Tendons: Time to Revisit Inflammation?

Rees, J D; Stride, M; Scott, Alexander

doi:10.1136/bjsports-2013-092459.9

Cited by 35 publications

(36 citation statements)

References 43 publications

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“…Schubert et al revealed demonstrated presence of macrophages and lymphocytes (using immunohistochemical techniques), in a chronic Achilles tendon pathology (duration of symptoms was 6-120 months) and granulocytes in a short time after acute rupture of the Achilles tendons [18]. Other authors demonstrated indirect signs of inflammatory response found in chronic tendons disorders -mediators of inflammation: IL-1, IL-6, TGF-β, substance P [19]. A smaller body of literature exists on chronic LHBT pathologies.…”

Section: Clusters Of Capillariesmentioning

confidence: 96%

“…This is illustrated by a review of literature focused on 32 studies evaluating effectiveness of NSAID in tendinopathy, whereas 9 of 32 were prospective and placebo controlled and only 5 of them revealed reduction of painful conditions [22]. Different study investigated effectiveness of corticosteroids injections -only short-term clinical improvement was reported [19]. Authors point at the side-effects of corticosteroids injections: skin atrophy, decreased tendon strength and integrity, infections, possibility of spontaneous tendon rupture.…”

Section: Clusters Of Capillariesmentioning

confidence: 99%

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Is the inflammation process absolutely absent in tendinopathy of the long head of the biceps tendon? Histopathologic study of the long head of the biceps tendon after arthroscopic treatment

Zabrzyński¹,

Paczesny²,

Łapaj³

et al. 2017

pjp

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Tendinopathy of the long head of the biceps tendon is a difficult medical issue. Its pathogenesis and etiology is multifactorial and unclear. Tendinopathy is thought to be primarily degenerative in nature, as tendons are characterized by impaired regeneration and healing. Thirty-five patients with preoperatively diagnosed tendinopathy of long head of the biceps tendon were referred to the Orthopedics Department. All patients underwent an arthroscopic-assisted biceps tenodesis or tenotomy. The intra-articular portion of the long head of the biceps tendon was obtained from each of the patients who underwent arthroscopy. A macroscopic and microscopic evaluation of biceps tendon samples revealed degeneration among all specimens. This study demonstrates the prevalence of the degeneration process and the presence of marginal inflammation process in tendinopathy of the long head of biceps tendon. The role, that inflammation process plays in tendinopathy is important in the early phase and gradually becomes secondary to the developing degeneration. The inflammatory cells, occasionally seen in pathological tendons, could be an evidence of re-injury and recent healing response.

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Section: Clusters Of Capillariesmentioning

confidence: 96%

Section: Clusters Of Capillariesmentioning

confidence: 99%

Is the inflammation process absolutely absent in tendinopathy of the long head of the biceps tendon? Histopathologic study of the long head of the biceps tendon after arthroscopic treatment

Zabrzyński¹,

Paczesny²,

Łapaj³

et al. 2017

pjp

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show abstract

“…Indeed, we found 96 DEGs to be annotated to "proteolysis" of which 67 were up-390 regulated in the HiO 2 HiT+ ( Figure 4C). Among them we found various extracellular proteases such as 391 matrix metalloproteinases (MMP 8,9,10,13,27), intracellular proteases involved in lysosomal 392 degradation such as cathepsins (cathepsin A, B, C, D, F, O, S, Z), and proteasome-related proteins 393 (PSMA 8, PSMB 3,8,9,).…”

mentioning

confidence: 99%

“…Tendinopathy severity is graded by its histopathological score, characterized by the extent of 36 disorganized collagen matrix, abnormal cell shape, presence of inflammation, increased cellularity, 37 vascularization and neuronal ingrowth [24][25][26][27][28]. These hallmarks of disease intimately involve tissue 38 turnover and proteolytic breakdown of the ECM [29][30][31][32].…”

mentioning

confidence: 99%

Tendon response to matrix unloading is determined by the patho-physiological niche

