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Interesting discussion on thatfootsite. Any comments?
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A patient of some years had a RTA 14 months ago and sustained multiple injuries, which resulted in hospitalisation for over a year with spinal injuries. Prior to the accident he had a long-standing corn over the 1st MPJ which he had reduced every 12 weeks. His last visit was the deay before the RTA.
I visited him at home a week after he left hospital (having not received any chiropody whilst on the ward) and was surprised to note his corn was still there and as big as ever. I was always under the impression that corns form as a result of pressure and that with appropriate pressure relief, they would soon disappear - surely the philosophy behind much of the advice we offer to patients in the form of insoles, orthotics and shoe modifications.
If I was being truthful, I have only ever seen a handful of corns disappear in my patients during my professional life (nearly 30 years now) and I like to think I keep up with all new developments. I use prescription orthoses when indicated, use substantive simple insoles and always advise patients to change footwear when it obviously contributes to their foot problem. But still my success rate in curative chiropody - for corns at least - remains low.
Reading some of the online emails, one forms the opinion that other colleagus achieve high rates of success in clearing these lesions. Given that my patient was non-weightbearing for 13 months - and his corn recurred regardless - what current measurement of efficacy does the profession employ in relation to this troublesome condition?
Can corns really be "cured" and if so, what is the definitive scientific method of eradicating them?
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I can't help with a "scientific method" because I don't think we have one.
Many of my biomech patients present with plantar callous or HD's. Often these take 3 to 6 months to resolve once custom orthoses have been fitted, but resolve they do (usually).
There seems to be a definite correlation between the duration of the lesion, the age and activity level of the patient, and the histiological characteristics of the lesion (ie how deep is it, is it neuro or neuro-vascular, is there a loss of underlying adipose tissue etc).
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Thank you for the speedy replies, however I don't think we are much further forward. Aside from the pathological changes that take place in the skin following a period of irritation or trauma, there will be many external factors that will influence whether or not a corn returns after treatment.
David, you mention some of these and I would suggest that the clinician must consider them filly when determining their management plan. If we assume that we are dealing with compliant patients for a moment and the external factors which contribute to the trauma are negated (such as in the instance of my RTA patient), we might expect the lesion to disappear within a reasonably short timeframe (3 months?). But that is rarely the case.
Are the histological changes that take place in the skin during the early stages of HD development irreversible? Or is it simply that once trauma occurs and a HD forms, the patient never really rests the foot sufficiently for the underlying inflammatory response to diminish sufficiently to allow the skin growth to return to normal?
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You said
"Are the histological changes that take place in the skin during the early stages of HD development irreversible? Or is it simply that once trauma occurs and a HD forms, the patient never really rests the foot sufficiently for the underlying inflamatory response to diminish sufficiently to allow the skin growth to return to normal?"
Not as simple as that I don't think. Each case is different. Certainly I would contend that histological changes are reversable in some patients. However, I believe there are simply too many variables for us to be able to present a clear-cut algorythmn of how to cure a corn.
Manesty (Forster) did some work with electrosurgery on neurovascular lesions a few years ago. The results were very good in some patients, but not in others. In fact I worked with Manesty and provided biomech correction for chronic plantar lesions which she removed using electrosurgery. Again, the results were hit-and-miss. My impression at the time was that we were not influencing certain variables, which was why some patients did not improve, or improve for very long.
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Yes I am familiar with this work and have used electrosurgery for a number of years, when appropriate. Without digressing too much I would only add that electrosurgery has its uses in a very limited number of patients and is not a panacea on its own. If mechanical stress is ther underlying cause, removing the corn by excision, electrosurgery, CO2 laser, or topical keratolytics, without addressing the mechanical problem, will be a complete waste of time.
On the other hand, my son plays classical guitar and had done for many years. As a result he has 4 corns on the tips of his left hand where he holds down the strings against the fretboard. This is essential for him to play - without these keratoses being present, he could only play for 20 mins or so at a time. Last year he took a gap year and didn't play for six months. When he returned home his fingers had returned to normal with no evidence of the keratoses.
