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Friction and blisters

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Asher, Nov 18, 2013.

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  1. Asher

    Asher Well-Known Member


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    Hi there,

    I've been writing an article for my website www.blisterprevention.com.au about friction and what it means to the cause and prevention of blisters. The aim is to make it easily understood by your average practitioner / athlete. I'd be interested to know if podiatrists find this helpful, too simplistic or inaccurate. To be honest, in spite of blisters being a special interest area, I find physics difficult. And I have a habit of over-simplifying things. Any feedback would be appreciated.

    FRICTION & BLISTERS
    People have different ideas of what friction is. Friction is the force that resists movement. It is not rubbing. Actually, my Dorland’s Pocket Medical Dictionary says friction is “the act of rubbing”. So in fact rubbing is one definition of friction. But it is not the one that is helpful to explaining how blisters form.

    The Merriam-Webster Dictionary has two definitions of friction:
    1) the act of rubbing one thing against another
    2) the force that resists relative motion between two bodies in contact

    To understand how friction causes blisters, we’re going to use the second definition. But we are going to get a bit more specific than that. It becomes much easier to understand what friction is and how it applies to blisters when you talk about static and dynamic friction.

    Definition of friction (static & dynamic)
    - Static friction is friction that occurs between two bodies in contact with one another while they are at rest. It's the friction which prevents an object from moving while it is still.
    - Dynamic friction is friction that opposes the movement of a body which is already in motion. It's the friction that slows or stops an object from moving. Reference

    Where is friction?
    When it comes to foot blisters, friction exists between two surfaces (an interface).
    skin-sock interface
    shoe-sock interface
    • or if you're wearing 2 pairs of socks, the sock-sock interface

    Measuring friction
    The level of friction between two surfaces is called the Coefficient of Friction (COF). The COF is a number usually below 1.0.

    • 0.9 = high COF = less motion between two surfaces = prolonged state of static friction
    • 0.2 = low COF = more motion between two surfaces = earlier state of dynamic friction

    How does friction cause blisters?
    Static friction causes blisters because it results in a lot of shear. Imagining the foot as a wobbly box helps to explain:

    Look at this wobbly box. The movement force at the top is from the bones as they move back and forth. And the force of friction is what keeps the bottom of the box stationary at the bottom - in a state of static friction. Everything in between the top and the bottom is made to stretch and distort. This is shear and this is what leads to blisters.

    [​IMG]

    Figure 1: Wobbly box and the effect of friction

    To stop blisters, we can either do something at the top of the wobbly box – that is, reduce bone movement. Or we can do something at the bottom of the wobbly box – like reduce the COF to make it more slippery. [This is what lubricants, powders, antiperspirants, tapes, ENGO patches, moisture-wicking socks and double-socks do]. And this is what we’re going to focus on right now.

    Static friction causes blisters
    A state of static friction is exactly what we see with the wobbly box. There’s a movement force at the top but no movement at the bottom. Lots of shear occurs in the middle though.

    Now, if that wobbly box was to move at the bottom (because the movement force at the top exceeded the friction force at the bottom) that’s what you’d call a state of dynamic friction. Makes sense – static means still, dynamic means motion.

    Here’s something you probably already know without realising. Have you ever tried to push a heavy box and found that a big effort is required to get it moving ... but once you get it going it’s easier to keep it moving? That’s because the force you need for the box to break free of static friction ... is HIGHER than that required to keep it on the move. Have a look at the table below. No matter what the combination of materials, the static COF is higher than the dynamic (kinetic) COF (except Teflon on Teflon which is the same).

    [​IMG]

    Figure 2: Some common values of coefficients of static and dynamic (kinetic) friction (these values are approximate). Source

    And this has special significance when describing the cause and prevention of blisters. Because when static friction is high and prolonged, there is going to be more shear. The wobbly box is going to have to stretch and distort further. If we’re talking about foot blisters, that means within the skin layers.

    Below is a representation of how shear develops (A). See how it increases to a maximum to what we call the shear peak. Shear builds and builds while there is a state of static friction. Now, see the dynamic section - as soon as there is movement, shear immediately reduces! So blisters form when there is a prolonged state of static friction – the longer two surfaces stay stuck together, the higher that shear is going to peak. And blisters are prevented when a state of dynamic friction occurs earlier (B) – because that gives us an earlier and hence lower shear peak.

    [​IMG]

    [​IMG]

    Figure 3: (A) Prolonged static friction; (B) Earlier dynamic friction

    What are you thinking right now?
    You must be thinking “Wait a minute, I thought rubbing causes blisters? You’re telling me that if I let rubbing go on in my shoes I can stop blisters?" Well, this rubbing thing is a widespread and understandable assumption. Rubbing doesn’t cause blisters, but it can damage the skin. Let me explain:

    • If the COF between the skin and sock is high when there is a state of dynamic friction, that motion (we tend to call rubbing) is going to be abrasive to the skin. If you already have a blister there, that abrasive motion will easily tear and dislodge your fragile blister roof and you’ll be left with a red raw sore on your foot. But the dynamic part of the process has not been responsible for forming the blister. It was already there because of the shear that resulted from static friction.

