot or cold packs, rest and NSAID's at first. If no improvement is made, a splint or brace can be used to keep the deviated arm straight. When none of the conservative treatments work surgical intervention is designated.

Arthroscopic repair of Bankart injuries have high success rates, with studies showing that nearly one-third of patients require re-intervention for continued shoulder instability following repair. Options for repair include an arthroscopic technique or a more invasive open Latarjet procedure, with the open technique tending to have a lower incidence of recurrent dislocation, but also a reduced range of motion following surgery.

Jaw dislocation is common for people who are in car, motorcycle or related accidents and also sports related activities. This injury does not pin point specific ages or genders because it could happen to anybody. People who dislocate their jaw do not usually seek emergency medical care. In most cases, jaw dislocations are acute and can be altered by minor manipulations. It was reported from one study that over a seven-year period at an emergency medical site, with 100,000 yearly visits, there were only 37 patients that were seen for a dislocated jaw.

Most temporomandibular disorders (TMDs) are self-limiting and do not get worse. Simple treatment, involving self-care practices, rehabilitation aimed at eliminating muscle spasms, and restoring correct coordination, is all that is required. Nonsteroidal anti inflammatory analgesics (NSAIDs) should be used on a short-term, regular basis and not on an as needed basis. On the other hand, treatment of chronic TMD can be difficult and the condition is best managed by a team approach; the team consists of a primary care physician, a dentist, a physiotherapist, a psychologist, a pharmacologist, and in small number of cases, a surgeon. The different modalities include patient education and self-care practices, medication, physical therapy, splints, psychological counseling, relaxation techniques, biofeedback, hypnotherapy, acupuncture, and arthrocentesis.

As with most dislocated joints, a dislocated jaw can usually be successfully positioned into its normal position by a trained medical professional. Attempts to readjust the jaw without the assistance of a medical professional could result in worsening of the injury. The health care provider may be able to set it back into the correct position by manipulating the area back into its proper position. Numbing medications such as general anesthetics, muscle relaxants, or in some cases sedation, may be needed to relax the strong jaw muscle. In more severe cases, surgery may be needed to reposition the jaw, particularly if repeated jaw dislocations have occurred.

In children, the results of early treatment are always good, typically normal or nearly so. If diagnosis is delayed, reconstructive surgery is needed and complications are much more common and results poorer. In adults, the healing is slower and results usually not as good.

Complications of ORIF surgery for Monteggia fractures can include non-union, malunion, nerve palsy and damage, muscle damage, arthritis, tendonitis, infection, stiffness and loss of range of motion, compartment syndrome, audible popping or snapping, deformity, and chronic pain associated with surgical hardware such as pins, screws, and plates. Several surgeries may be needed to correct this type of fracture as it is almost always a very complex fracture that requires a skilled orthopedic surgeon, usually a 'specialist', familiar with this type of injury.

Monteggia fractures may be managed conservatively in children with closed reduction (resetting and casting), but due to high risk of displacement causing malunion, open reduction internal fixation is typically performed.

Osteosynthesis (open reduction and internal fixation) of the ulnar shaft is considered the standard of care in adults. It promotes stability of the radial head dislocation and allows very early mobilisation to prevent stiffness. The elbow joint is particularly susceptible to loss of motion.

In the original description by Hume, where the olecranon fractures were not displaced, treatment consisted of closed reduction of the radial head dislocation under general anaesthesia by supination of the forearm. This was followed by immobilisation of the arm in a plaster cast with the elbow flexed at 90° and the forearm in supination for 6 weeks.

Where the olecranon fracture is displaced, open reduction internal fixation is recommended. Once the olecranon has been repaired, closed reduction of the radial head dislocation is usually possible. This is followed by immobilisation with the elbow flexed to 90° and the forearm in the neutral position. The duration of immobilisation depends on clinical assessment of the joint, and mobilisation may be possible after as little as 4 weeks.

Radioulnar synostosis is one of the more common failures of separation of parts of the upper limb. There are two general types: one is characterized by fusion of the radius and ulna at their proximal borders and the other is fused distal to the proximal radial epiphysis. Most cases are sporadic, congenital (due to a defect in longitudinal segmentation at the 7th week of development) and less often post-traumatic, bilateral in 60%, and more common in males. Familial cases in association with autosomal dominant transmission appear to be concentrated in certain geographic regions, such as Sicily.

The condition frequently is not noted until late childhood, as function may be normal, especially in unilateral cases. Increased wrist motion may compensate for the absent forearm motion. It has been suggested that individuals whose forearms are fixed in greater amounts of pronation (over 60 degrees) face more problems with function than those with around 20 degrees of fixation. Pain is generally not a problem, unless radial head dislocation should occur.

