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.

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

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.

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

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.

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.

Sprengel's deformity (also known as high scapula or congenital high scapula) is a rare congenital skeletal abnormality where a person has one shoulder blade that sits higher on the back than the other. The deformity is due to a failure in early fetal development where the shoulder fails to descend properly from the neck to its final position. The deformity is commonly associated with other conditions, most notably Klippel-Feil syndrome, congenital scoliosis including cervical scoliosis, fused ribs, the presence of an omovertebral bone and spina bifida. The left shoulder is the most commonly affected shoulder but the condition can be bilateral, meaning that both shoulders are affected. About 75% of all observed cases are girls. Treatment includes surgery in early childhood and physical therapy. Surgical treatment in adulthood is complicated by the risk of nerve damage when removing the omovertebral bone and when stretching the muscle tissue during relocation of the shoulder.

The scapula is small and rotated so that its inferior edge points toward the spine. There is a high correlation between Sprengel's deformity and the Klippel-Feil syndrome. Sometimes a bony connection is present between the elevated scapula and one of the cervical vertebrae, usually C5 or C6. This connection is known as the omovertebral bone.

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.

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.

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.

Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.

The healing time for a routine mandible fractures is 4–6 weeks whether MMF or rigid internal fixation (RIF) is used. For comparable fractures, patients who received MMF will lose more weight and take longer to regain mouth opening, whereas, those who receive RIF have higher infection rates.

The most common long-term complications are loss of sensation in the mandibular nerve, malocclusion and loss of teeth in the line of fracture. The more complicated the fracture (infection, comminution, displacement) the higher the risk of fracture.

Condylar fractures have higher rates of malocclusion which in turn are dependent on the degree of displacement and/or dislocation. When the fracture is intracapsular there is a higher rate of late-term osteoarthritis and the potential for ankylosis although the later is a rare complication as long as mobilization is early. Pediatric condylar fractures have higher rates of ankylosis and the potential for growth disturbance.

Rarely, mandibular fracture can lead to Frey's syndrome.

Proximal femoral focal deficiency (PFFD), also known as Congenital Femoral Deficiency (CFD), is a rare, non-hereditary birth defect that affects the pelvis, particularly the hip bone, and the proximal femur. The disorder may affect one side or both, with the hip being deformed and the leg shortened.

It is commonly linked with the absence or shortening of a leg bone (fibular hemimelia) and the absence of a kneecap. Other linked birth defects include the dislocation or instability of the joint between the femur and the kneecap, a shortened tibia or fibula, and foot deformities.

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.

Leri-Weill dyschondrosteosis is a pseudoautosomal dominant disorder which occurs more frequently in females and is due to a mutation, deletion or duplication of the SHOX gene. The SHOX gene plays a particularly important role in the growth and maturation of bones in the arms and legs. The SHOX gene is located within band Xp22.3 of the pseudoautosomal region of the X chromosome, which escapes X-inactivation. Homozygous SHOX gene mutations result in Langer mesomelic dysplasia.

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 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.

The cause of fibular hemimelia is unclear. Purportedly, there have been some incidents of genetic distribution in a family; however, this does not account for all cases. Maternal viral infections, embryonic trauma, teratogenic environmental exposures or vascular dysgenesis (failure of the embryo to form a satisfactory blood supply) between four and seven weeks gestation are considered possible causes.

In an experimental mouse model, change in the expression of a homeobox gene led to similar, but bilateral, fibular defects.

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.

It is a congenital subluxation or dislocation of the ulna's distal end, due to malformation of the bones. Sometimes, minor abnormalities of other bone structures, often caused by disease or injury, such as a fracture of the distal end of the radius with upward displacement of the distal fragment. The deformity varies in degree from a slight protrusion of the lower end of the ulna, to complete dislocation of the inferior radio-ulnar joint with marked radial deviation of the hand. Severe deformities are associated with congenital absence or hypoplasia of the radius.

The male:female rate of this disorder is 1:4. The incidence is unknown, and there is no described racial predominance. Even though Madelung's Deformity is considered a congenital disorder, symptoms sometimes aren't seen until adulthood. In most cases, symptoms find their onset during midchildhood. At this age, the relatively slower growth of the ulnar and palmar part of the radius, leads to an increasingly progressive deformity. Pain and deformity are the main symptoms patients present with. Typical clinical presentation consists of a short forearm, anterior-ulnar bow of the radius and a forward subluxation of the hand on the forearm. As mentioned before, the severity of the disorder varies greatly, which also leads to a spectrum of presentation.

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.

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.

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.