Dupuytren’s disease has a high recurrence rate, especially when a person has so called Dupuytren’s diathesis. The term diathesis relates to certain features of Dupuytren's disease and indicates an aggressive course of disease.

The presence of all new Dupuytren’s diathesis factors increases the risk of recurrent Dupuytren’s disease by 71% compared with a baseline risk of 23% in people lacking the factors. In another study the prognostic value of diathesis was evaluated. They concluded that presence of diathesis can predict recurrence and extension. A scoring system was made to evaluate the risk of recurrence and extension evaluating the following values: bilateral hand involvement, little finger surgery, early onset of disease, plantar fibrosis, knuckle pads and radial side involvement.

Minimally invasive therapies may precede higher recurrence rates. Recurrence lacks a consensus definition. Furthermore, different standards and measurements follow from the various definitions.

In one study, those with stage 2 of the disease were found to have a slightly increased risk of mortality, especially from cancer.

About 1.8 million people go to the emergency department each year due to hand injuries.

Burn scar contractures do not go away on their own, although may improve with the passage of time, with occupationaltherapy and physiotherapy, and with splinting. If persistent the person may need the contracture to be surgically released. Techniques may include local skin flaps (z-plasty) or skin grafting (full thickness or split thickness). There are also pharmacy and drug-store treatments that can be used to help scar maturation, especially silicone gel treatments. Prevention of contracture formation is key. For instance, in the case of a burned hand one would splint the hand and wrap each finger individually. In the instance of burns on the neck, hyperextension of the neck (i.e. no use of pillows) should be maintained during the healing process. Carbon dioxide laser therapy is now also used to aid in the loosening of surrounding skin, although is yet to form as part of an official global rehabilitation program.

Burn scar contracture refers to the tightening of the skin after a second or third degree burn. When skin is burned, the surrounding skin begins to pull together, resulting in a contracture. It needs to be treated as soon as possible because the scar can result in restriction of movement around the injured area.

Most hand injuries are minor and can heal without difficulty. However, any time the hand or finger is cut, crushed or the pain is ongoing, it is best to see a physician. Hand injuries when not treated on time can result in long term morbidity.

Antibiotics in simple hand injuries do not typically require antibiotics as they do not change the chance of infection.

There are few good estimates of prevalence for pes cavus in the general community. While pes cavus has been reported in between 2 and 29% of the adult population, there are several limitations of the prevalence data reported in these studies. Population-based studies suggest the prevalence of the cavus foot is approximately 10%.

Stenosing tenosynovitis is most commonly caused by overuse from chronic repetitive activities using the hand or the involved finger. Examples include work activities (e.g., computer use, materials handling) or recreational activities (e.g., knitting, golf, racket sports). Carpenters who use hammers suffer from this as well as those who continuously grip wood or other materials when cutting them due to having to use your hands as a clamp to hold things in place.

Primary stenosing tenosynovitis can be idiopathic, occurring in middle age women more frequently than in men, but can present also in infancy.

Secondary stenosing tenosynovitis can be caused by disease or entities that cause connective tissue disorders including the following:

- Rheumatoid arthritis and psoriatic arthritis—therefore the clinician must assess the hands for rheumatologic deformities.

- Gout

- Diabetes mellitus

- Amyloidosis

- Systemic lupus erythematosus

Others causes may include the following:

- Direct trauma to the site

- During the postpartum period

- Congenital

Pes cavus may be hereditary or acquired, and the underlying cause may be neurological, orthopedic, or neuromuscular. Pes cavus is sometimes—but not always—connected through Hereditary Motor and Sensory Neuropathy Type 1 (Charcot-Marie-Tooth disease) and Friedreich's Ataxia; many other cases of pes cavus are natural.

The cause and deforming mechanism underlying pes cavus is complex and not well understood. Factors considered influential in the development of pes cavus include muscle weakness and imbalance in neuromuscular disease, residual effects of congenital clubfoot, post-traumatic bone malformation, contracture of the plantar fascia, and shortening of the Achilles tendon.

