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.

Joint hypermobility syndrome shares symptoms with other conditions such as Marfan syndrome, Ehlers-Danlos Syndrome, and osteogenesis imperfecta. Experts in connective tissue disorders formally agreed that severe forms of Hypermobility Syndrome and mild forms of Ehlers-Danlos Syndrome Hypermobility Type are the same disorder.[""]

Generalized hypermobility is a common feature in all these hereditary connective tissue disorders and many features overlap, but often features are present that enable differentiating these disorders.

The inheritance pattern of Ehlers-Danlos syndrome varies by type. The arthrochalasia, classic, hypermobility and vascular forms usually have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance occurs when one copy of a gene in each cell is sufficient to cause a disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases result from new (sporadic) gene mutations. Such cases can occur in people with no history of the disorder in their family.

The dermatosparaxis and kyphoscoliosis types of EDS and some cases of the classic and hypermobility forms, are inherited in an autosomal recessive pattern. In autosomal recessive inheritance, two copies of the gene in each cell are altered. Most often, both parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.

Hypermobility syndrome is generally considered to comprise hypermobility together with other symptoms, such as myalgia and arthralgia. It is relatively common among children and affects more females than males.

Current thinking suggests four causative factors:

- The shape of the ends of the bones—Some joints normally have a large range of movement, such as the shoulder and hip. Both are ball and socket joints. If a shallow rather than a deep socket is inherited, a relatively large range of movement will be possible. If the socket is particularly shallow, then the joint may dislocate easily.

- Protein deficiency or hormone problems—Ligaments are made up of several types of protein fibre. These proteins include elastin, which gives elasticity and which may be altered in some people. Female sex hormones alter collagen proteins. Women are generally more supple just before a period and even more so in the latter stages of pregnancy, because of a hormone called relaxin that allows the pelvis to expand so the head of the baby can pass. Joint mobility differs by race, which may reflect differences in collagen protein structure. People from the Indian sub-continent, for example, often have more supple hands than Caucasians.

- Muscle tone—The tone of muscles is controlled by the nervous system, and influences range of movement. Special techniques can change muscle tone and increase flexibility. Yoga, for example, can help to relax muscles and make the joints more supple. Please note that Yoga is not recommended by most medical professionals for people with Joint Hypermobility Syndrome due to likelihood of damage to the joints. Gymnasts and athletes can sometimes acquire hypermobility in some joints through activity.

- Proprioception—Compromised ability to detect exact joint/body position with closed eyes, may lead to overstretching and hypermobile joints.

Hypermobility can also be caused by connective tissue disorders, such as Ehlers-Danlos Syndrome (EDS) and Marfan syndrome. Joint hypermobility is a common symptom for both. EDS has numerous sub-types; most include hypermobility in some degree. When hypermobility is the main symptom, then EDS/hypermobility type is likely. People with EDS-HT suffer frequent joint dislocations and subluxations (partial/incomplete dislocations), with or without trauma, sometimes spontaneously. Commonly, hypermobility is dismissed by medical professionals as nonsignificant.

About 25% of people over the age of 50 experience knee pain from degenerative knee diseases.

The exact cause is unknown. Mechanical factors, dietary and long term use of some antidepressants may be of significance. There is a correlation between these factors but not a cause or effect. The distinctive radiological feature of DISH is the continuous linear calcification along the antero-medial aspect of the thoracic spine. The disease is usually found in people in their 60s and above, and is extremely rare in people in their 40s and 30s. The disease can spread to any joint of the body, affecting the neck, shoulders, ribs, hips, pelvis, knees, ankles, and hands. The disease is not fatal, however some associated complications can lead to death. Complications include paralysis, dysphagia (the inability to swallow), and pulmonary infections. Although DISH manifests in a similar manner to ankylosing spondylitis, these two are totally separate diseases. Ankylosing spondylitis is a genetic disease with identifiable marks, and affects organs. DISH has no indication of a genetic link, and does not affect organs other than the lungs, which is only indirect due to the fusion of the rib cage.

Long term treatment of acne with vitamin derived retinoids, such as etretinate and acitretin, have been associated with "extraspinal" hyperostosis.