How so?
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"If mechanical stress is ther underlying cause, removing the corn by excision, electrosurgery, CO2 laser, or topical keratolytics, without addressing the mechanical problem, will be a complete waste of time."
Agreed. What I'm really saying is that there are many additional variables, probably different for each patient.
"As a result he has 4 corns on the tips of his left hand where he holds down the strings against the fretboard. This is essential for him to play - without these keratoses being present, he could only play for 20 mins or so at a time. Last year he took a gap year and didn't play for six months. When he returned home his fingers had returned to normal with no evidence of the keratoses. How so?"
His tissue tolerence to the mechanical exciting factor which caused the keratoses in the first place, allows the fingers to return to normal within a few months. I see the same when I canoe. I build a callous in the Summer, which clears within weeks during the Winter.
There is little published work on this in relation to feet, but it is a well-documented fact that biological tissue can and does alter in response to loading. Think of the thickened arm-bones by which the archers on Henry 8th's flagship The Mary Rose, were identified.
I don't think callousities or corns are much different. Remove the exciting factor (pressure) and they should clear, provided you've dealt with all the other variables which combine to keep the lesion in place. I think a few of these are: skin-type, age of patient, amount and duration of pressure, histological changes (we already mentioned that), the effect regular paring has (which we don't really know, I don't think).
We could also hypothesise about how regular paring of a lesion, combined with inadequate pressure relief, may actually cause a corn to worsen, but again - we don't have the research to back this up, or refute it.
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"We could also hypothesise about how regular paring of a lesion, combined with inadequate pressure relief, may actually cause a corn to worsen, but again - we don't have the research to back this up, or refute it."
I believe Jim Woodburn has done some work in this direction with rheumatology patients and has demonstrated that regular debridement of lesions in diabetic patients is less effective than providing adequate cushioning.
I suppose we have to consider whether corns or callosities are abnormal? I would contest that they are not - just the body's defence mechanism against adverse pressure or trauma. Which begs the question why we, as a profession, are dedicated to removing callosities when they themselves are not painful in many cases.
David, what is the pathological mechanism that initiates increased keratinisation. Is it the release of a chemical or enzyme from damaged or inflamed tissue - if so what is it called?
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Without looking it up I couldn't say what the current thought on which chemical or enzyme it is off the top of my head. Not that important either IMO, because I'm pretty sure we don't have a definitive "one enzyme does this" kind of answer. Happy to be corrected on that tho.
"Neales" 6th Ed seems not to know (just had a quick look). Mind you, Neales was pushing the idea that mepivacaine is a vaso-constrictor (it is too, in rat spinal-cord, and some mucous membrane, but not in feet) until recently, so I don't find it that good as a source of info.
What they do mention is physiological callous as opposed to pathological callous, which I guess may be the dividing line between do we treat or do we leave well alone?
I agree that corns and callous are natural body defenses, but against what?
Footwear, certainly, and walking on hard,flat surfaces, that too. How about throwing in the fact that biologically we start to age at around 30 years of age or so?
We haven't developed for life on a hard, flat surface, or to wear shoes either.
Our lower limb makeup is over a million years old.
Do a Google on Turkana Boy, check out the leg fossil bones.
This is where things become interesting. Why, for instance are the medial ankle ligaments at least as strong, or stronger than the lateral ankle ligaments.
Why, when you place a foot (any foot) into STJ neutral, is it always inverted?
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I've read a number of your articles on evolutionary changes in the skeletal structure and they are very interesting and well written. I would agree that there are many factors and forces at play in the adult foot, which can often lead to pathological changes. However, I would like to stay focussed on the localised skin & tissue mechanisms that are responsible for corn and callous formation rather than the primary or contributory mechanical defects.