Among the cases of neuromuscular pes cavus, 50% have been attributed to Charcot-Marie-Tooth disease, which is the most common type of inherited neuropathy with an incidence of 1 per 2,500 persons affected. Also known as Hereditary Motor and Sensory Neuropathy (HMSN), it is genetically heterogeneous and usually presents in the first decade of life with delayed motor milestones, distal muscle weakness, clumsiness, and frequent falls. By adulthood, Charcot-Marie-Tooth disease can cause painful foot deformities such as pes cavus. Although it is a relatively common disorder affecting the foot and ankle, little is known about the distribution of muscle weakness, severity of orthopaedic deformities, or types of foot pain experienced. There are no cures or effective courses of treatment to halt the progression of any form of Charcot-Marie-Tooth disease.

The development of the cavus foot structure seen in Charcot-Marie-Tooth disease has been previously linked to an imbalance of muscle strength around the foot and ankle. A hypothetical model proposed by various authors describes a relationship whereby weak evertor muscles are overpowered by stronger invertor muscles, causing an adducted forefoot and inverted rearfoot. Similarly, weak dorsiflexors are overpowered by stronger plantarflexors, causing a plantarflexed first metatarsal and anterior pes cavus.

Pes cavus is also evident in people without neuropathy or other neurological deficit. In the absence of neurological, congenital, or traumatic causes of pes cavus, the remaining cases are classified as being ‘idiopathic’ because their aetiology is unknown.

Prevention of the condition requires restoration of blood flow after injury and reduction of compartmental pressure on the muscles. Any splints, bandages, or other devices that might be obstructing circulation must be removed. A fasciotomy may be required to reduce pressure in the muscle compartment. If the contracture occurs, surgery to release the fixed tissues may help with the deformity and function of the hand.

Any fracture in elbow region or upper arm may lead to Volkmann's ischemic contracture, but it is especially associated with supracondylar fracture of the humerus.

Volkmann's contracture results from acute ischaemia and necrosis of the muscle fibres of the flexor group of muscles of the forearm, especially the flexor digitorum profundus and flexor pollicis longus. The muscles become fibrotic and shortened.

The condition is caused by obstruction on the brachial artery near the elbow, possibly from improper use of a tourniquet, improper use of a plaster cast, or compartment syndrome. It is also caused by fractures of the forearm bones if they cause bleeding from the major blood vessels of the forearm.

Garrod's pads (also known as "violinist's pads") are a cutaneous condition characterized by calluses on the dorsal aspect of the interphalangeal joints, i.e. the back side of the finger joints. They are often seen in violin, viola, and cello players, along with fiddler's neck and other dermatologic conditions peculiar to string musicians. Although Garrod’s pads are conventionally described as appearing on the proximal interphalangeal joint, Rimmer & Spielvogel document an instance on the distal interphalangeal joint of a cellist.

Garrod's pads are named after Archibald Garrod who first documented them in 1904 in association with Dupuytren's contracture. H.A. Bird described them as an incidental finding in a professional violinist and proposed that they arise in such cases due to repeated extreme tension of the extensor tendons over the interphalangeal joints. Bird noted that violin players use the left hand for a markedly different task than the right hand, with the extensor tendons in the left hand subjected to considerable tension, and that Garrod’s pads only arise on the left hand in such cases. This unilateral finding differentiates the occupational hazard of Garrod’s pads from more significant disorders. Among violinists and violists, Garrod’s pads apparently arise as a protective mechanism for the skin and subcutaneous tissues above the tendons; Bird notes that they do not protect against external trauma unlike most calluses.

Patients with Dupuytren's contracture are four times more likely to have coexisting Garrod's pads.

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).

Mechanical tension on a wound has been identified as a leading cause for hypertrophic scar formation.