Tendon injury and resulting tendinopathy are responsible for up to 30% of consultations to sports doctors and other musculoskeletal health providers. Tendinopathy is most often seen in tendons of athletes either before or after an injury but is becoming more common in non-athletes and sedentary populations. For example, the majority of patients with Achilles tendinopathy in a general population-based study did not associate their condition with a sporting activity. In another study the population incidence of Achilles tendinopathy increased sixfold from 1979-1986 to 1987-1994. The incidence of rotator cuff tendinopathy ranges from 0.3% to 5.5% and annual prevalence from 0.5% to 7.4%.

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.

Diffuse idiopathic skeletal hyperostosis (DISH) is a non-inflammatory spondyloarthropathy which predominantly affects the spine. It is characterized by ankylosis and enthesopathy (ossification of the ligaments and entheses). It most commonly affects the thoracic and thoraco-lumbar spine, but involvement is variable and can include the entire spine.

In the United States, more than US $3 billion is spent each year on arthroscopic knee surgeries that are known to be ineffective in people with degenerative knee pain.

People with diabetes mellitus are at higher risk for any kind of peripheral neuropathy, including ulnar nerve entrapments.

Cubital tunnel syndrome is more common in people who spend long periods of time with their elbows bent, such as when holding a telephone to the head. Flexing the elbow while the arm is pressed against a hard surface, such as leaning against the edge of a table, is a significant risk factor. The use of vibrating tools at work or other causes of repetitive activities increase the risk, including throwing a baseball.

Damage to or deformity of the elbow joint increases the risk of cubital tunnel syndrome. Additionally, people who have other nerve entrapments elsewhere in the arm and shoulder are at higher risk for ulnar nerve entrapment. There is some evidence that soft tissue compression of the nerve pathway in the shoulder by a bra strap over many years can cause symptoms of ulnar neuropathy, especially in very large-breasted women.

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 exact cause is unknown. Some doctors believe it is caused by abnormal metabolism of fat. Others think it may be caused by repetitive inflammation. Some feel that blood within the joint may cause the inflammatory change. Risk factors for PVNS developing are not yet understood. Very little research has been carried out. However, a common theme in patients is a trauma experienced to the joint prior to the onset of symptoms.

Treatment is frequently by means of removal of the loose bodies and of a partial or full synovectomy (removal of the synovium)

Full synovectomy is a moderately major operation and involves completely exposing the joint and removing the affected tissue. Partial synovectomy is normally done arthroscopically. Synovectomies are normally carried out by shaving the lining of the knee but there are other ways of achieving this by either freezing the synovium or by the use of radiation treatment.

The need for further procedures is greater than 25% although normally the frequency of the required removal of loose bodies is reduced by the previous synovectomy. There have been documented cases of malignant transformation however this is rare.

Whilst the condition can be described as a ‘benign growth’ it seldom affects more than one joint, and does not usually affect surrounding tissue.

Synovial chondromatosis (synonyms include synovial osteochondromatosis, primary synovial osteochondromatosis, and synovial chondrometaplasia) is a disease affecting the synovium, a thin flexible membrane around a joint. It is also known as Reichel's syndrome or Reichel-Jones-Henderson syndrome, named after Friedrich Paul Reichel, Hugh Toland Jones and Melvin Starkey Henderson.

Once established, periods of remissions and relapse can persist indefinitely.

While IH may remit spontaneously for most people the condition is long-lasting. Treatments as described above can be effective in reducing the frequency and degree of effusions. Deformative changes to joints are not a common feature of this mostly non-inflammatory condition.

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.

Specific populations at high risk of primary PFPS include runners, bicyclists, basketball players, young athletes and females.

Although the exact cause of Panner Disease is unknown, in recent research, it has been concluded that it may be associated with frequent throwing or other athletic activity. In the same article that talks about varying osteochondrosis diseases, it is pointed out that Panner Disease always involves alteration of the capitellum, which can be visualized by radiography. In another research article, the research team aimed to summarize the best available evidence for diagnosis and treatment for Panner Disease. In the article it was found that the most common symptoms that patients with Panner Disease present with are elbow stiffness and swelling, limited range of motion, and limited elbow extension. In alignment with the previously mentioned article, the team of researchers also concluded that Panner Disease involves irregularity of the capitellum, specifically that it appears flattened. Panner Disease often gets misdiagnosed as osteochondritis dissecans (OCD), and in this article they distinguish the difference between the two diseases are age difference and radiographic findings. In alignment with the two previously discussed articles, another article that reports on three case studies of Panner Disease, states that the primary treatment that is used for Panner Disease is rest and restriction from all physical and athletic activity that involves the use of the upper extremities; the activity is suggested to be ceased until the symptoms are relieved.

