Foot & Ankle International - 2017 FAI Supplement - 49S

would exist when less than 50% of the tendon remains
undamaged. Our objective was to analyze the mechanical
behavior of cadaveric peroneal tendons subjected to an artificially made damage, compromising 66% of its visible
width and tested in a cyclic and failure phase. Our hypothesis was that no failure would be observed in the cyclic phase.
Methods: 8 cadaveric foot- ankle - distal tibia specimens
were included in this study. A longitudinal full thickness
tendon defect was created, 3 cms in length, centered behind
the tip of the fibula, compromising 66% of the visible width
of the peroneal tendons as measured by a caliper. The peroneal retinaculum was kept intact. All specimens were
mounted onto a special frame specifically designed for the
study. All tendons were tested in a cyclic fashion using 100
repetitions between 50N and 200N. If no visual change or
tendon failure was observed after the initial testing, a load
to failure test was performed until tendon rupture or fixation
failure was observed. Tendon stiffness and load to failure
were registered. Statistical analysis was performed using
the SPSS software.
Results: No tendon failed during the cyclic testing. No defect
lengthening was observed after the cyclic phase. On the failure phase, the mean load resisted by the peroneus brevis was
416N, with a 95% confidence interval between 351N -481 N.
The mean load resisted by the peroneus longus was 723N,
with a 95% confidence interval between 578N - 868N. All
failures were at the level of the defect created. The coefficient
of variation was low for both tendons.
Conclusion: A 33% of remaining peroneal tendon was able
to resist very high tensile forces; therefore, it can be suggested that a 66% defect can be repaired and does not necessarily need a tenodesis as it has been historically
recommended. The high resistance offered by the peroneus
longus tendon offers the theoretical potential to use part of
it as a free graft to repair peroneus brevis tears. The 50%
rule, which determines when a peroneal tendon tear needs a
tenodesis or repair, should be revisited.
Foot & Ankle International, 38(S1)
DOI: 10.1177/1071100717S00047
©The Author(s) 2017

Application of Amniotic Membrane
Improves Repair in a Diabetic Animal
Model for Delayed Tendon Healing
Norman Waldrop, MD, Bonnie Mowry, PhD,
Mitchell Sanders, PhD, John McQuilling, PhD
Category: Basic Sciences/Biologics, Diabetes
AOFAS Annual Meeting 2017

Keywords: Amniotic Membrane, Diabetes, Tendon
Introduction/Purpose: Tendon injuries often heal with
significant scar formation and compromised biomechanical
function. For diabetics, these injuries are further complicated by changes in the extracellular matrix of the tendon,
leading to higher incidences of injury and slower healing.
Defective or delayed healing is a result of several factors
including an impaired ability to form a collagen matrix,
compromised angiogenesis, and inadequate production of
growth factors. Consequently, complications and re-rupture
rates are higher in diabetic patients. Amnion-derived cells
resulted in improved tendon healing in an otherwise healthy
animal model, in part due to their ability to provide numerous regenerative cytokines to the repair site. The purpose of
this study was to evaluate the effect of amniotic tissues on
tendon healing in a diabetic model with impaired healing.
Methods: For this study BBZDR/WOR animals, an insulin
dependent Type II diabetic rodent model, were used. After
appropriate anesthesia, a full thickness injury was made
through the Achilles tendon; immediately following injury,
the tendon was repaired using the modified Kessler method.
Repaired tendons were wrapped with a 0.5 x 0.5 cm section
of either a fresh hypothermically stored human amniotic
membrane (HSAM), a dehydrated human amnion chorion
membrane (dHACM), or left unwrapped as a control.
Contralateral tendons were used as sham controls, which
were exposed then immediately closed. Tendons were
retrieved at 14 or 28 days and evaluated using histology,
immunohistochemistry, and qPCR. At 28 days, both experimental tendons and contralateral controls from five rats per
group were harvested and tested to failure and peak force,
stiffness, energy uptake, and displacement at rupture were
then determined.
Results: At day 14, histological evaluation found significant increases in cellular recruitment at the site of injury in
both dHACM and HSAM treated animals (p=0.0001).
qPCR and immunofluorescence results confirmed several
biomarkers implicated in tendon repair were highly
expressed in the treatment groups, but not in untreated controls. In dHACM treated animals, TNF-a, TGFß-1, IL6,
FLAP, Tenascin-C, and Scleraxis expression was elevated
at 14 days. Control animals with only primary repair
resulted in a tendon repair failure rate of 20%; whereas animals treated with HSAM or dHACM had a 6% and 0%
failure rate, respectively. dHACM treated tendons also had
significant improvements in biomechanical properties
compared to controls including increases in the max force,
stiffness and strain (47±21%, 146±90%, and 59±35%
respectively).
Conclusion: Augmentation of tendon repair with placentalderived membranes may improve diabetic tendon repair
and reduce re-rupture rates. This study presents compelling
49S



