The inferior calcaneal spur—Anatomical and histological considerations

1. Introduction 

For the volume of literature relating to the inferior heel spur, there have been relatively few studies dedicated to defining the exact tissue into which the spur itself propagates [1], [2], [3], [4]. These few studies have all involved cadaveric or amputated limb dissection [1], [2], [3], [4] and the reported results have been varied, with the spur reported to reside within the flexor digitorum brevis and quadratus plantae [1]; within the flexor digitorum brevis and with small involvement from the abductor hallucis muscle [2]; within the plantar aponeurosis (PA) and superior to the aponeurosis, within the first layer musculature [3]; at the insertion sites of the abductor digiti minimi and the flexor digitorum brevis and to a lesser degree between the PA and these muscles and less frequently within the PA [4].

Regarding heel spur structure, McCarthy and Gorecki [1], in a cryomicrotomy study, evaluated a calcaneal spur with its insertion into the PA from one cadaver using electron microscopy. Observations included a calcified region that was characterized by an irregular oriented fibrillar network, parallel to the weight-bearing surface. The spur ended abruptly into the aponeurosis and its microstructure was also consistent with a highly irregular fibrillar network of collagen. The authors suggest this parallel nature of the calcified fibrillar network of the spur lends credence to the notion of traction as the mechanism of pathology, given the propensity of collagen to align themselves along lines of tension [1].

Separate studies [5], [6], [7] involving surgical cases of inferior heel pain, where a portion of the PA was submitted for histological investigation, all reported varying degrees of collagen degeneration demonstrated by a loss of collagen architecture and mucoid degeneration of dense collagenous tissue. Also reported was evidence of chondroid metaplasia of the aponeurotic enthesis and angiofibroplasia with increased numbers of fibrocytes and clusters of blood vessels as histological variations. Tountas and Fournasier [7] evaluated the histology of the calcaneal spurs in their series of surgical cases and reported the spurs to consist of mature lamellar bone with appositional periosteal woven bone deposition on its surface – also known as intramembranous ossification – a process where bone forms de novo (in this case on the surface of existing bone) [8]. Small foci of endochondral ossification – a different process in which bone replaces cartilage [8] – was also reported to exist at the apex of the spur.

A recent study by Lemont et al. [9] reported on histological samples of the PA from 50 cases of surgery for heel pain. In 16 PA samples, fibre fragmentation and myxoid degeneration were present. The authors conclude that there is substantial evidence for degeneration of the aponeurosis, but little evidence of inflammation within the PA in subcalcaneal pain diagnosed as insertional plantar fasciitis. Lemont et al. proposes fasciosis as a more appropriate description of this clinical entity [9]. While Lemont et al. examined 50 samples, they focused principally on PA pathology and described little of the features of the presumed resected heel spurs. Lemont et al. reports that 12 samples demonstrated apparent vascularization of the attached bone spur with multiple dilated vessels, suggesting bone contusion. Unfortunately, there is no further description or mention of the appearance of the heel spurs proper in their series [9].

A histological investigation by Kumai and Benjamin [10] into stages of heel spur formation and the subcalcaneal enthesis of the plantar fascia in cadaveric specimens reported spur formation to be heralded by degenerative changes within the PA, including fissuring and mucoid degeneration of collagen, similar to observations of previous studies [5], [6], [7], [9]. In comparing observations between small and large spurs, the authors propose that cartilage cell clustering and degeneration precedes the development of a spur, followed by subchondral plate thickening and the development of vertically oriented trabeculae abutting the proximal end of larger spurs [10]. Intramembranous ossification was noted, but not endochondral ossification. The spur itself was observed to form on the deep surface of the PA and, given this, the authors conclude that inferior heel spurs are not a product of traction but of degeneration within the PA [10].

The purpose of this study was to establish the anatomical and histopathological features of the inferior heel spur and the tissue in which it resides in otherwise healthy patients undergoing open heel surgery for recalcitrant heel spur syndrome.

2. Methods 

Approval for this study was obtained from the Curtin University of Technology Human Research Ethics Committee and was conducted from March 2004 through October 2004. Five consecutive patients undergoing open heel surgery for inferior calcaneal heel spur and plantar fascia resection were recruited. Participants were excluded from the study if the heel spur and pain were deemed to be caused by any pathology excepting mechanical origin. All patients were otherwise healthy with an unremarkable medical and family history.

Following informed consent, demographic, occupational and physical data were obtained. All subjects had recent (<6 months) weight-bearing radiographs (in standard angle and base of gait). Radiographic indices were obtained, including the presence of a saddle injury as described by Amis et al. [11], which is a concavity present on the calcaneal tuberosity that is posterior to a heel spur. Heel spur length was measured according to the technique reported by Özdemir et al. [12] (Fig. 1).