Heterotopic ossification of varying severity can be caused by surgery or trauma to the hips and legs. About every third patient who has total hip arthroplasty (joint replacement) or a severe fracture of the long bones of the lower leg will develop heterotopic ossification, but is uncommonly symptomatic. Between 50% and 90% of patients who developed heterotopic ossification following a previous hip arthroplasty will develop additional heterotopic ossification.

Heterotopic ossification often develops in patients with traumatic brain or spinal cord injuries, other severe neurologic disorders or severe burns, most commonly around the hips. The mechanism is unknown. This may account for the clinical impression that traumatic brain injuries cause accelerated fracture healing.

There are also rare genetic disorders causing heterotopic ossification such as fibrodysplasia ossificans progressiva (FOP), a condition that causes injured bodily tissues to be replaced by heterotopic bone. Characteristically exhibiting in the big toe at birth, it causes the formation of heterotopic bone throughout the body over the course of the sufferer's life, causing chronic pain and eventually leading to the immobilisation and fusion of most of the skeleton by abnormal growths of bone.

Another rare genetic disorder causing heterotopic ossification is progressive osseous heteroplasia (POH), is a condition characterized by cutaneous or subcutaneous ossification.

It is not always certain why arthritis of the knee develops. Most physicians believe that it is a combination of factors that can include muscle weakness, obesity, heredity, joint injury or stress, constant exposure to the cold, and aging. Cartilage in the knee begins to break down and leaves the bones of the knee rubbing against each other as you walk. Persons who work in a place that applies repetitive stress on the knees are at a high risk of developing this condition. Bone deformities increase the risk for osteoarthritis of the knee since the joints are already malformed and may contain defective cartilage. Having gout, rheumatoid arthritis, Paget's disease of bone or septic arthritis can increase your risk of developing osteoarthritis.

Some physicians and most podiatrist believe that Pes Planus (flat feet) cause increased rates and earlier incidence of knee osteoarthritis. In a study of army recruits with moderate to severe flat feet, the results showed that they had almost double the rate of knee arthritis when compared to recruits with normal arches.

In tennis players, about 39.7% have reported current or previous problems with their elbow. Less than one quarter (24%) of these athletes under the age of 50 reported that the tennis elbow symptoms were "severe" and "disabling," while 42% were over the age of 50. More women (36%) than men (24%) considered their symptoms severe and disabling. Tennis elbow is more prevalent in individuals over 40, where there is about a four-fold increase among men and two-fold increase among women. Tennis elbow equally affects both sexes and, although men have a marginally higher overall prevalence rate as compared to women, this is not consistent within each age group, nor is it a statistically significant difference.

Playing time is a significant factor in tennis elbow occurrence, with increased incidence with increased playing time being greatery for respondents under 40. Individuals over 40 who played over two hours doubled their chance of injury. Those under 40 increased it 3.5 fold compared to those who played less than two hours per day.

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

Most patients diagnosed with cubital tunnel syndrome have advanced disease (atrophy, static numbness, weakness) that might reflect permanent nerve damage that will not recover after surgery. When diagnosed prior to atrophy, weakness or static numbness, the disease can be arrested with treatment. Mild and intermittent symptoms often resolve spontaneously.

The cause is unknown but allergic and auto-inflammatory mechanisms have been proposed.

In a 1957 review of IH, Mattingly did not find evidence that the condition is inherited unlike Reimann who, in 1974, describes the condition as “heritable, non-inflammatory, and afebrile”.

More recently, specific association with the Mediterranean fever gene, MEFV, has been proposed. So, with some individuals carrying gene mutations (MEFV and also TRAPS-related genes), the native immune system seems to plays a role in the development of IH, i.e. there is an auto-immune component to the condition.

Elbow Dysplasia is a significant genetically determined problem in many breeds of dog, often manifesting from puppyhood and continuing for life. In elbow dysplasia, the complex elbow joint suffers from a structural defect, often related to its cartilage. This initial condition, known as a "primary lesion", causes an abnormal level of wear and tear and gradual degradation of the joint, at times disabling or with chronic pain. Secondary processes such as inflammation and osteoarthritis can arise from this damage which increase the problem and add further problems of their own.