Introduction

The enthesis is a specialized fibrocartilaginous structure that serves as the mechanical interface between soft tissues (tendons, ligaments, and joint capsules) and bone [1]. Its primary function is to efficiently transfer biomechanical forces, making it a critical site for load dissipation and adaptation [2]. Enthesitis, defined as inflammation at the enthesis, is a cardinal feature of spondyloarthritis (SpA) [3]. However, enthesopathies – a broader term encompassing both inflammatory and structural changes – are not exclusive to systemic inflammatory diseases. Repetitive microtrauma resulting from chronic mechanical overload, particularly in occupations or activities involving high physical demands, is a well-recognized non-inflammatory cause of entheseal pathology [4].

Elite athletes represent a unique population subjected to highly specific and intense mechanical loading patterns, often exceeding 10 h of training per week over many years. This chronic, repetitive stress can lead to structural remodeling and adaptive changes at the entheses, a process increasingly understood through the lens of mechanoinflammation [5]. Mechanoinflammation posits that excessive biomechanical stress can trigger a localized, non-infectious inflammatory cascade, leading to tissue damage and subsequent repair processes [6]. Differentiating between physiological entheseal adaptation (e.g., thickening, mild enthesophytes) and pathological enthesitis (e.g., active inflammation, erosions) in asymptomatic athletes is a significant clinical and research challenge [7].

Musculoskeletal ultrasound (US) was chosen as the primary imaging modality for this study due to its unique ability to provide high-resolution, real-time assessment of both inflammatory and structural entheseal changes. Unlike conventional radiography, which detects only late-stage structural damage, US allows visualization of early inflammatory features such as hypoechogenicity and power Doppler signal, as well as structural findings including enthesophytes and calcifications. Compared with magnetic resonance imaging, US offers greater feasibility for the simultaneous evaluation of multiple entheseal sites, enables dynamic and bilateral assessment, does not involve radiation exposure, and is more accessible in routine clinical practice. These characteristics make US particularly suitable for studying sport-related, load-dependent entheseal adaptations in elite athletes [8]. US provides high-resolution, real-time visualization of both inflammatory features (hypoechogenicity, increased thickness, Power Doppler [PD] signal) and structural damage (calcifications, erosions, enthesophytes) [9]. The Outcome Measures in Rheumatology (OMERACT) group has established consensus-based definitions and scoring systems for these elementary lesions, enhancing the reliability of US in this context [10]. Despite this, a global consensus on a single sonographic enthesitis index remains elusive, highlighting the complexity of US assessment in this area [11].

The literature remains limited regarding the differential impact of various sport-specific loading patterns on entheseal pathology. Previous studies have often grouped athletes broadly, obscuring the localized effects of distinct upper-versus lower-extremity dominant sports. Furthermore, the inclusion of non-inflammatory findings in enthesitis scoring indices remains a point of debate, particularly when evaluating athletes [12].

The primary objective of this study was to investigate the impact of sport-specific repetitive mechanical loading on entheseal inflammation and structural damage in elite athletes. We aimed to compare US-detected entheseal changes across different sports and extremity dominance groups relative to sedentary controls, thereby contributing to a better understanding of entheseal adaptation in this highly active population.

Material and methods

Results

Comparison of US scores

The US scores for entheseal inflammation and damage were compared for the upper extremity among Group A (upper extremity dominant), Group B (upper extremity non-dominant), and the sedentary Control Group, and for the lower extremity among Group C (lower extremity dominant), Group D (lower extremity non-dominant), and the sedentary Control Group (Table II). The frequencies of elementary lesions were compared between each elite athlete group and the sedentary control group, with the results shown in Supplementary Figures S3–S6. Overall, elite athletes exhibited significantly higher entheseal pathology (Figure 1) compared to sedentary controls, with differences varying by extremity and athlete specialization. The results of the regression analyses for lower and upper extremity inflammation and damage scores are presented in Table III.

Table II

Differences in inflammation and damage scores for upper extremity entheses across sports categories

Parameter	Group A (upper extremity dominant)	Group B (upper extremity non-dominant)	Control group	P-value
				All groups	Group A vs. Group B	Group A vs. Control	Group B vs. Control
Upper extremity inflammation score, median (IQR)	1 (0–3)	0.5 (0–3)	0 (0–1.5)	0.013	1.000	0.010	0.587
Upper extremity damage score, median (IQR)	0 (0–3)	0.5 (0–0.5)	0 (0–0)	< 0.001	0.129	< 0.001	1.000
Parameter	Group C (upper extremity dominant)	Group D (upper extremity non-dominant)	Control group	P-value
				All groups	Group C vs. Group D	Group C vs. Control	Group D vs. Control
Lower extremity inflammation score, median (IQR)	2 (1–4)	0.5 (0–2.75)	0 (0–1)	< 0.001	0.137	< 0.001	0.179
Lower extremity damage score, median (IQR)	4 (1–7.25)	2 (1–5.75)	2 (0–4.5)	0.055	N/A	N/A	N/A

