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  • Benn J S Boshell

Plantar Fasciitis or Heel Spur? The Chicken or The Egg?

Patients often ask "Do I have a heel spur or do I have plantar fasciitis?"

This is a conundrum which comes up time and time again and is possibly due to the two terms being used synonymously by different healthcare professionals when diagnosing patients with heel pain. It may also be due to a poor understanding of the pathophysiology of plantar heel spurs and/or plantar fasciitis by health professionals. The answer to the question is probably often "Both".

But when clinicians are asked which came first, this can be a little more difficult to answer. Let's start with definitions of the two conditions.

Heel spurs are defined as bony growths that extend from the skeleton into soft tissue (Benjamin et al 2006). Plantar fasciitis has been traditionally defined as inflammation of the thick tissue (plantar fascia) on the bottom of the foot. However Plantar ‘fasciitis’ is a misnomer since it is mostly a degenerative process, with little histological evidence of inflammation (Lemont et al 2003; Jarde et al 2003). Consequently, authors have termed it a fasciosis or fasciopathy since it encompasses both degenerative and inflammatory causes and is a general descriptor of pathology within the fascia. To discuss the semantics of the terminology is not the aim of this article and we shall leave this point here.

Heel Spur Pathophysiology

Osseous (bone) spurring of the plantar aspect of the calcaneus (heel) was first documented in 1900 by the German physician Plettner, who coined the term Kalkaneussporn. Translation - calcaneal spur. The pathophysiology of heel spurs is poorly understood. There are two popular reported hypotheses regarding the development of heel spurs.

Longitudinal traction hypothesis

It is hypothesised spurs may occur as a result of excessive repetitive traction by intrinsic muscles (small foot muscles), causing chronic microtrauma, which in turn, leads to periostitis (inflammation of the heel bone) and ossification (new bone growth). This is termed the 'longitudinal traction hypothesis' (Menz et al 2008). This hypothesis has been challenged due to a number of study findings. In one study it was found that the bony trabeculae (direction of growth) of spurs are not aligned in the direction of soft tissue traction (Li & Muehleman 2007). Another study found that excised (surgical removed) spurs can reform after surgical release of the plantar fascia, however, symptoms of heel pain did not return (Tountas & Fornasier 1996).

Vertical compression hypothesis

An alternative hypothesis is the vertical compression hypothesis which suggests calcaneal spurs develop in response to repetitive compression rather than traction. Specifically, they suggest that calcaneal spurs are fibrocartilaginous outgrowths which form in response to calcaneal stress fractures, in an attempt to protect the calcaneus against microcracks (Kumai & Benjamin 2002). Moreover, the location of the calcaneal spurs on the deep surface of the plantar fascia suggests compression is the main stressor. In addition, Li and Muehleman (2007) have documented that the trabeculae within these calcaneal spurs are not oriented in the direction of soft-tissue traction but rather in a vertical orientation.

Body weight

There is a consensus among researchers that body weight may play a significant role in the development of heel spurs in that overweight individuals are more likely to develop heel spurs due to increased compression stress (Sedat-Ali 1998; Kaplan et al 2003; Bartold 2004; Menz et al 2008). Menz and colleagues (2008) found from 216 participants 45% classified as obese had heel spurs, compared to only 9% of those who were not obese.


There is a fair level of evidence to suggest age plays a role in the development of heel spurs. A survey of 1,228 black Africans revealed that approximately 50% of patients who were more than 50 years of age had spurs. In the group of patients less than 30 years of age, the incidence dropped by 20%. A recent study including 1103 patients found a heel spur incidence rate of just 12.4% with the average age of the study group being 39 years of age.

Significance of heel spurs

The significance of a heel spur in patients with heel pain is a largely debated topic in podiatry. Heel spurs were originally considered to be an abnormality inextricably linked to heel pain. Even today, anecdotally, some General Practitioners, podiatrists, physiotherapists and other healt professionals believe that a plantar calcaneal spur causes plantar fasciitis pain, leading to referral for consideration of surgical removal of the spur (Johal & Milner 2012). On review of the literature, there is conflicting evidence regarding the significance of heel spurs in the role of plantar fasciitis. Some studies have reported a weak connection between heel spurs and plantar fasciitis whilst others have reported a strong link. It has been reported that the prevalence of heel spurs in the general population ranges from 8% to 18% (Shama et al 1983; Menz et al 2008). Shaman and colleagues (1983) reviewed 1000 radiographs and noted a 13.2% incidence of heel spurs but only 31% of these patients had symptoms of heel pain (Shama et al 1983). On the other hand, there are studies which found a high correlation between heel spurs and pain. Fakharian & Kalhor (2006) found in a sample of 625 that heel spurs developed in 33% of the general population and in nearly 80% of patients with painful heels. A recent study by Johal & Milner (2012) also found a significant association between heel spurs and plantar fasciitis (89%). It should be noted that this study was limited by a small population size (38 study participants).

In a large prospective study by Lee et al (2003) consisting of 435 patients with chronic proximal plantar fasciitis, 283 (65%) had an inferior calcaneal bone spur of variable size evident prior to treatment with high-energy extracorporeal shockwave therapy (ESWT). This included 308 patients who received ESWT and 127 placebo (not ESWT) patients. At both initial (3 months) and final (12 months) evaluations after receiving ESWT, no patient who received had significant disappearance or change in the radiographic appearance of the heel spur. Interestingly though, clinical outcome after ESWT was satisfactory in 168 patients (82%) with a radiographically demonstrable inferior heel spur and in 81 patients (79%) without such a heel spur. Therefore, the results showed no correlation between the presence or absence of the heel spur and the eventual treatment outcome. In essence, the presence or absence of a heel spur did not matter. Furthermore comparative surgical studies of plantar fascial release only vs heel spur resection with plantar fascial release reveal no major differences in outcome (Kinley et al 1993). Currently, to my knowledge, there is no evidence to prove a causal relationship between heel spurs and plantar fasciitis. furthermore, there is evidence against a causal link between plantar heel spurs and plantar fasciitis which comes from anatomical and MRI studies.

So which came first?

Although heel spurs have been described in association with plantar fasciitis, most publications conclude that they rarely cause this condition (Berkowitz 1991). Although a higher proportion of spurs is noted in plantar fasciitis, their presence is not causal. Plantar fasciitis may exist in the absence of a spur and asymptomatic spurs are common. It is believed that heel spurs develop secondary to plantar fasciitis as opposed to being a causative factor (Micke et al 2008).


What we do know is that age and body weight both play a significant role in the development of heel spurs. That is, they are particular more common in the older and obese populations. One theory to explain this pattern is that the development of heel spurs is a physiological (normal) process which happens very slowly over a lifetime and is thus not present until later years. It is the accumulation of physiological stress (normal weight bearing stress) being placed on the heels over the course of our lives which leads to the gradual development of heel spurs. It is evident that the prevalence of heel spurs in the younger population is very low by comparison regardless of whether they have plantar fasciitis or not. It is also known that obesity increases the compression stress on the heels which accelerates the "Wear and tear" of the heel bone leading to heel spurs in this population. Finally, heel spurs are overall undoubtedly more common in patients with plantar fasciitis than patients without plantar fasciitis. It is a logical notion that the causes of plantar fasciitis, a combination of traction stress and vertical stress will result overall in high levels of mechanical stress at the bottom of the heel. It is therefore of no surprise that heel spurs may develop secondary to these high-stress levels.


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