Most examples of radioulnar synostosis are isolated (non-syndromic). Syndromes that may be accompanied by radioulnar synostosis include X chromosome polyploidy (e.g., XXXY) and other chromosome disorders (e.g., 4p- syndrome, Williams syndrome), acrofacial dysostosis, Antley–Bixler syndrome, genitopatellar syndrome, Greig cephalopolysyndactyly syndrome, hereditary multiple osteochondromas (hereditary multiple exostoses), limb-body wall complex, and Nievergelt syndrome.

Craniosynostosis (from cranio, cranium; + syn, together; + ostosis relating to bone) is a condition in which one or more of the fibrous sutures in an infant skull prematurely fuses by turning into bone (ossification). Craniosynostosis has following kinds: scaphocephaly, trigonocephaly, plagiocephaly, anterior plagiocephaly, posterior plagiocephaly, brachycephaly, oxycephaly, pansynostosis.

With prompt treatment, particularly open reduction, and early mobilisation the outcome is generally good. High energy injuries and associated fractures worsen the outcome.

Plica syndrome treatment focuses on decreasing inflammation of the synovial capsule. A nonsteroidal anti-inflammatory drug (NSAID) is often used in conjunction with therapeutic exercise and modalities. Iontophoresis and phonophoresis have been utilized successfully against inflammation of the plica and synovial capsule. Failing these, surgical removal of the plica of the affected knee may be necessary.

A Bankart lesion is an injury of the anterior (inferior) glenoid labrum of the shoulder due to anterior shoulder dislocation. When this happens, a pocket at the front of the glenoid forms that allows the humeral head to dislocate into it. It is an indication for surgery and often accompanied by a Hill-Sachs lesion, damage to the posterior humeral head.

The Bankart lesion is named after English orthopedic surgeon Arthur Sydney Blundell Bankart (1879 – 1951).

A bony Bankart is a Bankart lesion that includes a fracture in of the anterior-inferior glenoid cavity of the scapula bone.

The incidence of Hill–Sachs lesion is not known with certainty. It has been reported to be present in 40% to 90% of patients presenting with anterior shoulder instability, that is subluxation or dislocation. In those who have recurrent events, it may be as high as 100%. Its presence is a specific sign of dislocation and can thus be used as an indicator that dislocation has occurred even if the joint has since regained its normal alignment. The average depth of Hill–Sachs lesion has been reported as 4.1 mm. Large, engaging Hill-Sachs fractures can contribute to shoulder instability and will often cause painful clicking, catching, or popping.

"Physiolysis"

Purpose of the treatment is the removal of the epiphysis that causes the abnormal growth of the wrist. This is done by making a small incision at the volar-radial side. This approach passes the Flexor pollicis longus and Palmaris longus and leaves the Median nerve and Radial artery protected. Then the Pronator quadratus muscle is found and detached from the radius. Here a cut into the bone will find the abnormal epiphysis. When the epiphysis is clearly defined more bone is removed so the radius is in its normal position and prevents a new bone bar from forming. This is the end of the physiolisis. This is always combined with a Vickers Ligament release.

"Dome osteotomy"

Purpose of this treatment option is to straighten the abnormal radius. To do this, an 8 cm incision is made from the wrist crease at the palmair radial side. The approach is made passing the Flexor carpi radialis with detachment of the Pronator quadratus muscle from the radius. Now the Vickers ligament release is done. After this the periosteum is elevated and a crescent-shaped osteotomy, concave at the end, is marked on the bone. Now the radius is cut dome shaped and straightened. The distal end of the radius stays attached to the ulna. The dome shape of the osteotomy allows adequate bony contact for stability and a subperiosteal void for rapid healing.

"Vickers Ligament Release"

This ligament causes the wrist to deform even more. The purpose of this release is to release the tension and leave the wrist straight in further growth. In both physiolysis and dome osteonomy there should be a clear view of the abnormal.

Synostosis (plural: synostoses) is fusion of two bones. It can be normal in puberty, fusion of the epiphysis, or abnormal. When synostosis is abnormal it is a type of dysostosis.

Examples of synostoses include:

- craniosynostosis – an abnormal fusion of two or more cranial bones;

- radioulnar synostosis – the abnormal fusion of the radius and ulna bones of the forearm;

- tarsal coalition – a failure to separately form all seven bones of the tarsus (the hind part of the foot) resulting in an amalgamation of two bones; and

- syndactyly – the abnormal fusion of neighboring digits.

Synostosis within joints can cause ankylosis.

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.

Although the precise mechanism of injury is unclear, the injury occurs in children who have fallen heavily with their arm trapped under the body. In his original description of the injury, Hume suggested that the injury occurred as a result of hyperextension of the elbow leading to fracture of the olecranon, with pronation of the forearm leading to the radial head dislocation.

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.

Treatment may be with or without surgery, depending on the type of fracture.

After an anterior shoulder dislocation, the risk of a future dislocation is about 20%. This risk is greater in males than females.