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.

Radial aplasia is a congenital defect which affects the formation of the radius bone in the arm. The radius is the lateral bone which connects to the wrist via articulation with the carpal bones. A child born with this condition has either a short or absent radius bone in one or both of his or her arm(s). Radial aplasia also results in the thumb being either partly formed or completely absent from the hand. Radial aplasia is connected with the condition VACTERL association. The cause for radial aplasia in unknown, but it widely believed to occur within the first ten weeks of gestation.

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.

Polydactyly or polydactylism (), also known as hyperdactyly, is a congenital physical anomaly in humans, dogs, and cats having supernumerary fingers or toes.

Polydactyly is the opposite of oligodactyly (fewer fingers or toes).

Radial dysplasia, also known as radial club hand or radial longitudinal deficiency, is a congenital difference occurring in a longitudinal direction resulting in radial deviation of the wrist and shortening of the forearm. It can occur in different ways, from a minor anomaly to complete absence of the radius, radial side of the carpal bones and thumb. Hypoplasia of the distal humerus may be present as well and can lead to stiffnes of the elbow. Radial deviation of the wrist is caused by lack of support to the carpus, radial deviation may be reinforced if forearm muscles are functioning poorly or have abnormal insertions. Although radial longitudinal deficiency is often bilateral, the extent of involvement is most often asymmetric.

The incidence is between 1:30,000 and 1:100,000 and it is more often a sporadic mutation rather than an inherited condition. In case of an inherited condition, several syndromes are known for an association with radial dysplasia, such as the cardiovascular Holt-Oram syndrome, the gastrointestinal VATER syndrome and the hematologic Fanconi anemia and TAR syndrome. Other possible causes are an injury to the apical ectodermal ridge during upper limb development, intrauterine compression, or maternal drug use (thalidomide).

Type VII of radial polydactyly is associated with several syndromes:

Holt–Oram syndrome, Fanconi anemia (aplastic anemia by the age of 6), Townes–Brocks syndrome, and Greig cephalopolysyndactyly (also known to occur with ulnar polydactyly).

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.

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.

Larsen syndrome (LS) is a congenital disorder discovered in 1950 by Larsen and associates when they observed dislocation of the large joints and face anomalies in six of their patients. Patients with Larsen syndrome normally present with a variety of symptoms, including congenital anterior dislocation of the knees, dislocation of the hips and elbows, flattened facial appearance, prominent foreheads, and depressed nasal bridges. Larsen syndrome can also cause a variety of cardiovascular and orthopedic abnormalities. This rare disorder is caused by a genetic defect in the gene encoding filamin B, a cytoplasmic protein that is important in regulating the structure and activity of the cytoskeleton. The gene that influences the emergence of Larsen syndrome is found in chromosome region, 3p21.1-14.1, a region containing human type VII collagen gene. Larsen syndrome has recently been described as a mesenchyme disorder that affects the connective tissue of an individual. Autosomal dominant and recessive forms of the disorder have been reported, although most cases are autosomal dominant. Reports have found that in Western societies, Larsen syndrome can be found in one in every 100,000 births, but this is most likely an underestimate because the disorder is frequently unrecognized or misdiagnosed.

Hemimelia comprises

- Fibular hemimelia, Congenital longitudinal deficiency of the fibula or Fibular longitudinal meromelia

- Tibial hemimelia, Congenital longitudenal deficiency of the tibia, Congenital aplasia and dysplasia of the tibia with intact fibula, Congenital longitudinal deficiency of the tibia or Tibial longitudinal meromelia

- Radial Hemimelia, Congenital longitudinal deficiency of the radius, Radial clubhand, Radial longitudinal meromelia or Radial ray agenesis

- Ulnar hemimelia, Congenital longitudinal deficiency of the ulna, Ulnar clubhand or Ulnar longitudinal meromelia

Liebenberg Syndrome is a rare autosomal genetic disease that involves a deletion mutation upstream of the PITX1 gene, which is one that's responsible for the body's organization, specifically in forming lower limbs. In animal studies, when this deletion was introduced to developing birds, their wing buds were noted to take on limb-like structures.

The condition was first described by Dr. F. Liebenberg in 1973 while he followed multiple generations of a South African family, but it has since been noticed in other family lineages across the world.

