Evidence of Neuronal Differentiation of Tendon Stromal Cells in Patients with Biceps Branchi Muscle Pain: A Histological and Immunohistochemical Study of 12 Patients (original) (raw)
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Tendon pain – what are the mechanisms behind it?
Scandinavian Journal of Pain
Objectives Management of chronic tendon pain is difficult and controversial. This is due to poor knowledge of the underlying pathophysiology of chronic tendon pain, priorly known as tendinitis but now termed tendinopathy. The objective of this topical review was to synthesize evolving information of mechanisms in tendon pain, using a comprehensive search of the available literature on this topic. Content This review found no correlations between tendon degeneration, collagen separation or neovascularization and chronic tendon pain. The synthesis demonstrated that chronic tendon pain, however, is characterized by excessive nerve sprouting with ingrowth in the tendon proper, which corresponds to alterations oberserved also in other connective tissues of chronic pain conditions. Healthy, painfree tendons are devoid of nerve fibers in the tendon proper, while innervation is confined to tendon surrounding structures, such as sheaths. Chronic painful tendons exhibit elevated amounts of pa...
Pathogenesis of tendinopathies: inflammation or degeneration?
Arthritis Research & Therapy, 2009
The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.
Review Pathogenesis of tendinopathies: inflammation or degeneration?
2009
The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.
The tendon unit: biochemical, biomechanical, hormonal influences
Journal of Orthopaedic Surgery and Research
The current literature has mainly focused on the biology of tendons and on the characterization of the biological properties of tenocytes and tenoblasts. It is still not understood how these cells can work together in homeostatic equilibrium. We put forward the concept of the “tendon unit” as a morpho-functional unit that can be influenced by a variety of external stimuli such as mechanical stimuli, hormonal influence, or pathological states. We describe how this unit can modify itself to respond to such stimuli. We evidence the capability of the tendon unit of healing itself through the production of collagen following different mechanical stimuli and hypothesize that restoration of the homeostatic balance of the tendon unit should be a therapeutic target.
Morpho-functional changes in human tendon tissue
European Journal of Histochemistry, 2009
Insertion tissue biopsies of right arm common extensor tendons from 11 patients with chronic lateral epicondylitis were processed for light and electron microscopy. The subjects were aged between 38 and 54 years (only one was 25). The specimens showed a variety of structural changes such as biochemical and spatial alteration of collagen, hyaline degeneration, loss of tenocytes, fibrocartilage metaplasia, calcifying processes, neovascularization and vessel wall modifications. Tissue alterations were evident in limited zones of the tendon fibrocartilage in which the surgical resection was generally visible. The areas where the degenerative processes were localized, were restricted and in spatial contiguity with morphologically normal ones. The observed cases presented histological and electron microscopic findings that characterize lateral epicondylitis as a degenerative phenomenon involving all tendon components.
Neuronal pathways in tendon healing and tendinopathy -update
The regulatory mechanisms involved in tendon homeostasis and repair are not fully understood. Accumulating data, however, demonstrate that the nervous system, in addition to afferent (sensory) functions, through efferent pathways plays an active role in regulating pain, inflammation, and tissue repair. In normal-, healing- and tendinopathic tendons three neurosignalling pathways consisting of autonomic, sensory and glutamatergic neuromediators have been established. In healthy tendons, neuromediators are found in the paratenon, whereas the proper tendon is practically devoid of nerves, reflecting that normal tendon homeostasis is regulated by pro- and antiinflammatory mediators from the tendon surroundings. During tendon repair, however, there is extensive nerve ingrowth into the tendon proper and subsequent timedependent appearance of sensory, autonomic and glutamatergic mediators, which amplify and fine-tune inflammation and tendon regeneration. In tendinopathy, excessive and protracted sensory and glutamatergic signalling may be involved in inflammatory, painful and hypertrophic tissue reactions. As our understanding of these processes improves, neuronal mediators may prove to be useful in the development of targeted pharmacotherapy and tissue engineering approaches to painful, degenerative and traumatic tendon disorders.
Tendon is a dense connective tissue that connects muscle to bone. Tendon can adapt to mechanical forces passing across it, through a reciprocal relationship between its cellular components (tenocytes and tenoblasts) and the extracellular matrix (ECM). In early development, the formation of scleraxis-expressing tendon progenitor population in the sclerotome is induced by a fibroblast growth factor signal secreted by the myotome. Tendon injury has been defined as a loss of cells or ECM caused by trauma. It represents a failure of cells and matrix adaptation to mechanical loading. Injury initiates attempts of tendon to repair itself, which has been defined as replacement of damaged or lost cells and ECM by new cells or new matrices. Tendon healing generally consists of four different phases: the inflammatory, proliferation, differentiation and remodelling phases. Clinically, tendons are repaired with a variety of surgical techniques, which show various degrees of success. In order to improve the conventional tendon repair methods, current tendon tissue engineering aims to investigate a repair method which can restore tissue defects with living cells, or cell based therapy. Advances in tissue engineering techniques would potentially yield to a cell-based product that could regenerate functional tendon tissue.
A Mini Review on the Basic Knowledge on Tendon: Revisiting the Normal Injured Tendon
Journal of Health and Translational Medicine, 2015
Tendon is a dense connective tissue that connects muscle to bone. Tendon can adapt to mechanical forces passing across it, through a reciprocal relationship between its cellular components (tenocytes and tenoblasts) and the extracellular matrix (ECM). In early development, the formation of scleraxis-expressing tendon progenitor population in the sclerotome is induced by a fibroblast growth factor signal secreted by the myotome. Tendon injury has been defined as a loss of cells or ECM caused by trauma. It represents a failure of cells and matrix adaptation to mechanical loading. Injury initiates attempts of tendon to repair itself, which has been defined as replacement of damaged or lost cells and ECM by new cells or new matrices. Tendon healing generally consists of four different phases: the inflammatory, proliferation, differentiation and remodelling phases. Clinically, tendons are repaired with a variety of surgical techniques, which show various degrees of success. In order to improve the conventional tendon repair methods, current tendon tissue engineering aims to investigate a repair method which can restore tissue defects with living cells, or cell based therapy. Advances in tissue engineering techniques would potentially yield to a cell-based product that could regenerate functional tendon tissue.