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Fig. 1. Black dashed arrow indicates saddle injury, a lytic antrum proximal to heel spur. Measurement of subcalcaneal spur length (A and B) indicates the most distal part of the medial calcaneal tuberosity; (C and D), the distal point of the subcalcaneal spur; (ϕ and π), the length of the subcalcaneal spur. Adapted from Özdemir et al. [12].

Surgery was performed under general anaesthesia with calf tourniquet haemostasis. Each participant was placed supine and an open approach to heel surgery was performed, as described by Malay [13]. Once excised, the thickness of the PA was measured with a micrometer and the separate heel spur tissue samples were then fixed with 4% buffered paraformaldehyde, decalcified, dehydrated with graded alcohol, cleared and embedded in paraffin wax. Sagittal and transverse sections were obtained at 8μm and stained with PAS-Alcian Blue, Haematoxylin and Eosin and Masson's Trichrome.

3. Results 

For the five participants included in this study, age ranged from 27 to 48 years (mean 38 years). Four women and one man participated in the study and of these five participants, four spent greater than 6h of daily weight-bearing for their respective occupations, including two whom averaged 10h/day. Four subjects were classified as being obese (mean BMI 32.4; obesity classified as BMI≥30) [14].

The average duration of heel pain ranged from 1.5 to 15 years (mean 4.7±11.6 years). However, subject 2, whose symptoms lasted 15 years, exceeds the other four subjects (1.5–3 years, mean 2.1±1.1 years).

Spur lengths ranged from 6 to 9mm (mean 7.1±1.1mm). This value is considered large when assimilated with the classification proposed by Özdemir et al. [12] (≥6mm considered large). All subjects demonstrated a degree of radiographic saddle injury (Fig. 2), which Amis et al. [11] found to occur in 60% of their cohort of 170 symptomatic heels. Of note, were the radiographic findings of a fracture through the base of the heel spur in two subjects (Fig. 2) and the intra-operative finding of an additional fracture through the base of a heel spur in a third subject that was not evident radiographically.

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Fig. 2. Closeup view of the heel spur of subject 3 taken from lateral weight-bearing radiograph. Dashed arrow indicates a small ‘saddle injury’. Solid arrow indicates subtle fracture line.

3.1. Intra-operative findings 

In each subject, it was observed intra-operatively that the heel spur propagated into the origin of the intrinsic musculature, namely the flexor digitorum brevis and to a lesser proportion, the abductor digiti minimi muscle (Fig. 3). Distal to the enthesis, the PA was consistently found to attach coherently with the flexor digitorum brevis muscle, agreeing with observations by Sarrafian [15] and Forman and Green [2], essentially organising the structures as a single unit. The PA was found consistently to course beneath the heel spur and insert just proximal and inferior to the origin of the spur. A large portion of the insertion of the PA was often correlated closely with the area of the saddle injury. The thickness of the PA samples ranged between 5 and 7mm (mean 6.1±0.7mm).

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Fig. 3. The excised spur. Muscle and adipose tissue attached to the calcaneal spur is highlighted.

3.2. Histological results 

In all samples there was clear evidence of skeletal muscle tissue distal and adjacent to the apex of the spur (Fig. 4). Adipose tissue was often noted to be evident within the muscle tissue. The skeletal muscle tissue is seen to attach to the spur by way of a fibrous–fibrocartilaginous enthesis (Fig. 4, Fig. 5). There were often vessels evident within this fibrous network. All but one spur demonstrated a chondroid cap that skirted the borders of the spur itself (Fig. 5). Florid endochondral ossification was evident at the apex and inferior flank of three of the heel spur samples, with trabeculae oriented vertically along the inferior margin and horizontally at the apex of the respective spurs (Fig. 4, Fig. 5, Fig. 6). None of the spurs demonstrated a cortical shell, but rather a mixture of fibrocartilage, cartilage and bony trabeculae. The area occupied by the PA enthesis, where it courses below the spur's inferior margin, was noted to send oblique fibres superiorly, which attach to the inferior aspect of the spur (Fig. 4). The entheses of the intrinsic musculature of the first layer of the foot and the PA was observed to amalgamate and form a common attachment for the respective structures (Fig. 4).

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Fig. 4. Longitudinal section of heel spur (Alcian Blue, ×25) Muscle tissue (M) is noted distal to the leading edge of the osseous spur (S). The muscle tissue is attached to the spur by a fibrous to fibrocartilaginous zone (F). A cartilage cap (C), is noted to be running inferiorly, distal and superiorly. (P) highlights the area where the plantar aponeurosis has been resected away before the heel spur can be resected during surgery. Pronounced endochondral ossification (arrowheads) is evident along the inferior margin and at the apex of the spur.