Wunderli

Blache

Piccoli

et al. 2019

Preprint

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1Aberrant matrix turnover with elevated matrix proteolysis is a hallmark of tendon pathology. While 2 tendon disease mechanisms remain obscure, mechanical cues are central regulators. Unloading of 3 tendon explants in standard culture conditions provokes rapid cell-mediated tissue breakdown. Here we 4 show that biological response to tissue unloading depends on the mimicked physiological context. Our 5 experiments reveal that explanted tendon tissues remain functionally stable in a simulated avascular 6 niche of low temperature and oxygen, regardless of the presence of serum. This hyperthermic and 7 hyperoxic niche-dependent catabolic switch was shown by whole transcriptome analysis (RNA-seq) to 8 be a strong pathological driver of an immune-modulatory phenotype, with a stress response to reactive 9 oxygen species (ROS) and associated activation of catabolic extracellular matrix proteolysis that 10 involved lysosomal activation and transcription of a range of proteolytic enzymes. Secretomic and 11 degradomic analysis through terminal amine isotopic labeling of substrates (TAILS) confirmed that 12 proteolytic activity in unloaded tissues was strongly niche dependent. Through targeted 13 pharmacological inhibition we isolated ROS mediated oxidative stress as a major checkpoint for matrix 14 proteolysis. We conclude from these data that the tendon stromal compartment responds to traumatic 15 mechanical unloading in a manner that is highly dependent on the extrinsic niche, with oxidative stress 16 response gating the proteolytic breakdown of the functional collagen backbone. tendon fibroblasts in a collagen-rich extracellular matrix (ECM). The fact that tendons bear 20 physiologically extreme mechanical stresses is reflected by its tightly packed and highly structured 21 ECM. The load bearing tendon core is comprised by hierarchically organized type-I collagen fibrils, 22 fibres and fascicles (or fibre bundles) [1], with fascicles representing the basic functional load-bearing 23 unit of stromal tissue [2,3]. Physiological mechanical signals are understood to regulate the lifelong 24 adaption of the tissue to individual functional demands [4][5][6][7][8], with a narrow gap between beneficial and 25 detrimental mechanical loads [9][10][11][12]. This threshold is often exceeded, with tendon disorders 26 accounting for 30 -50% of all musculoskeletal clinical complaints associated with pain [13]. 27Our basic knowledge of the molecular and cellular mechanisms behind tendon physiology and 28 pathology is limited [14][15][16], yet damage and inadequate repair are considered to be central to tendon 29 disease onset and progression [17][18][19]. The stimuli that trigger tissue healing responses remain unclear, 30 potentially being a direct effect of cellular activation by overloading or by unloading after isolated fibre 31 rupture with subsequently altered cell-matrix interaction [20]. However, the mechanisms of 32 overloading and underloading may not be mutually exclusive, with tissue damage resulting in localized 33 regions...

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“…Sharma & Maffulli, 2005) It is a cause of anterior knee pain and is primarily a clinical diagnosis, although Doppler ultrasound can have additional benefit in diagnosis (Peers & Lysens, 2005). The literature regarding the cause of tendinopathies is continually evolving and there is currently debated over whether it is a noninflammatory or inflammatory process (Khan et al, 2002;Rees et al, 2013). Differential diagnoses include patellofemoral pain syndrome, fat-pad syndromes, meniscal tears, and cartilage degeneration (Warden & Brukner, 2003).…”

mentioning

confidence: 99%

Equivalence of online and clinician administration of a patellar tendinopathy risk factor and severity questionnaire

Morton

Morrissey

Valle³

et al. 2014

Scandinavian Med Sci Sports

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The VISA-P is a questionnaire for assessing the severity of patellar tendinopathy (PT). Our study aim was to evaluate the equivalence of self-administration of the VISA-P online with the addition of risk factor questions to develop a tool suitable for high-volume remote use. A crossover study design with 107 subjects was used to determine equivalence between online and clinician administration. Three population groups were used to ensure construct validity. Online vs clinician administration revealed an intraclass correlation (ICC) of 0.79 [confidence interval (CI): 0.68-0.86] for the VISA-P with a systematic significant difference of 4.99, which is not clinically meaningful. Poor ICCs were seen for questions 7 and 8 of the VISA-P (0.37 and 0.47, respectively) in comparison with earlier questions. There were statistically significant differences between population groups for the VISA-P. The ICC for risk factor questions was excellent at 0.89 (CI: 0.84-0.93) with no mean difference (P = 1.00). The online questionnaire enables equivalent collection of VISA-P data and risk factor information and may well improve further with the suggested modifications to the instructions for questions 7 and 8. There is potential to use this questionnaire electronically to generate large databases in future research.

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Tendons: Time to Revisit Inflammation?

Cited by 35 publications

References 43 publications

Is the inflammation process absolutely absent in tendinopathy of the long head of the biceps tendon? Histopathologic study of the long head of the biceps tendon after arthroscopic treatment

Is the inflammation process absolutely absent in tendinopathy of the long head of the biceps tendon? Histopathologic study of the long head of the biceps tendon after arthroscopic treatment

Tendon response to matrix unloading is determined by the patho-physiological niche

Equivalence of online and clinician administration of a patellar tendinopathy risk factor and severity questionnaire

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