Study Summary
Background
Myofascial pain syndrome (MPS) is a common and costly chronic pain disorder affecting 30 to 85% of the population, yet its exact pathophysiologic mechanism remains poorly understood. Patients with MPS experience not only persistent muscle pain but also depression, anxiety, and reduced quality of life. While biochemical changes have been studied in various pain conditions, the specific roles of inflammation and oxidative stress in MPS—and how they relate to clinical symptoms like pain intensity and quality of life—have not been well established. Understanding these biological mechanisms could lead to better diagnostic approaches and targeted treatments for this prevalent condition.
What They Did
The researchers conducted a case-control study comparing 43 patients with primary myofascial pain syndrome to 42 healthy controls matched for age and body mass index. All participants were recruited from rehabilitation outpatient clinics at Tabriz University of Medical Sciences in Iran between October 2018 and May 2019. MPS patients had neck or shoulder pain lasting at least 3 months, active myofascial trigger points in specific shoulder muscles (trapezius, infraspinatus, and/or levator scapulae), pain scores above 4 on a 0-10 visual analog scale, and normal neurological examinations. The researchers measured five blood biomarkers: high-sensitivity C-reactive protein (hs-CRP) and phospholipase A2 (PLA2) as inflammatory markers; and malondialdehyde (MDA), total antioxidant capacity (TAC), and superoxide dismutase (SOD) as oxidative stress markers.
They also assessed pain intensity at rest, during activity, and at night using visual analog scales; measured pressure pain threshold with an electronic algometer; and evaluated quality of life using the SF-36 questionnaire. Statistical analyses compared biomarker levels between groups and examined correlations with clinical outcomes.
What They Found
MPS patients showed significantly higher levels of inflammatory and oxidative stress markers compared to healthy controls. Specifically, serum hs-CRP was 4.68 ± 4.36 vs. 2.92 ± 4.55 μg/ml (p = 0.011), PLA2 was 6.81 ± 2.22 vs. 4.73 ± 2.97 pg/ml (p < 0.001), and MDA was 2.63 ± 0.71 vs. 1.98 ± 0.90 nmol/ml (p < 0.001). Conversely, antioxidant levels were lower in MPS patients: TAC was 2.46 ± 0.49 vs. 2.83 ± 0.82 mmol/L (p = 0.011) and SOD was 78.89 ± 37.93 vs. 154.25 ± 115.93 U/ml (p < 0.001). Quality of life was substantially worse in MPS patients across most SF-36 domains, with particularly large differences in physical health (202.97 ± 85.09 vs. 278.30 ± 88.36, p = 0.001) and mental health (213.44 ± 79.18 vs. 264.61 ± 65.87, p = 0.001).
Importantly, hs-CRP levels were positively associated with resting pain (r = 0.349, p = 0.019), activity pain (r = 0.295, p = 0.049), night pain (r = 0.304, p = 0.043), and pain duration (r = 0.283, p = 0.007). TAC was negatively associated with resting pain intensity (r = -0.312, p = 0.037). Quality of life measures correlated positively with TAC and negatively with hs-CRP and PLA2 levels.
What This Means
This study provides compelling evidence that systemic inflammation and oxidative stress are not just present in myofascial pain syndrome but are directly linked to how much pain patients experience and how poor their quality of life becomes. The findings suggest that MPS involves whole-body biological changes, not just localized muscle problems. For patients, this means that future treatments targeting inflammation or boosting antioxidant defenses might help reduce pain and improve daily functioning beyond conventional muscle-focused therapies. For clinicians, measuring these biomarkers could potentially help assess disease severity or monitor treatment response.
However, because this was a case-control study, it cannot prove that inflammation causes MPS—only that the two are associated. The small sample size and single-center design mean these findings need confirmation in larger, longitudinal studies before biomarker-guided treatments become standard practice.