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Fig. 5. Longitudinal section of apex of heel spur (Alcian Blue, ×200). Area of the extreme apex of the spur. Arrowheads indicate segments of endochondral ossification taking place. The cartilage (C) is clearly seen. The transition to fibrocartilage (F) is denoted more distal.

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Fig. 6. Longitudinal section of inferior spur Margin (Alcian Blue, ×100). Higher power view of inferior margin of the heel spur. Endochondral ossification is noted (white arrowheads). There is an obvious fibrocartilaginous (F) enthesis inferior to the spur margin. The compact bone (B) of the spur itself is seen by the pink staining islands, surrounded in parts by a rather fibrous marrow tissue (fm). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of the article.)

Marrow constituents ranged from adipose tissue (subjects 1 and 3), to fibrous and highly vascular (subjects 3 and 4), to cartilage remnants in the leading edge of one spur (subject 2).

4. Discussion 

In all heel spur sections, it was observed that the PA traversed the area inferior to the spur with insertion along the inferior margin of the spur by means of a fibrous–fibrocartilaginous enthesis. The apex and superior aspect of the spur was found consistently to reside within the enthesis of the intrinsic muscles of the first layer of the plantar aspect of the foot, specifically the flexor digitorum brevis and abductor digiti minimi. At low magnification, it was evident that the enthesis of the intrinsic musculature and PA were amalgamated and fashioned a broad conjoined enthesis.

There was a prolific number of fibrocytes present at the distal portion of the entheses in these samples, reflective of a high amount of fibroplasia. Indeed, previous studies have demonstrated a consistent increase in the thickness of the aponeurosis in persons suffering inferior heel pain with, or without, the presence of a heel spur when compared with controls [10], [16], [17], [18], [19], [20]. Thicknesses of the resected proximal portion of the PA from subjects involved in this study (6.1±0.7mm) were consistent with previous reported pathologic values of 3–6mm (normal reported values range between 2 and 4mm) [16], [17], [18], [19], [20]. The observation of increased thickness beyond normal reported values of the PA in persons with plantar fasciitis/enthesopathy is commonly accepted as a product of repetitive overload of the PA and intrinsic musculature and has been described as heralding the manifestation of a spur [10].

The actual insertion site of the PA in this subject group was observed to interface closely with the saddle injury described by Amis et al. [11]. Both in this series of cases and those reported by Amis et al. [11], the saddle injuries were noted just proximal to the heel spur, though unlike Amis et al. [11], who believes this point to represent a fatiguing of the tuberosity where the flexor digitorum brevis muscle originates, the findings in this study would suggest this region to represent a possible fatiguing of the tuberosity from stress at the point where the PA proper inserts. Further investigation would be desirable to confirm this and describe histological features of this ‘saddle injury’; to elucidate if it is an osseous injury per se, or just a simple antrum (a natural cavity or hollow in bone) for attachment of the PA enthesis.

At the level of the proximal portion of the entheses, fibrocartilage was observed where it flares to insert inferiorly on the medial calcaneal tubercle and inferior and distal portion of the heel spur. There is a prolific blue staining of the enthesis with PAS-Alcian Blue reflecting a high proportion of proteoglycan, though it is not known whether this proteoglycan content is inherent to its normal structure or an adaptation to daily weight-bearing pressure. This type of fibrocartilaginous structure is analogous with wrap-around regions of tendons and ligaments which change direction when coursing around osseous pulleys [21], [22] and has been likened to a pad by Kumai and Benjamin [10]. They describe this area of the subcalcaneal enthesis where the heel ‘articulates’ with the ground as similar to articular cartilage in a weight-bearing joint. The high concentration of proteoglycan in this region would support this suggestion. Added to this, in a paper on fatigue perturbation of the calcaneus, Smith et al. [23] believe the presence of heel spurs are analogous with buttress callous, commonly seen in the periphery of joints in degenerative joint disease. Similarly, Kumai and Benjamin [10] viewed spurs as skeletal adaption to weight-bearing stress – not traction stress – but an adaptive response to loading patterns on the weight-bearing enthesis. This notion is lent credence with previous research demonstrating the high proportion of inferior heel pain and spur development to occur with age [24], [25], [26], [27], [28], [29], obesity [25], [27], [30], [31], [32], [33] and prolonged weight-bearing [25], [33], [34]. Both obesity and prolonged weight-bearing would overload the medial calcaneal tubercle, ultimately resulting in osseous perturbance and wear and tear. In this study, four of the five subjects were deemed obese and spent greater than 6h/day weight-bearing.