When a normal wound heals, the body produces new collagen fibres at a rate which balances the breakdown of old collagen. Hypertrophic scars are red and thick and may be itchy or painful. They do not extend beyond the boundary of the original wound, but may continue to thicken for up to six months. They usually improve over one or two years, but may cause distress due to their appearance or the intensity of the itching; they can also restrict movement if they are located close to a joint.

Some people have an inherited tendency to this type of scarring, for example, those with Ehlers–Danlos syndrome, classic type. It is not possible to completely prevent hypertrophic scars, so those with a history of them should inform their doctor or surgeon if they need surgery. Scar therapies may speed up the process of change from a hypertrophic scar to a flatter, paler one.

Stenosing tenosynovitis (also known as trigger finger or trigger thumb) is a painful condition caused by the inflammation (tenosynovitis) and progressive restriction of the superficial and deep flexors fibrous tendon sheath adjacent to the A1 pulley at a metacarpal head. Repetitive forceful compression, tensile stress, and resistive flexion, causes inflammation, swelling, and microtrauma, that results in thickening (commonly a nodular formation) of the tendon distal to the pulley and stenosis of the tendon sheath leading to a painful digital base, limitation of finger movements, triggering, snapping, locking, and deformity progressively.

Patients report a popping sound at the proximal interphalangeal joint (PIP), morning stiffness with/without triggering, delayed and sometimes painful extension of the digit, and when more advanced, a locking position that requires manipulation to extend the affected finger. This condition more commonly affects the middle and ring fingers (occasionally the thumb), and the flexor rather than extensor tendons in the hand.

In rheumatic trigger finger (or in diabetes), more than one finger may be involved. Cases of stenosing peroneal tenosynovitis, have been reported where the patient presents with pain over the lateral malleolus, both with active and passive range of motion and no physical of radiographic evidence of instability.

The following factors may be involved in causing this deformity:

- Inherent laxity of the knee ligaments

- Weakness of biceps femoris muscle

- Instability of the knee joint due to ligaments and joint capsule injuries

- Inappropriate alignment of the tibia and femur

- Malunion of the bones around the knee

- Weakness in the hip extensor muscles

- Gastrocnemius muscle weakness (in standing position)

- Upper motor neuron lesion (for example, hemiplegia as the result of a cerebrovascular accident)

- Lower motor neuron lesion (for example, in post-polio syndrome)

- Deficit in joint proprioception

- Lower limb length discrepancy

- Congenital genu recurvatum

- Cerebral palsy

- Multiple sclerosis

- Muscular dystrophy

- Limited dorsiflexion (plantar flexion contracture)

- Popliteus muscle weakness

- Connective tissue disorders. In these disorders, there are excessive joint mobility (joint hypermobility) problems. These disorders include:

- Marfan syndrome

- Ehlers-Danlos syndrome

- Benign hypermobile joint syndrome

- Osteogenesis imperfecta disease

A hypertrophic scar is a cutaneous condition characterized by deposits of excessive amounts of collagen which gives rise to a raised scar, but not to the degree observed with keloids. Like keloids, they form most often at the sites of pimples, body piercings, cuts and burns. They often contain nerves and blood vessels. They generally develop after thermal or traumatic injury that involves the deep layers of the dermis and express high levels of TGF-β.

AC is caused by chronic and excessive exposure to ultraviolet radiation in sunlight.

Risk factors include:

- Outdoor lifestyle: e.g. farmers, sailors, fishermen, windsurfers, mountaineers, golfers, etc. This has given rise to synonyms for this condition such as "sailor's lip" and "farmer's lip". The prevalence in agricultural workers in a semi-arid region of Brazil is reported to be 16.7%.

- Light skin complexion: the condition typically affects individuals with lighter skin tones, particularly Caucasians living in tropical regions. In one report, 96% of persons with AC had phenotype II according to the Fitzpatrick scale.

- Age: AC typically affects older individuals, and rarely those under the age of 45.

- Gender: the condition affects males more commonly than females. Sometimes this ratio is reported as high as 10:1.

