Weight-bearing and ambulation force the soft tissues in the heel to react to compressive and tractional forces at the same time. Understanding the anatomic relationship of structures in this tightly packed area of the foot can help the practitioner to understand the possible causes of heel pain. Compression of the heel pad occurs at the beginning of each weight-bearing period, followed by traction on both the plantar and posterior calcaneus during the middle to late stance periods. Depending on body structure and activity, those forces may exceed tissue tolerances and may create painful and disabling symptoms.

At the anterior aspect of the calcaneal tuberosity are the attachments of the plantar fascia, or plantar aponeurosis, and the intrinsic musculature of the foot. These structures extend the length of the longitudinal arch and envelop the metatarsophalangeal joints inserting on the phalanges (1). The plantar structures are tightened whenever the metatarsophalangeal joints are dorsiflexed, thus raising the longitudinal arch of the foot. The secondary effect is traction on the calcaneal origins of the plantar intrinsic musculature (1).

The plantar fascia is a broad, dense band of longitudinally arranged collagen fibers that begins as a thick mass attached to the anterior aspect of the calcaneal tuberosity (2). The central band spreads into a broad sheet as it extends distally and divides into five digital bands at the metatarsophalangeal joints (2). Each digital band divides to pass on either side of the flexor tendons and inserts dorsally into the periosteum at the base of the proximal phalanges. Fibers of the plantar fascia blend with the dermis, transverse metatarsal ligament, flexor tendon sheaths, and other adjacent ligamentous structures (1,2). The central portion of the plantar fascia is continuous with the medial and lateral portions. At these junctions are two strong intermuscular septa that are broader distally than proximally (2).

The lateral portion of the plantar fascia is found superficial to the abductor digiti minimi muscle (2,3). This portion of the fascia is thicker proximally and forms a strong band between the lateral process of the tuberosity of the calcaneus and the base of the fifth metatarsal bone. The lateral band of the plantar fascia is continuous with the central portion medially and with the fascia on the dorsum of the foot laterally (2) (Fig. 39.1).

The medial portion of the plantar fascia lies superficial to the abductor hallucis muscle and is thin. It is continuous with the central portion of the plantar fascia laterally and with the fascia on the dorsum of the foot medially. This medial portion is also attached to the flexor retinaculum (2).

The plantar fascia itself is largely inelastic. This inelasticity means that tension experienced on one end is immediately transmitted to the other. As the foot moves through midstance to toe-off, the metatarsophalangeal joints are dorsiflexed, thus creating tension on both intrinsic muscle and the plantar fascial origins at the calcaneal tuberosity. Simultaneously, additional tension is created by the soleus as it pulls the heel posteriorly, stabilizing the ankle for forefoot stance (4).

No natural bursae exist beneath the plantar surface of the heel. Adventitial bursae may exist, but they are uncommon. Barrett et al (5), in a dissection of 200 cadaver legs, were able to identify only a single inferior calcaneal bursa.

Over the years, many authors have described the classic heel spur (8,9,10 and 11). The heel spur or calcaneal spur is an osteophytic outgrowth anterior to the medial calcaneal tuberosity that usually extends its entire width or about 2.0 to 2.5 cm (11). This condition most often exists without producing symptoms, although in some selected patients it may become a source of symptoms.

Although some surgeons believe that the apex of the spur lies in the origin of the plantar fascia, McCarthy and Gorecki (8) countered that the spur lies in the origin of the flexor digitorum brevis muscle, superior to the plantar fascia. Furthermore, they asserted that the origin of the flexor digitorum brevis muscle, the quadratus plantae, the long plantar ligament, the abductor hallucis muscle, and the abductor digiti minimi muscle are all sites of potential spur formation.

Foreman and Green studied cadaveric specimens and found that the plantar fascia “slings underneath the calcaneus and remains plantar to the spur at the calcaneal tuberosities. The flexor digitorum brevis lies above the aponeurosis and attaches into the apex of the spur at the medial tuberosity” (9). They also believed that the abductor hallucis origin attaches at the apex of the spur and contributes to its formation. From their cadaveric specimen studies, these investigators found that the abductor digiti minimi and quadratus plantae origins were lateral to and superior to the spur, respectively.

Graham stated that the plantar fascia and the flexor brevis muscle attach to the calcaneal tubercle proximal to where technetium-99m scans show increased uptake His belief was that the intrinsics pull on the tubercle and eventually collapse the anterior lip of the tubercle. Graham’s contention is that the “spurs” seen on radiographs are a “manifestation of the healing effort and reflect a layering out of the calcification on top of the flexor muscle and not a traction spur as commonly believed” (12).

Many authors believe that the constant pulling of the plantar fascia causes an inflammatory process. The constant strain results in periostitis followed by osteogenesis (13,14 and 15). Histologic studies have demonstrated that the periosteum displays “low-grade chronic inflammation as evidenced by thickening and edema, proliferation of fibroblasts, and round cell infiltration.” In addition, investigators noted that the bone spur itself showed “fibrosis of marrow tissues, small areas of necrosis, hyaline or gelatinous degeneration, and at places, proliferation of fibroblasts and sclerosis of cortical bone” (16).

