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Biomarkers in Pain: 2nd Edition

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 15 November 2026 | Viewed by 8420

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Dr. Mats B. Eriksson

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Department of Surgical Sciences, Anaesthesiogy and Intensive Care Medicine, Uppsala University, 751 85 Uppsala, Sweden
Interests: anesthesiology; biomarkers; coagulation; cytokines; endotoxin; critical care medicine; intensive care; leptin; inflammation; intraosseous; sepsis; SAPS3; shock
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Prof. Dr. Anders O. Larsson

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Department of Medical Sciences, Clinical Chemistry, Uppsala University, 751 85 Uppsala, Sweden
Interests: endotoxin; intensive care; acute kidney injury; glomerular filtration rate markers; kidney tubular damage markers; cardiovascular risk markers; neutrophil activation markers; calprotectin
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Dear Colleagues,

Acute and chronic pain are two major reasons that patients seek healthcare. Approximately 20% of the world’s population suffers from chronic pain, and in the USA alone, annual economic losses due to chronic pain are estimated to be USD 600 billion. Apart from being a major economic burden for society, chronic pain is also a major cause of decreased quality of life.

Chronic pain is often difficult to treat, and we have few objective measures for evaluating pain levels. Patients in pain therefore often struggle to have their pain problems acknowledged, as pain is a subjective experience that is difficult to verify. During the last decade, biomarkers related to chronic pain have been investigated. The discovery of such markers could not only be used to improve the diagnoses and prognostication of patients with chronic pain, but could also support those who file an insurance claim after an injury. Biomarkers of pain could also be used to distinguish different causes of pain, allowing for an improved selection of treatments. Such markers could also provide pharmaceutical companies with a tool for evaluating pain relief effects in clinical trials.

The focus of this Special Issue of Biomedicines is on the value of biomarkers of pain from a broad perspective.

Biomarkers of pain may be used to identify and quantify pain of various origins in order to facilitate adequate therapeutic interventions. Extensive prescriptions of analgesics, especially opioids, are associated with overdose deaths. Although pain is a subjective experience, the use of determinants of pain as an end point in clinical trials may help to predict the safety as well as the analgesic efficacy of new drugs.

Dr. Mats B. Eriksson
Prof. Dr. Anders O. Larsson
Guest Editors

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Keywords

analgesia
biomarker
CSF
cytokine
inflammation
neuropathy
neurotransmitter
pain
QoL
sensitization
sensory

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Biomarkers in Pain in Biomedicines (8 articles)

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Research

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14 pages, 1309 KB

Open AccessArticle

Pain Phenotypes, Treatment Patterns, and Utilization Burden Among Patients with Inflammatory Bowel Disease Referred to a Tertiary Pain Clinic: A Retrospective Cohort Study

by Shachar Zion Shemesh, Paz Kelmer, Bella Ungar, Yotam Hadari and Lior Ungar

Biomedicines 2026, 14(7), 1422; https://doi.org/10.3390/biomedicines14071422 (registering DOI) - 23 Jun 2026

