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

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%.

There can be several concurrent causes. Trauma, auto-immune disorders, infection and iatrogenic (medicine-related) factors can all cause bursitis. Bursitis is commonly caused by repetitive movement and excessive pressure. Shoulders, elbows and knees are the most commonly affected. Inflammation of the bursae may also be caused by other inflammatory conditions such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus and gout. Immune deficiencies, including HIV and diabetes, can also cause bursitis. Infrequently, scoliosis can cause bursitis of the shoulders; however, shoulder bursitis is more commonly caused by overuse of the shoulder joint and related muscles.

Traumatic injury is another cause of bursitis. The inflammation irritates because the bursa no longer fits in the original small area between the bone and the functionary muscle or tendon. When the bone increases pressure upon the bursa, bursitis results. Sometimes the cause is unknown. It can also be associated with various other chronic systemic diseases.

The most common examples of this condition:

- Prepatellar bursitis, "housemaid's knee"

- Infrapatellar bursitis, "clergyman's knee"

- Trochanteric bursitis, giving pain over lateral aspect of hip

- Olecranon bursitis, "student's elbow", characterised by pain and swelling in the elbow

- Subacromial bursitis, giving shoulder pain, is the most common form of bursitis.

- Achilles bursitis

- Retrocalcaneal bursitis

- Ischial bursitis, "weaver's bottom"

- Iliopsoas bursitis

- Anserine bursitis

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.

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".

Trochleitis is diagnosed based on three criteria: 1) demonstration of inflammation of superior oblique tendon/ trochlea region, 2) periorbital pain and tenderness to palpation in the area of the sore trochlea, and 3) worsening of pain on attempted vertical eye movement, particularly with adduction of the eye. It is important to identify trochleitis because it is a treatable condition and the patient can benefit much from pain relief. Treatment consists of a single injection of corticosteroids to the affected peritrochlear region. A specific "cocktail" consisting of 0.5 ml of depomedrol (80 mg/ml) and 0.5 ml of 2% lidocaine can be injected into the trochlea; immediate relief due to the effects of the local anesthetic indicates successful placement. However, great care must be taken as the injection is in the region of several arteries, veins and nerves. The needle should not be too small (so as not to penetrate tiny structures), the surgeon should draw back on the syringe (to ensure not have pierced a vessel), the lidocaine should not contain epinephrine (which could cause vasospasm), and the pressure of the injection must always be controlled. Only a limited number of injections can be made as they would otherwise lead to muscle atrophy. Diagnosis can be confirmed by response to this treatment; pain and swelling are expected to disappear in 48–72 hours. Some patients experience recurrence of trochleitis.

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.

Bicipital tenosynovitis is tendinitis or inflammation of the tendon and sheath lining of the biceps muscle. It is often the result of many years of small tears or other degenerative changes in the tendon first manifesting in middle age, but can be due to a sudden injury. Calcification of the tendon, and osteophytes ("bone spurs") in the intertubercular groove can be apparent on x-rays. The condition (which can also occur in dogs) is commonly treated with physical therapy and cortisone and/or surgery.

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.

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.

The literature on the pathophysiology of bursitis describes inflammation as the primary cause of symptoms. Inflammatory bursitis is usually the result of repetitive injury to the bursa.

In the subacromial bursa, this generally occurs due to microtrauma to adjacent structures, particularly the supraspinatus tendon. The inflammatory process causes synovial cells to multiply, increasing collagen formation and fluid production within the bursa and reduction in the outside layer of lubrication (Ishii et al., 1997).

Less frequently observed causes of subacromial bursitis include hemorrhagic conditions, crystal deposition and infection.

Many causes have been proposed in the medical literature for subacromial impingement syndrome. The bursa facilitates the motion of the rotator cuff beneath the arch, any disturbance of the relationship of the subacromial structures can lead to impingement. These factors can be broadly classified as intrinsic such as tendon degeneration, rotator cuff muscle weakness and overuse. Extrinsic factors include bone spurs from the acromion or AC joint, shoulder instability and neurologic problems arising outside of the shoulder.

The cause of trigger finger is unclear but several causes have been proposed. It has also been called stenosing tenosynovitis (specifically "digital tenosynovitis stenosans"), but this may be a misnomer, as inflammation is not a predominant feature.

It has been speculated that repetitive forceful use of a digit leads to narrowing of the fibrous digital sheath in which it runs, but there is little scientific data to support this theory. The relationship of trigger finger to work activities is debatable and scientific evidence for and against hand use as a cause exist. While the mechanism is unclear, there is some evidence that triggering of the thumb is more likely to occur following surgery for carpal tunnel syndrome. It may also occur in rheumatoid arthritis.

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.

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.

According to a study in the Journal of Orthopaedics the prevalence of a rotator cuff tear was considerably greater in males than in females within the ages of 50–60 years old, within the ages of 70–80 years old there wasn’t much difference in prevalence. The data of this study showed that the prevalence of a rotator cuff tear in the general population is 22.1% Yamamoto et al. performed a medical examination on 683 people whom live in a mountain village. The purpose of this study was to determine the prevalence of a rotator cuff tear among a population. Yamamoto found that among the mountain village population, rotator cuff tears were present in 20.7% of the village population. In both of these studies we see that the percentages of the prevalence of a rotator cuff tear are very close in number so these numbers show us the prevalence of rotator cuff tears in the general population.

In an autopsy study of rotator cuff tears, the incidence of partial tears was 28%, and of complete rupture 30%. Frequently, tears occurred on both sides and the frequency increased with age. The frequency was also higher in females. Other cadaver studies have noted intratendinous tears to be more frequent (7.2%) than bursal-sided (2.4%) or articular-sided tears (3.6%). However, clinically, articular-sided tears are found to be 2 to 3 times more common than bursal-sided tears and among a population of young athletes, articular-sided tears constituted 91% of all partial-thickness tears.

