Children younger than 6 have the best prognosis, since they have time for the dead bone to revascularize and remodel, with a good chance that the femoral head will recover and remain spherical after resolution of the disease. Children who have been diagnosed with Perthes' disease after the age of 10 are at a very high risk of developing osteoarthritis and coxa magna. When an LCP disease diagnosis occurs after age 8, a better outcome results with surgery rather than nonoperative treatments. Shape of femoral head at the time when Legg-Calve Perthes disease heals is the most important determinant of risk for degenerative arthritis; hence, the shape of femoral head and congruence of hip are most useful outcome measures.

Perthes' disease is one of the most common hip disorders in young children, occurring in roughly 5.5 of 100,000 children per year. The lifetime risk of a child developing the disease is about one per 1,200 individuals. Boys are affected about three to five times more often than girls. New cases of Perthes' disease rarely occur after age 14 years (if diagnosed after 14 years of age, then it is usually old disease from early in childhood or avascular necrosis from an alternative cause).

White northern Europeans appear to be affected more frequently than other races, though a paucity of reliable epidemiology exists in the Southern Hemisphere. Children of sufferers of the disease themselves may have a very slightly increased risk, though it is unclear if this is because of a genetic predisposition, or a shared environmental factor. It is most commonly seen in persons aged three to 12 years, with a median of six years of age. The UK incidence rates show an intriguing pattern with low incidence rates in London, and a progressive increase in disease in more northerly areas (maximal in Scotland). Some evidence suggests, at least in developed countries, more socioeconomically deprived communities have a greater risk of disease (a similar trend to diseases such as adult heart disease), though the reason for this remains unknown. One possible explanation that has been considered is tobacco smoke exposure, though this is significantly confounded by the strong socioeconomic gradient common to both smoking and Perthes' disease. Dietary factors of the child, and of the mother during pregnancy, are of interest to the research groups.

The exact cause of Kienböck's is not known, though there are thought to be a number of factors predisposing a person to Kienböck's.

Recent studies have made a correlation between Kienböck's sufferers and Western European ancestry, but no definitive link can be positively confirmed.

The necrosis of the lunate bone can frequently be traced to a trauma to the wrist, like a compound fracture, which could cause the lunate's blood supply to be interrupted. Blood flows to the lunate through several arteries, each supplying a percentage. When one of these pathways is severed, the likelihood the patient will develop necrosis increases.

Despite a preponderance of evidence, no particular cause has been conclusively verified.

Data exists on the internet that most people suffering from Kienböck's are affected in their dominant hand, though about one-third of sufferers report the condition in their non-dominant hand. In very few cases have there been people that have acquired it in both wrists.

Kienböck's disease is classified as a "rare disorder," meaning that it affects fewer than 200,000 people in the U.S. population.

Many Kienböck's patients are frustrated by the lack of consensus among hand surgeons about optimal treatments for Kienböck's. No matter what the disease's stage of progression, there is no one best treatment, and the decision is often based partially, or even mostly, on incidental factors such as the patient's pain tolerance, the patient's desire to return to active use of the hand (such as in manual occupations), and the surgeon's level of expertise with different treatments.

Though, since each case of Kienböck's is different, the makeup of the wrist and arm bones are important factors which are individualized to each patient. Therefore, one surgery will never be able to solve all the problems associated with the disease. Thus, no consensus can be reached among surgeons.

Being an extremely rare disease, it is unknown as to what exactly causes Panner Disease. It is believed that the disease may be brought on by continuous overuse of the elbow and that puts pressure on the elbow and also strains the elbow in children during the period of rapid bone growth. The overuse of the elbow can be due to the involvement in sports such as baseball, handball, and gymnastics where these sports involve throwing or putting a lot of pressure on the joints. These repeated activities cause microtraumas and results in the affected elbow being swollen, irritated, and in pain. Panner Disease results when the blood supply to the capitellum is disrupted and therefore the cells within the growth plate of the capitellum die and it becomes flat due to the softening and collapsing of the surrounding bone. To prevent future instances of Panner Disease the child is instructed to cease all physical and sports activities that involve the use of the affected elbow until the symptoms are relieved.