Abstract

Background: Pain is a prominent and disabling manifestation of inflammatory bowel disease (IBD), including abdominal, pelvic, musculoskeletal, axial, and neuropathic pain phenotypes. Patients referred to pain clinics represent a selected subgroup with clinically meaningful, persistent, refractory, or diagnostically complex pain. Objective: To characterize pain phenotypes, treatment patterns, interventional pain-care exposure, and utilization burden among patients with IBD evaluated in tertiary pain-clinic settings and to explore differences between Crohn’s disease and ulcerative colitis patients. Methods: We performed a retrospective electronic medical-record cohort study of patients with documented IBD who were evaluated in pain-clinic settings between 24 October 2010 and 14 May 2026. Repeated clinical entries were aggregated into unique visit dates and patient-level variables. IBD diagnosis, pain phenotypes, treatment documentation, interventional procedures, and pain-clinic utilization were summarized descriptively using counts, percentages, means, medians, interquartile ranges, and ranges as appropriate. Crohn’s disease and ulcerative colitis subgroups were compared using univariable odds ratios with 95% confidence intervals and two-sided p-values. Because repeated clinical entries could belong to the same patient, the primary analytic unit was the patient rather than the individual note. Results: The source dataset included 19,615 clinical entries representing 7053 unique pain-clinic visits among 596 unique patients with IBD. The cohort included 314 patients with Crohn’s disease (52.7%), 247 with ulcerative colitis (41.4%), and 35 with IBD-unclassified (5.9%). The mean number of pain-clinic visits per patient was 11.8, with a median of four visits (interquartile range, 1–11). The dominant patient-level pain phenotypes were limb or peripheral joint pain (395/596, 66.3%), back or axial spine pain (358/596, 60.1%), and abdominal or pelvic pain (246/596, 41.3%). Overall, 437 patients (73.3%) had documentation of at least one interventional pain procedure. Compared with ulcerative colitis, Crohn’s disease was associated with higher documentation of abdominal or pelvic pain (148/314, 47.1% vs. 82/247, 33.2%; odds ratio, 1.79; 95% confidence interval, 1.27–2.53; p = 0.001) and fibromyalgia-like or widespread pain (83/314, 26.4% vs. 39/247, 15.8%; odds ratio, 1.92; 95% confidence interval, 1.25–2.93; p = 0.0027). In contrast, radiofrequency procedures (59/314, 18.8% vs. 78/247, 31.6%; odds ratio, 0.50; 95% confidence interval, 0.34–0.74; p = 0.0005) and facet or medial branch procedures (79/314, 25.2% vs. 87/247, 35.2%; odds ratio, 0.62; 95% confidence interval, 0.43–0.89; p = 0.012) were less frequently documented in Crohn’s disease than in ulcerative colitis. Conclusions: Among patients with IBD referred to tertiary pain-clinic evaluation, pain was heterogeneous and predominantly musculoskeletal, axial, neuropathic, and procedurally targetable rather than exclusively visceral. These findings support structured, mechanism-based pain assessment integrated with gastroenterology, rheumatology, and pain-medicine care. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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16 pages, 841 KB

Open AccessArticle

Circulating Brain-Derived Neurotrophic Factor (BDNF) and Multimodal Opioid-Based Analgesia in Chronic Pain: Plasma BDNF as an Indicator of Pain Intensity and Neuropathic Pain

by Urszula Kosciuczuk, Piotr Jakubow and Damian Misiuk

Biomedicines 2026, 14(6), 1313; https://doi.org/10.3390/biomedicines14061313 - 10 Jun 2026

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Abstract

Background: Brain-derived neurotrophic factor (BDNF) is crucial in the nociception and mechanisms underlying chronic and neuropathic pain. The evaluation of circulating BDNF in patients with multimodal analgesia has not been reported previously. We hypothesized that opioid-based multi-analgesia induces changes in BDNF values and that BDNF correlates with pain intensity in neuropathic pain. Methods: Adult patients who met low back pain (LBP) criteria and received multimodal opioid-based therapy were included. The control group included patients with LBP who did not receive any pharmacotherapy. Plasma measurements obtained with the ELISA test were analyzed. The study was registered at Clinical Trials.gov (NCT 04227223). Results: Patients with multimodal opioid-based analgesia had significantly higher BDNF values compared to the monotherapy: 3.6 ng/mL vs. 2.7 ng/mL, p = 0.01. No statistical differences were observed compared to the non-pharmacologically treated group: 3.6 ng/mL vs. 5.0 ng/mL, p = 0.75. The median BDNF values were lowest in the mild-pain group, and significant differences were observed between the severe and moderate-pain groups (p = 0.006) and the mild-pain group (p = 0.0001). BDNF was significantly higher in the neuropathic-pain group compared to the group of patients without neuropathic pain (p = 0.0005). A significant correlation was demonstrated between the BDNF and numerical rating pain score (NRS) in the neuropathic-pain component (rho = 0.6, p = 0.001). Conclusions: Multimodal opioid-based analgesia decreases plasma BDNF concentrations less than opioid monotherapy, which offers an opportunity to limit opioid-induced adverse effects. BDNF influences pain intensity and predicts neuropathic pain in multimodal opioid-based analgesia. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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27 pages, 5731 KB