Additional factors may also play a role, including tobacco use, lip irritation, poor oral hygiene, and ill-fitting dentures.

The name is derived from the ancient Greek words "kamptos" ("bent") and "daktylos" ("finger").

Camptodactyly is a medical condition that causes one or more fingers to be permanently bent. It involves fixed flexion deformity of the proximal interphalangeal joints. The fifth finger is always affected.

Camptodactyly can be caused by a genetic disorder. In that case, it is an autosomal dominant trait that is known for its incomplete genetic expressivity. This means that when a person has the genes for it, the condition may appear in both hands, one, or neither. A linkage scan proposed that the chromosomal locus of camptodactyly was 3q11.2-q13.12.

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 )

Classification of radial dysplasia is practised through different models. Some only include the different deformities or absences of the radius, where others also include anomalies of the thumb and carpal bones. The Bayne and Klug classification discriminates four different types of radial dysplasia. A fifth type was added by Goldfarb et al. describing a radial dysplasia with participation of the humerus. In this classification only anomalies of the radius and the humerus are taken in consideration. James and colleagues expanded this classification by including deficiencies of the carpal bones with a normal distal radius length as type 0 and isolated thumb anomalies as type N.

Type N: Isolated thumb anomaly

Type 0: Deficiency of the carpal bones

Type I: Short distal radius

Type II: Hypoplastic radius in miniature

Type III: Absent distal radius

Type IV: Complete absent radius

Type V: Complete absent radius and manifestations in the proximal humerus

The term absent radius can refer to the last 3 types.

A muscle contracture is a permanent shortening of a muscle or joint. It is usually in response to prolonged hypertonic spasticity in a concentrated muscle area, such as is seen in the tightest muscles of people with conditions like spastic cerebral palsy.

Contractures are essentially muscles or tendons that have remained too tight for too long, thus becoming shorter. Once they occur, it is often argued that they cannot be stretched or exercised away (they must be released with orthopedic surgery). Most of the physical therapy, occupational therapy, and other exercise regimens targeted towards people with spasticity focuses on trying to prevent contractures from happening in the first place. However, research on sustained traction of connective tissue in approaches such as adaptive yoga has demonstrated that contracture can be reduced, at the same time that tendency toward spasticity is addressed.

Contractures can also be due to ischemia, as in Volkmann's contracture.

Excessive matrix metalloproteinase and myofibroblast accumulation in the wound margins can result in contracture.

To prevent AC from developing, protective measures could be undertaken such as avoiding mid-day sun, or use of a broad-brimmed hat, lip balm with anti UVA and UVB ingredients (e.g. para-aminobenzoic acid), or sun blocking agents (e.g. zinc oxide, titanium oxide) prior to sun exposure.

Dead arm syndrome starts with repetitive motion and forces on the posterior capsule of the shoulder. The posterior capsule is a band of fibrous tissue that interconnects with tendons of the rotator cuff of the shoulder. Four muscles and their tendons make up the rotator cuff. They cover the outside of the shoulder to hold, protect and move the joint.

Overuse can lead to a buildup of tissue around the posterior capsule called hypertrophy. The next step is tightness of the posterior capsule called posterior capsular contracture. This type of problem reduces the amount the shoulder can rotate inwardly.

Over time, with enough force, a tear may develop in the labrum. The labrum is a rim of cartilage around the shoulder socket to help hold the head of the humerus (upper arm) in the joint. This condition is called a superior labrum anterior posterior (SLAP) lesion. The final outcome in all these steps is the dead arm phenomenon.

The shoulder is unstable and dislocation may come next. Dead arm syndrome will not go away on its own with rest—it must be treated. If there is a SLAP lesion, then surgery is needed to repair the problem. If the injury is caught before a SLAP tear, then physical therapy with stretching and exercise can restore it.

It is common among baseball pitchers as they age, and it can also occur with quarterbacks in football and handball players also as they age.