I've had a look through my old notes and textbooks at the weekend and have come across no mention what biochemical changes take place to stimulate keratinisation as a result of repeated minor trauma. I assumed. like you, that Donald Neale and Isobel Adams would have dealt with this in the first edition and I find it curious that even by the 6th edition, no mention of skin and tissue pathogenisis is made. Given that corns and callosities are central to much of the work that we see, don't you find this odd?
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You wrote:
"but what biochemical reaction takes place to cause hyperkeratosis? Does the inflammatory response following trauma act as a precursor which releases an enzyme stimulating cell production? Or does another mechanism take place?"
What I was trying to say in my last post was that perhaps there is no enzyme. Maybe the process is purely mechanical?
Anyway, I have a reference book (Ian - if you read this, bring the book back!) which may shed a little more light on this. If so I'll reply more fully over the next couple of days. I have a feeling though, that the initial hyperkeratosis is simply a build-up of compacted keratin which is not being allowed to slough off naturally.
An inflammatory response in the early stages would simply lead to a blister, surely?
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Thanks and I am grateful for your interest. I would have thought that there would have to some form of biochemical response at cellular level. Walter & Israel's General Pathology on acute inflammation states " Inflammation is the reaction of the vascular and supporting elements of a tissue to injury, and results in the formation of a protein-rich exudate, provided the injury has not been so severe as to destroy the area.” The functions of this fibrin rich exudate are many, but the primary function is to aid healing. Whilst I do not think this exudate is directly responsible for the stimulation of increased epidermal cell activity as found in foot lesions, perhaps something similar occurs with chronic inflammation.
However, this still doesn’t explain fully why corns recur in patients where chronic inflammation is not present, such as my RTA patient. I can see that the skin architecture may change over a period of time so that callous and corns may be considered the “norm” – and that being the case I would have to question the efficacy of many of our traditional treatments such as insoles & orthotics as well as shoe modifications. “They may not cure the corn but they could give some relief” is probably a more accurate statement to give patients instead of some of the more evangelical claims that are made.
Have we been overestimating our clinical ability in the eradication of these simple lesions?
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Very interesting discussion and threatening to exceed my limited understanding.
Being a simple soul I see only a huge number of potential influences developing into a multitude of synergies far to complex for my poor little brain to grasp.
We can't hope to fully understand the complexities of the healing process any more than we can fully understand causation. This doesn't mean that we shouldn't try but I have a real problem in accepting the word "cure".
The best we can hope for is greater understanding of process and therefore better management which makes discussions like this so valuable.
and then
We help the patient by influencing them and their environment so that optimum self healing can occur.
For what it's worth, I subscribe to the 'purely mechanical theory' and resultant altered blueprint. "Less being more" even a small irritant will prevent or delay the reversal of hyperkeratinosis.
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I would agree that the cellular response mechanism is complex and is subject to many variables, but I think it could be important enough for the clinician to give some thought to. If we could determine what biochemical changes occur when skin changes result in callus formation, we might go some way in determining if a suitable antagonist might be employed to reverse the process. Just imagine the day when, after enucleating a painful and long-standing HD, you could inject or apply an appropriate solution, confident in the knowledge that the lesion would not recur - unless off course the mechanical stresses were reintroduced and further injury occurred. I think we might be able to justify a small fee increase then!
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I have to admit defeat on this one - I can't find a reference to any enzyme/chemical which stimulates the growth of callous or the proliferation of hyperkeratosis.
I think I'll stick to my original theory.
It's all mechanical.
Last edited by Mark Russell : 23rd February 2006 at 05:27 AM.
Corns are biomechanical.What could be happening here is a plantarflexed MT or a long metatarsal.
You raise a good question regarding the use of keratolytics.I find that a once a day application of Aldara cream can help in some cases.
As for your other point:Well,yes you can "cure" a corn with surgery,but in my experience,a transfer lesion post op is rather common.You are altering the biomechanics of the foot by,say,a shortening osteotomy of a metatarsal.If this corn is a dorsal corn,an arthroplasty can help to relieve pressure points,but,again,you are changing the shape of the foot to fit into a shoe.Without the proper shoe modifications,these corns will recur.
