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Abstract

Objectives

Plantar calcaneal spur (PCS) is a bony outgrowth of the calcaneal tuberosity frequently associated with chronic heel pain. Although its precise etiology remains uncertain, mechanical stress and repetitive traction forces are frequently implicated. Haglund’s deformity, defined as a bony enlargement on the posterosuperior calcaneus, results in retrocalcaneal impingement of the Achilles tendon. While both conditions involve stress-related alterations of the calcaneus, their potential association has not been clearly established. This study aimed to evaluate the relationship between PCS and Haglund’s deformity by determining the incidence of Haglund’s deformity in symptomatic PCS patients and investigating associated factors.

Methods

In this retrospective case–control study, 377 patients aged ≥18 years who underwent weight-bearing lateral foot radiographs between March 2023 and March 2024 were included. The case group (n = 94) consisted of patients with symptomatic PCS, and the control group (n = 283) comprised patients without PCS. Haglund’s deformity was assessed radiographically using the BRINK angle, with values >20° considered diagnostic. Demographic characteristics and comorbidities were analyzed.

Results

Haglund’s deformity was significantly more prevalent in the PCS group (62/94; 66.0%) compared with controls (53/283; 18.7%) (p = 0.001). Diabetes mellitus showed a significant association with Haglund’s deformity (p = 0.01). No significant differences were observed in age, sex, body mass index, or other comorbidities.

Conclusion

Our findings demonstrate a strong radiological association between PCS and Haglund’s deformity, suggesting shared biomechanical stress pathways involving the plantar fascia and Achilles tendon. Prospective studies incorporating biomechanical evaluation are warranted to clarify underlying mechanisms and clinical implications.

Keywords

BRINK angle Haglund’s deformity plantar calcaneal spur radiological assessment

Background

Heel pain is a common complaint in the general population, frequently diagnosed as plantar calcaneal spur (PCS).¹ PCS is a bony outgrowth that develops from the calcaneal tuberosity.² It typically originates from the medial part of the calcaneal tuberosity but may also occur on the lateral side.^2–4 The exact pathophysiology of PCS remains unclear, and multiple hypotheses have been proposed.⁵ According to the traditional hypothesis, repetitive traction of the plantar fascia leads to inflammation and reactive ossification, ultimately resulting in PCS formation.⁶ However, a study by Kumai et al. suggested that PCS develops primarily due to vertical compression forces, arguing that traction forces do not play a role in its formation since PCS does not develop within the plantar fascia.⁷ Similarly, Weiss demonstrated that prolonged standing, excessive body weight, calcaneal morphology, and arthritis contribute to PCS development.⁸ Etiological factors associated with PCS include calcaneal morphology, obesity, metabolic disorders, chronic irritation, and arthritis.⁹ The incidence of PCS varies between 11% and 45%, depending on age.^8,9 Although approximately 10% of individuals with PCS are asymptomatic, the primary symptoms include pain and tension in the heel region.

Haglund’s deformity was first described by Patrick Haglund in 1927 as an abnormal bony prominence on the posterior-superior aspect of the calcaneus.¹⁰ Continuous impingement between the Achilles tendon and the calcaneal prominence can lead to retrocalcaneal bursitis, a major cause of posterior heel pain.^11,12 Patients with Haglund’s deformity typically describe their pain as localized to the retrocalcaneal region. The posterior-superior calcaneal prominence associated with retrocalcaneal pain and tenderness is commonly referred to as Haglund’s disease.¹³