Table III

Determinants of US scores (multivariate linear regression analysis)

US score	Associated factor	B (95% CI)	P-value
Upper extremity inflammation	Age	0.117 (0.056–0.178)	< 0.001
	Weekly training duration	0.055 (0.017–0.094)	0.005
Upper extremity damage	Age	0.215 (0.145–0.286)	< 0.001
Lower extremity inflammation	Body mass index (BMI)	0.449 (0.223–0.676)	< 0.001
Lower extremity damage	Age	0.173 (0.098–0.249)	< 0.001
	Body mass index (BMI)	0.248 (0.020–0.476)	0.033

Figure 1

Elementary lesions in different enthesis areas: A – erosion on subscapularis enthesis area, B – erosion on supraspinatus enthesis area, C – enthesophyte on supraspinatus enthesis area, D – enthesophyte on Achilles tendon enthesis area, E – enthesophyte on quadriceps tendon enthesis area, F – erosion on lateral epicondyle

Discussion

This study provides compelling evidence that sport-specific, chronic mechanical loading in elite athletes is associated with a significantly higher burden of entheseal changes – both inflammatory and structural – detectable by US, compared to sedentary controls. Crucially, our findings highlight the differential impact of loading patterns, with upper extremity-dominant sports leading to higher upper limb scores and lower extremity-dominant sports correlating with higher lower limb inflammation.

Our finding of a higher prevalence of entheseal abnormalities in elite athletes compared to sedentary controls is consistent with a growing body of literature. For instance, Lanfranchi et al. [14] conducted a cross-sectional study comparing entheses US findings in axial spondyloarthritis patients, athletes, and healthy controls, similarly reporting a higher frequency of entheseal changes in athletes than in controls. More recently, Perrotta et al. [15] compared entheseal fibrocartilage in psoriatic arthritis patients, athletes, and healthy controls, noting distinct adaptive patterns in athletes, which reinforces the idea that mechanical demand drives structural changes. Our study extends these findings by demonstrating that this increased burden is not uniform but is specifically localized to the most stressed extremity, providing a more granular view of sport-specific adaptation.

The observed effect of limb dominance is a key strength of our study. The significantly higher upper extremity scores in Group A (upper dominant) directly reflect the high-velocity, repetitive, and eccentric loading inherent in sports such as archery and climbing. This localized effect is mirrored in studies focusing on specific joints, such as Benítez-Martínez et al. [16], who found differences in patellar tendon abnormalities based on lower limb dominance in elite basketball players. Our results, which encompass a wider range of entheseal sites, consolidate the principle that the enthesis adapts locally to the specific biomechanical demands placed upon it.

The multivariate analysis provides critical insights into the factors driving entheseal changes.

The high prevalence of asymptomatic US abnormalities in our cohort is a crucial finding that necessitates careful clinical interpretation. This finding is at the heart of the debate regarding enthesitis scoring. Mascarenhas et al. (2021) [12] reviewed enthesitis scoring indices and highlighted the challenge of including non-inflammatory findings (such as enthesophytes) when assessing for inflammatory disease. In our athletic population, these findings are likely a manifestation of physiological adaptation or mechanoinflammation – a subclinical, adaptive inflammatory response – rather than systemic inflammatory disease [5]. Clinicians must therefore contextualize US findings within the athlete’s specific sport, training history, and symptom status to avoid misdiagnosis or unnecessary intervention.

An important conceptual consideration in the present study relates to the interpretation of the OMERACT US ‘damage’ domain in an athletic population. While the OMERACT definitions were applied to ensure methodological standardization, structural findings such as enthesophytes and calcifications – classified as ‘damage’ within inflammatory arthritis frameworks – may represent physiological or load-related structural adaptations in elite athletes rather than true pathology. In this context, US features reflecting active inflammation, particularly power Doppler signal and erosions, are likely to be more specific for inflammatory enthesitis when interpreted alongside clinical symptoms and disease probability. Recognizing this distinction is essential to avoid pathologizing adaptive entheseal changes in physically active individuals [10].

This study has several notable strengths. First, entheseal assessment was performed using standardized OMERACT definitions, ensuring methodological consistency and alignment with the current international consensus. Second, a comprehensive US protocol covering multiple bilateral entheseal sites was applied, allowing a detailed evaluation of both inflammatory and structural changes. Third, athletes were analyzed according to sport-specific mechanical loading patterns, providing a more nuanced understanding of localized entheseal adaptations. Finally, the inclusion of largely asymptomatic elite athletes reflects real-world clinical practice, where US abnormalities are often detected in the absence of overt symptoms, thereby enhancing the clinical applicability of our findings.