At the risk of being argumentative (me? ), I think you pose a very interesting question, Mark. Indeed I would have to say the most fundamental question to all skin care specialists. I have chaired several debates on related topics and by far this is the one which get the greatest division and strongest argument.
There is much research on epitheliasation and although it is neoplasms which take the majority of attention there is sufficient evidence to support epithelial rates are directed by biochemistry. Triggered initially through damage to the keratin nuclear envelope (causation still unknown, all be it intermittent pressure and friction are commonly cited), enzyme type control in the blood (genetic predisposition ) results and determines local epithelial growth rates. The physical presentation (of a corn) is conical but rarely is the indentation directly over the constant resistance (i.e. as defined by the geometric centre of the bone head) more often than not it sits to the side. This cannot be by chance.
If we take a trophic ulceration pattern as a comparison. The interruption to the skin is direct and perforates straight down into the bone. This is more likely to be caused by remitting pressure whereas corns are intermittent. If we takes the effects of three dimensional movement over the corny nucleus (dreadful term), and apply Newton's Laws and the principles of moments you soon derived a corkscrew effect which takes the skin surface and twists it laterally against the bone beneath. The position of the corkscrew reaction is determined by the magnitude of reactive forces occurring around the lesion which explains why corns differ from individuals.
The base of the nucleus describes the point of greatest resistance. Traditionally corns were though to have roots or grow from the base and hence the silly term nucleus. In effect you have a compromised skin surface which is corkscrewed against a resistance during stance phase. Biochemistry does the rest and controls the rate of epithelisation and this is why there are no cures for corns.
Hydrating the skin will improve desquamation and anecdotal stories abound of people on prolonged bed rest where the corn just falls off. However put them back on their feet again and bingo the lesion return in time . Local application of hydrating creams are incredibly effective but for only a short period. Within hours of application the water content of the keratin cell increased dramatically. However within a short number of days the skin cell refuses to maintain increased water levels artificially introduced by bland or barrier creams. Hydrophilic and lypophilic preparations are limited through their penetrative properties. Ambiphilic which passes through water and fat are more likely to act as an effective vechile but are rarely used in podiatry.
This is why there is nothing in a bottle or tube yet which will rid the populous of corns. Changing creams may temporarily extend the hydration but inevitable in a short period of time hydrating creams are nil and void. Routine massage may have beneficial effects on the peripheral circulation, which is as good a reason as any to apply cream Chemical creams such as those which contain keratoplastics like salicylic acid and or lactic acid , or urea interact with the acid mantle or the long chains of the side salt linkages of the keratin molecule suffice to change the pliability of hard keratin but these creams have side effects such as uticaria and therefore have limited use in sensitive skins. The creams are more likely to be used in chthonic hyperkeratosis.
Electro surgery was a hopeful development a few years back. Basically it introduced an epidermal/ epidermal-dermal blister under the corn formation. Pressure cannot travel through fluids and the temporary relief was remarkable. Once the blister burst then the skin above would appear to fall off leaving a granulated new skin. When combined with foot orthoses initial results were encouraging but long term reports indicated a return of the original lesion. The return to the staus quo was more than likely due to the permanent pattern change in epithelialisation foot orthotic control being a complete red herring.
