Myofascial pain syndrome (MPS) is a leading cause of chronic musculoskeletal pain, yet its mechanisms remain debated. Traditional models emphasized muscle contracture or central sensitization, but growing evidence highlights fascia as a biologically active, pain-relevant tissue. Pathological alterations such as densification, fibrosis, and inflammation may generate nociceptive input and sustain persistent symptoms. To explore this perspective, we conducted a conceptual narrative review of studies published between 2000 and 2025 in PubMed, Embase, Scopus, and Google Scholar. Eligible publications included anatomical, histological, imaging, biomechanical, and clinical investigations, and evidence was synthesized narratively into an integrative model of mechanisms. This mini-review followed the SANRA guidelines for narrative reviews. The literature demonstrates that fascia is richly innervated by nociceptors and sympathetic fibers and undergoes pathological changes in patients with MPS. Imaging and histological studies confirm fibrosis, densification, and inflammatory activity in symptomatic fascia. Mechanistic pathways linking fascia to pain include impaired sliding, abnormal mechanotransduction, and neuroinflammatory sensitization. Clinically, patients exhibit tenderness on fascial palpation, imaging evidence of stiffness, and symptomatic improvement after fascia-focused therapies. These findings suggest that fascia functions as a key peripheral driver in MPS. This concept was first formalized as the ‘integrated hypothesis’ by Simons in 2004. Integrating fascia into existing frameworks reconciles muscle-based and central sensitization models, providing a plausible substrate that initiates nociceptive signaling, perpetuates central adaptations, and interacts with psychosocial influences. This integrative model may explain the heterogeneity of MPS and supports multimodal treatment strategies that combine fascial therapies with central and psychosocial interventions. Although current evidence remains preliminary and heterogeneous, recognizing fascia as a central but interconnected contributor to MPS offers a more comprehensive understanding of this syndrome and a clinically relevant framework for future diagnostic and therapeutic innovation in pain medicine.

Equine lameness diagnosis is dominated by a joint- and tendon-centric paradigm. The standard diagnostic algorithm relies on gait observation, perineural and intrasynovial anesthesia, and cross-sectional imaging. It is directed almost exclusively at skeletal and articular structures. Myofascial trigger points (MTrPs) are hypersensitive, hyperirritable loci within taut bands of skeletal muscle. They produce local and referred pain on compression or contraction. In horses, MTrPs are a clinically relevant but systematically overlooked source of primary lameness. This review synthesises evidence from equine and comparative research. We argue that MTrPs can act as the primary-not merely secondary-cause of gait asymmetry, performance deficits, and pain behavior in horses. Key mechanisms include the energy crisis model of MTrP formation, peripheral and central sensitization, referred pain projection mimicking distal limb pathology, and the biomechanical consequences of MTrP-induced muscle inhibition on gait. Electrophysiological studies confirm that equine MTrPs show the same spontaneous electrical activity as human and animal MTrPs. Prevalence studies indicate that MTrPs are present in many sport horses. Dressage horses show particularly high prevalence in the cervical and thoracolumbar musculature. Of clinical importance is the referred pain phenomenon: MTrPs in proximal muscles such as the gluteus medius, longissimus lumborum, and biceps femoris may produce apparent distal limb pain. Such pain can be clinically indistinguishable from joint or tendon pathology. This has direct and underappreciated implications for diagnostic accuracy. We propose that systematic myofascial palpation should be integrated into the routine equine lameness workup as a first-tier diagnostic step. Rapid resolution of gait asymmetry following targeted MTrP treatment should be interpreted as supportive evidence of myofascial origin. We further delineate the clinically relevant trigger point activity spectrum from active to latent states, address differential diagnoses such as Lyme-associated diffuse myalgia and primary myopathies (PSSM2, MIM, IMM), summarise the principal therapeutic modalities used in equine MTrP management, and examine biotensegrity as a mechanobiological framework explaining the multisegmental fascial effects of myofascial dysfunction.

Background: Myofascial Pain Syndrome (MPS) is a common, overlooked, and underdiagnosed condition and has significant burden. MPS is often dismissed by clinicians while patients remain in pain for years. MPS can evolve into fibromyalgia, however, effective treatments for both are lacking due to absence of a clear mechanism. Many studies focus on central sensitization. Therefore, the purpose of this scoping review is to systematically search cross-disciplinary empirical studies of MPS, focusing on mechanical aspects, and suggest an organic mechanism explaining how it might evolve into fibromyalg

Myofascial pain syndrome (MPS) is one of the most common causes of chronic pain. It is characterized by trigger points (TrPs) that are located within palpable taut bands (TBs) in muscles and their fascial structures. Traditionally, this clinical condition has been regarded as a dysfunction of the musculoskeletal system, commonly associated with mechanical overload, such as acute strain, repetitive movements, and/or abnormal posture holding. However, the intrinsic mechanisms underlying its development remain a subject of debate. This review proposes a paradigm shift: to consider MPS as a physiological protective response rather than a pathological disorder. From this perspective, the TrP-TB complex may represent a dual contributor to structural and functional protection. On the one hand, it might limit potentially harmful movements through local and segmental sensitization mechanisms. On the other hand, it could enhance joint stability by increasing the tension of the muscle fibers that form the TB and its intramuscular connective tissue, potentially augmenting proprioceptive input. This new perspective offers a revised conceptual framework in which phenomena traditionally interpreted as purposeless manifestations of painful dysfunction may instead be understood as defensive and/or compensatory responses. Such a perspective both broadens understanding of MPS and may encourage the development of treatment protocols that go beyond classical techniques, which focus mainly on inactivating TrPs and managing pain. This new perspective suggests incorporating strategies to modulate load, perform functional training, and address both peripheral and central sensitization within a comprehensive, multilevel framework. Ultimately, this perspective may help achieve more durable and sustainable therapeutic outcomes, possibly contributing to a reduction in the prevalence of pain-related disability associated with MPS.