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Canadian Medical Alliance for the Preservation of the Lower Extremity


How Skin Breaks Down In Ulcer Formation

We talk a lot about ulcer formation on this website, so it's worth
spending a little time on the actual mechanism of ulcer formation. 
What happens to the skin?  And why?  

As discussed on our page on diabetic and neuropathic ulcers, these
ulcers are caused by the mechanical forces of pressure and shear
(friction) combined with sensory neuropathy (in particular), with
contributions of motor neuropathy and autonomic neuropathy



On the neuropathy side, altered nerve function of sensory nerves
diminishes the ability of the patient to feel when something is wrong
with the foot.  This is known as sensory neuropathy, and is the single
biggest factor in neuropathic ulcer formation.  

However, neuropathy can affect more than just sensory nerves.  It may
also affect the autonomic nerves--the nerves that control functions we
don't think about.  In the foot, this autonomic neuropathy may present
as an abnormal moisture content in the skin. 

As seen to the right, a patient with autonomic neuropathy may have dry
skin, susceptible to cracks, fissures and abrasions.  This may lead to
fungal and bacterial infiltration that can further weaken the skin.






Altered nerve function of motor nerves (those running from the brain

down to the muscles of the foot) can cause the muscles in the leg and
foot to pull irregularly. This is known as motor neuropathy, and can
result in misalignments of the foot that can lead to crooked toes,
contracted joints, and abnormal bony prominences.  

To the right is an example of the long flexor tendons firing excessively
from motor neuropathy.  The toes curl, creating pressure on the tips of
the toes.  

We discuss the basics of the biomechanics in ulcer formation at greater
length here, but as one quick example, to the right we see the toes of
the foot clutching the ground irregularly. 


Contractures like this can place excessive pressure on the tips of the toes

that can lead to corns or calluses (below left), damaging the skin to the
degree of foot ulcers (below center). 

This can lead to infection and a greater likelihood of amputation.  Even
small amputations can have a domino effect.  They may lead to new sites
of increased pressure, new ulcers, new infections, and additional risk of
further amputation.  In the example below right, the 2nd toe would now
be in most significant danger.

















How Do Pressure and Shear (Friction) Break Down

Skin To Create An Ulcer?

Let's begin by looking at a close-up, cross-sectional
view of normal skin.  

Skin is composed of several layers.  The deepest
layer is the dermis.  The word 'dermis' is Greek
for 'skin,' and is represented by the lighter pink
layer marked D in the image to the right.  (It's
not pink in real life--the color is given by the stain
applied to the slide to enhance its visibility.) 

The dermis layer houses structures like blood
vessels, nerve endings, sweat glands and hair
follicles.  It also contains collagen, a protein that 
gives strength and elasticity to our soft-tissue

The upper layer, (the wavy, darker, purple layer marked E in the image above), is known as the epidermis (Greek for 'upon the skin.')  This layer serves as the body's barrier to the outside world. 


You can see that the epidermis has finger-like projections extending down into the dermis.  These projections, marked RR on the image above, are known as rete ridges (pronounced "ree-tee") or rete pegs.  (Rete is derived from the Latin, meaning 'net.')


Rete ridges serve a couple important purposes. 

First, they increase the surface area between the dermis and epidermis,

allowing better transfer of nutrients from the blood, which lie in the dermis

and extend up into the pink extensions between the rete ridges.  (See right.)

Without rete ridges providing nutrients deep into the epidermis, your
epidermis couldn't be so thick, and you'd have a thinner barrier to the
outside world.

Rete ridges also serve as anchors to hold the epidermis onto the dermis.  The

importance of this will become evident in a moment.

The epidermis, itself, is composed of several layers.  The outermost layer

is the stratum corneum, and it consists of a flattened layer of dead skin

cells.  It is the same material your hair and your nails are made from.  In fact,
a rhinoceros' horn is made of the same tissue.  So it's quite strong.

In most of the skin throughout the body, this stratum corneum layer is relatively

thin, as shown above.  






However, skin on the bottom of the foot, the plantar surface, has a

much thicker layer of stratum corneum than regular skin, as seen to
the right.  (We've oriented the slide so the thick stratum corneum
layer is on the bottom, as it is in the foot.)  

This thick layer is required because the skin on the bottom of the foot
bears the entirety of our body weight with each step, and encounters
more trauma from the outside world. 


(The palms of the hand also exhibit a thickened outer layer of skin like
this, as the hands, too, often undergo a lot of stress and trauma and
need a thicker layer of protection.) 

The difference in skin thick is the major reason skin grafts taken from
other parts of the body don't do well on the bottom of the foot.  The
skin from the rest of the body just isn't thick enough to hold up to the
pressures of weight bearing. 



So lets now talk about the effect of pressure on neuropathic skin.


Because we live in a world governed by gravity, some part of the
body is always under pressure.  When you're in bed, it's whatever
surface you sleep on.  When you sit, it's on the rear end.  When
you stand, the pressure is on your feet.  

The pressure will push the skin down onto a hard surface, pushing
the blood from the capillaries between the rete ridges and
deeper vessels.  You may be able to see this when you press your
own skin for a moment, then let go.  With pressure, your skin
turns white, as the blood is pushed from the skin.   You can see
the difference in the photo to the right, taken through a pane
of glass.   One finger is pushing down on the glass and looks
white.  The other finger is not touching the glass.  That finger
retains capillary flow and, hence, it keeps its pink color.   