Silicone implants (exactly the same principle of introducing viscoelastics, sub dermally) were heralded as a successful care plan until they discovered the silicone products were unstable and crystallised. The techniques are still used today with more stable compounds. A radical procedure when compared to external silicone plugging. The lesion is enucleated and the removed keratin replaced by homogenous viscoelastic silicone material. Filled like a crack in the plaster wall the physical properties of the visco-elastic (a solid which contains both fluid and gas) acts as waterbed reducing peek points of pressure, As the skin reproduces itself in the normal 28 cycle, the plug is physically push out. Serial management of corn treated with silicone plugs physically present a conical lesion which opens up like a rose in full bloom. Hypertrophy of the keratin layer remains the same but the physical indentation of the nucleus reduces in depth. To illustrate this take a hankerhief or paper tissue and lay it flat over the hand with the thumb and forefinger set in a 0 shape. Use you index finger on the other hand to simulate a clockwise turning effect into the centre of the 0 until there is an indentation (the nucleus). Now gently tease out the overlying edges of the tissue and observe the base of the indentation rise to the horizontal. This is the physical effect of serial care using silicone plugs
Plugging over 36 weeks (usually at 6 weekly intervals ) will reduce the size (depth of the corn). Painful lesion become much less of a concern and complicated skin protrusion such as vascular or neurovascular involvement can easily be treated with protein precipitants to encourage reabsorption. Often after three or four treatment the lesion is quantitatively smaller but the client reports a return of acute symptoms. Maintaining the regime unabated results in eradication of this pain . Skin care can be used in conjunction with biomechanical care however it is unlikely maintaining middle range motion has any effect on established corny lesions (which are determined by biochemistry controlled by enzymes in the blood stream)
Relating to another post on Arena concerning old podiatry text. Books of the fist half of the twentieth century contained oodles of information on corn management whereas text appearing in the later half of the century have avoided the topic despite the volume of hard data research available in this most interesting subject so pertinent to foot physicians
You were half-way through this answer last July when you got completely distracted by a lithesome waitress with 4" canary-yellow toeless mules. Thanks for finishing it now! Going back to the point about tissue specific enzymes which stimulate keratinisation, is there/has there been any research looking at ways of influencing their behaviour?
I get the bit about the pathological changes in the skin and can see how the mechanics you describe result in changes to the physical appearance, but it's the biochemical changes that I find interesting. Would it be possible to develop a geneticly modified antagonist that can be administered to reverse the process, for example? Or an enzyme specific cream that can block the messenger mechanism and prevent an increase in the rate of keratinisation?
Be no use to guitarists though.
Kind regards
Mark
Last edited by Mark Russell : 23rd February 2006 at 05:50 PM.
>Going back to the point about tissue specific enzymes which stimulate keratinisation, is there/has there been any research looking at ways of influencing their behaviour?
The yin and ten Chaoliine throery has been around for decades now
Jarrett did a lot of work in the 60s and early 70s and published a much on what they thought controled epithelial rates. He was interested in neoplasms and I briefly spoke to him in 1980 at a conference and he said he was unaware of corn pathology but thought his work on epithelialisation would apply. There has been an explosion of research since them and if Kate Springette is a subscriber she would be more able to give chapter and verse.
Karen Roberts researched the effects of ambiphilic preparations used to take active agents such as fungacides into deeper layers of the dermis. Karen was an Edinburgh student who went on to read a doctorate in pharmacology. Bill "Tubby " Kerr did prilimentary work on water uptake in keratin cell as did Stephen Jackson in Australia. Although the studies were small and used different methodologies, the results were remarkably similar. Frank McCourt from Manchester also published his work on keratinisation about a decade or so ago.
I suppose it is my turn to pick up the tab next time we meet.
>I get the bit about the pathological changes in the skin and can see how the mechanics you describe result in changes to the physical appearance, but it's the biochemical changes that I find interesting. Would it be possible to develop a geneticly modified antagonist that can be administered to reverse the process, for example? Or an enzyme specific cream that can block the messenger mechanism and prevent an increase in the rate of keratinisation?
To achieve that objective would I suggest be like solving the enigma of the Holy Grail and make us richer than Bill Gates. Of course in the search for skin cancer cures individual antagonists have been tagged but obviously it is not an easy process and nothing yet seems to have emerged with any practical purpose for corn cures.