Open AccessArticle

Betanin from Beta vulgaris Attenuates Complete Freund’s Adjuvant-Induced Inflammatory Pain: Integrated Preclinical and In Silico Insights

by Ahmed Massoud, Amina E. Essawy, Mohammed A. Alfredan, Ashraf M. Abdel-Moneim, Rehab A. Gomaa and Sherine Abdel Salam

Biomedicines 2026, 14(6), 1202; https://doi.org/10.3390/biomedicines14061202 - 27 May 2026

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Abstract

Background/Objectives: Betanin (BET), a prominent phytochemical mainly derived from Beta vulgaris, exhibits strong anti-inflammatory and antioxidant activities owing to its distinctive chemical structure. Nevertheless, its potential analgesic effect in the context of inflammatory pain remains insufficiently explored. Accordingly, this study investigated the analgesic effects of BET in a complete Freund’s adjuvant (CFA)-induced rat model of inflammatory pain. Methods: Rats received a single subcutaneous injection of 100 µL CFA to induce inflammatory pain, followed by oral administration of BET at doses of 40 or 80 mg/kg/day for 14 days. Results: BET treatment significantly reduced paw edema and improved HPL (hot plate latency) in CFA-injected rats. Biochemically, in the ipsilateral spinal cord of rats, BET at both 40 and 80 mg/kg significantly increased IL-4, and only the 80 mg/kg dose significantly reduced oxidative stress (MDA) and IL-1β. TNF-α levels were slightly reduced at both doses and did not reach statistical significance versus CFA. At the molecular level, miR-107 was significantly downregulated by BET at 80 mg/kg (but not 40 mg/kg), while miR-145 was significantly upregulated by both 40 mg/kg and 80 mg/kg compared to CFA. Pearson’s correlation indicated that miR-107 was positively correlated with MDA, IL-1β and TNF-α but negatively with IL-4, whereas miR-145 was positively correlated with IL-4 but negatively with IL-1β. PCA biplot analysis corroborated these findings, showing simultaneous presence of MDA, IL-1β, TNF-α, and miR-107 with CFA, and IL-4 and miR-145 were only related to control and CFA+BET80 groups. In addition, using transmission electron microscopy imaging, we found that BET alleviated neuronal damage in CFA-treated rats. Furthermore, molecular docking analysis predicted that BET may exhibit stable binding interactions with several inflammation- and apoptosis-related targets, including AKT1, mTOR, IKKβ, TNF-α, IL-1β, COX-2, caspase-3, caspase-7, and caspase-8, supporting its multi-target anti-inflammatory and antiapoptotic effects. Conclusions: Overall, our data suggest that BET can possibly exert analgesic effects in CFA-induced inflammatory pain by modulating oxidative stress and favoring a shift toward an anti-inflammatory status. These effects coincided with downregulation of miR-107, overexpression of miR-145, and improvements in inflammatory pain behaviors. Further investigations are required to validate the involvement of specific miRNA- and pathway-mediated effects. Nevertheless, our findings highlight BET as a promising natural candidate for future development of anti-inflammatory and analgesic strategies. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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11 pages, 534 KB

Open AccessArticle

Autonomic Receptor Autoantibodies in Complex Regional Pain Syndrome and Other Chronic Pain Conditions: A Cross-Sectional Analysis

by Daniël P. C. van der Spek, Renée H. Hoffenkamp, Frank J. P. M. Huygen, Krishna D. Bharwani, Niels Eijkelkamp and Maaike Dirckx