Various radiological measurement techniques have been developed to confirm the presence of Haglund’s deformity. Among these, Fowler’s angle is one of the most commonly used parameters. However, a study by Lu et al. found no statistically significant difference in Fowler’s angle between symptomatic Haglund’s disease patients and healthy controls.¹⁴ Other measurements, such as the Cheveaux-Liet angle, Ruch calcaneal inclination, and the Heneghan-Pavlov test, have also been reported to have low specificity and sensitivity.¹⁵ Among various radiographic measurements used to assess Haglund’s deformity, the BRINK angle has recently gained prominence due to its simplicity, reproducibility, and strong clinical relevance. Traditional angles, such as Fowler’s or Cheveaux-Liet, have been criticized for their low specificity and limited reliability in differentiating symptomatic deformities. In contrast, the BRINK angle offers excellent intra- and inter-observer agreement (κ ≈ 0.8) and allows accurate quantification of posterior calcaneal morphology on standard weight-bearing radiographs. By reflecting the anatomical prominence most associated with retrocalcaneal impingement, this measurement not only facilitates early diagnosis but also aids surgical planning in patients with symptomatic Haglund’s deformity. In this study, the BRINK angle was chosen because it provides a precise, clinically meaningful tool for investigating potential biomechanical associations, particularly between plantar calcaneal spurs and posterior calcaneal changes..^16,17

Although the precise etiology of Haglund’s deformity remains unclear, it has been associated with factors such as Achilles tendon tightness, cavus foot, genetic predisposition, calcaneal morphology, obesity, and arthritis.¹⁸

The aim of this study was to evaluate the potential association between plantar calcaneal spur (PCS) and Haglund’s deformity. Specifically, the study sought to determine the incidence of Haglund’s deformity in patients with symptomatic PCS and to identify factors associated with this relationship.

Patients and methods

Ethical Approval

This study was conducted in accordance with the principles of the Declaration of Helsinki and was approved by the Non-Interventional Clinical Research Ethics Committee of Gaziantep City Hospital (Approval No: 127/2025). Informed consent was obtained from all patients prior to their inclusion in the study.

Study population

Patients aged 18 years or older who presented to the outpatient clinic with heel pain and underwent weight-bearing lateral foot radiographs at Gaziantep Şehitkamil State Hospital between March 2023 and March 2024 were consecutively analyzed. Clinical data, foot radiographs, and relevant imaging records were retrieved from the Picture Archiving and Communication System (PACS) and the hospital database.

Patients were excluded if they had:

• Incomplete clinical data,

• A history of fractures, malunion, or congenital malformations,

• Low-quality foot radiographs, defined as images where:

∘ All metatarsals and phalanges were not visible,

∘ The distal ends of the talus and calcaneus were not included,

∘ Both feet were captured in a single cassette.

Additionally, patients who presented to the emergency department between March 2023 and March 2024 due to acute ankle trauma, but had no prior history of foot or ankle disorders, were also consecutively selected from the institutional clinical database. Their foot radiographs were retrieved from PACS and evaluated for standard positioning and suitability for radiographic measurements.

Exclusion criteria for this group included:

• History of fractures, malunion, or congenital malformations,

• Low-quality radiographs,

• Inability to be contacted via telephone follow-up.

In this retrospective design, we included all patients without PCS who met the strict inclusion criteria during the same study period, resulting in a 1:3 case-to-control ratio. This strategy minimized selection bias and enhanced statistical power, allowing more robust estimation of associations. Statistical analyses used (Chi-square, Mann-Whitney U) are valid for unequal sample sizes, and Bonferroni correction was applied where needed.

Study groups and variables

As a result, two distinct study groups were formed:

(1) The case group comprised 94 patients diagnosed with symptomatic PCS.

(2) The control group included 283 patients without PCS.

The groups were compared in terms of:

• Age,

• Sex,

• Body mass index (BMI),

• Presence of chronic diseases,

• Presence of Haglund’s deformity.

A flowchart illustrating the inclusion and exclusion criteria of the study is presented in Figure 1.

Figure 1.

Patient selection flowchart for case and control groups.

Each BRINK angle measurement was performed twice by the senior author at an interval of at least 3 weeks, and the mean of these two measurements was used for subsequent analysis. This method was chosen to enhance measurement precision and minimize random error. Inter-observer reliability was not assessed because measurements were performed by a single experienced orthopedic surgeon; however, previous studies have demonstrated excellent intra- and inter-observer agreement for the BRINK angle (κ ≈ 0.8).¹⁷

Radiographic measurements

The BRINK angle was measured using lateral foot radiographs, with a value greater than 20° considered diagnostic for Haglund’s deformity (Figure 2). For statistical analyses, the mean of the two independent measurements was used.