Moons ago I was interested in seeking a solution and got as far as discovering ambiphilic preparations. I did have a trial run with one subject ( n = 1). The young lady was the lead singer of a well known Scottish pop group that had peaked but were living in reasonable luxury on the outskirts of Glasgow. She had mild callous and I advised her to use Ungenum Merk. Both she and me were delighted with the result. I moved to Sussex and became a heath service manager for podiatry services. There I introduced Ungenum Merk as the vehicle for salicylic acid (for warts), unfortuantley I was unable to organise clinical trials.
the only 'dumb' question is the one that is not asked
I am not sure what DrPod meant, but I initially reacted very negativly to the word "corn" in the title of the thread and thought "Oh my god". This is a professional and not a lay forum - how embarrasing. Then, in a flash, the "inverted commas" were added around "corn" in the title, which makes it a bit more palatable.
I am not sure what DrPod meant, but I initially reacted very negativly to the word "corn" in the title of the thread and thought "Oh my god". This is a professional and not a lay forum - how embarrasing. Then, in a flash, the "inverted commas" were added around "corn" in the title, which makes it a bit more palatable.
I had meant to use the inverted commas around cuarable and indeed changed them on the post header as you will have noted. Could you explain why you felt embarrassed and why the term corn is so unpalatable?
Mark - I will respond as I had a couple of others PM me about it as well. They basically suggested changing the thread title (which I didn't). I think what it is, is that "corns" is layperson terminology, we are "professionals" and should be using professional terminology, which I assume is DaVinci's and DrPod's issues (...I think, but stand to be corrected).
Craig - how interesting. I guess where I come from plain speaking is very much the norm. Apologies if my terminology caused offence. Perhaps Dr Pod and DaVinci will be kind enough to elaborate on their views so that I may learn from the error of my ways.
I would not worry about. The quality of content in the thread here and at ThatFootSite speaks for itself.
I do "pull my hair out" when students speak to me about "corns", "thins the blood" etc, when we try to drill into them apropriate terminology for a healh professional to use.
Mhmm. I did think about the terminology before I started the post and came to the conclusion that “corn” was most appropriate. Why the embarrassment? Sure I could have used “heloma durum” or “lesion” but I thought that almost verged on being snobbishly elitist. Not my style. And as it has been pointed out this is a public forum and as such is a valuable resource for many seeking information about common foot disorders. It is simply a fact of life that the vast majority of the general public will know these problems as “corns”. So why confuse the issue? I suppose we have to accept that global online forums will be subject to regional variation – in a way that’s what makes them interesting – but I have to say I found the comments by the aforementioned contributors curiously condescending. But of course I may be mistaken.
I suppose we have to accept that global online forums will be subject to regional variation
You are right. I have changed the title of a number of threads to better reflect that global outlook -- (eg how many outside the UK know what the "NHS" is?). I got berated on another forum (non-podiatry) that I moderate at because I could not spell - I simply used the word "optimise" .... guess which country the person who launched into me (and made a fool of themselves) was from as they insisted it be spelt "optimize"? How come everyone from outside that country knows about these differences in spelling and those from that country do not?
I think we could be on thin ice when it comes to calling a corn, a heloma durum, as precise scientific terminology. Intracable keratoma is also a bit iffy but more acceptable since it does give a blanket term to localised hyperkeratosis with a range of dermal protrusions and localised hydration varients.
The term corn comes from the latin term, clavis (meaning nail as in hammer and nail). Nothing lay about that , nor is the term anything to be embarrassed about. Treatment of corns was developed by the Ancient Greeks and Aristotle, himself, is thought to have crafted the first skin knives (precursor of the surgical scalpel) specifically to scrape the hard skin. He certainly recognised the need for regular minute disectioning and upheld this as the only treatment available for corns and callous . Not wrong there either. Corn cuttering was a well established trade by the time of the Great Fire of London. Later corn operators became more popular term until Lowe introduced Chiropodist in the eighteenth century. Chiropodists and podiatrists are one of the same and all look to caring for foot morbidity, irrespective of the scope of practice.
There is another aspect of this discussion I would like to explore, namely the use of simple insoles in the treatment of pathological corns and callous. For many patients - especially the elderly - the use of functional orthoses is not as effective (indeed sometimes contra-indicated) as simple cushioning insoles using materials like poron or cleron. However, when calculating the most appropriate prescription, many clinicians abandon evidence based protocols in favour of practical considerations - i.e. making the insole fit the shoe rather than suit the patient.