Biomedicines 2026, 14(4), 945; https://doi.org/10.3390/biomedicines14040945 - 21 Apr 2026

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Abstract

Objectives: Complex regional pain syndrome (CRPS) is a heterogeneous pain disorder with incompletely understood immunoinflammatory features. This study investigated whether autonomic receptor autoantibodies differentiate CRPS from other chronic pain conditions and healthy controls. Methods: We conducted a cross-sectional analysis of serum samples from patients referred with suspected CRPS. Patients were subsequently classified as having either CRPS or another chronic pain condition, based on the Budapest criteria. Healthy controls were included for comparison. Serum levels of autoantibodies targeting the muscarinic M2 receptor (M2R), β1-adrenergic receptor (β1AR), and the β2-adrenergic receptor (β2AR) were assessed using enzyme-linked immunosorbent assay. All analyses were performed blinded to group assignment. Results: Seventy participants were analyzed (CRPS = 22, other chronic pain = 25, healthy controls = 23). M2R autoantibody levels were higher in both CRPS and other chronic pain compared with healthy controls (mean difference [MD] = 0.37, 95%CI 0.22–0.51; and MD = 0.31 95%CI 0.19–0.44, respectively). β2AR levels were higher in other chronic pain compared with healthy controls (MD = 0.29, 95%CI 0.04–0.54), whereas no significant difference was observed in CRPS (MD = 0.21 95%CI −0.01–0.42). No meaningful differences were observed between CRPS and other chronic pain for any receptor. β1AR levels did not differ between groups. Seropositivity for any autoantibody was 55% in CRPS, 44% in other chronic pain, and 22% in healthy controls. Conclusions: Elevated autonomic receptor autoantibody levels were observed across chronic pain conditions but were not specific for CRPS. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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19 pages, 1899 KB

Open AccessArticle

Peripheral Blood Cells and Clinical Profiles as Biomarkers for Pain Detection in Palliative Care Patients

by Hugo Ribeiro, Raquel Alves, Joana Jorge, Bárbara Oliveiros, Tânia Gaspar, Inês Rodrigues, João Rocha Neves, Joana Brandão Silva, António Pereira Neves, Ana Bela Sarmento-Ribeiro, Marília Dourado, Ana Cristina Gonçalves and José Paulo Andrade

Biomedicines 2026, 14(1), 176; https://doi.org/10.3390/biomedicines14010176 - 14 Jan 2026

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Abstract

Background/Objectives: Patients in need of specialized palliative care are clinically highly complex, with pain being the most prevalent problem. Furthermore, in these patients, a self-report for characterization of pain could be difficult to obtain. This cross-sectional, exploratory study investigates the use of clinical parameters and peripheral blood biomarkers for potentially identifying and characterizing pain (assessed using Pain Assessment in Advanced Dementia (PAINAD) and Numeric Scale (NS)) in patients under palliative care, including a population with dementia where pain is often underdiagnosed. Methods: Fifty-three patients with non-oncological diseases were analyzed in a cross-sectional study using medical and nursing records. Among previous biomarkers related to monocytes and platelets assessed by flow cytometry, we selected the most significative ones for pain characterization in a logistic regression analysis (multivariate analysis), alongside patient-specific characteristics such as renal function, nutritional status, and age. Results: Our exploratory findings suggest strong relationships between chronic pain and advanced age, reduced glomerular filtration rate (GFR), and malnutrition within this cohort. Furthermore, the percentage of lymphocytes, total and classical monocytes, the relative expression in monocytes of CD206, CD163, the CD163/CD206 ratio, and the relative expression in platelets of CD59 emerged as potential predictors of pain. Statistical analyses highlighted the challenges of multicollinearity among variables such as age, GFR, and nutritional status. A classification model further suggested that all patients over 65 years in our specific sample reported pain. Conclusions: This pilot study provides preliminary support for prior evidence linking chronic pain to aging, nutritional deficits, and renal impairment, and highlights potential novel peripheral blood biomarkers for pain assessment. This work emphasizes the promise of clinical and molecular biomarkers to improve pain detection and management, contributing to personalized and effective palliative care strategies. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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14 pages, 7946 KB