In 1997 Morrison et al.

published a study that reviewed the cases of 616 patients (636 shoulders) with impingement syndrome (painful arc of motion) to assess the outcome of non-surgical care. An attempt was made to exclude patients who were suspected of having additional shoulder conditions such as, full-thickness tears of the rotator cuff, degenerative arthritis of the acromioclavicular joint, instability of the glenohumeral joint, or adhesive capsulitis. All patients were managed with anti-inflammatory medication and a specific, supervised physical-therapy regimen. The patients were followed up from six months to over six years. They found that 67% (413 patients) of the patients improved, while 28% did not improve and went to surgical treatment. 5% did not improve and declined further treatment.

Of the 413 patients who improved, 74 had a recurrence of symptoms during the observation period and their symptoms responded to rest or after resumption of the exercise program.

The Morrison study shows that the outcome of impingement symptoms varies with patient characteristics. Younger patients ( 20 years or less) and patients between 41 and 60 years of age, fared better than those who were in the 21 to 40 years age group. This may be related to the peak incidence of work, job requirements, sports and hobby related activities, that may place greater demands on the shoulder. However, patients who were older than sixty years of age had the "poorest results". It is known that the rotator cuff and adjacent structures undergo degenerative changes with ageing.

The authors were unable to posit an explanation for the observation of the bimodal distribution of satisfactory results with regard to age. They concluded that it was "unclear why (those) who were twenty-one to forty years old had less satisfactory results". The poorer outcome for patients over 60 years old was thought to be potentially related to "undiagnosed full-thickness tears of the rotator cuff".

The cause of snapping hip syndrome is not well understood, and confusion exists within the medical community regarding causation. Athletes appear to be at an enhanced risk for snapping hip syndrome due to repetitive and physically demanding movements.

In athletes such as ballet dancers, gymnasts, horse riders, track and field athletes and soccer players, military training, or any vigorous exerciser, repeated hip flexion leads to injury. In excessive weightlifting or running, the cause is usually attributed to extreme thickening of the tendons in the hip region. Snapping hip syndrome most often occurs in people who are 15 to 40 years old.

The cause of trochleitis is often unknown (idiopathic trochleitis), but it has been known to occur in patients with rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, enteropathic arthropathy, and psoriasis. In his study, Tychsen and his group evaluated trochleitis patients with echography and CT scan to demonstrate swelling and inflammation. Imaging studies showed inflammation of superior oblique tendon/ trochlear pulley. It was unclear whether the inflammation involved the trochlea itself, or the tissues surrounding the trochlea.

Although strains are not restricted to athletes and can happen while doing everyday tasks, however, people who play sports are more at risk for developing a strain. It should also be noted that it is common for an injury to develop when there is a sudden increase in duration, intensity, or frequency of an activity.

Retrocalcaneal bursitis is an inflammation of the bursa located between the calcaneus and the anterior surface of the Achilles tendon. It commonly occurs in association with rheumatoid arthritis, spondyloarthropathies, gout, and trauma.

The pain is usually on the back of the heel and swelling appears on lateral or medial side of the tendon.

OSD occurs from the combined effects of tibial tuberosity immaturity and quadriceps tightness. There is a possibility of migration of the ossicle or fragmentation in Osgood-Schlatter patients. The implications of OSD and the ossification of the tubercle can lead to functional limitations and pain for patients into adulthood.

Of people admitted with OSD, about half were children who were between the ages of 1 and 17. In addition, in 2014, a case study of 261 patients was observed over 12 to 24 months. 237 of these people responded well to sport restriction and non-steroid anti-inflammatory agents, which resulted in recovery to normal athletic activity.

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.

Extra-articular snapping hip syndrome is commonly associated with leg length difference (usually the long side is symptomatic), tightness in the iliotibial band (ITB) on the involved side, weakness in hip abductors and external rotators, poor lumbopelvic stability and abnormal foot mechanics (overpronation). Popping occurs when the thickened posterior aspect of the ITB or the anterior gluteus maximus rubs over the greater trochanter as the hip is extended.

The condition is usually self-limiting and is caused by stress on the patellar tendon that attaches the quadriceps muscle at the front of the thigh to the tibial tuberosity. Following an adolescent growth spurt, repeated stress from contraction of the quadriceps is transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple subacute avulsion fractures along with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump which can be very painful, especially when hit. Activities such as kneeling may also irritate the tendon.

The syndrome may develop without trauma or other apparent cause; however, some studies report up to 50% of patients relate a history of precipitating trauma. Several authors have tried to identify the actual underlying etiology and risk factors that predispose Osgood–Schlatter disease and postulated various theories. However, currently it is widely accepted that Osgood–Schlatter disease is a traction apophysitis of the proximal tibial tubercle at the insertion of the patellar tendon caused by repetitive micro-trauma. In other

words, Osgood–Schlatter disease is an overuse injury and closely related to the physical activity of the child. It was shown that children

who actively participate in sports are affected more frequently as compared with non-participants. In a retrospective study of adolescents, old athletes actively participating in sports showed a frequency of 21% reporting the syndrome compared with only 4.5% of age-matched nonathletic controls.

The symptoms usually resolve with treatment but may recur for 12–24 months before complete resolution at skeletal maturity, when the tibial epiphysis fuses. In some cases the symptoms do not resolve until the patient is fully grown. In approximately 10% of patients the symptoms continue unabated into adulthood, despite all conservative measures.