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%.

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.

A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear. According to a study in the Journal of Orthopaedic Surgery and Traumatology the frequency of rotator cuff tears can increase with age. The study shows the participants that were the ages of 70–90 years old had a rate of rotator cuff tears that were 1 to 5. The participants who were 90+ years old the frequency of a rotator cuff tear jumped to 1 to 3. This study shows that with an increase in age there is also an increase in the probability of a rotator cuff tear.

While people with rotator cuff tears may not have any noticeable symptoms, studies have shown that over time 40% will have enlargement of the tear over a five-year period. Of those whose tears enlarge, 20% have no symptoms while 80% eventually develop symptoms.

There is no irrefutable evidence that rotator cuff surgery benefits patients more than non-surgical management and a percentage of patients never regain full range of motion after surgery.

Epidemiological studies strongly support a relationship between age and cuff tear prevalence. In a recent study the frequency of such tears increased from 13% in the youngest group (aged 50–59 y) to 20% (aged 60–69 y), 31% (aged 70–79 y), and 51% in the oldest group (aged 80–89 y). This high rate of tear prevalence in asymptomatic individuals suggests that rotator cuff tears could be considered a "normal" process of aging rather than a result of an apparent pathological process.

Another factor of tennis elbow injury is experience and ability. The proportion of players who reported a history of tennis elbow had an increased number of playing years. As for ability, poor technique increases the chance for injury much like any sport. Therefore, an individual must learn proper technique for all aspects of their sport. The competitive level of the athlete also affects the incidence of tennis elbow. Class A and B players had a significantly higher rate of tennis elbow occurrence compared to class C and novice players. However, an opposite, but not statistically significant, trend is observed for the recurrence of previous cases, with an increasingly higher rate as ability level decreases.

Other ways to prevent tennis elbow:

- Decrease the amount of playing time if already injured or feeling pain in outside part of the elbow.

- Stay in overall good physical shape.

- Strengthen the muscles of the forearm: (pronator quadratus, pronator teres, and supinator muscle)—the upper arm: (biceps, triceps)—and the shoulder (deltoid muscle) and upper back (trapezius). Increased muscular strength increases stability of joints such as the elbow.

- Like other sports, use equipment appropriate to your ability, body size, and muscular strength.

- Avoid any repetitive lifting or pulling of heavy objects (especially over your head)

Vibration dampeners (otherwise known as "gummies") are not believed to be a reliable preventative measure. Rather, proper weight distribution in the racket is thought to be a more viable option in negating shock.

Several risk factors of CMC OA of the thumb are known. Each of these risk factors does not cause CMC OA by itself, but acts as a predisposing factor influencing the process of OA in some way. Risk factors include: female gender, suffering from obesity, repetitive heavy manual labor, familial predisposition and hormonal changes, such as menopause.

The exact etiology of tendinopathy has not been fully elucidated and different stresses may induce varying responses in different tendons. There are multifactorial theories that could include: tensile overload, tenocyte related collagen synthesis disruption, load-induced ischemia, neural sprouting, thermal damage, and adaptive compressive responses. The intratendinous sliding motion of fascicles and shear force at interfaces of fascicles could be an important mechanical factor for the development of tendinopathy and predispose tendons to rupture. Obesity, or more specifically, adiposity or fatness, has also been linked to an increasing incidence of tendinopathy.

The most commonly accepted cause for this condition however is seen to be an overuse syndrome in combination with intrinsic and extrinsic factors leading to what may be seen as a progressive interference or the failing of the innate healing response. Tendinopathy involves cellular apoptosis, matrix disorganization and neovascularization.

Tendinopathy can be induced in animal models by a surgical injury to the tendon. In both sheep shoulder (infraspinatus) and horse forelimb (superficial digitor flexor) tendons, a mid-tendon transection caused pathology in the entire tendon after four and six weeks respectively.

