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Tendon pain : what are the mechanisms behind it?

Ackermann, Paul W. (författare)
Karolinska Institutet,Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.;Karolinska Univ Hosp, Trauma Acute Surg & Orthopaed, S-17176 Stockholm, Sweden.
Alim, Md Abdul, 1983- (författare)
Uppsala universitet,Allmänmedicin och preventivmedicin,Institutionen för medicinsk biokemi och mikrobiologi,Karolinska Inst, Dept Dent Med, Stockholm, Sweden
Pejler, Gunnar (författare)
Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi,Swedish Univ Agr Sci, Dept Anat Physiol & Biochem, Uppsala, Sweden
visa fler...
Peterson, Magnus, 1966- (författare)
Uppsala universitet,Allmänmedicin och preventivmedicin,Reg Uppsala, Acad Primary Hlth Care, Uppsala, Sweden
visa färre...
Karolinska Institutet Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden;Karolinska Univ Hosp, Trauma Acute Surg & Orthopaed, S-17176 Stockholm, Sweden. (creator_code:org_t)
2022-07-18
2023
Engelska.
Ingår i: Scandinavian Journal of Pain. - : Walter de Gruyter. - 1877-8860 .- 1877-8879. ; 23:1, s. 14-24
  • Forskningsöversikt (refereegranskat)
Abstract Ämnesord
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  • ObjectivesManagement 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.ContentThis 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 pain neuromediators, such as glutamate and substance p as well as up-regulated expression and excitability of pain receptors, such as the glutamate receptor NMDAR1 and the SP receptor NK1, found on ingrown nerves and immune cells. Increasing evidence indicates that mast cells serve as an important link between the peripheral nervous system and the immune systems resulting in so called neurogenic inflammation.SummaryChronic painful tendons exhibit (1) protracted ingrowth of sensory nerves (2) elevated pain mediator levels and (3) up-regulated expression and excitability of pain receptors, participating in (4) neuro-immune pathways involved in pain regulation. Current treatments that entail the highest scientific evidence to mitigate chronic tendon pain include eccentric exercises and extracorporeal shockwave, which both target peripheral neoinnervation aiming at nerve regeneration.OutlookPotential mechanism-based pharmacological treatment approaches could be developed by blocking promotors of nerve ingrowth, such as NGF, and promoting inhibitors of nerve ingrowth, like semaphorins, as well as blocking glutamate-NMDA-receptor pathways, which are prominent in chronic tendon pain.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Ortopedi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Orthopaedics (hsv//eng)

Nyckelord

mast cells
nerve tissue proteins
neuronal plasticity
pain
receptors
tendon

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