Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle

This scoping review systematically examines 799 studies on myofascial pain syndrome (MPS) and fibromyalgia, proposing a new theoretical model for understanding these conditions. The author suggests that both conditions represent manifestations of a common pathologic process centered on the fascia, termed 'fascial armoring.' Fascia is a connective tissue that permeates the entire body, surrounding muscles, bones, and organs. It has unique viscoelastic properties that allow reversible adaptation to mechanical stress through tensional relaxation. When subjected to prolonged stress or immobilization, fascia undergoes changes in hyaluronic acid concentration and myofibroblast activity.

Myofibroblasts are specialized cells that differentiate from normal fibroblasts in response to mechanical stress, developing alpha-actin fibers that generate sustained contraction in the tissue. Unlike reversible muscle contraction, myofibroblast contraction can persist for long periods through extracellular matrix remodeling. The 'fascial armoring' model proposes that trigger points represent areas where myofibroblasts have created 'tensional shielding' to protect tissues from excessive stress. However, this protective adaptation can become pathologic when generalized.

Fascial tension can propagate through tensegrity principles, in which structures are stabilized by continuous tension with discontinuous compression. This would explain how local dysfunction can cause distant symptoms and why fibromyalgia presents a specific pattern of painful points adjacent to bony prominences. Sedentary lifestyle emerges as a principal risk factor, since fascia evolutionarily adapted to continuous movement. Immobilization leads to changes in collagen, increased myofibroblast density, and formation of pathologic adhesions as early as the first week.

Paradoxically, movement and exercise prevent and reverse these changes through multiple mechanisms: fascial energy dissipation, mechanical disruption of fibers, local heating that breaks down hyaluronic acid, increased lymphatic flow, and natural pandiculation. Clinically, MPS manifests through trigger points with abnormal electrical activity and palpable taut bands. The 'satellite' phenomenon — in which trigger points induce new distant points — can be explained by fascial tensional propagation. When this process generalizes, it can progress to fibromyalgia, characterized by elevated intramuscular pressures (mean 33.5 mmHg vs.

12.2 mmHg in controls) that exceed the criteria for chronic compartment syndrome. Cardiovascular evidence in fibromyalgia includes reduced peripheral blood flow, capillary dilations, and arterial alterations, consistent with generalized fascial compression. Metabolic findings show elevation of interstitial lactate, glutamate, and pyruvate, suggesting low-grade ischemia. Genomic studies identify mitochondrial polymorphisms associated with increased risk.

Intriguing phenomena such as complete resolution of fibromyalgia after laparoscopic surgeries or parathyroidectomy may be explained by inadvertent fasciotomy releasing tension from the tensegrity network. The model predicts that different surgeries will have variable effects depending on how they affect fascial tensegrity — some relieving, others exacerbating symptoms. Therapeutically, needling emerges as a common modality, possibly functioning as 'global percutaneous fasciotomy' that disrupts pathologic connections in the tensegrity network. The proposed mechanism involves creating weak points where internal forces rupture fibers, releasing tension and inducing myofibroblast apoptosis.

The approach should respect tensegrity principles, releasing tension gradually from the periphery toward the center to avoid pathologic redistribution of forces. This model unifies several 'functional syndromes' under a common mechanism of tension-tensegrity generated by myofibroblasts, explaining the epidemiologic overlap between fibromyalgia, irritable bowel syndrome, chronic fatigue, and other conditions. Risk factors include not only sedentary lifestyle but also diet, medications, and environmental exposures that induce myofibroblasts. The model has limitations, not fully explaining central neurologic aspects or psychosocial factors, but it offers a unifying framework for understanding mechanical aspects often neglected in these prevalent conditions.