Sports Med U | Educating Minds, Elevating Potential

Overuse injuries in sport: a comprehensive overview

Aicale, R., Tarantino, D. and Maffulli, N., 2018. Overuse injuries in sport: a comprehensive overview. Journal of orthopaedic surgery and research, 13, pp.1-11.

In today’s letter

• Overview of overuse injuries we see in sport

• Rapid Results =

1. Tendinopathy: Load modification and appropriate (depended on discomfort levels) exercises can effectively reduce pain and support tendon recovery, though full tissue healing may take time.

2. Stress Fracture: Early detection and activity modification are essential, as immediate offloading can prevent the progression of a stress reaction into a full fracture.

3. Juvenile Osteochondritis Dissecans: Early diagnosis combined with restrictions in activity can help stabilise the lesions in young athletes, allowing spontaneous healing in many cases. (YOUNG athletes only)

• 3 resources to check out to further you knowledge about overuse injuries

• Meme of the week: I’m in! ✅

Whats New in SportsMed U

Aim of the study

• The aim of this study is to explore the causes, symptoms, diagnostic tools, and treatments for the most common overuse injuries in sports.

• The focus is particularly on tendinopathy, stress reactions and juvenile osteochondritis dissecans—each of which can result from repetitive strain.

Did you know?

• Overuse injuries generally occur without a specific traumatic event, meaning there’s no one big incident that causes them; instead, these injuries build up over time.

• Besides overloading and lack of recovery, underpreparedness can also increase the risk. This happens when athletes face sudden increases, or "spikes," in training or match load that their bodies aren’t ready for.

Tendinopathy

• Overuse tendinopathy leads to pain and swelling in the affected tendon, reducing its ability to handle load and limiting movement during exercise.

• Healing relies on the tendon cells (tenocytes) responding to the injury by activating processes like cell death (apoptosis), cell movement (chemotaxis), and growth and specialisation (proliferation and differentiation).

• Tendinopathy is often considered a “failed healing response.” This means that, after an initial tendon injury, what should be a quick, efficient healing process becomes prolonged and less effective, leading to tendon degeneration and altered structure.

Stress Fractures

• Inadequate training techniques and other risk factors make players prone to bone-related overuse injuries, for example stress reactions that can develop into stress fractures.

The body adapts to stress based on Wolff’s law, which says:

“Bones adjust their structure according to the loads they experience”

• Stress fractures are small cracks in the bone’s outer layer (cortical bone), and they’re common among athletes, affecting thousands every year.

• If untreated, a stress fracture can worsen and eventually break the bone completely, which may require surgical repair.

• That being said, our tissues can adapt in complex ways, both weakening from overuse and strengthening in response to repetitive strain (It just needs to be monitored and progressed sensibly).

Juvenile Osteochondritis Dissecans (JOCD)

• It causes pain in teenagers, affecting both athletes and non-athletes.

• This condition involves damage (delamination) and localised cell death (necrosis) in the bone just beneath the cartilage, sometimes including the cartilage itself.

• While the exact cause isn’t known, repetitive microtrauma—like that seen in overuse injuries—is thought to be a major contributing factor.

What is going on under the surface with tendons?

Why does tendon healing succeed for some people but fail for others?

• There are factors that make healing less effective: For instance, tendinopathy rates are higher in people with obesity or lower insulin sensitivity, such as those with type 1 or type 2 diabetes.

• Obesity is linked to a low-grade, ongoing inflammatory state, mainly shown by increased levels of pro-inflammatory cytokines in the blood.

• Since inflammation has a big role in healing, prolonged, low-grade inflammation (common in obesity) impacts tendon healing after an injury.

• Even under ideal conditions, tendon healing is slow and complex; any slight disruption in the stages can make the recovery process much longer and more complicated.

• Right after a tendon injury, there’s an acute inflammatory phase in the first few days, where inflammatory cells like macrophages and monocytes migrate to the injury site.

• In obesity, chronic inflammation often reduces the number of circulating macrophages. With fewer of these cells available, the initial response to injury may be weaker, affecting early healing.

• This “failed healing” state results in disorganised tissue, with more extracellular ground substance and less alignment among collagen fibers.

• This relationship might clarify how mechanical overuse contributes to the development of tendinopathy, as it likely interferes with a tendon’s natural healing response.

Molecular factors in overuse injury

• When tendons don’t experience enough regular, healthy stress over time—a process called "underloading" starts to occur — which ironically makes the tendon more vulnerable to injury when suddenly exposed to higher demands.

• Tendons that are underloaded aren’t well-prepared to handle increased physical load, making them more prone to injuries when demands spike.

