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11 Articles in Volume 10, Issue #9
Activated Glia: Targets for the Treatment of Neuropathic Pain
Acute Herpes Zoster Neuritis and Postherpetic Neuralgia
Acute Treatment of Cluster Headache
Chronic Overuse Sports Injuries in the Adolescent/Pediatric Population
Clinical Recognition of Central Abnormal Neuroplasticity
H-Wave® Stimulation: A Novel Approach In Electromedicine
Homeopathy Enters Contemporary Pain Practice
Immune-modulating Effects of Therapeutic Laser
Pain and Addiction: Words, Meanings, and Actions in the Age of the DSM-5
Partial Plantar Fasciectomy With Autologous Platelet Concentrate
Tethered Spinal Cord Syndrome: Pathophysiology and Radiologic Diagnosis

Partial Plantar Fasciectomy With Autologous Platelet Concentrate

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Chronic heel pain can be extremely complex and debilitating. Very subtle, and some not so subtle, lower extremity biomechanical compensations frequently occur resulting in symptom complexes that can be extensive and difficult to treat and not isolated to the heel. These multi-factorial pain syndromes can be confusing to the practitioner in the initial diagnosis and work up of the patient.

The American Podiatric Medical Association Practice Survey in 2003 found that up to 44% of patient visits to a foot and ankle practitioner every year present with a chief complaint of heel pain.1 The vast majority of these patients will be diagnosed with plantar fasciitis. No one really knows how many people are affected by heel pain. It has been estimated that greater than two million people every year in the United States suffer from heel pain and one study suggested 10 percent of the population.2 It has been estimated that 93% of all cases of heel pain can be attributed to plantar fasciitis (fasciopathy).

The etiology of heel pain can be complex and multi-factorial including such diagnoses (some erroneous) as plantar fasciitis/fasciosis, inferior calcaneal fat pad atrophy, infracalcaneal bursitis and medial calcaneal nerve entrapment. When misdiagnosed, the patient often receives unnecessary treatment including steroid injections and surgery. There is no current universal standard by which this diagnosis is made and also no agreed-upon staging and grading scheme to determine appropriate treatment.

Understanding the Heel

The human plantar fascia is a dense aponeurosis that originates from the inferior aspect of the calcaneus. It is often confluent anatomically with the distal insertion of the Achilles tendon fibers on the inferior surface of the calcaneus and provides the majority of the biomechanical structural support for the foot during stance and especially gait. It is dynamic and terminates distally in the forefoot and toes with a complex integration into the soft tissues of the fat pad on the sole of the foot and in the submetatarsal head area.3 The plantar fascia provides a critically important digital stabilization mechanism with subsequent offloading of the metatarsal heads during the late midstance and the propulsive phases of gait. The histology and appearance of the plantar fascia with high resolution diagnostic ultrasound is similar to that found for tendon4 (see Figure 1).

Figure 1. Diagnostic ultrasound of a non-symptomatic plantar fascia with normal thickness.


Chronic plantar heel pain has been documented to have a severe negative impact on the general quality of life as reported by Irving, et al in a 2008 article in the Journal of the American Podiatric Medical Association.5

Plantar Fasciopathy (Plantar Fasciosis)

While it is still generally and erroneously believed that the plantar fascia becomes chronically inflamed because it is subjected to an excessive mechanical axial tension that is subsequently often treated by the misguided use of steroids and NSAID’s, it is known that the condition is degenerative.6,7 In 2003, Lemont published a study in the Journal of the American Podiatric Medical Association,7 where it was objectively determined that the condition that has been mistakenly attributed to an inflammation of the plantar fascia is, in fact, a degenerative condition similar to tendinopathy. In specimens taken at the time of plantar fasciectomy, no histologic mediators of inflammation were seen microscopically. Similar findings in tendinopathy confirm what Lemont observed.8-10 This was further demonstrated in tendon animal studies.11 Histological separation and disruption of collagen fibrils both lengthwise and crosswise, an increase in tenocytes—combined with vascular hyperplasia—has been repeatedly observed. Visualization with high-resolution diagnostic ultrasound of this tissue response—as hypoechoic signal intensity—has been previously and erroneously attributed to inflammation within the tissue. An example of this can be seen in Figure 2.


Figure 2. Abnormally thickened plantar fascia with hypoechoic signal intensity. Tendon or aponeurosis can only handle an eccentric force to approximately 4-6% of its original length without pathologic damage occurring.12 This results in tissue breakdown within 2-3 weeks and is a degenerative rather than an inflammatory response.7 It is known that the plantar fascia can handle high tensile loads and has a stress modulus between that of ligament and tendon.1 The concept of high axial tension forces acting as the primary etiological factor in the development of this condition needs to be scrutinized. In strong support of the cause of plantar fasciosis more likely being due to compressive and shearing type forces, as opposed to axial ones, is Li and Muehleman’s histological study which demonstrated that the trabeculae within the inferior calcaneal exostosis are not aligned with the tension force of the plantar fascia (which has always been perceived to be the etiology of the breakdown of the plantar fascia) but instead are due to the stress placed on the inferior surface of the calcaneus with weight bearing.13 It is likely that within the first few weeks when the plantar fascia starts to become symptomatic, it may be initially due to an inflammatory response. However, it has been shown in animal studies that when the tendon is subjected to a lengthwise tensile force that stretches the tendon to more than its normal tolerance (which is only about 4-6 percent of its length), there are no cellular signs of inflammation after two to three weeks. These areas of tendonous or ligamentous structures that become damaged remain in this chronic state of degeneration unable to heal. The appearance of degeneration of the plantar fascia with ultrasound highly correlates to the symptomatic presentation of pain. However, people can have degeneration without pain just the same as people can have pain without degeneration. As can be seen in Table 1, the presence of hypoechoic signal intensity visualized in the substance of the plantar fascia is highly correlated with the presence of plantar fasciosis.

Table 1. Compilation of Studies that Evaluate the Hypoechoic Signal Correlated with Symptomatic Plantar Fascia Thickness (fasciosis)

Author, Year

Number of sympto-
matic heels

Average PF thickness (mm)

Hypoechoic findings

Number of unilateral cases

Last updated on: March 7, 2011