    • If you had this same amount of movement between the skin and sock but this time the COF is low, that’s not going to be abrasive to the skin. Rather than ‘rubbing’ with its connotations of abrasiveness, this is more like what you might call ‘sliding’. Not only are you less likely to get a blister because of the shorter state of static friction, even if you did, you are less likely to suffer abrasion of the blister roof.

    This differentiation between static and dynamic friction, as well as high and low COF is very important as the effect each has is different. Below is a summary of skin-sock permutations and resultant effect to skin:

    • State of static friction + high COF = blister-causing
    • State of dynamic friction + high COF = abrasion injury
    • State of dynamic friction + low COF = blister prevention
    • State of static friction + low COF = no skin injury threat

    The above pertains to the skin-sock interface. It's similar at the shoe-sock interface in that:

    • A low shoe-sock COF provides early motion between the shoe and sock to reduce shear ie: blister prevention
    • But there is no risk of abrasion. If shoe-sock COF is lower than skin-sock COF, the skin and sock remain stuck together. If no movement occurs between skin and sock, there can be no abrasion.

    Take home messages
    1. Friction is easier to understand when considering it as static and dynamic.
    2. A prolonged state of static friction leads to blisters.
    3. An earlier onset of dynamic friction is a blister prevention strategy.

    Many thanks
    Rebecca Rushton
     
  2. Asher

    Asher Well-Known Member

  3. Lab Guy

    Lab Guy Well-Known Member

    Hi Rebecca,

    Question for you. Diabetic patient with callus/preulcer plantar IPJ of hallux. Hallux hyperextended at IPJ. I will off-load the IPJ to decrease pressure but do you think an Engo patch overlying the IPJ on top of the Plastazote will help to decrease shear?
    Thanks,

    Steven
     
  4. Asher

    Asher Well-Known Member

    Yes Steven, it will.

    Both pressure and the coefficient of friction (COF) combine to produce the friction conditions that result in shear. They are mutually dependent. Shear is unlikely to reach damaging levels with a low COF. And shear is unlikely to reach damaging levels with low pressure. The problem for feet is we walk on them so on weight bearing areas, there is by default a fair amount of pressure. If this can be reduced, it should be. But it is advisable not to neglect the COF part of it. Try this:

    Step 1: Place the tip of your right index finger on the back of your left hand.
    Step 2: Wobble it back and forth but keep it stuck to the same bit of skin. Notice how your skin stretches? This is shear and this is what causes foot blisters. Keep wobbling as you read:

    Shear might look like rubbing but it’s not. Notice how your finger tip has not moved relative to the skin of the back of your hand? But your hand skin has moved relative to the underlying bone. This is shear. When shear is excessive and repetitive blisters form - it's that last little bit of shear that is damaging, when there is maximum stretch.

    Step 3: Wobble back and forth again but this time press really firmly with your finger tip. Notice how there is more shear when you press harder. Low pressure allows your fingertip to slide across the skin before shear becomes excessive. High pressure sees your fingertip remain stuck to your hand for longer which causes a lot more shear. This is the relevance of pressure to the frictional force that causes shear.
    Step 4: Now put a drop of oil on the back of your hand and wobble your fingertip back and forth again. Press really hard as you do this. I’m doing it right now and I can compress the tissues like crazy yet only a tiny bit of shear is produced! You have to do this to believe it. When there is a low COF (as provided by the oil in this experiment) even extreme pressure will fail to produce significant shear. This is the relevance of the COF to the frictional force that causes shear.

    Does that make sense?

    Here are a few quotes that provide some perspective:

    "With only a few recent exceptions, researchers typically mention that shear forces are an important factor in skin breakdown but then proceed to measure and relate to peak pressure values and factors." Carlson, 2006

    "There are two types of force which occur on the sole of the foot, one is vertical force at right angles to the foot, which causes direct pressure on the tissues. The other is horizontal force, or shear stress, which is parallel to the surface of the foot and occurs in association with acceleration and deceleration. Of the two forces shear stress is more damaging than pressure." Brand, 1983

    Rebecca
     
  5. Lab Guy

    Lab Guy Well-Known Member

    Rebecca,

    Thank you very much for your prompt, informative and educational response. Great demonstration.

    I have a lab and make quite a few diabetic custom orthotics and will try the Engo patches to decrease shear and off-load to decrease pressure. I am in the USA, any idea on where to buy to obtain a better volume discount for a business? Thanks again, Rebecca.

    Steven
     
  6. Asher

    Asher Well-Known Member

  7. Lab Guy

    Lab Guy Well-Known Member


    Rebecca,

    Thanks for info. I have used Shear Ban before for my diabetic orthotics and they worked well. I did not know they too were made by Tamarack.

    Is there a difference between Shear Ban and Engo Patches that appear to be made by the the same company? Is one better than another? I need to educate the Podiatrists to spend a little extra money for these patches. Thanks again.

    Steven
     
  8. Asher

    Asher Well-Known Member

    Steven,

    As far as I know, the polytetrafluoroethylene (PTFE) surface and the adhesive is exactly the same. I believe the bit in between the two (the backing) is marginally thicker on the Shearban. I'm sure Jason will be able to give you all the details.