Open AccessArticle

Neuropathic Pain and Related Depression in Mice: The Effect of a Terpene and a Minor Cannabinoid in Combination

by Jose Rios, Mohammed Alnoud, Mohammad S. Hussain, Zayd Ayas, Emmanuel Franco, Justin Mills, Joshua Nwose, Maria Sophia Malbas, Hiram Garcia, Manish K. Tripathi and Khalid Benamar

Biomedicines 2025, 13(12), 3103; https://doi.org/10.3390/biomedicines13123103 - 16 Dec 2025

Cited by 1 | Viewed by 1133

Abstract

Background/Objectives: Neuropathic pain is one of the most severe types of chronic pain. Although it is difficult to manage, it often co-occurs with depression. Yet, no medication addresses the neuropathic pain and depression comorbidity. Therefore, developing integrated treatment strategies that address both pain and depression is a major public health priority and an unmet need affecting millions. Methods: In this study, we investigated the effect of combining a terpene, Beta-Caryophyllene (BCP), and cannabidiol (CBD) on neuropathic pain and associated depression. We employed a chronic constriction injury (CCI) neuropathic pain model and a series of behavioral tests to evaluate how oral administration of this combination influences neuropathic pain and depression-like behaviors in mice. We employed immunohistochemistry and proteomics approaches to explore the mechanism. Results: The analgesic effect of combining CBD and BCP is synergistic in neuropathic pain and also shows an antidepressant effect. Additionally, we found that this combination decreases neuroinflammation associated with CCI and affects specific genes involved in the inflammation. Conclusions: This work provides preclinical scientific evidence supporting the potential usefulness of this combination for neuropathic pain and associated depression. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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Review

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15 pages, 611 KB

Open AccessReview

From Prediction to Monitoring: Toward a Translational Framework of Biomarkers in Spinal Cord Stimulation

by Gustavo Fabregat-Cid, Natalia Escrivá-Matoses and José De Andrés

Biomedicines 2026, 14(6), 1307; https://doi.org/10.3390/biomedicines14061307 - 9 Jun 2026

Viewed by 237

Abstract

Spinal cord stimulation (SCS) is an established therapy for chronic pain, yet treatment response remains highly variable and patient selection largely empirical. The identification of biomarkers with the potential to predict and monitor therapeutic response is therefore critical for advancing toward precision neuromodulation. This study provides a structured narrative synthesis of current evidence on biomarkers in SCS, focusing on their predictive and monitoring roles and their translational potential. Available studies were analysed across electrophysiological, neuroimaging, autonomic, and molecular domains and conceptually organized into predictive biomarkers—reflecting baseline biological states associated with treatment susceptibility—and monitoring biomarkers, capturing physiological and molecular adaptations following stimulation. Among predictive approaches, intraoperative electroencephalography (EEG) and resting-state functional magnetic resonance imaging (rs-fMRI) have shown promising but exploratory discriminative performance. However, EEG findings are derived from intraoperative settings, limiting their applicability to pre-implantation patient selection. In contrast, monitoring biomarkers—including heart rate variability, metabolic imaging, and immunological parameters—provide objective measures of treatment-induced changes but do not currently support predictive use. Molecular and genomic biomarkers, while mechanistically informative, remain exploratory and lack validated clinical utility. A central limitation of the field is the fragmentation of biomarker research, with most studies evaluating single modalities in isolation. To address this gap, we propose a translational framework integrating predictive and monitoring biomarkers through a two-stage model combining baseline stratification with longitudinal response assessment. Although biomarker research in SCS is rapidly evolving, its clinical application remains limited. The development of multimodal, validated biomarker strategies may support improved patient selection and more objective evaluation of treatment response, enabling a transition toward mechanism-based neuromodulation. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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22 pages, 485 KB