Overt osseous perturbance was identified in three of the five subjects, with evidence of a fracture through the heel spur itself and, of these fractures, two extended from the aforementioned saddle area. The presence of a fracture through the spur could well explain the persistence of symptoms in patients that fail conservative measures and ultimately undergo surgical intervention. Furthermore, MR studies of subjects suffering insertional plantar fasciitis and heel spur syndrome [16], [35] have reported marrow oedema at the region correlating with the common enthesis of the PA and intrinsic musculature, suggesting bony injury. Indeed, endochondral ossification, observed at the margins of a proportion of the spurs within subjects of this study, is a prominent feature of long bone fracture healing [36]. However, endochondral ossification was noted in specimens without radiographic or intra-operative evidence of a fracture and vice versa. A larger series of surgical samples would be desirable to determine the significance of this finding.

In those samples that demonstrated endochondral ossification, the osteogenic activity was present most abundantly at both the apex and the inferior margin of the spur. The orientation of the trabeculae of this osseous proliferative process provides information about the forces acting on the spur. In the samples in this study, trabeculae are oriented both vertically, along the inferior margin of the spur and horizontally at its apex. This suggests: (1) longitudinal traction stress from the intrinsic musculature is influencing the morphology of the bone formation distally and/or (2) the vertically oriented trabeculae is an adaptive response to repetitive buttressing of the enthesis and the adjacent medial calcaneal tubercle from daily weight-bearing buttress forces as suggested by Kumai and Benjamin [10]. Shear stresses and stretching has been shown to accelerate endochondral ossification [37], [38].

Ultimately, confidence in the patho-histogenesis of heel spurs is undermined by a lack of control samples and small sample size of this study. At this point in time, there is no published research that delineates in detail the normal histological architecture of the inferior and anterior aspect of the medial calcaneal tubercle, specifically in the region of the enthesis of the PA and intrinsic musculature. Lemont et al. [9] described the PA aponeurosis as fibrocartilaginous, though was no more specific than this. Kumai and Benjamin's study [10] on heel spur formation does iterate three potential phases of development of the heel spur, however they used embalmed elderly cadavers of unknown medical history and with an unknown history of the existence of inferior heel pain. It is well established that the incidence of heel spurs increases with increasing age and the spurs in Kumai and Benjamin's series [10] (elderly embalmed cadavers) may not reflect those heel spurs excised in surgery of living patients.

A proposed explanation of the genesis of the inferior heel spur, supported by these histological samples and agreeing with previous reports [1], [2], [3], [10], is based on a foundation of repetitive insults—either traction to, or compressive buttressing causing fatigue of the medial calcaneal tubercle at the conjoined fibrocartilaginous enthesis of the intrinsic muscles and PA. Reactive fibroplasia of the enthesis, continued osseous fatigue and microtrabecular fracture occur in this local area. Given the presumed avascular nature of the fibrocartilage-periosteal interface, osteoprogenitor cells in the periosteal tissue proliferate and differentiate into chondroblasts forming a cartilage sleeve or cap (chondroid metaplasia). This process – seen in the heel spur samples – is similar to that of the process of fracture callus formation. This cartilage collar is then replaced by bone by virtue of endochondral ossification (chondrocyte calcification of cartilage matrix) [8]. However, while not observed in this series of samples, direct ossification of the connective tissue enthesis (intramembranous ossification) should not be discounted and has been noted on the superior aspects of heel spurs in previous studies [7], [10]. However, the presence of cartilage would suggest a predominant influence of endochondral ossification, although the two processes can occur simultaneously and do, in fact, in fracture repairs [36].

5. Conclusion 

The results of this study of five participants undergoing open heel surgery for persistent inferior heel pain has demonstrated the inferior calcaneal spur lies within the origin of the intrinsic musculature, specifically the flexor digitorum brevis and abductor digiti minimi. At a microscopic level, the skeletal muscle tissue has attachment by virtue of a fibrous to fibrocartilaginous enthesis to the apex of the spur. Skirting the inferior surface of the spur, the PA directs part of its enthesis superiorly to amalgamate to the muscular enthesis. The exact tissue in which the spur resides is largely academic given the firm apposition of the flexor digitorum brevis to the PA. It seems logical that both of these structures act as a single unit pulling at the more proximal infero-medial calcaneal tubercle, thus rendering both repetitive, persistent traction and weight-bearing compressive fatigue in the pathology of heel spurs. At a cellular level, more research is required to describe and quantify the normal histological features of the respective plantar rear foot structures involved in inferior heel pain. It is accepted that the radiographic presence of a heel spur is not exclusively associated with inferior heel pain, nor is the manifestation of a heel spur always painful. However, in the event of persistent inferior heel pain, one should maintain suspicion for fracture of the spur itself and, in light of this, more aggressive conservative care in the form of a period of non-weight-bearing cast immobilization may be more readily employed before seeking surgical intervention.

Conflict of interest 

There was, nor is, any financial and personal relationship with other people or organizations that inappropriately influenced this study or the production of this article.