    Rebecca
     
  9. Lab Guy

    Lab Guy Well-Known Member

    I will call Jason and tell him you referred me. Thanks for info.

    Steven
     
  10. efuller

    efuller MVP

    Hi Rebecca, I don't really see the need for the discussion of dynamic vs static friction. I don't see how it adds to the discussion. In both static and dynamic frictional states there will be horizontal forces acting on the skin and whatever the skin is touching. It's the horizontal force that is probably causing the damage. The skin will probably be damaged with both static and dynamic friction. I don't think the treatment will be changed whether it is static or dynamic.

    Thoughts?
    Eric
     
  11. To avoid confusion, and increase clarity, I think it is better to get a definition of friction from a physics textbook.

    Friction is the force component acting parallel to the surface of an object when an object moves or attempts to move along a surface (Cutnell JD, Johnson KW: Physics. (3rd ed). John Wiley & Sons, New York, 1995, p. 106).

    Frictional force comes in two types: static frictional force and kinetic frictional force (also known as sliding frictional force).

    The maximum static frictional force is dependent on the magnitude of the normal force (i.e. force which acts perpendicular to the object's surface) and not on the surface area of contact between the object and the surface.

    The kinetic frictional force is also independent on the contact area between the object and the surface, it is independent of the speed of the sliding motion, if the speed is small and is dependent on the magnitude of the frictional force ((3rd ed). John Wiley & Sons, New York, 1995, p. 106-9).

    Also, we did have an excellent discussion on this subject earlier this year on Podiatry Arena: Blisters and Taping

    Can't agree with you here, Rebecca. I believe that rubbing one object on another object, which causes kinetic frictional forces (what you call dynamic frictional forces) do play a large part in the production of "friction blisters". High frictional forces over time increase local tissue temperature which may lead to increased risk of delamination of skin and blistering. You seem to be implying here in your website that only static frictional forces cause blistering but I really don't see any data here which supports your hypothesis.

    If only static frictional forces are important in the production of "friction blisters" and the external skin heat generating mechanism of increased kinetic frictional forces are not important then why do athletes tend to get more blisters on their feet in hot climate/hot weather?

    Also, why did one study show that "a temperature increase of 4ºC will speed up the rate of blister formation by 50 percent" (Hall M, Schurr DG, Zimmerman MB, et al. Plantar foot surface temperatures with use of insoles. Iowa Orthop J 2004;24:72-5)?

    When I rub my finger back and forth across the palm of my hand, my finger and palm of my hand get hotter because of kinetic frictional forces. However, if I just wiggle my finger back and forth on one spot of the palm of my hand (not moving it so only static frictional forces are occurring), I can detect no increase in skin temperature either under my finger or on that one spot of my palm.

    Also, rubbing two sticks together forcefully, which causes increased heat due to kinetic frictional forces, not static frictional forces, will generate enough heat to start a fire. Certainly heat generated by repetitive rubbing the shoe on a sock or the sock on the skin can increase the heat of the skin enough to increase the risk of blister formation, versus having no increase in skin temperature.

    Now since research has shown that increased temperature does play a role in increased friction blister formation in feet, and kinetic frictional forces are known to cause very significant increases in local temperatures in the objects being rubbed back and forth, how can you now conclude that "Rubbing doesn’t cause blisters, but it can damage the skin."?? Do you have any research evidence to support this statement? I would be interested in reading any scientific research that shows that the kinetic frictional forces and increased local skin temperatures caused by "rubbing" does not lead, at least in part, to increased friction blister formation.
     
  12. Asher

    Asher Well-Known Member

    Hi Eric,

    If you believe shear can be damaging to the skin, then static friction is important because it determines peak shear.

    What do you mean by horizontal forces? I assume you refer to shear, in which case, I'd repeat my previous sentence.

    Yes, the skin can be damaged in both situations. But:

    a) If you adhered a protective layer to the skin (eg: dressing / tape) and it did not change the COF, then shear would be unchanged and shear injury (eg: a blister which is a delamination within the stratum spinosum) would not be prevented. What would be prevented is the ability of the dynamic friction state to abrade the skin (rub of layers from the outermost stratum corneum, progressing deeper with continued injuring force).

    b) A state of dynamic friction can prevent skin injury if the COF is low (eg: lubricants)
    [/QUOTE]

    What do you think?

    Rebecca
     
  13. Asher

    Asher Well-Known Member

    Hi Kevin,

    I’m not sure we share the same conclusion of the 'Blisters and Taping' thread. Just because heat has been found to be associated with higher incidence of blister formation, doesn’t mean heat caused the blister by way of thermal burn. An alternative reasoning could be that heat causes increased perspiration which increased friction coefficients, which increase the duration of static friction, which increases shear damage (Nacht et al, 1981; Naylor, 1955).

    But you are quite right, we need to see the research:

    First there was Naylor in 1955 that suggested friction blisters are not a burn. In his experimental blister research, Naylor compared blister rates at two rubbing speeds - the faster rubbing speed did not cause blisters to form any quicker than the slower rubbing speed. Separately, he compared two materials that provided the rubbing force that differed in thermoconductivity (one had the ability to absorb heat away from the skin). No difference in blistering was found.