Filamins are cytoplasmic proteins that regulate the structure and activity of the cytoskeleton. These proteins serve as scaffolds on which intracellular signaling and protein trafficking are organized. Filamin B has been found to be expressed in human growth plate chondrocytes, which are especially important in vertebrae segmentation and skeleton morphogenesis. Genetic analysis of patients with Larsen syndrome has found the syndrome is caused by missense mutations in the gene that codes for filamin B. These mutations cause an accelerated rate of apoptosis in the epiphyseal growth plates of individuals with the mutation. The defects can cause short stature and other symptoms associated with Larsen syndrome.

Colles fractures occur in all age groups, although certain patterns follow an age distribution.

- In the elderly, because of the weaker cortex, the fracture is more often extra-articular.

- Younger individuals tend to require a higher energy force to cause the fracture and tend to have more complex intra-articular fractures. In children with open epiphyses, an equivalent fracture is the "epiphyseal slip", as can be seen in other joints, such as a slipped capital femoral epiphysis in the hip. This is a Salter I or II fracture with the deforming forces directed through the weaker epiphyseal plate.

- More common in women because of post-menopausal osteoporosis.

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.

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.

Perthes lesion is variant of Bankart lesion, presenting as an anterior glenohumeral injury that occurs when the scapular periosteum remains intact but is stripped medially and the anterior labrum is avulsed from the glenoid but remains partially attached to the scapula by intact periosteum.

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

The etiology of the Galeazzi fracture is thought to be a fall that causes an axial load to be placed on a hyperpronated forearm. However, researchers have been unable to reproduce the mechanism of injury in a laboratory setting.

After the injury, the fracture is subject to deforming forces including those of the brachioradialis, pronator quadratus, and thumb extensors, as well as the weight of the hand. The deforming muscular and soft-tissue injuries that are associated with this fracture cannot be controlled with plaster immobilization.

Surgery is an option to correct some of the morphological changes made by Liebenberg Syndrome. Cases exist where surgery is performed to correct radial deviations and flexion deformities in the wrist. A surgery called a carpectomy has been performed on a patient whereby a surgeon removes the proximal row of the carpal bones. This procedure removes some of the carpal bones to create a more regular wrist function than is observed in people with this condition.

More severe types (Bayne type III en IV) of radial dysplasia can be treated with surgical intervention. The main goal of centralization is to increase hand function by positioning the hand over the distal ulna, and stabilizing the wrist in straight position. Splinting or soft-tissue distraction may be used preceding the centralization.

In classic centralization central portions of the carpus are removed to create a notch for placement of the ulna. A different approach is to place the metacarpal of the middle finger in line with the ulna with a fixation pin.

If radial tissues are still too short after soft-tissue stretching, soft tissue release and different approaches for manipulation of the forearm bones may be used to enable the placement of the hand onto the ulna. Possible approaches are shortening of the ulna by resection of a segment, or removing carpal bones. If the ulna is significantly bent, osteotomy may be needed to straighten the ulna. After placing the wrist in the correct position, radial wrist extensors are transferred to the extensor carpi ulnaris tendon, to help stabilize the wrist in straight position. If the thumb or its carpometacarpal joint is absent, centralization can be followed by pollicization. Postoperatively, a long arm plaster splinter has to be worn for at least 6 to 8 weeks. A removable splint is often worn for a long period of time.

Radial angulation of the hand enables patients with stiff elbows to reach their mouth for feeding; therefore treatment is contraindicated in cases of extension contracture of the elbow. A risk of centralization is that the procedure may cause injury to the ulnar physis, leading to early epiphyseal arrest of the ulna, and thereby resulting in an even shorter forearm. Sestero et al. reported that ulnar growth after centralization reaches from 48% to 58% of normal ulnar length, while ulnar growth in untreated patients reaches 64% of normal ulnar length. Several reviews note that centralization can only partially correct radial deviation of the wrist and that studies with longterm follow-up show relapse of radial deviation.

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.

The injury is immediately fatal in 70% of cases, with an additional 15% surviving to the emergency room, but perishing during their hospital stay. A basion-dental interval of 16mm or greater is associated with mortality. In those with neurologic deficits, survival is unlikely.