The ultimate cause for these conditions is unknown, but the most commonly cited cause factors are rapid growth, heredity, trauma (or overuse), anatomic conformation, and dietary imbalances; however, only anatomic conformation and heredity are well supported by scientific literature. The way that the disease is initiated has been debated. Although failure of chondrocyte differentiation, formation of a fragile cartilage, failure of blood supply to the growth cartilage, and bone necrosis all have been proposed as the starting point in the pathogenesis, recent literature strongly supports failure of blood supply to growth cartilage as most likely.

Training of the feet, utilizing foot gymnastics and going barefoot on varying terrain, can facilitate the formation of arches during childhood, with a developed arch occurring for most by the age of four to six years. Ligament laxity is also among the factors known to be associated with flat feet. One medical study in India with a large sample size of children who had grown up wearing shoes and others going barefoot found that the longitudinal arches of the bare-footers were generally strongest and highest as a group, and that flat feet were less common in children who had grown up wearing sandals or slippers than among those who had worn closed-toe shoes. Focusing on the influence of footwear on the prevalence of pes planus, the cross-sectional study performed on children noted that wearing shoes throughout early childhood can be detrimental to the development of a normal or a high medial longitudinal arch. The vulnerability for flat foot among shoe-wearing children increases if the child has an associated ligament laxity condition. The results of the study suggest that children be encouraged to play barefooted on various surfaces of terrain and that slippers and sandals are less harmful compared to closed-toe shoes. It appeared that closed-toe shoes greatly inhibited the development of the arch of the foot more so than slippers or sandals. This conclusion may be a result of the notion that intrinsic muscle activity of the arch is required to prevent slippers and sandals from falling off the child’s foot.

Dysbaric osteonecrosis is a significant occupational hazard, occurring in 50% of commercial Japanese divers, 65% of Hawaiian fishermen and 16% of commercial and caisson divers in the UK.

Its relationship to compressed air is strong in that it may follow a single exposure to compressed air, may occur with no history of DCS but is usually associated with significant compressed air exposure. The distribution of lesions differs with the type of exposure - the juxta-articular lesions being more common in caisson workers than in divers.

There is a definite relationship between length of time exposed to extreme depths and the percentage of divers with bone lesions. Evidence does not suggest that dysbaric osteonecrosis is a significant risk in recreational scuba diving.

Flat feet can also develop as an adult ("adult acquired flatfoot") due to injury, illness, unusual or prolonged stress to the foot, faulty biomechanics, or as part of the normal aging process. This is most common in women over 40 years of age. Known risk factors include obesity, hypertension and diabetes. Flat feet can also occur in pregnant women as a result of temporary changes, due to increased elastin (elasticity) during pregnancy. However, if developed by adulthood, flat feet generally remain flat permanently.

If a youth or adult appears flatfooted while standing in a full weight bearing position, but an arch appears when the person plantarflexes, or pulls the toes back with the rest of the foot flat on the floor, this condition is called flexible flatfoot. This is not a true collapsed arch, as the medial longitudinal arch is still present and the windlass mechanism still operates; this presentation is actually due to excessive pronation of the foot (rolling inwards), although the term 'flat foot' is still applicable as it is a somewhat generic term. Muscular training of the feet is helpful and will often result in increased arch height regardless of age.

Metallosis is the putative medical condition involving deposition and build-up of metal debris in the soft tissues of the body.

Metallosis has been hypothesized to occur when metallic components in medical implants, specifically joint replacements, abrade against one another.

Metallosis has also been observed in some patients either sensitive to the implant or for unknown reasons even in the absence of malpositioned prosthesis. Though rare, metallosis has been observed at an estimated incidence of 5% of metal joint implant patients over the last 40 years. Women may be at slightly higher risk than men. If metallosis occurs, it may involve the hip and knee joints, the shoulder, wrist, or elbow joints.