    In 1973, Comaish ruled out the potential causes of wear, heat, enzymes, pressure, stretching and ischaemia to conclude blisters were a mechanical tear within the epidermis.

    Knapik et al (1995) did a literature review and state “Skin temperature appears to be a minor factor in blister formation. Blisters form somewhat more rapidly when the skin temperature is higher but blisters also occur when the skin temperature is low. In experimental rubbing studies, local heat is produced and skin temperatures have been reported between 41 degrees Celsius and 50 degrees Celsius. However, friction blisters do not resemble second degree thermal burns either clinically or histologically.”

    And Hashmi et al (2013) concluded that the temperature rise associated with blistering is a result of the blister (inflammatory response), it's not causative. (Hashmi, 2013).

    Rebecca

    - Akers, WA, Sulzberger MB. 1972. The Friction Blister. Military Medicine. 137:1-7.
    - Comaish, JS. 1973. Epidermal Fatigue as a Cause of Friction Blisters. The Lancet. Jan 13: 81-83.
    - Hashmi, F, Richards, BS, Forghany, S, Hatton, AL and Nester, CJ. 2013. The Formation of Friction Blisters on the Foot: The Development of a Laboratory-Based Blister Creation Model. Skin Research and Technology. 19: e479-e489.
    - Knapik, JJ, Reynolds, K, Duplantis, KL and Jones, BH. 1995. Friction blisters – pathophysiology, prevention and treatment. Sports Medicine. 20 (3): 136-147.
    - Nacht, S, Close, J, Yeung, D and Gans, EH. 1981. Skin friction coefficient: changes induced by skin hydration and emollient application and correlation with perceived skin feel. Journal of the Society of Cosmetic Chemists. 32 (March-April): 55-65.
    - Naylor, P. 1955. Experimental friction blisters. British Journal of Dermatology. 67: 327 – 42.
    - Naylor, P. 1955. The skin surface and friction. British Journal of Dermatology. 67: 239 – 48.
     
  14. Rebecca:

    Any time you propose a theory to explain a phenomenon, then your theory should take into account all experimental findings, not just some of them. According to your theory published on your website you state:

    As I stated before, experimental findings showed that "a temperature increase of 4ºC will speed up the rate of blister formation by 50 percent" (Hall M, Schurr DG, Zimmerman MB, et al. Plantar foot surface temperatures with use of insoles. Iowa Orthop J 2004;24:72-5). Since rubbing causes increased heat and since blisters are 50% more likely to form with even a small 4ºC increase in temperature, don't you think that a 10ºC increase in temperature would lead to an even greater likelihood of friction blister formation?

    There is also the widely noticed, anecdotal findings that blistering in shoes is created more in hot weather than in cold weather. From my personal experiences of running for over 40 years in very hot weather to very cold weather, nearly all the blisters I ever got on my feet were when running in very hot weather, never in cold weather

    Tell me how your theory of blister formation incorporates these two observations that blisters are more likely to form when the temperature is increased. Are you saying that the local heat produced that the skin of the foot rubbing on a sock or shoe creating an increased kinetic frictional force has absolutely no effect in producing friction blisters in feet when you make the claim: "Rubbing doesn’t cause blisters, but it can damage the skin."?

    In other words, are you saying that a local increase in skin temperature has nothing to do with the production of friction blisters in feet?

    The reason I ask, is because my knowledge of physics and thermal effects on body tissues leads me to believe that local temperature increases in tissues will alter the mechanical characteristics of the viscoelastic structures of the human body, skin being one of them.
     
  15. Asher

    Asher Well-Known Member

    Hi Kevin,

    Respectfully Kevin, I thought I just did. What are your comments on the array of evidence I provided.

    It's not my theory Kevin, I didn't come up with this. And it's not new (Naylor, 1955). And yes, I'm saying it's not the heat produced by dynamic (kinetic) friction that causes blisters by way of thermal burn.

    Yes, but not because it burns the skin. Because it increases the COF via increased perspiration which leads to a higher shear peak due to a prolonged state of static friction.


    “Skin temperature appears to be a minor factor in blister formation. Blisters form somewhat more rapidly when the skin temperature is higher but blisters also occur when the skin temperature is low. In experimental rubbing studies, local heat is produced and skin temperatures have been reported between 41 degrees Celsius and 50 degrees Celsius. However, friction blisters do not resemble second degree thermal burns either clinically or histologically.” Knapik et al, 1995.

    It's not my theory Kevin and it's not new. And yes, I'm saying it's not the heat produced by dynamic (kinetic) friction that causes blisters by way of thermal burn.

    The action we refer to as rubbing has a static friction component and a dynamic friction component. But we tend to think of just the dynamic part. Blisters are a mecahincal tear within the stratum spinosum layer of the epidermis caused by shear. Shear peaks in a phase of static friction and is relieved by a state of kinetic friction. Static friction determines the degree to which shear will peak.

    Yes it does, because it increases perspiration which leads to a higher coefficient of friction which prolongs a state of static friction which causes a higher peak in shear.

    Yes Kevin, you are a knowledgeable guy and you trump me 100 times over as far as physics goes. But there is a decent body of research that opposes the "blisters are a thermal burn" assumption.

