Imaging of plantar fascia disorders: findings on plain radiography, ultrasound and magnetic resonance imaging

The PF (Fig. 1), also called the plantar aponeurosis, is a strong connective tissue structure that helps maintain the longitudinal arch of the foot [3, 4]. The PF consists of three bundles: central, lateral and medial. The central component is proximally thick and distally thin and is the thickest of the three. It arises from the medial tubercle of the calcaneus and extends distally becoming broader and covering the plantar surface of the flexor digitorum brevis muscle. Distally, it divides into five digitations that insert into the metatarsophalangeal joints. The lateral portion is also proximally thick and distally thin. It arises from the lateral margin of the medial calcaneal tubercle, covers the plantar surface of the abductor digiti minimi muscle and inserts into the fifth metatarsal joint capsule. The medial portion is thinner than the others. It arises from the midportion of the central bundle, covers the plantar surface of the abductor hallucis muscle and inserts into the first metatarsal joint capsule [5]. The mean maximal thickness of the PF has been reported as 4.0 mm in its central bundle, 2.3 mm in its lateral bundle and 0.6 mm in its medial bundle [6]. Overall, PF thickness is greater in men than in women [6]. Histologically, the PF is mostly composed of type I collagen fibres forming bundles arranged in a proximal-distal direction, with a few transverse and vertical collagen fibres. These large fibrous bundles are embedded within a matrix of loose connective tissue containing type III collagen and a few elastic fibres [5].

Plantar fasciitis (Figs. 2, 3, and 4) is the most common injury of the PF and is estimated to induce more than 1 million patients to seek treatment annually [7]. Despite its name, plantar fasciitis has a degenerative rather than inflammatory nature and is related to overuse trauma leading to microtears [8]; thus, the term “plantar fasciopathy” is often preferred. The proximal third of the central bundle of the PF is classically involved; however, distal plantar fasciitis has recently been recognised as a cause of recalcitrant heel pain [9]. The aetiology of plantar fasciitis is multifactorial. Biomechanical risk factors include those causing repetitive stress on the PF, such as foot deformities, improper footwear, increased body mass index and activities that involve prolonged walking, running or standing [10‐12]. Among the medical conditions associated with plantar fasciitis, the most notable are seronegative spondyloarthropathies and rheumatoid arthritis [13‐16]. Plantar calcaneal spurs, also known as calcaneal enthesophytes, have been investigated in great detail as a possible cause of plantar fasciitis [17‐20], but they are not specific and also occur in asymptomatic individuals. The diagnosis of plantar fasciitis generally relies on clinical history and physical examination. The main symptoms include pain and stiffness in the morning, or pain at the beginning of activity after rest. Physical examination reveals tenderness at the origin of the PF and impaired dorsiflexion of the ankle and extension of the toes [21‐24]. Although generally self-limiting, plantar fasciitis may result in physical inactivity and impact quality of life. Imaging can aid in the diagnosis, particularly in recalcitrant cases or may rule out other heel pathology [9, 22].

Plantar fibromatosis or Ledderhose disease (Fig. 5) is a benign nodular formation due to fibroblastic proliferation in the PF. It tends to involve the distal two thirds of the PF, usually in its central bundle, although proximal nodules are not uncommon. Nodular lesions may be multiple and bilateral and typically measure less than 3 cm in diameter [25‐27]. Plantar fibromatosis is frequently seen as an isolated disease, but an association with Dupuytren’s disease has been noted [28]. Clinically, plantar fibroma appears as a firm thickening or a single nodule, generally localised in the medial portion of the sole, which is occasionally painful [25‐27].

Tears of the PF (Fig. 6) are uncommon and can be partial or complete. Traumatic tears are often related to forcible plantar flexion of the foot in competitive athletes, mostly runners and jumpers; these are typically distal to calcaneal insertion of the PF and chronic overuse is considered an aetiological factor [29‐32]. Spontaneous ruptures may occur at the calcaneal attachment of the PF in patients with previous history of plantar fasciitis and local treatment with steroid injections [33‐35]. Clinical presentation includes acute pain, usually accompanied by a “snap” noise, and local swelling [36].

