Tendinopathies share the same pathogenesis regardless of anatomical location
the verdict
REFUTED
the evidence says no
refutedsupported
the weight of evidence
2 sources for · 2 against
Published literature refutes the claim, demonstrating that tendinopathies comprise distinct subtypes with different pathogenic mechanisms and molecular pathways depending on anatomical and cellular features.
The presence of pain sensitisation has been documented and reported as being a possible cause of treatment failure and pain chronicity in several musculoskeletal conditions, such as tendinopathies. The aim of the present study is to analyse existing evidence on pain sensitisation in tendinopathies comparing the local and distant pain thresholds of healthy and affected subjects with distinct analysis for different tendinopathies. PubMed, Cochrane Central Register, Scopus, and Web Of Science were systematically searched after registration on PROSPERO (CRD42020164124). Level I to level IV studies evaluating the presence of pain sensitisation in patients with symptomatic tendinopathies, documented through a validated method, were included. A meta-analysis was performed to compare local, contralateral, and distant pain thresholds between patients and healthy controls with sub-analyses for different tendinopathies. Meta-regressions were conducted to evaluate the influence of age, activity level, and duration of symptoms on results. Thirty-four studies out of 2868 were included. The overall meta-analysis of local pressure pain thresholds (PPT) documented an increased sensitivity in affected subjects (p < 0.001). The analyses on contralateral PPTs (p < 0.001) and distant PPTs (p = 0.009) documented increased sensitivity in the affected group. The results of the sub-analyses on different tendinopathies were conflicting, except for those on lateral epicondylalgia. Patients’ activity level (p = 0.02) and age (p = 0.05) significantly influenced local PPT results. Tendinopathies are characterized by pain sensitisation, but, while features of both central and peripheral sensitisation can be constantly detected in lateral epicondylalgia, results on other tendinopathies were more conflicting. Patients’ characteristics are possible confounders that should be taken into account when addressing pain sensitisation.
Rotator cuff tendinopathy is the most common tendinopathy type with the worst prognosis. Conventional treatments often elicit heterogeneous drug responses due to the diversity of tendinopathy. Hence, this study attempted a classification of 126 diseased tendons into three distinct subtypes with opposite pathogenic mechanisms based on transcriptomic and clinical features. The hypoxic atrophic subtype with white appearance (Hw) exhibits downregulated neovascularization pathways. The inflammatory proliferative subtype with white appearance (Iw) shows a moderate upregulation of inflammatory characteristics. The inflammatory proliferative subtype with red appearance (Ir) exhibits the highest levels of upregulated neovascularization and inflammatory pathways, along with severe joint dysfunction. We then established research models, including subtype-specific simulations in animal models and clinical data analysis. These revealed that glucocorticoid, a controversial commonly used drug, was only effective in treating the Ir subtype. Hence, the tendinopathy subtypes elucidated in this study have significant implications for developing precision treatment of tendinopathy.
Tendinopathy is a common musculoskeletal disorder causing significant pain and functional impairment. High-intensity laser therapy (HILT) has increasingly been employed for tendinopathy. However, further research is required to elucidate therapeutic efficacy differences across various subtypes, determine optimal treatment parameters, and assess long-term effects. To evaluate the effectiveness of HILT for tendinopathy. PubMed, Embase, Cochrane Library, China Biology Medicine, Web of Science, CNKI, and SCOPUS databases were searched to include randomised controlled trials comparing HILT with placebo or other treatments up to 20 October 2025. Primary outcome measures included pain intensity and disability, analyzed as MD and SMD with 95% confidence intervals, respectively. Risk of bias was assessed using the Cochrane Tool and Physiotherapy Evidence Database scale. Heterogeneity was assessed with I², and random-effects models were used. 15 studies involving 629 patients were included: lateral epicondylitis (53%), rotator cuff tendinopathy (27%), and others (20%). Studies showed moderate quality (mean PEDro score 6.3), with strong randomisation (100% low risk) but weaknesses in allocation concealment (20% low risk) and blinding. HILT significantly improved pain (MD: -1.15; 95%CI: -1.73 to -0.58) and disability (SMD: -1.00; 95%CI: -1.77 to -0.22, p < 0.05). Pain reduction exceeded the MCID, though the lower confidence interval bound suggests marginal benefit in some. For disability, subgroup analysis by anatomical site revealed greater improvement in shoulder-related conditions (MD: -2.54) than in elbow-related conditions (MD: -0.91). Stress pain showed the most substantial relief (MD: -2.30), and treatment effects increased over time, peaking after 16 weeks. HILT effectively improves pain and disability in tendinopathy, with site-specific and cumulative benefits. Given methodological limitations, future high-quality studies are needed to optimize parameters and confirm long-term benefits.
Rotator cuff calcific tendinopathy and arthrofibrosis of the shoulder (adhesive capsulitis) are debilitating musculoskeletal disorders that significantly impact joint function and impair quality of life. Despite its high prevalence and common clinical presentation, the metabolic mechanisms underlying these conditions characterized by pain, and reduced mobility, remain poorly understood. This review aims to elucidate the role of metabolic processes implicated in the pathogenesis of calcific tendinopathy and shoulder arthrofibrosis. We will be focusing on the mechanistic role of how these processes contribute to disease progression and can direct potential therapeutic targets. Calcific tendinopathy is marked by aberrant calcium deposition within tendons, influenced by disrupted calcium and phosphate homeostasis, and altered cellular responses. Key molecular pathways, including bone morphogenetic proteins (BMPs), Wnt signaling, and transforming growth factor-beta (TGF-β), play crucial roles in the pathophysiology of calcification, calcium imbalance, and muscle fibrosis. In contrast, shoulder arthrofibrosis involves excessive collagen deposition and fibrosis within the shoulder joint capsule, driven by metabolic dysregulation and inflammation. The TGF-β signaling pathway and inflammatory cytokines, such as interleukin-6 (IL-6), are central to the fibrotic response. A comparative analysis reveals both shared and distinct metabolic pathways between these conditions, highlighting the interplay between inflammation, cellular metabolism, extracellular matrix remodeling, calcific deposition, and calcium migration to the glenohumeral joints, resulting in adhesive capsulitis, thereby providing insights into their pathophysiology. This review discusses current therapeutic approaches and their limitations, advocating for the development of targeted therapies that address specific metabolic dysregulations. Future therapeutic strategies focus on developing targeted interventions that address the underlying metabolic dysregulation, aiming to improve patient outcomes and advance clinical management. This review offers a comprehensive overview of the metabolic mechanisms involved in calcific tendinopathy and shoulder arthrofibrosis, providing a foundation for future research and therapeutic development.
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This check searched the claim as stated. It did not run a separate search for evidence against it.