Causes of Heel Pain

The Achilles tendon, connecting the calf muscles to the calcaneus, can be the source of pain at the back of the heel. We mainly distinguish between insertional tendinitis and calcific tendinopathy.

Insertional tendinitis causes localized pain at the calcaneal insertion of the Achilles tendon. This pain intensifies when walking uphill, running, or jumping. In our patients, we regularly observe posterior swelling and marked tenderness to palpation.

The causes include sport overuse (intensive running, jumping sports), wearing shoes with rigid heel counters, and tightness in the calf muscles. In patients over 50, being overweight is a contributing factor. We find that an abrupt change in physical activity often precedes the onset of symptoms.

Calcific tendinopathy is characterized by calcium deposits within the tendon, visible on X-rays. These calcifications, although sometimes asymptomatic, can cause friction with the heel counter of the shoe and trigger local inflammation. Calcifications are regularly located at the calcaneal insertion of the Achilles tendon. Ultrasound allows localization of these deposits and assessment of the tendon’s condition. MRI provides an overall analysis of the Achilles tendon.

Symptoms include morning pain during the first steps, swelling of the area, and stiffness after rest. Stretching the tendon (standing on tiptoes) reproduces the pain.

Haglund’s disease corresponds to an association of 3 potential pains:

• Pain in the Achilles tendon: mid-portion tendinopathy
• Pain in the calcaneal tuberosity: pre-Achilles bursitis
• Pain at the Achilles calcaneal insertion: insertional tendinopathy

The morphology of the foot, the posterior calcaneal tuberosity, as well as the torsion of the calcaneal tuberosity, are contributing factors to Haglund’s disease.

A bony outgrowth on the posterior part of the calcaneus can create a visible and palpable bump. We encounter it mainly in young adults, with a predisposition in patients with a high-arched foot.

This bony deformity comes into conflict with the rigid heel counter of shoes, particularly safety shoes, boots, and certain sports shoes. Repeated friction causes inflammation of the synovial bursa located between the bone and the skin, called retro-Achilles bursitis, and inflammation of the synovial bursa located between the calcaneal tuberosity and the Achilles tendon, called pre-Achilles bursitis. This inflammation results in a red, hot, and painful swelling to the touch.

Contributing factors include hereditary bone morphology, high-arched feet which accentuate the bump, and prolonged wearing of shoes with a rigid heel counter.

Characteristic symptoms include a visible bump at the back of the heel, local skin redness, pain when putting on shoes, and sometimes inflammatory bursitis with a sensation of warmth. The pain generally improves when barefoot, which is a distinguishing sign compared to Achilles tendinopathies.

The diagnosis is mainly based on clinical examination, and lateral X-rays of the ankle and foot which assess the morphology of the foot and calcaneus.

The calcaneal spur is a bony growth visible on X-rays, located at the insertion point of the plantar aponeurosis on the calcaneus. Contrary to popular belief, this outgrowth is not the direct cause of pain in most cases, but rather a reflection of the significant tension exerted at the calcaneal insertion of the plantar fascia.

Calcaneal spurs are regularly found on X-rays of completely asymptomatic patients. Studies show that 10 to 25% of the general population has a calcaneal spur without any pain. Conversely, many patients suffering from plantar heel pain have strictly normal X-rays.

This ossification results from chronic pulling by the plantar fascia on its bony insertion. It is therefore a consequence, not a cause. When pain is present, it results from excessive tension in the fascia (plantar fasciitis) or other structures, not from the spur itself.

Surgical removal of the spur requires wide detachment of the plantar aponeurosis, which is generally undesirable. We prefer stretching of the posterior muscle chains, cushioning orthotic insoles, and treatments for inflammation.

The calcaneal stress fracture occurs following repeated strain that exceeds the bone's capacity to adapt. We frequently diagnose it in long-distance runners, military personnel during intensive training, and people who have suddenly increased their physical activity.

Symptoms appear gradually. The pain occurs on weight-bearing, worsens with walking and over the course of the day, unlike plantar fasciitis which improves after warming up. Limping appears quickly, and the patient avoids placing the heel fully on the ground. Lateral pressure on the calcaneus (compression between both hands) reproduces the pain, a characteristic clinical sign. The pain can also become nocturnal.

Standard X-rays are normal during the first 2 to 3 weeks. MRI allows early diagnosis by visualizing the bone fissure and bone marrow edema. Bone scintigraphy also shows increased uptake at the fracture site.

This condition requires rest for at least 6 to 8 weeks, and adaptation when resuming physical activities.

The lateral plantar branch of the posterior tibial nerve passes between the plantar aponeurosis and the heel bone. Its compression generates neurological symptoms often mistaken for plantar fasciitis.

The pain is located on the inner side of the heel, with a burning, tingling, or electric shock-like sensation. In our patients, we observe maximal intensity in the morning during the first steps, then a partial decrease during the day. Some describe numbness or tingling radiating to the arch of the foot with increased intensity at night.

Nerve compression occurs in a narrow anatomical passage. Causes include muscle hypertrophy, the presence of a thickened, inflamed, or retracted aponeurosis, and compression of the posterior tibial nerve within its osteofibrous tunnel.