Peculiar lesions of the PF should be kept in mind as differential diagnoses of the main PF disorders and include xanthoma, diabetic fascial disease, foreign-body reactions and plantar infections. Xanthomas (Fig. 7) are described in many hyperlipidaemia states; they typically involve tendons and are occasionally located within the PF. They are usually asymptomatic and tend to recur after surgical removal [3]. Some studies have found that the thickness and stiffness of the PF and Achilles tendon are increased in patients with type I and type II diabetes mellitus [37, 38]. PF thickness is considered a predictor of the development of late complications in type I diabetes mellitus [38, 39]. Moreover, a relationship between PF thickening in type II diabetes mellitus and body mass index values has also been demonstrated [37]. Occasionally, foreign material is present within or adjacent to the PF and presents with symptoms of plantar fasciitis. It derives from penetrating injuries even though history of trauma or puncture is not always reported [3]. Infectious fasciitis (Fig. 8) may occur as a result of spread from a contiguous source of infection, penetrating wounds due to iatrogenic (surgical procedures) and accidental causes (foreign body, punctures), or in diabetics’ feet [2, 40]; atypical infections may result from haematic diffusion of microorganisms, particularly in immunosuppressed patients [41]. As fascial inflammation can cause destruction of mechanical barriers, infection may spread and affect perifascial structures including soft tissues, bone and muscles [42].

Plain radiography is widespread, cost-effective and panoramic, thus often representing the imaging modality of first choice for the evaluation of painful heel.

Several findings suggestive of plantar fasciitis can be detected on conventional radiographs. Despite this, plain radiography should not be used to make a diagnosis of plantar fasciitis without knowledge of clinical history or physical examination findings [19]. PF thickness can be measured with accuracy on lateral plain radiographs of the ankle and foot [3, 4, 19]. PF mean thickness at its calcaneal origin, in the central fascicle, is 4.0 mm [6]. Increased thickness of the PF measuring more than 4–5 mm within 5 mm of its calcaneal attachment is evident on lateral plain radiographs of individuals with plantar fasciitis (Figs. 2, 3 and 4) and represents a reliable sign of plantar fasciitis [19]. Deep below the PF, at its calcaneal origin, a fat pad is seen and usually has a triangular shape on lateral non-weight-bearing plain radiographs. This fat pad becomes narrowed or is absent in individuals with plantar fasciitis, maybe owing to both mechanical and inflammatory mechanisms, thus representing a further sign of plantar fasciitis [19]. The combination of thickened PF and fat pad abnormalities on lateral plain radiography has a sensitivity of 85% and specificity of 95% for plantar fasciitis [19]. Changes in the cortex of the calcaneus at the attachment of the PF, with or without spur formation, have been correlated with plantar fasciitis (Fig. 4). These are cortical irregularities presenting with loss of the smooth contour of the bone and both cortical lucency and sclerosis [19].

Plantar calcaneal spurs and calcifications within the PF are uncommon occurrences in patients with plantar fasciitis [19, 20]. The significance of calcaneal spurs as a cause of plantar fasciitis has received considerable attention in the literature [17‐20], and currently their importance in terms of the diagnosis and prognosis of plantar fasciitis is debatable. Calcaneal spurs associated with plantar fasciitis include those located within the plantar fascia (Fig. 4) [20]. These are however very uncommon, as the most common site of plantar calcaneal spurs is in the abductor hallucis and flexor digitorum brevis origins, deep below the PF (Figs. 3 and 4) [18, 20]. Thus, evidence of calcaneal spurs on conventional radiographs is not a pathognomonic sign of plantar fasciitis.

Apart from highlighting indirect signs of plantar fasciitis and calcaneal spurs, conventional radiography is useful in overviewing anatomical and pathological changes of the bone and soft tissues. Radiopaque foreign material, such as metals, may be easily revealed [43]. In the case of infectious fasciitis, plain radiography shows soft-tissue swelling and blurring of soft-tissue planes. Concomitant osteomyelitic changes in bone morphology can also be detected and mainly include lytic lesions, osteopenia, loss of trabecular architecture, new bone apposition and periosteal thickening (Fig. 8) [40]. Finally, stress fractures may be associated with PF injuries and should be ruled out [44].