Table of Contents for the Digital Edition of Foot & Ankle International - 2017 FAI Supplement

TOC 1
TOC 2
TOC 3
TOC Page 4 + Verso
Editorial Board
President's Introduction
AOFAS Annual Meeting Abstracts 2017
AOFAS Annual Meeting Abstracts 2017
Foot & Ankle International - 2017 FAI Supplement - CT1
Foot & Ankle International - 2017 FAI Supplement - CT2
Foot & Ankle International - 2017 FAI Supplement - Cover1
Foot & Ankle International - 2017 FAI Supplement - Cover2
Foot & Ankle International - 2017 FAI Supplement - i
Foot & Ankle International - 2017 FAI Supplement - TOC 1
Foot & Ankle International - 2017 FAI Supplement - iii
Foot & Ankle International - 2017 FAI Supplement - TOC 2
Foot & Ankle International - 2017 FAI Supplement - 1A
Foot & Ankle International - 2017 FAI Supplement - 1B
Foot & Ankle International - 2017 FAI Supplement - v
Foot & Ankle International - 2017 FAI Supplement - TOC 3
Foot & Ankle International - 2017 FAI Supplement - vii
Foot & Ankle International - 2017 FAI Supplement - TOC Page 4 + Verso
Foot & Ankle International - 2017 FAI Supplement - Editorial Board
Foot & Ankle International - 2017 FAI Supplement - x
Foot & Ankle International - 2017 FAI Supplement - President's Introduction
Foot & Ankle International - 2017 FAI Supplement - AOFAS Annual Meeting Abstracts 2017
Foot & Ankle International - 2017 FAI Supplement - 3S
Foot & Ankle International - 2017 FAI Supplement - 4S
Foot & Ankle International - 2017 FAI Supplement - 5S
Foot & Ankle International - 2017 FAI Supplement - 6S
Foot & Ankle International - 2017 FAI Supplement - 7S
Foot & Ankle International - 2017 FAI Supplement - 8S
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Foot & Ankle International - 2017 FAI Supplement - 10S
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Foot & Ankle International - 2017 FAI Supplement - 14S
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Foot & Ankle International - 2017 FAI Supplement - 18S
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Foot & Ankle International - 2017 FAI Supplement - 38S
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Foot & Ankle International - 2017 FAI Supplement - 40S
Foot & Ankle International - 2017 FAI Supplement - 41S
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Foot & Ankle International - 2017 FAI Supplement - 43S
Foot & Ankle International - 2017 FAI Supplement - 44S
Foot & Ankle International - 2017 FAI Supplement - 45S
Foot & Ankle International - 2017 FAI Supplement - 46S
Foot & Ankle International - 2017 FAI Supplement - AOFAS Annual Meeting Abstracts 2017
Foot & Ankle International - 2017 FAI Supplement - 48S
Foot & Ankle International - 2017 FAI Supplement - 49S
Foot & Ankle International - 2017 FAI Supplement - 50S
Foot & Ankle International - 2017 FAI Supplement - 51S
Foot & Ankle International - 2017 FAI Supplement - 52S
Foot & Ankle International - 2017 FAI Supplement - 53S
Foot & Ankle International - 2017 FAI Supplement - 54S
Foot & Ankle International - 2017 FAI Supplement - Cover3
Foot & Ankle International - 2017 FAI Supplement - Cover4
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