The abrasion of metal components may cause metal ions to be solubilized. The hypothesis that the immune system identifies the metal ions as foreign bodies and inflames the area around the debris may be incorrect because of the small size of metal ions may prevent them from becoming haptens. Poisoning from metallosis is rare, but cobaltism is an established health concern. The involvement of the immune system in this putative condition has also been theorized but has never been proven.

Purported symptoms of metallosis generally include pain around the site of the implant, pseudotumors (a mass of inflamed cells that resembles a tumor but is actually collected fluids), and a noticeable rash that indicates necrosis. The damaged and inflamed tissue can also contribute to loosening the implant or medical device. Metallosis can cause dislocation of non-cemented implants as the healthy tissue that would normally hold the implant in place is weakened or destroyed. Metallosis has been demonstrated to cause osteolysis.

Women, those who are small in stature, and the obese are at greater risk for metallosis because their body structure causes more tension on the implant, quickening the abrasion of the metal components and the subsequent build-up of metallic debris.

Bone mineral density decreases with increasing age. Osteoporotic bone loss can be prevented through an adequate intake of vitamin C and vitamin D, coupled with exercise and by being a non-smoker. A study by Cheng et al. in 1997, showed that greater bone density indicated less risk for fractures in the calcaneus.

Kienböck's disease is a disorder of the wrist. It is named for Dr. Robert Kienböck, a radiologist in Vienna, Austria who described osteomalacia of the lunate in 1910.

It is breakdown of the lunate bone, a carpal bone in the wrist that articulates with the radius in the forearm. Specifically, Kienböck's disease is another name for avascular necrosis (death and fracture of bone tissue due to interruption of blood supply) with fragmentation and collapse of the lunate. This has classically been attributed to arterial disruption, but may also occur after events that produce venous congestion with elevated interosseous pressure.

Panner disease is an osteochondrosis of the capitellum of the elbow. Panner disease is primarily seen in boys between the ages of five and ten years old. Panner disease is often caused by excessive throwing due to valgus stress. The disease causes pain and stiffness in the affected elbow and may limit extension; the affected elbow is usually on the dominant arm the child uses. The disease may be associated with pitching and athletic activity. On radiographs, the capitellum may appear irregular with areas of radiolucency. Treatment is symptomatic, with a good prognosis. Treatment is minimal and includes restricting athletic activity to allow for the elbow to heal and for pain to be relieved. The disease is named after the Danish radiologist Hans Jessen Panner (1871–1930).

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.

OCD is a relatively rare disorder, with an estimated incidence of 15 to 30 cases per 100,000 persons per year. Widuchowski W "et al." found OCD to be the cause of articular cartilage defects in 2% of cases in a study of 25,124 knee arthroscopies. Although rare, OCD is noted as an important cause of joint pain in active adolescents. The juvenile form of the disease occurs in children with open growth plates, usually between the ages 5 and 15 years and occurs more commonly in males than females, with a ratio between 2:1 and 3:1. However, OCD has become more common among adolescent females as they become more active in sports. The adult form, which occurs in those who have reached skeletal maturity, is most commonly found in people 16 to 50 years old.

While OCD may affect any joint, the knee—specifically the medial femoral condyle in 75–85% of knee cases—tends to be the most commonly affected, and constitutes 75% of all cases. The elbow (specifically the capitulum of the humerus) is the second most affected joint with 6% of cases; the talar dome of the ankle represents 4% of cases. Less frequent locations include the patella, vertebrae, the femoral head, and the glenoid of the scapula.

In humans, these conditions may be classified into three groups:

1. Spinal: Scheuermann's disease (of the interspinal joints) which is a curve in the thoracic spine.

2. Articular: Legg-Calvé-Perthes disease (or, avascular necrosis of the femoral head in the hip), Köhler's disease (of the tarsal navicular bone of the foot), Panner's disease (of the capitulum of the elbow), and Freiberg's infraction (of the second or third metatarsal of the foot and less frequently the first or fourth; sometimes called Freiberg's Infraction or Freiberg's disease)

3. Non-articular: This group includes Sever's disease (of the calcaneus, or heel), and Kienbock's disease of the hand, and other conditions not completely characteristic of the osteochondrosis, such as Osgood-Schlatter's disease (of the tibial tubercle) and Osteochondritis dissecans.