Quinolone antibiotics are associated with increased risk of tendinitis and tendon rupture. A 2013 review found the incidence of tendon injury among those taking fluoroquinolones to be between 0.08 and 0.2%. Fluoroquinolones most frequently affect large load-bearing tendons in the lower limb, especially the Achilles tendon which ruptures in approximately 30 to 40% of cases.

It is an overuse injury from repetitive overloading of the extensor mechanism of the knee. The microtears exceed the body's healing mechanism unless the activity is stopped.

Among the risk factors for patellar tendonitis are low ankle dorsiflexion, weak gluteal muscles, and muscle tightness, particularly in the calves, quadriceps muscle, and hamstrings.

The injury occurs to athletes in many sports.

Tendinosis, sometimes called chronic tendinitis, chronic tendinopathy, or chronic tendon injury, is damage to a tendon at a cellular level (the suffix "osis" implies a pathology of chronic degeneration without inflammation). It is thought to be caused by microtears in the connective tissue in and around the tendon, leading to an increase in tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of tendon rupture. Tendinosis is often misdiagnosed as tendinitis because of the limited understanding of tendinopathies by the medical community. Classic characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity, and a lack of inflammatory cells which has challenged the original misnomer "tendinitis".

Tendinosis of the common extensor tendon of the elbow (“tennis elbow”), as of the Rotator Cuff, is a common cause of pain in the elbow or shoulder.

The general opinion is that tendinosis is due to tendon overuse, and failed healing of the tendon. In addition, the extensor carpi radialis brevis muscle plays a key role.

In horses tendinitis is called a bowed tendon from the appearance of the affected tendon after it heals without treatment. Mesenchymal stem cells, derived from a horse's bone marrow or fat, are currently being used for tendon repair in horses.

CMC OA is the most common form of OA affecting the hand. Dahaghin et al. showed that about 15% of women and 7% of men between 50 and 60 years of age suffer from CMC OA of the thumb. However, in about 65% of people older than 55 years, radiologic evidence of OA was present without any symptoms. Armstrong et al. reported a prevalence of 33% in postmenopausal women, of which one third was symptomatic, compared to 11% in men older than 55 years. This shows CMC OA of the thumb is significantly more prevalent in women, especially in postmenopausal women, compared to men.

Tendinitis (also tendonitis), meaning inflammation of a tendon, is a type of tendinopathy often confused with the more common tendinosis, which has similar symptoms but requires different treatment. (The suffix "-itis" denotes diseases characterized by inflammation.) The term tendinitis is generally reserved for tendon injuries that involve larger-scale acute injuries accompanied by inflammation. Tendinitis is typically referred to in combination with the body part involved, such as Achilles tendinitis (affecting the Achilles tendon), or patellar tendinitis (jumper's knee, affecting the patellar tendon).

The cause of de Quervain's disease is not established. Evidence regarding a possible relation with occupational risk factors is debated. A systematic review of potential risk factors discussed in the literature did not find any evidence of a causal relationship with occupational factors. However, researchers in France found personal and work-related factors were associated with de Quervain's disease in the working population; wrist bending and movements associated with the twisting or driving of screws were the most significant of the work-related factors. Proponents of the view that De Quervain syndrome is a repetitive strain injury consider postures where the thumb is held in abduction and extension to be predisposing factors. Workers who perform rapid repetitive activities involving pinching, grasping, pulling or pushing have been considered at increased risk. Specific activities that have been postulated as potential risk factors include intensive computer mouse use, trackball use, and typing, as well as some pastimes, including bowling, golf, fly-fishing, piano-playing, sewing, and knitting.

Women are affected more often than men. The syndrome commonly occurs during and after pregnancy. Contributory factors may include hormonal changes, fluid retention and—more debatably—lifting.

Electroanalgesia, ice therapy, and heat offer symptomatic relief. The benefit of ultrasound in calcific tendinitis is debated; most studies are negative but a study by Ebenbichler et al. (1999) showed resolution of deposits and clinical improvement.

