APMA News - September/October 2017 - S1

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SEP T EMBER / O C T O BER 2017 / ISSUE 48

BRING YOUR EXPERTISE TO THE NATIONAL
The Call for Speakers is now open for the APMA 2018 Annual Scientific Meeting
(The National), taking place July 12-15 in Washington, DC. To learn more and
apply, visit www.apma.org/callforspeakers.
The wound care topics featured in this issue were presented during this year's
meeting in Nashville, TN. If you want to share your research with your colleagues
at the must-attend meeting for every podiatrist, act now; applications are due
October 2.

MATRIX METALLOPROTEINASE AND WOUND CARE
Brock Liden, DPM, Pinkerington, OH

atrix metalloproteinase (MMPs) are
enzymes that play critical roles in the
normal healing process, including
assisting in the removal of denatured matrix,
degrading capillary basement membrane to
allow new vessels to form in angiogenesis,
enabling contraction of scar matrix and
Repeated
Tissue Injury

Image 1

Ischemia
and
Bioburden-Biofilm

Prolonged
Elevated
Inflammation
↑Neutrophils
↑Macrophages
↑Mast cells

Chronic Wound
Pathophysiology

Imbalanced
Proteases and
Inhibitors
↑Proteases
↓ Inhibitors

extracellular matrix (ECM) by myofibroblasts,
migration of epidermal cells, and remodeling
of scar tissue. However, MMPs need to be
present in the right amounts, at the right
places, and at the right times to function
properly in normal healing.
In chronic wounds, the major factor driving inflammation is
the bioburden-biofilm.
The inflammation leads
to massive up-regulation of MMPs, leading
to significant impact
Destruction of
on the wound environEssential Proteins
ment. The chronic
↑ECM degradation
↓Growth factors/receptors
↓Cell migration
wound pathophysiolo↓Cell proliferation
gy starts with repeated
tissue injury, allowing
biofilm-bioburden
establishment. This
situation leads to prolonged inflammation,

Your APMA is supported through a generous
educational grant from Spenco Medical by Implus.
Editor
Design

Will Scott; wpscott@apma.org
Suzanne Kleinwaks Design

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Mast, B., & Schultz, G. (1996). Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Repair
and Regeneration, 4(4), 411-420.

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allowing up-regulation of MMPs and
down-regulation of tissue inhibitory metalloproteinase. The increase in MMPs damages
ECM, destroys growth factors and growth
factor receptors, and decreases cell proliferation and migration. The cascade is an
amplifying cycle, which means that with each
pass, the amount of MMPs increases.
MMPs have been shown to have a direct
relationship to wound volume/healing.
MMPs fluctuate greatly in the wound bed
over a relatively short period of time. As
MMPs decrease, wounds will typically progress toward healing. Conversely, as MMPs
increase, wounds will stall or increase.
Dressings can help regulate MMPs back
to a more normal level. Several accepted
approaches exist to address MMPs in the
wound bed:
1. Collagen is the most accepted dressing
to alter MMPs. It acts as a sacrificial
substrate, allowing the MMPs to eat the
collagen dressing instead of the patient's
own tissue. The issue with collagen is that
it must be applied at the appropriate rate
to address the quantity of MMPs in the
wound bed. If there is too little collagen,
the MMPs overwhelm the dressing and
return to the wound bed, doing damage.
If there is too much, the collagen is not
optimized for the wound's benefit.
2. Debridement physically removes the MMPs
from the wound bed and, depending on
the debridement depth, will impact the
biofilm, slowing the cascade.
Continued on Page 2

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