Figure 2.

Brink angle on lateral foot radiograph.

Statistical methods

The normality of numerical variables was assessed using the Shapiro-Wilk test. The Mann-Whitney U test was employed for comparisons between two groups when variables did not follow a normal distribution. Associations between categorical variables were analyzed using the Chi-square test, with Bonferroni correction applied where necessary. All statistical analyses were conducted using SPSS 22.0 software (IBM Corp., Armonk, NY, USA) for Windows. A p-value <0.05 was considered statistically significant.

Results

A total of 377 patients were included in the study and analyzed. The case group consisted of 94 patients (25%), while the control group comprised 283 patients (75%). Both groups were comparable in terms of age, sex, body mass index (BMI), and comorbidities (Table 1). The mean BMI was 31 in the case group and 29 in the control group, indicating high BMI levels in both groups.

Table 1.

Comparison of case and control groups.

Variable	Control group (n, %)	Case group (n, %)	p-value
Gender			0.301
Female	198 (70.0)	71 (75.5)
Male	85 (30.0)	23 (24.5)
Haglund’s deformity			0.001*
Present	53 (18.7)	62 (66.0)
Absent	230 (81.3)	32 (34.0)
Comorbidities			0.243
Ankylosing spondylitis	4 (1.4)	2 (2.1)
Diabetes mellitus	88 (31.1)	25 (26.6)
Rheumatoid arthritis	6 (2.1)	6 (6.4)
None	185 (65.4)	61 (64.9)
Age (mean±SD)	43 ± 13.78	42.77 ± 13.27	0.998
BMI (mean±SD)	29.4 ± 6.16	30.82 ± 6.57	0.062

Note. p < 0.05 is considered statistically significant. Statistical analyses were performed using the Chi-square test, Mann-Whitney U test, and Bonferroni correction.

The prevalence of Haglund’s deformity was significantly higher in the case group (62 patients, 66%) compared to the control group (53 patients, 18.7%) (p = 0.001, Table 2). Additionally, among the 115 patients diagnosed with Haglund’s deformity, 45 patients (39.1%) had diabetes mellitus, a finding that was also statistically significant (p = 0.01, Table 2).

Table 2.

Factors associated with Haglund’s deformity.

Variable	Haglund’s deformity present (n, %)	Haglund’s deformity absent (n, %)	p-value
Group			0.001*
Control	53 (46.1)	230 (87.8)
Case	62 (53.9)	32 (12.2)
Comorbidities
Ankylosing spondylitis	2 (1.7)	4 (1.5)
Diabetes mellitus	45 (39.1)	68 (26.0)	0.01
Rheumatoid arthritis	6 (5.2)	6 (2.3)
None	62 (53.9)	184 (70.2)

Note. p < 0.05 is considered statistically significant. Statistical analyses were performed using the Chi-square test and Bonferroni correction.

Discussion

Our study demonstrated a significant association between plantar calcaneal spurs (PCS) and Haglund’s deformity. We found that Haglund’s deformity was significantly more prevalent in the PCS group (66%) compared to the control group (18.7%) (p = 0.001). This finding supports the hypothesis that PCS may contribute to the development of Haglund’s deformity by increasing tensile forces on the Achilles tendon. Additionally, we observed a significant association between diabetes mellitus and Haglund’s deformity (p = 0.01), suggesting a potential role of metabolic factors in its pathogenesis.

Previous studies have primarily focused on the relationship between Achilles tendon pathology and Haglund’s deformity. Lu et al. identified a link between calcific Achilles tendinitis and Haglund’s deformity.¹⁹ Similarly, Lee et al. reported that the size of Haglund’s deformity was not directly related to insertional Achilles tendinitis (IAT) but that Achilles tendon calcifications and an increased calcaneal inclination angle might contribute to more severe cases.²⁰ In a more recent study, Nakajima et al. found that Haglund’s deformity morphology and its proximity to the Achilles tendon were related to the development of insertional Achilles tendinopathy.²¹ In the radiological study conducted by Tang et al., Haglund’s deformity was identified as a risk factor for insertional Achilles tendinopathy requiring surgery, and the radiographic parameters of bump height and the bump–calcaneus ratio were found to be valuable in predicting the presence of insertional Achilles tendinopathy on MRI.²²