• Certain molecular agents are thought to connect tendon degeneration and poor healing with an ongoing production of reactive oxygen species (ROS) within and around tendon cells. Lifestyle choices, like diet and exercise habits, have a big influence on ROS production.

ROS are reactive oxygen-based molecules, and a free radical is a molecule that has one or more unpaired electrons, making it highly reactive. Think of ROS as “live wires”—when they aren’t balanced, they can cause disruptions similar to how loose wires can spark and damage nearby structures

• ROS are mainly produced in the mitochondria during normal respiration. They’re byproducts of cells making energy and can help cells grow and adapt. But if levels get too high, ROS can lead to cell death.

• They were originally thought to be mostly as harmful, damaging cell parts like lipids, DNA, and proteins. Even though some ROS (like superoxide and hydrogen peroxide) are mild, they can still alter proteins enough to cause trouble.

• High levels are associated with major health issues like cancer, heart disease, autoimmune disorders, and injuries from over-exercising.

• They affect connective tissues (like tendons) by impacting their structure and function. During intense exercise, reactive oxygen species production spikes due to both mitochondrial activity and immune responses.

• When tendons go through repeated cycles of loading and unloading (like in running), this creates ischemia-reperfusion cycles, meaning periods of low and then high oxygen. This pattern raises ROS levels in tendons, contributing to stress and potential damage.

• In addition, exercise heats up the body, with muscle temperatures reaching up to 47°C. This increased temperature boosts ROS production in muscles and tendons, making them more vulnerable to damage.

• But they are not all bad - Reactive oxygen species from immune cells help in healing by promoting collagen production and fibrotic (scar-like) tissue formation. They also influence tendon cells, or tenocytes, which affects both tendinopathy and recovery after tendon injuries.

Tendinopathy

• Tendinopathy is thought to result from inflammation in the tendon due to repeated or excessive use.

• However, anti-inflammatory medication don’t generally work well for tendinopathy, and studies now suggest that degeneration—not inflammation—drives this condition.

• In tendinopathy, the collagen fibers, which are usually well-organised and parallel, lose their alignment, and the collagen itself becomes thinner and less dense.

• Collagen in a healthy tendon is neatly bundled, but in tendinopathy, it’s disorganised, irregularly wavy, and includes more type III collagen, which is a weaker form produced during repair.

• Blood flow to tendinopathic tendons is also abnormal, with blood vessels arranged randomly and sometimes perpendicular to the collagen fibers.

Tendinopathy in Athletes

• Tendinopathy is common among both elite and recreational athletes, often due to repetitive, intense loading of the tendons

• Achilles tendinopathy, specifically, is one of the most frequent overuse injuries in athletes and has been on the rise over the last few decades.

• Sports that involve a lot of running and jumping, like soccer, tend to see higher rates among players.

• Tendons may handle a certain amount of micro-damage from repetitive loads, but when these demands are too high and consistent, the tendon’s ability to repair can’t keep up, resulting in injury.

Pain & Diagnosis

• The exact source of pain in tendinopathy isn’t fully understood, but both the local tendon cells and peripheral nerves seem to contribute in how pain develops.

• Studies suggest that tendinopathy involves changes in how nerves respond to tendon damage, affecting both the local site and central pain pathways.

• Diagnosing tendinopathy typically involves a clinical history and physical exam. Key signs are pain, swelling (localized or diffuse), and a drop in performance.

• Pain usually starts early in a training session and can return shortly after finishing. Over time, it may persist throughout exercise and, in severe cases, affect everyday activities.

• For non-insertional Achilles tendinopathy diagnosis, tests include palpation (for pain or thickening of the tendon), the Royal London Hospital (RLH) test, the painful arc sign, and tendon-loading tests like passive dorsiflexion, single heel raises, or hopping.

Managing Achilles Tendinopathy

• First-line treatments for Achilles tendinopathy are conservative, covering a range of options:

1. NSAIDs

2. Physical therapy

3. Cryotherapy

4. Shock wave therapy

5. Heat therapy.

• There isn’t a lot of high-quality research supporting one treatment over another for Achilles tendinopathy, and up to 25% of people don’t respond to conservative treatments alone.

• Eccentric exercises are widely used and often helpful for th achilles, though they don’t work for everyone, and the exact mechanism behind their success is still being studied.

• Shock wave therapy has shown similar results to eccentric strengthening exercises, with about 60% of patients reporting significant improvement in both treatment groups.

• When Shock wave is available, it may be a good second-line option, especially if eccentric exercises alone aren’t effective

Stress Fracture

• Stress reactions are considered early indicators that could eventually lead to stress fractures.