    Rebecca
     
  16. Rebecca:

    This will be my last post on this subject since you are obviously irritated with me and can see my disagreement with your analysis is going nowhere. By the way, I never said "blisters are a thermal burn" unless you can find the thread where you think I said that.

    What I did say was that increased skin temperature will lead to increased risk of friction blisters developing so that skin temperature is a factor, but not the only factor in their production. Friction blisters are multifactorial and since heat is produced by kinetic frictional forces, then these "rubbing forces" are another factor that may increase the risk of friction blisters developing.

    I believe that friction blisters would be better biomechanically modeled using the idea of external and internal shearing forces and the microscopic mechanical internal skin layer trauma that these forces produce. However, I really don't have desire to discuss this subject any further at this point in time. I thought my comments would help, which they obviously didn't.

    Good luck with your website.
     
  17. Asher

    Asher Well-Known Member

    Hi Kevin,

    I extend my most sincere apologies. I totally misinterpreted you. That was my mistake. And I am definitely not irritated with you!

    So you’re thinking along the lines of this quote from Comaish (1973):

    “Fatigue and heat trauma are not mutually exclusive, they could be additive in their traumatic effect on the epidermis or there may be a direct effect of temperature on the endurance limit of the epidermis, as with inorganic materials such as steel.”

    I guess the question is how important is heat to the primary cause (mechanism of injury) of blisters.

    Would it be accurate to say that there are 3 proposed theories of blister causation:

    1) Mechanical fatigue within the prickle layer due to the shear strain associated with static friction - This is supported by the literature
    2) Mechanical fatigue within the prickle layer precipitated by localised heating of dynamic friction - Not supported by the literature
    3) A combination of the above - Plausible, requires further evidence ​

    Cheers Kevin and apologies again. I hope you can forgive my mistake.

    Rebecca
     
  18. Rebecca:

    No worries. You are obviously more knowledgeable on this subject than I am so I don't think I can be of any more help to you.

    Keep up the good work.:drinks
     
  19. blinda

    blinda MVP

    Whilst I cannot add anything of further value than that already covered in the great discussion we had in the original blisters & taping thread (from which I learnt a great deal from both Rebecca and Kevin), I think we can agree that heat and friction are most certainly significant contributing factors to the mechanical forces associated with separation of epidermal layers at the stratum spinosum.

    As I stated before, I don`t believe there is any evidence to suggest that friction, or increase in heat alone, is substantial enough to promote the production of cytokine/proteins which fill the bulla associated with second degreeand deeper burns (which occur below the epidermis). However, couple the evident increase in heat associated with inflammation and vasodilation, etc, we have to conclude that causation of epidermal blistering is multi-factoral.

    I for one, am glad that someone like Rebecca is taking the time to share her thoughts as she continues to research this fascinating area of dermatological biomechanics.:drinks

    Cheers,
    Bel
     
  20. efuller

    efuller MVP

    Yes, by horizontal forces I mean shear.

    Who is the audience that this writing is intended for? The reason that I ask is that a lay audience may not get any additional benefit from knowing there are two kinds of shear. Is it possible to reduce one kind of shear without reducing the other. Does the discussion of shear types help you make your point. Does the extra discussion help explain your treatment? One of your final points was "Friction is easier to understand when considering it as static and dynamic." However, I did not see how that made it easier to understand.

    Eric
     
  21. Asher

    Asher Well-Known Member

    Hi Eric,

    Quite simply, I'd like to fully understand how and why friction blisters form on the feet and how blister prevention strategies work. It's not as easy as it seems.

    I used to think blisters were caused by rubbing, that is, dynamic friction.

    I didn't consider that a state of static friction existed before the dynamic friction state.

    Considering peak shear is determined by the static COF, and blisters are an injury of shear, an understanding of static friction seems important and actually makes blister causation easier for me to comprehend.

    I do understand what you are saying though Eric.

    Rebecca
     
  22. Asher

    Asher Well-Known Member

    Here is some more info on heat, friction and blisters.

    I have assumed that when foot blister discussions mention heat as a causative factor, the reference is to heat’s effect on producing the moist environment that leads to an increase in COF. However, when it comes to friction blisters on the feet, heat can be relevant in several ways:

    a) The hot and humid in-shoe environment – The in-shoe environment can get hot. Hall et al (2004) measured the plantar temperature in normal subjects and found the temperature increases when walking (more particularly they sought to see if using different insole materials caused higher temperatures. They found that temperatures increased similarly for all materials used).

    An increased temperature causes increased perspiration. This perspiration provides a ‘moist’ environment (Naylor, 1955) and a moist environment (neither very wet nor very dry) is known to increase friction coefficients (Naylor, 1955; Akers and Sulzberger, 1972; Nacht et al 1981) which increases blister incidence (Sulzberger et al, 1966; Akers, 1985) by way of shear force (Comaish, 1973). As a result, the reduction of COF is the aim of many blister management strategies (Akers, 1977; Knapik et al, 1995; Knapik et al, 1998; Carlson, 2006; Polliack and Scheinberg, 2006; Herring and Richie, 1990; Carlson 2011).

    b) The inflammatory process that occurs with blister development – Inflammation increases skin temperature. Hashmi et al (2013) aimed to understand surface vasodilation due to inflammation in response to the frictional force applied to the posterior heel. They documented temperature increases from baseline to blister formation and temperature reductions for 5.5 hours afterwards.

    c) Blisters are more common in warmer conditions than colder conditions - Griffin et al (1969) compared friction blister formation on monkey palms and soles in an arctic chamber at 14 degrees Celsius, a tropical chamber at 46 degrees Celsius and a “normal” environment at 30 degrees Celsius. It took a longer time for friction blister formation on chilled sites and shorter time on warm skin than on normal skin temperature sites.