Several limitations of this study should be acknowledged. First, the cross-sectional design precludes any causal inference regarding the relationship between mechanical loading and entheseal changes. Second, the absence of a spondyloarthritis comparator group limits direct differentiation between mechanically driven entheseal adaptation and inflammatory enthesitis. Third, US assessments were performed by a single experienced examiner, which may limit generalizability despite the use of standardized OMERACT definitions. In addition, although age was included in multivariate analyses, residual confounding related to age differences between certain athlete groups and the control population cannot be entirely excluded. These limitations should be considered when interpreting the results [9]. Although the present study did not include a spondyloarthritis comparator arm, the differentiation between mechanically driven entheseal adaptation and inflammatory enthesitis remains a key clinical challenge. Previous comparative studies have shown that athletes may exhibit a high prevalence of US-detected entheseal abnormalities that overlap with findings seen in inflammatory arthritis, despite the absence of systemic disease or symptoms. In particular, Lanfranchi et al. and Perrotta et al. demonstrated that while structural changes such as enthesophytes and calcifications are common in athletes, features reflecting active inflammation – especially persistent power Doppler signal and erosions – are more suggestive of true inflammatory enthesitis. Our findings should therefore be interpreted within the context of sport-specific mechanical loading, clinical presentation, and disease probability, to avoid misclassification of physiological adaptation as pathological enthesitis [14, 15]. An additional limitation of this study relates to age differences between certain athlete subgroups and the sedentary Control Group. Although age was included as a covariate in the multivariate regression analyses and was identified as an independent predictor of entheseal damage, residual confounding related to age cannot be fully excluded in a cross-sectional design. Structural entheseal changes such as calcifications and enthesophytes are known to accumulate with age and may therefore partially contribute to higher damage scores observed in older athlete groups, particularly climbers, compared with a younger control population. Consequently, the observed differences should be interpreted as associations rather than definitive evidence of sport-related causality

US reliability is a critical methodological consideration in entheseal imaging studies. In the present study, all examinations were performed by a single experienced sonographer using standardized OMERACT definitions; however, formal intra- and inter-observer reliability analyses were not repeated within this dataset, which should be acknowledged as a limitation. Nevertheless, in a previously published study by our group applying the same OMERACT-based US definitions for entheseal assessment, intra- and inter-observer reliability were excellent, with intraclass correlation coefficients exceeding 0.80 across all entheseal sites. These findings support the reproducibility of the applied methodology when performed by trained assessors, although future studies should ideally incorporate reliability testing within the study cohort [2].

Given the cross-sectional design of the present study, causal relationships between sport-related mechanical loading and US-detected entheseal changes cannot be established. The observed associations should therefore be interpreted with caution. An alternative explanation may involve reverse causality or selection bias, whereby individuals with inherently robust musculoskeletal or entheseal characteristics are more likely to engage in and sustain elite-level athletic activity. Consequently, the findings of this study should be understood as associations rather than evidence of direct causation, highlighting the need for longitudinal studies to clarify the temporal relationship between mechanical loading and entheseal adaptation.

The clinical relevance of the present findings lies in their implications for daily rheumatology practice. With the expanding use of musculoskeletal US, entheseal abnormalities are increasingly detected in asymptomatic or minimally symptomatic individuals, particularly among physically active populations. Elite athletes may demonstrate US findings that resemble inflammatory pathology, despite these changes representing biomechanical adaptation rather than disease. Previous studies have highlighted the significant impact of mechanical loading, neuromuscular control, and postural factors on musculoskeletal tissue behavior, underscoring that structural and functional adaptations may occur in the absence of systemic inflammation. Therefore, our results emphasize that US findings in athletes should always be interpreted in conjunction with sport-specific loading patterns, clinical symptoms, and overall disease probability, in order to avoid misdiagnosis and unnecessary therapeutic escalation [17, 18].

The clinical significance of the observed statistically significant differences should be interpreted with caution. In certain comparisons, particularly for upper extremity damage scores, the median value was zero in both athletes and controls, indicating that statistical significance was driven by a subset of individuals with higher scores rather than a uniform group-wide shift. Importantly, a high prevalence of ultrasound-detected entheseal abnormalities was observed in largely asymptomatic elite athletes. These findings should not be automatically interpreted as pathological enthesitis requiring clinical intervention. In physically active populations, many structural entheseal changes likely reflect physiological or load-related adaptation rather than inflammatory disease. Therefore, ultrasound findings in athletes must always be interpreted in conjunction with clinical symptoms, sport-specific mechanical loading patterns, and overall disease probability to avoid misdiagnosis and unnecessary treatment.

Future longitudinal studies are warranted to track the evolution of US-detected entheseal changes over an athlete’s career and to determine which specific US features predict the onset of clinical symptoms. Research incorporating advanced imaging techniques (e.g., MRI) and molecular biomarkers of inflammation could further elucidate the biological distinction between physiological entheseal adaptation and early pathological mechanoinflammation.

Sport-specific mechanical loading is a powerful driver of localized entheseal changes in elite athletes, detectable by high-resolution US. The differential associations of entheseal scores with age, weekly training duration, and BMI underscore the complex interplay of cumulative stress and systemic factors in entheseal remodeling. These findings reinforce the need for a nuanced interpretation of US results in the athletic population, recognizing that many imaging abnormalities represent subclinical adaptation rather than overt disease.