• The exact cause of stress fractures isn’t fully clear. Mechanical stress is a factor, but other elements like physical fitness, nutrition, and hormonal balance also seem to contribute

• Diagnosing stress reactions early can significantly improve healing timeframes. Treatment for stress reactions generally mirrors that of stress fractures.

• When the bone faces repetitive stress, osteoclastic activity (which breaks down bone) can outpace new bone formation, temporarily weakening the bone.

• If the stress load continues or the body doesn’t get adequate rest, a stress reaction can progress into a stress fracture.

There are two main types of stress fractures:

1. Fatigue fractures (due to overuse in individuals with normal bone density)

2. Insufficiency fractures (found in those with low bone density).

• Fatigue fractures are typical in athletes and military recruits, where repetitive stress and inadequate rest lead to accumulated microdamage in the bone.

• Insufficiency fractures occur in individuals with low bone mineral density, like those with osteoporosis or the female athlete triad. Here, the bone can’t remodel properly even under normal levels of stress.

• Research has shown that elite female athletes, particularly in sports like football, are prone to stress fractures and may experience menstrual irregularities or delayed menarche despite normal body composition.

• Education on energy balance, nutrition, and menstrual health can help prevent stress fractures in the short term and reduce the risk of osteoporosis over the long term.

• Stress fractures usually start with localised pain that worsens toward the end of a run. As the fracture progresses, pain may appear even during everyday activities.

• Increasing training frequency, duration, or intensity too quickly is a primary risk factor for stress fractures.

• Hard surfaces and worn-out shoes (over 6 months old) are also associated with a higher risk of stress fractures, as old shoes lose shock-absorbing.

• Certain intrinsic factors can raise the likelihood of stress fractures. Studies have found that female runners with smaller calf girth or less lower limb muscle mass are at a higher risk.

• Biomechanics are also important; runners with excessive hip adduction or rearfoot eversion are more likely to develop tibial stress fractures.

Diagnosing Stress Fractures and Treatment Options

• A telltale sign of a stress fracture is localised tenderness along the bone. Other possible symptoms include swelling, warmth, and redness in the affected area.

• Tests like the fulcrum test or hop test may help diagnose long bone fractures, though they’re not as sensitive (specific to stress farctures).

• A functional assessment of the kinetic chain, including muscle strength imbalances, leg-length discrepancies, and foot mechanics, can help identify biomechanical factors linked to stress fractures.

• Rest and protection are key in recovery, but understanding the underlying causes and addressing them is just as important to prevent future injuries.

Juvenile osteochondritis dissecans (JOCD)

• JOCD is a common cause of knee pain in adolescents, affecting both athletes and non-athletes, with boys having a higher incidence than girls.

• It’s thought to be driven by repetitive microtrauma, similar to other overuse injuries.

• In around 85% of cases, the lesion affects the medial femoral condyle of the knee.

• Despite the term “osteochondritis” suggesting inflammation, histology shows damage to the bone and cartilage with little to no inflammation.

• Symptoms often develop gradually and include knee pain, typically in the anterior region, which worsens with activity. Intermittent swelling (effusion) can follow physical activities.

• On examination, there may be mild swelling or restricted knee movement, depending on the disease stage.

• In early JOCD stages, symptoms are non-specific if the cartilage over the femoral condyle is intact. In advanced stages, the cartilage may break away, forming a loose body in the joint.

Diagnosis and Treatment of JOCD

• In advanced cases, loose cartilage fragments can cause joint pain, swelling, and even locking of the knee joint.

• JOCD lesions in the medial femoral condyle often trigger pain when the knee is flexed and internally rotated from full extension to around 30 degrees, relieved by external rotation.

• X-rays are a common first step in diagnosing JOCD. To compare, images of both knees are often taken, with a "tunnel view" providing a clearer look at the lesion.

• In cases where there’s significant swelling, discomfort, or trouble bearing weight, an MRI is typically ordered. MRI can detect instability in the lesion.

• Early diagnosis and treatment with activity restriction and pain management can promote healing in about 8-12 weeks.

• In younger patients with an open distal femoral growth plate, spontaneous healing is common, and the long-term outlook is generally excellent.

• If the lesion is unstable or symptoms persist despite conservative treatment, surgical options like drilling, reattachment, or removing the lesion may be necessary.

Top 3 resources to check out

To learn about overuse injuries

1. Overuse injury handout (PDF) - LINK

2. Athletic youth development (Article) - LINK

3. How overuse injuries happen (Video)

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