    Kiistala’s (1969) study on suction blisters found a 50% faster blistering rate with a 4 degree increase in temperature. This might be applied to friction blisters, not in regard to the epidermal injury but in blister filling time. [There are two independent stages of blister development a) the intra-epidermal split; b) filling with fluid (Naylor, 1955; Sulzberger et al, 1966)].

    d) The act of rubbing produces heat – The study quoted by Richie (2010) that demonstrated “a temperature increase of 4 degrees Celsius will speed up the rate of blister formation by 50%” was by Kiistala (1972) and is actually a study of suction blisters, not friction blisters. As heat is not imparted to the skin surface by way of dynamic friction for the formation of suction blisters to form, these results cannot be applied to this theory of heat’s relevance. But they could be relevant as described above in regard to blister filling time.

    The following hypothesis was put forward by Kevin in the blisters and taping thread (post #62):

    “The build up of increased temperature at the stratum spinosum, which is directly caused by the dynamic frictional forces at the superficial skin surface, help weaken the molecular bonds of the stratum spinosum. At normal skin temperatures, these molecular bonds are able to prevent low magnitude or low frequency dynamic shearing forces from shearing the stratum spinosum skin layer apart and causing friction blisters. However, at higher skin termperatures, these molecular bonds weaken which then more easily allows dynamic shearing forces at the skin surface to separate the stratum spinosum, which, in turn, leads to increased frequency of friction blister formation.”​

    Comaish (1973) considered friction blisters from an engineering perspective to determine causative factors. He concluded that mechanical fatigue within the epidermis is the main factor causing blisters, but considers the additional effect of heat resulting from friction:
    “Fatigue and heat trauma are not mutually exclusive, they could be additive in their traumatic effect on the epidermis or there may be a direct effect of temperature on the endurance limit of epidermis, as with inorganic materials such as steel.”​

    Naylor (1955: Experimental Friction Blisters) questions the involvement of heat in friction blister formation:

    “If a rise in temperature at the skin surface were responsible for the damage to the prickle cells, a silver friction head which has a high thermal conductivity should afford protection to the skin compared with polythene, which has a low thermal conductivity. The results show that at comparable frictional forces, silver and polythene were equally damaging.

    Rubbing the skin at an increased speed should produce higher local rises in temperature by producing more heat and allowing less time for its dissipation between successive rubs. The results show that a 50% increase in the speed of the friction head produces no increase of epidermal damage at comparable frictional forces.

    Although no attempt has been made to measure directly any rise of temperature at the skin surface caused by the friction, these two series of experiments make local rise of temperature, as a cause of prickle cell necrosis, appear unlikely.”​

    And Hashmi et al (2013) produced experimental posterior heel blisters and measured temperature before, during and after blister formation. They sought to minimise the effect of heat resulting from friction as they assessed the inflammatory response in blister development.

    “We assumed that heat and temperature change generated by pure surface friction was short lived, ie: dissipated within a few seconds. This was visually apparent on live thermal imaging footage during pilot testing. Since the skin temperature increased after repeated applications of load it is reasonable to assume that a physiological inflammatory response was initiated and responsible for the recorded skin temperature increases. This demonstrates that our method quantified the pre- and post-blister physiological inflammatory changes that occur in response to the external loads. Also, that these temperature changes were not due to superficial frictional heat nor changes in environmental temperature (for up to 30 mins post-blister).”​

    If heat transfer from the skin surface to the stratum spinosum is a major factor in blister development, one would expect the thicker corneum of the soles and palms would afford a level of blister protection. In fact, a thick corneum and adhered deeper structures are requisites for blister formation (Naylor, 1955; Akers and Sulzberger, 1972). Sulzberger et al (1966) was best placed to assess this potential protective function as they tested many sites on the body (back, buttocks, shins, forearms, upper arms, thighs, palms, and soles). Unfortunately, they did not present any data or make any comment on this aspect. It is known that there is a delay in blister formation becoming clinically apparent where the corneum is thick (Naylor, 1955). This is compared to a blister roof on ‘thin and loose’ skin that is less resistant to continued frictional forces and tends to shear off in a single rub (Naylor, 1955, Sulzberger et al, 1966).

    Although it is thoroughly plausible, I don’t think it can be said that research to date supports the theory that local surface heat generated by dynamic friction is a significant factor in blister formation. Perhaps there is other research I'm not aware of.

