522 J WOCN ■ September/October 2011 Copyright © 2011 by the Wound, Ostomy and Continence Nurses Society
Copyright © 2011 Wound, Ostomy and Continence Nurses Society. Unauthorized reproduction of this article is prohibited.
WOUND CARE
Effect of Oxidized Regenerated
Cellulose/Collagen Matrix on
Proteases in Wound Exudate of
Patients With Diabetic Foot Ulcers
Dietmar Ulrich Ralf Smeets Frank Unglaub Michael Wöltje Norbert Pallua
PURPOSE: The aim of this study was to investigate the influence
of oxidized regenerated cellulose/collagen matrix on the con-
centration and activity of gelatinases, elastase, and plasmin in
wound exudate.
SUBJECTS AND SETTING: The study included 32 patients with dia-
betic foot ulcers. Ten patients with a mean age of 66 9 years
(mean SD) were treated with hydrocolloid dressings; 22 patients
with a mean age of 57 12 years were treated with oxidized
regenerated/collagen matrix and hydrocolloid dressings.
METHODS: Wound exudate was collected on days 0, 5, 14, and
every 14 days thereafter for 12 weeks. Total protein was deter-
mined according to Bradford’s technique. The levels of elastase
and plasmin were measured spectrofluorometrically. Besides,
gelatinase activity and matrix metalloproteinase-2 concentration
were analyzed. The surface area of all ulcers was measured by
planimetry.
RESULTS: Patients treated with oxidized regenerated cellulose/
collagen matrix showed a significant decrease in elastase, plasmin,
and gelatinase activities in wound exudates. The matrix metal-
loproteinase-2 concentration was significantly reduced on days
14, 28, 42, and 56 in comparison to day 0. Furthermore, wound
size was significantly reduced at days 14 and 28 in oxidized
regenerated cellulose/collagen matrix-treated patients (P .05).
CONCLUSION: Our results showed a significant and immediate
reduction in the levels of all tested proteases in the wound
exudate of diabetic foot ulcer patients treated with oxidized
regenerated cellulose/collagen matrix. These patients also
experienced a significantly greater reduction in wound size.
■ Introduction
Foot ulcers are one of the most common complications of
diabetes mellitus. It not only is a typical complication in
later stages of diabetes but can also occur in patients with
newly diagnosed disease.
1
Despite the postulations of the
St Vincent Declaration, which stated that within 5 years
the amputation rate should be reduced by 50%, there are
30,000 amputations reported each year in Germany due to
diabetic foot ulcers.
2-11
Normal wound healing relies on a balance between the
processes that lead to new tissue formation and processes
necessary to remove damaged tissue. Tissue formation and
removal are regulated by growth factors and proteases that
control the biologic processes necessary to achieve normal
wound repair.
12
Abnormalities in the levels of growth fac-
tors and proteases are thought to be one of the factors con-
tributing to wound chronicity and failure to heal.
13
This
hypothesis is supported by studies of diabetic foot ulcers,
which consistently reveal persistent inflammation and an
imbalance in protease/protease-inhibitor levels.
14
Alterations
in the levels of these regulatory factors can lead to a non-
healing state and the formation of a chronic wound.
15
Chronic wounds fail to follow the normal pattern of
wound repair, which involves inflammation, granulation,
J Wound Ostomy Continence Nurs. 2011;38(5):522-528.
Published by Lippincott Williams & Wilkins
Dietmar Ulrich, MD, PhD, Department of Plastic and
Reconstructive Surgery, Erasmus University Hospital, Rotterdam,
The Netherlands.
Ralf Smeets, MD, DDS, PhD, Interdisciplinary Centre of Clinical
Research “BIOMAT”.
Frank Unglaub, MD, PhD, Department of Plastic Surgery, Hand
Surgery, Burn Unit, University Hospital Aachen, Pauwelsstrasse 30,
Aachen, Germany.
Michael Wöltje, PhD, Department of Plastic Surgery, Hand
Surgery, Burn Unit, University Hospital Aachen, Pauwelsstrasse 30,
Aachen, Germany.
Norbert Pallua, MD, PhD, Department of Plastic Surgery, Hand
Surgery, Burn Unit, University Hospital Aachen, Pauwelsstrasse 30,
Aachen, Germany.
Dietmar Ulrich and Ralf Smeets contributed equally to the study.
Correspondence: Ralf Smeets, MD, DDS, PhD, Interdisciplinary
Centre of Clinical Research “BIOMAT,” University Hospital
Aachen, Pauwelsstrasse 30, Aachen D-52074, Germany
(rasmeets@ukaachen.de).
DOI: 10.1097/WON.0b013e31822ad290