Improving the biomechanics of the shoulder will reduce the tension on the fault muscles allowing a decrease in symptoms. Improved biomechanics are thought to reduce the amount of calcification that occurs especially in the case on supraspinatus where it can be caused from repetitive compression against the acromion.

Patellar tendinitis (patellar tendinopathy, also known as jumper's knee), is a relatively common cause of pain in the inferior patellar region in athletes. It is common with frequent jumping and studies have shown it may be associated with stiff ankle movement and ankle sprains.

In those with calcific tendinitis of the shoulder high energy extracorporeal shock-wave therapy (which uses sound waves) can be useful. It is not useful in other types of tendinitis. This procedure may be known as .

De Quervain syndrome, is a tenosynovitis of the sheath or tunnel that surrounds two tendons that control movement of the thumb.

Tenosynovitis most commonly results from the introduction of bacteria into a sheath through a puncture or laceration wound, though bacteria can also be spread from adjacent tissue or via hematogenous spread. The clinical presentation is therefore as acute infection following trauma. The infection can be mono- or polymicrobial and can vary depending on the nature of the trauma. The most common pathogenic agent is staphylococcus aureus introduced from the skin. Other bacteria linked to infectious tenosynovitis include Pasteurella multocida (associated with animal bites), Eikenella spp. (associated with IV drug use), and Mycobacterium marinum (associated with wounds exposed to fresh or salt water). Additionally, sexually active patients are at risk for hematogenous spread due to Neisseria gonorrhea (see infectious arthritis).

Noninfectious tenosynovitis can arise from overuse or secondary to other systemic inflammatory conditions such as [rheumatoid arthritis] or [reactive arthritis]. If left untreated, the tendons may undergo stenosis, causing conditions such as de Quervain’s and trigger finger.

The most common manifestation of infectious tenosynovitis is in the flexor tendons of the fingers, though infections of other tendon sheaths have been reported as well. The four cardinal signs of infectious flexor tenosynovitis are tenderness to touch along the flexor aspect of the finger, symmetric enlargement of the affected finger, the finger being held in slight flexion at rest, and severe pain with passive extension. Fever may also be present but is uncommon.

The congenital absence of the gluteal muscle was described in 1976, as occurring in a brother and sister with absence of gluteal muscles and with spina bifida occulta. It was thought to be caused by an autosomal recessive gene.

Edgar "et al." (2012) reported the case of a 15-year-old white male with congenital absence of the "gluteus maximus" muscles associated with spina bifida occulta, learning disability, optic nerve hypoplasia, scoliosis, and central nervous system hamartomas.

If gluteal muscles were absent the following actions would not be possible. The "gluteus maximus" extends the thigh at the hip in actions like stair climbing, running or walking. It also abducts the thigh, elevates the trunk and also prevents the trunk of a person from moving forward or backward when the rest of the body is in movement. The "gluteal maximus" also aids in stabilizing the femur and the tibia. The "gluteas minimus" and "medius" are also part of the gluteal muscles. If these muscles were missing, the leg would not be able to abduct or medial rotate the thigh. The body would also not be able to shift weight from one side to the other when one foot is on the ground but not another. Considering this a rare congenital disease with other complications, walking would also not be possible in the list of additional symptoms above.

Pathology is insertional tendinopathy of the medius and tendons and enlargement of the associated bursa.

Gluteals remain inactive in a seated position. Movements that require muscles become more difficult; stress is put on the spine.

Multiple epiphyseal dysplasia (MED) encompasses a spectrum of skeletal disorders, most of which are inherited in an autosomal dominant form. However, there is an autosomal recessive form.

Associated genes include COL9A1, COL9A2, COL9A3, COMP, and MATN3.

Types include:

Fairbank's disease or multiple epiphyseal dysplasia (MED) is a rare genetic disorder (dominant form: 1 in 10,000 births) that affects the growing ends of bones. Long bones normally elongate by expansion of cartilage in the growth plate (epiphyseal plate) near their ends. As it expands outward from the growth plate, the cartilage mineralizes and hardens to become bone (ossification). In MED, this process is defective.