Open AccessReview

Neuroinflammatory Biomarkers in Chronic Low Back Pain: Mechanisms, Clinical Evidence, and Translational Challenges

by João Pinheiro, Pedro Lima, Ricardo Pestana, Miriam Sousa, José Alves, Hugo Ribeiro, Gonçalo Neto D’Almeida and Isabel Santana

Biomedicines 2026, 14(3), 557; https://doi.org/10.3390/biomedicines14030557 - 28 Feb 2026

Cited by 2 | Viewed by 1164

Abstract

Background: Chronic low back pain (CLBP) is a leading cause of disability worldwide and remains clinically challenging due to its marked heterogeneity and limited correlation between structural pathology and symptoms. Increasing evidence suggests that neuroinflammatory mechanisms and central sensitization (CS) contribute to pain persistence in a clinically relevant subset of patients. This narrative review critically evaluates the current evidence on neuroinflammatory biomarkers in CLBP and discusses their translational potential for mechanism-based patient stratification. Methods: A comprehensive literature search was conducted in PubMed, Scopus, and Google Scholar using terms related to neuroinflammation, biomarkers, CLBP, CS, and glial activation. Studies were preferentially selected according to the following hierarchical criteria: (1) human studies directly investigating neuroinflammatory biomarkers in CLBP; (2) mechanistic human imaging or cerebrospinal fluid studies; (3) translational preclinical investigations providing direct mechanistic relevance; and (4) high-quality systematic reviews providing synthesis of biomarker evidence. As this was a narrative review, study selection was guided by conceptual relevance and translational significance rather than by formal systematic review methodology. Results: Converging evidence supports the involvement of neuroinflammatory processes in subgroups of patients with CLBP. In vivo TSPO-PET imaging and experimental data support glial activation in pain-processing regions. Cerebrospinal fluid studies report elevated chemokines, particularly interleukin-8 and monocyte chemoattractant protein-1, highlighting periphery-to-central nervous system inflammatory cross-talk and the concept of compartmentalized neuroinflammation. In parallel, epigenetic markers such as brain-derived neurotrophic factor DNA methylation have emerged as indirect correlates of CS-related pain phenotypes. In contrast, traditional systemic inflammatory markers show inconsistent and nonspecific associations. Conclusions: Neuroinflammatory biomarkers hold promise for mechanism-based stratification of CLBP, particularly for identifying patients with CS-driven pain. However, major methodological and translational challenges remain, including lack of standardization, limited accessibility of central nervous system-compartment measures, and the need for longitudinal and interventional validation. Future research should prioritize multi-marker and multi-compartment approaches integrated with functional phenotyping to establish clinical utility. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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31 pages, 1085 KB

Open AccessReview

The Role of the CCR5 Receptor in Neuropathic Pain Modulation: Current Insights and Therapeutic Implications

by Mario García-Domínguez

Biomedicines 2025, 13(11), 2650; https://doi.org/10.3390/biomedicines13112650 - 29 Oct 2025

Cited by 1 | Viewed by 2624

Abstract

Neuropathic pain, a chronic condition arising from injury or dysfunction of the somatosensory nervous system, is characterized by persistent hypersensitivity and spontaneous pain. The chemokine receptor CCR5 (C-C motif chemokine receptor 5) has recently been identified as a critical mediator in neuroinflammation and neuropathic pain signaling pathways. Expressed on immune cells and neurons, CCR5 regulates immune cell recruitment and activation, thereby contributing to neuronal sensitization and maintenance of pain states. This review examines the currently characterized molecular mechanisms through which CCR5 modulates neuropathic pain pathophysiology and assesses the potential of CCR5 antagonists as novel therapeutic agents for the management of chronic neuropathic pain. Understanding the involvement of CCR5 in pain modulation may facilitate the development of targeted treatments with improved efficacy and safety profiles. Full article

(This article belongs to the Special Issue Biomarkers in Pain: 2nd Edition)

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