Investigators have stated that of all adult foot complaints, 15% result from heel pain (8). Over the years, many causes of heel
pain have been proposed. In the 1930s, gonorrhea, syphilis, tuberculosis, and streptococcal infections were commonly believed to be major causes (16). Later, many of the theories on gonorrhea were discredited (17,18). Hauser (14) surmised that the heel spur acts like a truss, pointing down into the muscle belly and causing pain. Some investigators postulated that the subcalcaneal fat pad loses its compressibility secondary to thinning and loss of structural integrity of the septa. Graham considered the pain to be related to cortical fatigue fractures of the medial tubercle of the calcaneus (12). Smith et al (19) suggested “microtrabecular stress fractures (“fatigue perturbation”) of the calcaneus which occur with secondary soft tissue involvement such as enthesopathy, periostitis, myositis, bursitis, and finally the formation of a buttress callus (bone spur) to stabilize a microcortical crack.”

Hauser and Hicks had similar ideas regarding the traction forces acting at the insertion of the plantar fascia and intrinsic musculature (15,20). These tension forces are increased during the later part of stance, when the windlass mechanism is a major contributor to the tension. Many authors have shown that not all heel spurs are typically in and of themselves painful (11,21).

Lemont et al (22) histologically examined 50 heel spur resection samples performed for refractory plantar heel pain and found that there was no evidence of inflammation present in any of the specimens. Based on these observations, they recommended that the disorder of recurrent heel pain that is unresponsive to any type of conservative treatment be classified as plantar fasciosis instead of plantar fasciitis.

It is important to note that Lamont’s study only involved submission of heel spurs for microscopic examination, not segments of plantar fascia. Ten specimens were normal, sixteen demonstrated fiber fragmentation with myxoid degeneration of the attached fascia and the remaining samples “were submitted in sections, preventing adequate pathologic analysis.” Myxoid degeneration can be nonpathologic and is often an age-related observation. Lamont’s findings were not stratified by age, sex, or length of symptoms. Based upon this study alone, the characterization of heel pain as the result of “fasciosis” and its therapeutic options should be approached with caution.

In 1981, Przylucki and Jones (7) described a more accurate course of the first branch of the lateral plantar nerve. They noted that the nerve actually passes in proximity to the calcaneal tuber. Thus, it was believed that, in patients with recalcitrant heel pain, this nerve could be the sole or concomitant cause of the painful condition, and these investigators obtained relief in three patients by nerve excision. Sections of the nerve from cadavers, as well as from surgical patients, demonstrated histologic evidence of perineural hypertrophy. This work provided the clinical confirmation for the anatomic studies performed by other investigators (23,24,25 and 26).

Rondhuis and Huson (26) concluded that the site of entrapment was between the deep taut fascia of the abductor hallucis muscle and the medial or caudal head of the quadratus muscle. They presented strong evidence that nerve is a mixed type, providing sensory fibers to the calcaneal periosteum, including over the medial tuberosity, and the long plantar ligament, as well as motor fibers to the quadratus plantae, flexor digitorum brevis, and abductor digiti quinti muscles. This evidence may help to explain the more neuralgic symptoms that are characteristic of this cause of heel pain.

Baxter and Pfeffer (27) referred to the heel spur as an unlikely cause of direct mechanical heel pain. However, they believed that inflammation in the area of the spur is a theoretic source of compression of the first branch of the lateral plantar nerve as it passes superior to the spur. Patients exhibiting maximal tenderness over the area between the abductor hallucis and quadratus plantae muscles were proposed to suffer from nerve entrapment, and this test could be considered the “hallmark of this compression neuropathy.” In their study of 69 heels in 53 patients undergoing operative decompression of the inferior calcaneal nerve, 89% of these patients’ heels experienced good to excellent results, with 83% achieving complete resolution of pain after an average of 49 months.

Chronic exertional compartment syndrome has become recognized as a potential source of pain and disability in the lower extremity (28,29,30,31 and 32). Some research has focused on the possibility of compartment syndromes in the foot. Mollica described chronic exertional compartment syndrome as a transient, symptomatic pressure increase within a myofascial compartment that is precipitated by exercise and subsiding with cessation of athletic activity (50). The medial compartment appears most susceptible to chronic exertional compartment syndrome in the foot (33). This compartment contains the following: the abductor hallucis and flexor hallucis brevis muscles; the tendons of the flexor hallucis longus, peroneus longus, and tibialis posterior; and the medial planter nerve. In addition, this medial compartment does not communicate with any other compartment of the foot or ankle. Patients may report “cramp-like” pain and tightness in the arch (33). Pain may be preceded or followed by tingling or numbness. These symptoms may mimic classic plantar fasciitis pain when the medial compartment of the foot is involved. Palpation of the abductor hallucis muscle belly, medial to the plantar fascia, elicits a painful response.

Most of the current literature points to abnormal foot mechanics as a major influence in producing the heel pain syndrome. Excessive traction of the plantar fascia and intrinsic musculature are responsible for the majority of cases of heel pain. Bone scintography and MRI typically demonstrate inflammation of bone and soft tissue in the area of the calcaneal tuberosity.

Bergmann (34) concluded that “any force that causes an excessive pull at the origin of the plantar fascia or muscle can cause heel spur syndrome.” He referred to the various biomechanical abnormalities causing abnormal or excessive pronation (tibial varum, short Achilles tendon, compensated rearfoot varus, forefoot varus, flexible and partially flexible forefoot valgus, or a combination) as potential causes of heel spur syndrome.