Short-term pressure to skin is no issue.  But were a tissue to
have blood removed for a long period of time, the cells would
eventually die.  Fortunately, we have nerves to let us know the
tissue under pressure is getting uncomfortable.  So you turn
over in bed.  You adjust your seated position, or stand up for
a while.  You shift your body weight on to the other foot or sit
down.  And you do this without really even thinking about it.  

But this is not true in a patient with sensory neuropathy.  If you
have sensory loss, you don't get a warning when there is too
much pressure on a foot.  They experience a loss of protective
sensation, or LOPS.  The cells of the skin, or beneath the skin
may become damaged and die, creating an ulcer.  

With an inability to feel the ground, even normal skin can break
down and experience an ulcer. But imagine the patient has thick
skin, like a corn or callus, as seen to the right.  It would be like
walking on a rock.  And the pressure would be many times greater,
increasing the likelihood of an ulcer through pressure.


This is one reason calluses are an indicator of potentialulcer sites.


Besides direct pressure, there is another form of trauma that
can cause an ulcer to form--shear. Shear is essentially friction
caused by motion of the foot on the ground, combined with
body weight pressure applied to the skin.

A common example of a force that would create excessive shear
is a foot that pronates (rolls inwards) excessively, as seen to the


Misaligned or abnormally-moving toes are another common

Motions like this can cause problems for thick skin.  The
plantar skin encountering the ground will stop first, and
the body, along with the deeper layers of skin closest to
the body, keeps moving. 

This means the different layers of the stratum corneum

are moving at different speeds relative to each other.









As a result, tissues layers may separate or shred, as seen

to the right. 


This is shear.



When this shear occurs in superficial layers of the stratum corneum,
you may develop a blister, as seen to the right.

If the blister ruptures, you'll often see the underlying tissue is red
and sensitive.  This is because the deeper levels of skin, those
where the blood vessels and nerves reside, are exposed.



But tissues may shear at deeper levels.  

In an insensate foot (one with neuropathy), the tearing of the 
layers of tissue may extend more deeply without the patient
being aware.  





Here we see a clinical example of tearing of the outer layer
of skin. 


Note the bleeding and pink layers inside the tears.  We're
looking through tears in the epidermis to the dermis, the
layer with blood vessels.  

This is early ulcer formation.  




The thicker the skin--as with thick calluses--the greater the 

sensitivity to shear.  Tissues may rip very deeply.  












Because we may not be able to see what's going on under these damaged tissues, we have to remove the dead skin to fully examine and assess the degree of damage. 































Aging, often seen with diabetes and other neuropathic conditions,

can make matters worse. 

Even without diabetes or neuropathy, the epidermis tends to
shrink with age, making a thinner barrier to the outside world.  

Note how thin the skin is in this older patient seen to the right. 
The skin is so thin you can almost see through it.   

Skin like this is less resistant to pressure and shear. 



You can see the thinning of the epidermis on microscopic view, too.

And you can see those rete ridges (the extensions of epidermis into
the dermis) will often extend less deeply into the dermis with age,
providing aging skin with less strength to combat shear.  

Below left is young skin, with a thick epidermal layer and deep

rete ridges.  Those projections anchor the skin, making it resistant
to shear forces. 

Below right is old skin, with a thin, epidermis and little in the 
way of rete ridges to anchor the epidermis onto the dermis.

























Further, in elderly people, the layer of fat that resides beneath the dermis on the bottom of the foot can atrophy, placing the bones into closer contact to the already-thin skin.  Less fat means less cushioning and more pressure on the bones.  

High sugar, poor nutrition, and vascular disease, particularly from smoking may adversely affect the skin's ability to resist pressure and shear, as well as inhibit healing.  Steroid use has the same harmful effect on skin.

When you add all this together, dry or compromised skin (from autonomic neuropathy), contractures and misalignments (from
arthritis and motor neuropathy), abnormal motions (from motor neuropathy or biomechanical abnormalities) and an inability to
feel what's going on (from sensory neuropathy), often in older, diabetic patients with compromised skin, high sugar and
diminished blood flow, you can see how ulcers may form. 

To see a clinical example of the effects of sugar on wound healing, click here.  

To learn more about some of the biomechanical factors involved with wounds, click here.  

To learn more about neuropathic wounds, click here

To return to the top of the page, click on the maple leaf.





Histology Skin 5.jpg
Histology Normal Skin 1.jpg




Stratum Corneum

Stratum Corneum

Plantar skin 2.jpg
Histology Skin 5.jpg
heel callus_edited.png


colorful autumn maple leaf isolated on w
ulcer tip of 3rd toe.jpg
Histology old and new skin.png
Histology Skin 1.jpg

Young skin, with thick epidermis (purple layer) 
with deep rete ridge projections into the dermis

Old skin, with a thin epidermis and negligible rete ridges projecting into the dermis.

Rete Ridges.jpg

Photo courtesy of


"Turn your wounds into wisdom."

--Oprah Winfrey

This page written by Dr. S A Schumacher
Podiatric Surgeon
Surrey, British Columbia  Canada

All clinical photographs are owned and provided
by Dr. S A Schumacher.  They may be reproduced
for educational purposes with attribution to: 
Dr. S A Schumacher, Surrey, BC Canada 
and a link to this website,

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