It is more common in females over the age of 50 with possible risk factors of corticosteroid use, Lupus, alcoholism, pancreatitis, sickle cell anemia, and rheumatoid arthritis.

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high dose steroids. Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gaucher’s disease, and Caisson disease. The condition may also occur without any clear reason.

Bisphosphonates are associated with osteonecrosis of the mandible. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.

Freiberg disease, also known as a Freiberg infraction, is a form of avascular necrosis in the metatarsal bone of the foot. It generally develops in the second metatarsal, but can occur in any metatarsal. Physical stress causes multiple tiny fractures where the middle of the metatarsal meets the growth plate. These fractures impair blood flow to the end of the metatarsal resulting in the death of bone cells (osteonecrosis). It is an uncommon condition, occurring most often in young women, athletes, and those with abnormally long metatarsals. Approximately 80% of those diagnosed are women.

Initial treatment is generally 4–6 weeks of limited activity, often with crutches or orthotics. In rare cases, surgery is necessary to reduce the bone mass of the metatarsal.

The condition was first described by Dr. Alfred H. Freiberg in 1914. He initially thought the condition was caused by acute physical trauma, which is why it was initially called an infraction.

In 1991, Kathol conducted a study which showed a correlation between calcaneal insufficiency avulsion fractures (a fracture in which the Achilles tendon removes a portion of the bone as it rescinds) and diabetes mellitus. The diabetic population is more susceptible to the risks of fracture and potential healing complications and infection that may lead to limb amputation. Diabetes can be regulated and prevented through diet and exercise.

If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).

Despite much research, the causes remain unclear but include repetitive physical trauma, ischemia (restriction of blood flow), hereditary and endocrine factors, avascular necrosis (loss of blood flow), rapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and problems of bone formation. Although the name "osteochondritis" implies inflammation, the lack of inflammatory cells in histological examination suggests a non-inflammatory cause. It is thought that repetitive microtrauma, which leads to microfractures and sometimes an interruption of blood supply to the subchondral bone, may cause subsequent localized loss of blood supply or alteration of growth.

Trauma, rather than avascular necrosis, is thought to cause osteochondritis dissecans in juveniles. In adults, trauma is thought to be the main or perhaps the sole cause, and may be endogenous, exogenous or both. The incidence of repetitive strain injury in young athletes is on the rise and accounts for a significant number of visits to primary care; this reinforces the theory that OCD may be associated with increased participation in sports and subsequent trauma. High-impact sports such as gymnastics, soccer, basketball, lacrosse, football, tennis, squash, baseball and weight lifting may put participants at a higher risk of OCD in stressed joints (knees, ankles and elbows).

Recent case reports suggest that some people may be genetically predisposed to OCD. Families with OCD may have mutations in the aggrecan gene. Studies in horses have implicated specific genetic defects.

Tarsal coalition is almost exclusively a product of an error during the dividing of embryonic cells in utero. Other causes of synostosis (bone fusion) could include a surgical 'screwing together' of two bones, a very advanced case of arthritis leading to self-fusion of a joint by an internal process within the body or some other very traumatic event. The birth defect responsible for tarsal coalition is thought to often be an autosomal dominant genetic condition. This means that if you have a parent with the disorder it is highly likely to be passed on to offspring.

Persons suffering from metallosis can experience any of the following symptoms:

- Extreme pain (even when not moving);

- Swelling and inflammation;

- Loosening of the implant;

- Dislocation;

- Bone deterioration;

- Aseptic fibrosis, local necrosis;

- Hip replacement failure;

- Metal toxicity from grinding metal components; and

- Necessary subsequent hip replacement revision or surgeries.

Chopart's fracture–dislocation is usually caused by falls from height, traffic collisions and twisting injuries to the foot as seen in basketball players.

Spontaneous osteonecrosis of the Knee, also known as Ahlback's disease is the result of vascular arterial insufficiency to the medial femoral condyle of the knee resulting in necrosis and destruction of bone. It is often unilateral and can be associated with a meniscal tear.