85
n=43
Case group with primary myofascial pain syndrome
n=42
Age- and BMI-matched healthy subjects
MPS Patients
Case group with primary myofascial pain syndrome
Healthy Controls
Age- and BMI-matched healthy subjects
Results Comparison
hs-CRP (μg/ml)
μg/mlSOD (U/ml)
U/mlMDA (nmol/ml)
nmol/mlKey Findings
| Finding | Detail | Impact |
|---|---|---|
| Elevated inflammatory markers in MPS | Serum hs-CRP (4.68 ± 4.36 vs. 2.92 ± 4.55 μg/ml, p = 0.011) and PLA2 (6.81 ± 2.22 vs. 4.73 ± 2.97 pg/ml, p < 0.001) were significantly higher in MPS patients compared to healthy controls. | High |
| Increased oxidative stress with reduced antioxidant capacity | MDA was higher (2.63 ± 0.71 vs. 1.98 ± 0.90 nmol/ml, p < 0.001) while TAC (2.46 ± 0.49 vs. 2.83 ± 0.82 mmol/L, p = 0.011) and SOD (78.89 ± 37.93 vs. 154.25 ± 115.93 U/ml, p < 0.001) were lower in MPS patients. | High |
| hs-CRP correlates with multiple pain measures | Serum hs-CRP was positively associated with resting pain (r = 0.349, p = 0.019), activity pain (r = 0.295, p = 0.049), night pain (r = 0.304, p = 0.043), pressure pain threshold (r = 0.210, p = 0.047), and pain duration (r = 0.283, p = 0.007). | High |
| Antioxidant levels linked to pain and quality of life | TAC was negatively associated with resting pain intensity (r = -0.312, p = 0.037), and quality of life scales correlated positively with TAC and negatively with hs-CRP and PLA2. | Medium |
| Quality of life substantially impaired in MPS | All SF-36 scales and subscales were significantly lower in MPS patients except physical function, energy/fatigue, and emotional wellbeing. Physical health: 202.97 ± 85.09 vs. 278.30 ± 88.36 (p = 0.001); Mental health: 213.44 ± 79.18 vs. 264.61 ± 65.87 (p = 0.001). | High |
Serum hs-CRP (4.68 ± 4.36 vs. 2.92 ± 4.55 μg/ml, p = 0.011) and PLA2 (6.81 ± 2.22 vs. 4.73 ± 2.97 pg/ml, p < 0.001) were significantly higher in MPS patients compared to healthy controls.
MDA was higher (2.63 ± 0.71 vs. 1.98 ± 0.90 nmol/ml, p < 0.001) while TAC (2.46 ± 0.49 vs. 2.83 ± 0.82 mmol/L, p = 0.011) and SOD (78.89 ± 37.93 vs. 154.25 ± 115.93 U/ml, p < 0.001) were lower in MPS patients.
Serum hs-CRP was positively associated with resting pain (r = 0.349, p = 0.019), activity pain (r = 0.295, p = 0.049), night pain (r = 0.304, p = 0.043), pressure pain threshold (r = 0.210, p = 0.047), and pain duration (r = 0.283, p = 0.007).
TAC was negatively associated with resting pain intensity (r = -0.312, p = 0.037), and quality of life scales correlated positively with TAC and negatively with hs-CRP and PLA2.
All SF-36 scales and subscales were significantly lower in MPS patients except physical function, energy/fatigue, and emotional wellbeing. Physical health: 202.97 ± 85.09 vs. 278.30 ± 88.36 (p = 0.001); Mental health: 213.44 ± 79.18 vs. 264.61 ± 65.87 (p = 0.001).
Strengths
- Matched case-control design with age and BMI matching
- Multiple validated biomarkers assessed simultaneously
- Comprehensive clinical assessment including pain at rest, activity, and night
- Use of validated outcome measures (VAS, PPT, SF-36)
Limitations
- Relatively small sample size (85 total participants)
- Case-control design cannot establish causality
- Single-center study from Iran limits generalizability
- No serial biomarker measurements to assess dynamic changes
- No dietary assessment of anti-inflammatory micronutrients
Key Takeaways for Patients
What This Means for You
- 01Your blood may show signs of increased inflammation and oxidative stress if you have myofascial pain syndrome
- 02Higher inflammation levels appear linked to more severe pain and worse daily functioning
- 03Antioxidant levels in your body may be lower than in people without this condition
- 04Future treatments might target these biological processes, not just the painful muscles
- 05More research is needed to confirm whether reducing inflammation directly improves symptoms