To our knowledge, our study is the first to investigate the potential association between PCS and Haglund’s deformity. While previous research has focused on dorsal calcaneal morphology, our findings suggest that plantar traction forces may also play a role in the pathogenesis of Haglund’s deformity. This new perspective highlights the need for further research into how PCS-induced mechanical stress affects the Achilles tendon and posterior calcaneus over time.

The development of Haglund’s deformity has been linked to various biomechanical factors that contribute to calcaneal remodeling and tensile stress on the Achilles tendon.^23,24 These factors include compensated rearfoot varus, forefoot valgus, plantar flexion of the first metatarsal, cavus foot, tibial varum, restricted joint motion, a steeper subtalar joint axis, excessive frontal plane motion, excessive pronation, and leg length discrepancy.²³ Additionally, abnormal calcaneal morphology, childhood apophysitis, vascular insufficiency, and trauma have been proposed as contributing factors to posterior heel deformities.²⁴

Furthermore, the role of excessive loading and mechanical stress in Haglund’s deformity formation has been emphasized in previous studies.²⁵ The interaction between plantar and posterior calcaneal structures remains unclear, but evidence suggests that tensile loading on the plantar fascia may influence Achilles tendon mechanics. This may lead to adaptive bony changes at the posterior calcaneus, contributing to the development of Haglund’s deformity over time. Given the overlap in biomechanical stressors between PCS and Haglund’s deformity, future research should focus on how plantar traction forces impact posterior calcaneal morphology and Achilles tendon strain.

This study has some limitations. Its retrospective design introduces the possibility of selection bias, and the relatively small case group size may have limited the statistical power of our findings. Additionally, our study did not include longitudinal follow-up to assess whether PCS precedes the development of Haglund’s deformity over time. Future prospective studies with biomechanical analyses are needed to further clarify the causal relationship between PCS and Haglund’s deformity.

Conclusion

Our study demonstrated a significant association between plantar calcaneal spurs (PCS) and Haglund’s deformity, with the prevalence of Haglund’s deformity being significantly higher in the PCS group compared to the control group. Additionally, we observed a significant association between diabetes mellitus and Haglund’s deformity, suggesting that metabolic factors may influence its occurrence.

Although our study is limited by its retrospective design and sample size, these findings provide a foundation for future research. Further prospective studies with larger cohorts are needed to better understand the relationship between PCS and Haglund’s deformity and its clinical implications.

Footnotes

ORCID iDs

Volkan Özel

Nevzat Gönder

Ethical considerations

This study was conducted in accordance with the Declaration of Helsinki and was approved by the Non-Interventional Clinical Research Ethics Committee of Gaziantep City Hospital (Approval No: 127/2025).

Consent to participate

Informed consent was obtained from all participants prior to their inclusion in the study.

Consent for publication

Not applicable. This study does not include individual patient data in any form (images, videos, or case reports) that would require specific consent for publication.

Author contributions

V.Ö. contributed to the study design, data collection, statistical analysis, and manuscript writing.

N.G. contributed to the data collection and manuscript writing.

İ.H.D. participated in data interpretation and critical revision of the manuscript.

F.G. supervised the study and provided final approval for submission.

All authors read and approved the final manuscript.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The datasets used and analyzed during the current study are available from the corresponding author upon reasonable request*.

Appendix

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Radiological association between Haglund’s deformity and plantar calcaneal spur: A retrospective case-control study

Abstract

Objectives

Methods

Results

Conclusion

Keywords

Background

Patients and methods

Ethical Approval

Study population

Study groups and variables

Radiographic measurements

Statistical methods

Results

Discussion

Conclusion

Footnotes

ORCID iDs

Ethical considerations

Consent to participate

Consent for publication

Author contributions

Funding

Declaration of conflicting interests

Data Availability Statement

Appendix

References