Neuronal pathways in tendon healing and tendinopathy - update

Paul, Wright

doi:10.2741/4280

Cited by 50 publications

(50 citation statements)

References 90 publications

(122 reference statements)

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“…However, a closer look into the repair capacity of tendon reveals that it is actually a complex physiological system, with tightly coordinated interplay between an ''intrinsic compartment" that comprises the fibrous collagen core (tendon cells and the multiscale arrangement of collagen assemblies), and an ''extrinsic tendon compartment" that consists of synovium-like tissues connecting the immune, vascular, and nervous systems [18][19][20] (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

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Tendon injury and repair – A perspective on the basic mechanisms of tendon disease and future clinical therapy

2017

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Section: Introductionmentioning

confidence: 99%

“…1). The extent of intrinsic and extrinsic compartment coordination in functional repair, and discord in degenerative processes, is still poorly understood [20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Tendon injury and repair – A perspective on the basic mechanisms of tendon disease and future clinical therapy

2017

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“…Peripheral nerve endings at the site of injury can emit potent neuromediators with the ability to modify the function of fibroblast-like cells in the healing tendon tissue (Ackermann et al 2014;Murphy and Hart 1993). Emitted neuronal substances may also interact with resident mast cells (MCs) and macrophages to affect their function (Chiu et al 2012;Murphy and Hart 1993).…”

Section: Introductionmentioning

confidence: 99%

“…Glutamate is the primary excitatory mediator of the nervous system and has, via its preferred receptor, NMDAR1, been implicated in regulating tendon healing (Ackermann et al 2014;Molloy et al 2006b) and various pain conditions (Freemont et al 1997) including tendinopathy (Ackermann et al 2014). In tendon healing as well as in tendinopathic patients, a 10-fold up-regulation of NMDAR1 expression has been established (Greve et al 2012;Molloy et al 2006a).…”

Section: Introductionmentioning

confidence: 99%

Increased mast cell degranulation and co-localization of mast cells with the NMDA receptor-1 during healing after Achilles tendon rupture

et al. 2017

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The role of inflammation and the mechanism of tendon healing after rupture has historically been a matter of controversy. The purpose of the present study is to investigate the role of mast cells and their relation to the NMDA receptor-1 (a glutamate receptor) during healing after Achilles tendon rupture. Eight female Sprague Dawley rats had their right Achilles tendon transected. Three weeks after rupture, histological quantification of mast cell numbers and their state of degranulation was assessed by histochemistry. Co-localization of mast cell tryptase (a mast cell marker) and NMDA receptor-1 was determined by immunofluorescence. The intact left Achilles tendon was used as control. An increased number of mast cells and a higher proportion of degranulated mast cells were found in the healing Achilles tendon compared to the intact. In addition, increased co-localization of mast cell tryptase and NMDA receptor-1 was seen in the areas of myotendinous junction, mid-tendon proper and bone tendon junction of the healing versus the intact tendon. These findings introduce a possible role for mast cells in the healing phase after Achilles tendon rupture.

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“…Провоспалитель-ным потенциалом обладают такие нейромедиаторы, актив-но синтезируемые нейроглией и самими нервными оконча-ниями, как кальцитонин-родственный пептид, тахикинины (в частности, субстанция Р), меланокортины, вазоактивный интестинальный пептид, гипофизарный полипептид, акти-вирующий аденилатциклазу (PACAP), грелин и др. [7][8][9].…”

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Dissatisfaction with management of musculoskeletal pain: A global problem and methods of its solution

Каратеев¹

2017

RJTAO

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Идеальная стратегия терапии любого заболевания предполагает этиотропный и патогенетический подход. Всегда следует искать причину болезни (например, если ее развитие вызвано инфекционным агентом), а когда это не-возможно (как в подавляющем большинстве случаев при хронических заболеваниях), четко выделить основные зве-нья ее патогенеза. Точное знание направления фармакоте-рапии ориентирует на очень высокий результат, которого можно достичь в процессе лечения: полное прекращение прогрессирования болезни, т. е. стойкая медикаментозная, а при благоприятном стечении обстоятельств и безмедика-ментозная ремиссия или даже полное выздоровление. (non-steroidal anti-inflammatory drugs (NSAIDs), opioids, local glucocorticoid injections, duloxetine, etc.) Effective control of musculoskeletal pain (MSP) is one of the main tasks of medical care for the most common rheumatic diseases, such as osteoarthritis (OA) and non-specific back pain (NSBP). Epidemiological surveys have shown that a substantial proportion (about 40-50%) of patients consider their assigned treatment to be ineffective and are dissatisfied with its results. The reasons for this are a phenotypic diversity of MSP, individual responses to analgesic drugs, and comorbidities (particularly metabolic disorders and depression). Placebo-controlled trials have demonstrated that monotherapy with the most popular drugs

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Neuronal pathways in tendon healing and tendinopathy - update

Cited by 50 publications

References 90 publications

Tendon injury and repair – A perspective on the basic mechanisms of tendon disease and future clinical therapy

Tendon injury and repair – A perspective on the basic mechanisms of tendon disease and future clinical therapy

Increased mast cell degranulation and co-localization of mast cells with the NMDA receptor-1 during healing after Achilles tendon rupture

Dissatisfaction with management of musculoskeletal pain: A global problem and methods of its solution

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