Age-Related Changes in the Cellular, Mechanical, and Contractile Properties of Rat Tail Tendons

Lavagnino, Michael; Gardner, Keri; Arnoczky, Steven P.

doi:10.3109/03008207.2012.744973

Cited by 36 publications

(37 citation statements)

References 41 publications

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“…Our histological analysis of the ossified region of the adult tendon confirmed typical patterns of ageing seen in other models (Lavagnino et al. ). A lack of crimp morphology was observed in all adult samples, as well as a reduced number of cells per mm 2 .…”

Section: Discussionsupporting

confidence: 88%

“…This would indicate that additional tendon cells are created following hatching of the chick but are reduced gradually with aging. Our histological analysis of the ossified region of the adult tendon confirmed typical patterns of ageing seen in other models (Lavagnino et al 2012). A lack of crimp morphology was observed in all adult samples, as well as a reduced number of cells per mm 2 .…”

Section: The Ossified Avian Tendon Tissuesupporting

confidence: 84%

“…Both these regions displayed a loss in collagen crimp morphology in comparison with embryonic tendon, characteristic of ageing and injury in tendon (Lavagnino et al. ). The clear boundary between the ossified and non‐ossified regions of the adult tendon, suggest tendon ossification could be patterned on the process of formation of the enthesis, as in cases of calcific tendinopathy (Benjamin et al.…”

Section: Discussionmentioning

confidence: 99%

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Investigating tendon mineralisation in the avian hindlimb: a model for tendon ageing, injury and disease

2013

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Mineralisation of the tendon tissue has been described in various models of injury, ageing and disease. Often resulting in painful and debilitating conditions, the processes underlying this mechanism are poorly understood. To elucidate the progression from healthy tendon to mineralised tendon, an appropriate model is required. In this study, we describe the spontaneous and non-pathological ossification and calcification of tendons of the hindlimb of the domestic chicken (Gallus gallus domesticus). The appearance of the ossified avian tendon has been described previously, although there have been no studies investigating the developmental processes and underlying mechanisms leading to the ossified avian tendon. The tissue and cells from three tendons -the ossifying extensor and flexor digitorum longus tendons and the non-ossifying Achilles tendon -were analysed for markers of ageing and mineralisation using histology, immunohistochemistry, cytochemistry and molecular analysis. Histologically, the adult tissue showed a loss of healthy tendon crimp morphology as well as markers of calcium deposits and mineralisation. The tissue showed a lowered expression of collagens inherent to the tendon extracellular matrix and presented proteins expressed by bone. The cells from the ossified tendons showed a chondrogenic and osteogenic phenotype as well as tenogenic phenotype and expressed the same markers of ossification and calcification as the tissue. A molecular analysis of the gene expression of the cells confirmed these results. Tendon ossification within the ossified avian tendon seems to be the result of an endochondral process driven by its cells, although the roles of the different cell populations have yet to be elucidated. Understanding the role of the tenocyte within this tissue and the process behind tendon ossification may help us prevent or treat ossification that occurs in injured, ageing or diseased tendon.

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Section: Discussionsupporting

confidence: 88%

Section: The Ossified Avian Tendon Tissuesupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

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Investigating tendon mineralisation in the avian hindlimb: a model for tendon ageing, injury and disease

2013

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“…One way, this may be comprised is by declining cell numbers with increasing age. A number of previous studies have reported a decrease in cell number with increasing age in rat Achilles tendon (Yu et al., ), rat tail tendon (Lavagnino et al., ), and mice patellar tendons (Dunkman et al., ). However, it is difficult to separate maturation and ageing effects in short‐lived species such as rats where growth plates remain open throughout life (Kilborn et al., ).…”

Section: Discussionmentioning

confidence: 93%

Ageing does not result in a decline in cell synthetic activity in an injury prone tendon

Thorpe

McDermott

Goodship

et al. 2015

Scandinavian Med Sci Sports

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1Advancing age is a well-known risk factor for tendon disease. Energy storing tendons, (e.g. 2human Achilles, equine superficial digital flexor tendon (SDFT)) are particularly vulnerable 3 and it is thought that injury occurs following an accumulation of micro-damage in the 4 extracellular matrix (ECM). Several authors suggest that age-related micro-damage 5 accumulates due to a failure of the aging cell population to maintain the ECM or an 6 imbalance between anabolic and catabolic pathways. We hypothesised that ageing results in a 7 decreased ability of tendon cells to synthesise matrix components and matrix degrading 8 enzymes, resulting in a reduced turnover of the ECM and a decreased ability to repair micro-9 damage. The SDFT was collected from horses aged 3-30 years with no signs of tendon 10 injury. Cell synthetic and degradative ability was assessed at the mRNA and protein levels. 11Telomere length was measured as an additional marker of cell ageing. There was no decrease 12 in cellularity or relative telomere length with increasing age, and no decline in mRNA or 13 protein levels for matrix proteins or degradative enzymes. The results suggest that the 14 mechanism for age-related tendon deterioration is not due to reduced cellularity or a loss of 15 synthetic functionality and that alternative mechanisms should be considered.

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“…Consistent with healing in other tendons, our data demonstrate that aging impairs restoration of mechanical properties and results in decreased matrix deposition. 21,22 Tendon cell number decreases over the lifespan of mature tendons, as seen in mice patellar tendons, 23 rat Achilles tendon, 6,24 and rat tail tendon, 25 likely due to a dramatic reduction in cell proliferation post-natally. [26][27][28] Moreover, the remaining cells have an altered morphology, with rounder cells in the young tendon giving way to a thinner, more elongated phenotype in aged tenocytes, which is associated with a lower metabolic activity.…”

Section: Discussionmentioning

confidence: 99%

Aging does not alter tendon mechanical properties during homeostasis, but does impair flexor tendon healing

Ackerman

Bah

Jonason

et al. 2017

Journal Orthopaedic Research

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Aging is an important factor in disrupted homeostasis of many tissues. While an increased incidence of tendinopathy and tendon rupture are observed with aging, it is unclear whether this is due to progressive changes in tendon cell function and mechanics over time, or an impaired repair reaction from aged tendons in response to insult or injury. In the present study we examined changes in the mechanical properties of Flexor Digitorum Longus (FDL), Flexor Carpi Ulnaris (FCU), and tail fascicles in both male and female C57Bl/6 mice between 3-27 months of age to better understand the effects of sex and age on tendon homeostasis. No change in max load at failure was observed in any group over the course of aging, although there were significant decreases in toe and linear stiffness in female mice from 3-months to 15, and to 22-27-months. No changes in cell proliferation were observed with aging, although an observable decrease in cellularity occurred in 31-month old tendons. Given that aging did not dramatically alter tendon mechanical homeostasis we hypothesized that a disruption in tendon homeostasis, via acute injury would result in an impaired healing response. Significant decreases in max load, stiffness, and yield load were observed in repairs of 22-month old mice, relative to 4-month old mice. No changes in cell proliferation were observed between young and aged, however a dramatic loss of bridging collagen extracellular matrix was observed in aged repairs suggest that matrix production, but not cell proliferation leads to impaired tendon healing with aging.

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Age-Related Changes in the Cellular, Mechanical, and Contractile Properties of Rat Tail Tendons

Cited by 36 publications

References 41 publications

Investigating tendon mineralisation in the avian hindlimb: a model for tendon ageing, injury and disease

Investigating tendon mineralisation in the avian hindlimb: a model for tendon ageing, injury and disease

Ageing does not result in a decline in cell synthetic activity in an injury prone tendon

Aging does not alter tendon mechanical properties during homeostasis, but does impair flexor tendon healing

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