Clinical examination reveals pain on pressing a precise point on the inner edge of the heel, different from the painful area in fasciitis. Tapping the nerve (Tinel’s sign) triggers paresthesia. Ultrasound can sometimes visualize nerve thickening, and electromyogram confirms nerve impairment, although it is normal in 20 to 30% of cases. MRI rules out any obstacle compressing the nerve.

Sever’s disease specifically affects children aged 8 to 13, mostly athletic boys. This condition affects the posterior ossification center of the calcaneus, located at the back of the heel.

Repeated microtrauma related to intensive sports (football, basketball, gymnastics, dance) create microtrauma and inflammation of the growth cartilage. The pull of the Achilles tendon on this still-immature bone center worsens the process.

The child complains of pain at the back of the heel, worsened by sports and running. Limping on the tiptoes to avoid heel contact may be observed. Direct pressure on the posterior area of the calcaneus triggers sharp pain, a pathognomonic sign of the disease.

X-rays sometimes show densification or fragmentation of the posterior ossification center, but these signs may be absent. The diagnosis remains essentially clinical.

This condition is benign and resolves spontaneously at the end of bone growth. Treatment is based on adapting sports activities (2 to 3 months), applying ice after exercise, regular calf muscle stretching, and wearing cushioning heel pads. Symptoms usually disappear within 6 to 12 months without after-effects.

Certain mild cases of heel pain, related to temporary overuse or unsuitable footwear, can improve spontaneously with rest and adjustment of activities. We observe this favorable progression with mild tendonitis or pain linked to unusual exertion.

However, the absence of treatment carries a risk of chronicity. Untreated or poorly treated plantar fasciitis can persist for several years and become harder to manage. An ignored stress fracture may develop into a more complex fracture. Prolonged nerve compression can lead to permanent damage.

We recommend consulting a specialist if the pain persists beyond 3 weeks despite rest and self-management measures. Early diagnosis enables tailored treatment and prevents long-term complications.

Continuing sports activities when experiencing acute or persistent pain is not recommended. Every impact worsens tissue damage and delays healing. We regularly observe that patients who continue their sport despite pain develop chronic conditions requiring several months of treatment.

A specialist consultation provides an early diagnosis, and allows you to continue sports activities in a supervised manner.

We advise temporarily replacing your usual sport with low-impact activities. Swimming, cycling, aqua aerobics, or ellipticals help you maintain fitness while protecting your heel. Gradually returning to sports only after complete disappearance of symptoms, under medical supervision, reduces the risk of recurrence.

Orthopedic insoles have proven highly effective for heel pain caused by mechanical issues. They correct static foot disorders (flat feet, high arches), redistribute pressure, absorb shocks, and relieve painful areas.

However, their benefit is limited for nerve conditions or bone injuries. In such cases, other treatments may be more appropriate.

The podiatrist carries out a full postural assessment and designs custom orthoses according to your specific needs. "Generic" insoles sold without a medical prescription rarely provide lasting relief.

The duration varies greatly depending on the condition and the speed of treatment. Early-stage tendonitis treated promptly heals in 2 to 3 weeks. Recent plantar fasciitis usually responds to treatment in 6 to 12 weeks. Haglund's disease often needs 3 to 6 months of conservative treatment before significant improvement.

Calcaneal stress fractures require strict rest for at least 6 to 8 weeks, followed by a gradual return to activity over an additional 4 to 6 weeks. Nerve compressions improve more slowly, with progressive improvement over 3 to 6 months.

Our experience shows that patients who seek early consultation and strictly follow recommendations heal faster. On the other hand, chronic heel pain neglected for several months requires longer and sometimes more invasive treatments.

An X-ray is not always necessary for recent heel pain with typical symptoms of plantar fasciitis in a young patient. The clinical examination alone is often sufficient for diagnosis and starting treatment.

However, we systematically request weight-bearing X-rays of the ankles and feet at the first consultation. For us, these X-rays are an extension of the clinical examination.

We systematically prescribe X-rays in cases of trauma (suspected fracture), persistent pain despite well-managed treatment (looking for large heel spurs, Haglund's disease), suspected stress fracture, or atypical symptoms suggesting a bone condition.

Weight-bearing (standing) X-rays of both feet (front and side views) constitute the minimal workup. They visualize bone architecture, any bony outgrowths, and static disorders. CT scan or MRI is reserved for complex situations requiring a more detailed analysis of bone structures and soft tissues.

Athletes involved in activities with repeated impact (running, jumping, basketball, volleyball, tennis) do indeed have an increased risk of heel pain. Repetitive mechanical stress leads to plantar fasciitis, Achilles tendonitis, and stress fractures.

However, sedentary individuals are not immune. Overweight, prolonged standing at work, and wearing unsuitable footwear also expose people to heel pain.

Common risk factors include inadequate footwear (shoes without arch support, high heels, unstable shoes), postural disorders (flat feet, high arches, leg length discrepancy), tight calf muscles, and age (reduced tissue elasticity after age 50).

The foot specialist orthopedic surgeon first makes a precise diagnosis through a detailed clinical exam and analysis of appropriate imaging tests (X-rays, ultrasound, MRI if needed).

Conservative treatment is the first line of management in over 90% of cases. Medical treatment is generally offered first.

Surgery is reserved for cases resistant to well-managed medical treatment for 3 to 12 months, depending on the underlying condition.