On ultrasound, similarly to ligaments, PF shows a fibrillar pattern due to the hyperechoic appearance of type I collagen fibre bundles embedded within a background of hypoechoic matrix [45, 46].

Sonographic characteristics of plantar fasciitis include loss of fibrillar structure, increased thickness over 4 mm, perifascial collections and calcifications within the PF (Figs. 2 and 4) [16, 47‐57]. Hyperaemia is a well-known feature of tendinopathy due to neurovascular growth and may contribute to pain. It can be assessed using Doppler ultrasound. Similarly, Doppler ultrasound can identify hyperaemia in the PF, near its proximal insertion and in the perifascial soft tissue, in patients with plantar fasciitis (Fig. 4); hyperaemia can also correlate with treatment [58‐61]. As an additional finding, in patients with plantar fasciitis the PF is less elastic under real-time sonoelastography, and this might increase the accuracy of ultrasound [62, 63].

The sonographic presentation of plantar fibromatosis (Ledderhose disease) includes typically single, rarely multiple iso-hypoechoic, well-demarcated, nodular thickenings of the PF, with no calcifications or fluid collection. Doppler ultrasound generally shows no vascular flow inside the lesion (Fig. 5) [64].

Sonographic findings of PF rupture include complete or partial interruption of the PF, with hypoechoic tissue at the site of rupture related to local haemorrhage and inflammation (Fig. 6) [3].

Among other disorders of the PF, plantar xanthomas appear as nodules with a speckled pattern [3]. Increased thickness of the PF can be sonographically detected in the early stages of diabetes mellitus [37‐39]. Ultrasound can aid in the diagnosis of foreign body reaction by identifying echoic extraneous material within or adjacent to the PF. Sometimes posterior acoustic shadowing and, in cases of metal objects, comet tail reverberation artefacts may also be seen [65]. Ultrasound is useful in the assessment of musculoskeletal infections, particularly in distinguishing acute or chronic infections from tumours or non-infective conditions. In the case of infectious fasciitis, the PF is increased in volume with loss of fibrillar pattern and perifascial oedema and is hyperaemic on Doppler evaluation [40].

In healthy individuals, the PF is homogeneously hypointense on both T1-weighted and fluid-sensitive sequences [6].

MRI findings of plantar fasciitis include: thickening of the PF, most commonly at its calcaneal origin; intrasubstance areas of intermediate signal on T1-weighted sequences and increased signal on fluid-sensitive sequences; oedema in the adjacent soft tissue; bone marrow oedema of the calcaneal attachment of the PF suggestive of enthesopathy (Figs. 2 and 3) [2, 4].

In plantar fibromatosis (Ledderhose disease), the common MRI appearance of plantar fibroma is a lobulated mass of low signal intensity on both T1- and T2-weighted sequences due to its fibrous nature (Fig. 5). In some instances, plantar fibroma may show high signal on fluid-sensitive sequences [4].

MRI findings of acute PF tear are complete or partial interruption of the low signal of the PF and signal changes at the site of lesion including high signal on fluid-sensitive sequences and intermediate signal on T1-weighted sequences. High-signal intensity may be an additional finding on fluid-sensitive sequences in the soft tissues surrounding the site of rupture (Fig. 6); this reflects local haemorrhage, inflammation and oedema [2, 66, 67].

Among other lesions of the PF, xanthomas appear as fusiform enlargement of the PF showing heterogeneous signal intensity on both T1- and T2-weighted sequences (Fig. 7) [66]. In the case of foreign body reaction, MRI appearance is variable: low signal intensity on T1-weighted images is frequently noted, while surrounding granulation tissue often has high signal intensity on T2-weighted images [3]. In the case of plantar infection, MR imaging allows identification, localisation and assessment of the extent of the inflammatory process. On MRI, the PF, perifascial soft tissues and adjacent bone show abnormal high signal intensity on fluid-sensitive sequences, low signal intensity on T1-weighted sequences and significant contrast enhancement (Fig. 8) [2, 67].