    All experimental friction blister studies have used “rubbing” as the blister generator. This involves both static and dynamic friction components. Conceptually, shear peaks when there is a state of static friction. Static coefficients of friction are (almost) always higher than dynamic coefficients of friction. Heat is not a significant factor when there is a state of static friction. Conversely, heat generation is an obvious result of a state of dynamic friction (when there is a high COF). Producing blisters using only static friction versus standard “rubbing’’ procedures could be revealing.

    Any thoughts?

    Rebecca
     
  23. efuller

    efuller MVP



    from Wikipeia
    The Coulomb friction F_\mathrm{f}\, may take any value from zero up to \mu F_\mathrm{n}\,, and the direction of the frictional force against a surface is opposite to the motion that surface would experience in the absence of friction. Thus, in the static case, the frictional force is exactly what it must be in order to prevent motion between the surfaces; it balances the net force tending to cause such motion. In this case, rather than providing an estimate of the actual frictional force, the Coulomb approximation provides a threshold value for this force, above which motion would commence. This maximum force is known as traction.

    Here is some theoretical thought on static versus dynamic. Think of the box on the floor. You apply a horizontal force, it doesn't move and it doesn't move. the frictional force is equal to the applied horizontal force. (It has to be because F = ma and a = 0) Now add some more horizontal force. Still not moving, the frictional force is bigger, but not bigger than the coefficient of friction. Add, some more horizontal force and it does start to move. If the box were on a table and you had a rope tied to it and the other end of the rope was wound around a pulley so that the other end of the rope could have a tray attached to it. In that tray you could put some weights. So, you keep adding weights into the tray and when the weights create a larger force that the static coefficient of friction the box will start to move. Since the dynamic coefficient of friction is less than he static the box will accelerate under the force from the weights. If the coeficient of friction did not change from static to dynamic the box would move at constant velocity. The shear force is the resistance to sliding of the box. The box doesn't know the difference between static and dynamic force. It just knows that force is applied.

    So, now lets look at the skin and make the assumption that at some value of shear force the stuff that it holding the two layers of skin together breaks and you get a blister. To get a blister the breaking point would probably have to be below the static coefficient of friction. If you were to add some lubricant that lowered the static coefficient of friction then you might be able to keep the shear force below the breaking point of the layers of skin. If, with the lubricant, your dynamic coefficient of friction is greater than the breaking point you still probably going to get blisters. (dependent on velocity of motion seen.) So that's all theoretical and you are welcome to apply it to the research.

    Eric
     
  24. Asher

    Asher Well-Known Member

    Thanks for this Eric, I appreciate it.

    I’m not sure I’m with your here when you say “The shear force is the resistance to sliding of the box. The box doesn't know the difference between static and dynamic force. It just knows that force is applied.”

    The way I understand it is the movement force is at the top of the box, the force resisting movement of the box along the table is the frictional force (which is a combination of pressure and the COF between the two surfaces). And shear is what’s going on in between. It is an internal force that occurs between layers within the box - I guess it’s the force that resists deformation of the box.

    The box will deform (shear) more when the movement force acting at the top of the box exceeds a high frictional force at the bottom. Conversely, the box will deform (shear) less when the movement force acting at the top of the box exceeds a low frictional force at the bottom. In the first instance, a state of static friction lasts longer because of the high frictional force and there is more chance of the deformation reaching a blister-causing level. In the second instance, a state of static friction is shorter because of the low frictional force and there is less chance of the deformation reaching a blister-causing level.

    If I understand you correctly Eric, I agree with you. I have ignored the part of dynamic friction that exists from the shear peak to the blister threshold. This dynamic friction will be blister-causing.

    [​IMG]

    Thinking in terms of blister prevention, it’s the static friction between the blister threshold and the shear peak that is important. If you negate this with an earlier onset of dynamic friction (below the blister threshold), there is no dynamic friction that is blister-causing.

    [​IMG]

    Please let me know if I misunderstand you or where I'm going wrong.

    Thanks again Eric.
    Rebecca

    PS: I just figured out how to insert images - these are two from the original post
     
    Last edited: Nov 24, 2013
  25. efuller

    efuller MVP

    So, we are doing free body diagram analysis here. The first step is to define the body. Let's define the body as the box. Gravity is pulling the box down, the table is pushing upward on the box with a force equal to that of gravity ( the accelration is zero, so the net vertical force is zero) In our diagram let's say that the rope is applying a force to the box from the left to the right. The box is not moving therefore the surface of the table is applying a horizontal force to the bottom of the box. This is the shear force between the table and the box. The shear force is different than the shear strain.

    Now we can also look at the box itself. The rope is at a distance above the table and pulling the box to the to the right. The table is applying a force to the box to the left. This will create forces within the box that have to resist the shear strain. If the box is strong/solid enough there will be no deformation of the box. If the box is flexible it will deform. This is independent of whether or not motion occurs between the bottom of the box and the table. Motion of the bottom of the box, relative to the table, will occur when the rope force exceeds the maximum static friction force. The maximum static friction force is the coefficient of friction times the normal force. The normal force, in this example, is the force of gravity acting on the box.

    In thinking about the skin, the maximum shear force that can be applied is determined by the static coefficient of friction. If your lubricant/sock/intervention reduces the static coefficient of friction it will reduce the maximum horizontal force that can be applied to the skin. In this discussion we have been making the assumption that there is a level of force at which the skin layers will separate. The theory then goes our goal is to reduce the level of peak possible force. Hopefully, it will be reduced to a level below the theoretical level at which damage occurs. The static frictional coefficient describes the maximum possible shear force because once sliding starts to occur, you have to use the dynamic coefficient which is usually less than the static coefficient.


    The surface may be static, but there may be deformation in the skin above surface. See the discussion of the box above. The deformation in the skin above may have high enough forces that the separation of the layers occurs. So, it's not dynamic friction at the skin / surface interface, but shear strain on the skin.


    Same concept here. There is a difference between frictional forces at the skin surface interface and shear deformation within the skin. However, it does appear that you got what I'm saying, but with wording that's not quite right.

    I had some issues with the diagrams, but when you quote them it's hard to see them at the same time. I have to go kick a cardboard box that's full of papers that need filing.

    Eric
     
  26. Asher

    Asher Well-Known Member

    Thank you for your explanation Eric, it sounds like we’re on the same page.

    “When discussing forces upon the surface of the skin, the terms “friction force”, “shear force” and “traction force” are, as used in the medical literature, essentially the same. The term “shear stress” is a bit different because it refers to force per unit area. The medical literature has been a little loose in the usage of these terms, but that has not caused any significant misunderstanding” (Carlson, 2011).​

    When you’re not the sharpest tool in the shed (I’m referring to myself), it doesn’t take much to cause misunderstanding!

    Rebecca
     
  27. jharrison

    jharrison Welcome New Poster

    Hi Rebecca,


    I enjoyed reading your posts, and all the following posts, and have learnt something! Thanks.
    Julie
     
  28. IntentionallyAnonymous

    IntentionallyAnonymous Welcome New Poster

    Kevin,

    I did not find your quote (regarding the increase in blister formation) in the reference you provided. Here's the link to your referenced article:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888418/

    However, I did find that same blister formation quote used by Doug Richie in this Podiatry Today article, but his reference was (Kiistala U. Dermal-epidermal separation. Ann Clin Res 1972;4:236).

    Unfortunately, I have been unable to find even the abstract to that article. Can someone dig that up for me, or perhaps find the correct article?

    I'm always interested in examining methodologies of studies with (at first glance) opposing conclusions.

    Thanks in advance for any help in finding the actual source for that claim!

    Cheers!

    Intentionally Anonymous (for now)
     
  29. Asher

    Asher Well-Known Member

    Dermal-epidermal separation. II. External factors in suction blister formation with special reference to the effect of temperature.
     
  30. alessandro costa

    alessandro costa Active Member

    THERE IS A MESS IN THIS DISCUSSION AND IT IS ALMOST IMPOSSIBLE TO COMPREND wich one is blister's cause....OMG
     
  31. alessandro costa

    alessandro costa Active Member

    As I stated before, I don`t believe there is any evidence to suggest that friction, or increase in heat alone, is substantial enough to promote the production of cytokine/proteins which fill the bulla associated with second degreeand deeper burns (which occur below the epidermis). However, couple the evident increase in heat associated with inflammation and vasodilation, etc, we have to conclude that causation of epidermal blistering is multi-factoral.

    I for one, am glad that someone like Rebecca is taking the time to share her thoughts as she continues to research this fascinating area of dermatological biomechanics.:drinks

    Cheers,
    Bel[/QUOTE]

    BLINDA how can u say that heat promote the production of cytokine/proteins wich fill the bulla associated with second degreeand deeper burns (which occur below the epidermis).??? references ? :bash:
     
  32. blinda

    blinda MVP

    I really don't understand your question.

    Maybe this post;http://www.podiatry-arena.com/podiatry-forum/showpost.php?p=292800&postcount=47 will help, or try reading the whole thread here;http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=85834 where we discussed blistering at length.....or maybe even try to rephrase your question to me, seasoned with a little courtesy.
     
  33. alessandro costa

    alessandro costa Active Member

    ok sorry I didn't want to offend you I was misunderstood.
    you wrote "heat promote the production of cytokine/proteins wich fill the bulla associated with second degreeand deeper burns (which occur below the epidermis)"
    but I can't find any reference in leterature about production of cytokine wich fill the bulla in friction blister. where did you find it out? thank you
     
  34. blinda

    blinda MVP

    No worries.

    I was referring to the original “blisters and taping” thread (which I recommend you read through) where we discussed the literature on blister formation. My comment related to the fact that blistering associated with a thermal burn is completely different to that of a blister caused through friction and shear.

    This difference is observed in the structures involved as blistering, or separation of the epidermal layers which become fluid filled, occurs at the stratum spinosum and granulosum layers in friction/shear blisters. In contrast, blistering resulting from a thermal burn occurs sub-epidermally. Classification of thermal burns are based upon the depth and effect of the injury. Here`s your reference:http://www.ncbi.nlm.nih.gov/pubmed/19200248

    My point was merely a reiteration of our previous agreement in the "blisters and taping" thread that whilst there is obviously an increase in skin temperature, heat alone is not solely responsible for the formation of the epidermal blistering observed during friction and shear stress.

    Hope that`s a bit clearer.

    Cheers,
    Bel
     
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