Frequently I see patients who have simple foot problems - for example, atrophy of the plantar adipose tissue resulting in forefoot callous and corns in patients whose weight is inxs of 200lbs - being fitted with 3mm thick insoles into shoes with solid composite or leather soles. The primary consideration being something which fits into the existing footwear rather than addressing all the pathophysiological factors - weight, tissue loss, skin changes, mechanical problems & etc.
Given the previous comments regarding histological changes that take place in the skin, what considerations do colleagues make when calculating prescriptions?
> Given the previous comments regarding histological changes that take
place in the skin, what considerations do colleagues give when
calculating prescriptions?
I am of the opinion the shoe is the ultimate orthoses and provided it fits the foot comfortably, is appropriately for the activities and contains the required support for weightbearing and non weightbearing events then you can ask for little else foir the vast majority of the populus. Although conditions apply
As you know I taught "Appliances aka foot orthotics and prosthetics" for longer than the Train Robbers were incarcerated but was never happy with traditional insoles manufacture, To the uninitiated the fabricated metatarsal pads stuck to leatherboard and delighted when thermoplastic materials became available. I shall refrain from wining on but would refer anyone interested to the review of insoling "what I wrote" and had published in 1988 (The Chiropodist - UK). There I wax eloquent on the benefits of elastic memory and isobaric and isotactic effect in the serial management of prominences on the sole of the foot. Well worth the read (but of course I would say that).
When I was a manager of a diabetic unit a thousand years ago I used 6mm plastazote templates fitted cold to the shoe then left to dianomically form through wear. The devices were replaced at each treatment and I kept the originals for comparison. Good compliance from the client was surpassed only by the record of the foot contour which was then, early 80s adequate palliation for ulceration. For fun I used different colours of plastazote to help me register the stage of care.
What I was pleased to see go were the perenial tradional insoles lovingly crafted over years, but stained with contaminated exudate.
Management of chronic leasion (ie fibrous corns) I used silicone plugs and plastazote insoles in tandum and wrote up these experiences in the Chiropodist throughout the eighties.
The more cases I became involved with the more I found silione props could be used to reduce peak pressures on plantar lesions. Often this was sufficient and a plastazote insole was not necessary. In the nineties companies began to produce viscoeslastic inlays which were intellegent materials and took off the peg insoles to a new level.
In summary my findings were thermoplastic inlays were servicable, economical and as good therapeutically as bespoke traditional insloes. Patients would respond to comfort and more likely to comply when lesions showed improvement. Many podiatrists were offended at the thought bespoke accommodative insoles were outmoded.
Mark wrote "There is another aspect of this discussion I would like to explore, namely the use of simple insoles in the treatment of pathological corns and callous."
Is it a callus or a callous?
The Concise Medical Dictionary 3rd edition, says its a callus.
The origins of both words derive from the Latin word 'callum' meaning, hard skin, and are the masculine form. Middle English, from the Old French word 'cailleux', meaning hard skin. They first appeared, as a variant, in the English language in and around the 16th century, just as corn cutters were becoming popular in Europe and Britain. Practitioners flourished after the Quack Act (UK), when non-medical persons were legally able to treat open sores with almost anything and everything that made the patient better. Scathingly medical practitioners referred to these alternative persons as 'quacks' and hence the Quack Act. The popularity of non-medical skin healers was brought about directly by the plague epidemics of that time, Syphilis (large pox) and small pox were rife, as was Hansen's Disease. Lack of understanding among physics meant many doctors refused to treat patients suffering form venereal diseases and hence this sector of the population sought alternative medicine and occult remedies. Many claims corresponded to disease remission as the disease process ran its course to secondary and tertiary stages. Among this ground swell the corn cutter emerged. To them callus (singular noun) described and area of thickened skin or area of bony tissue formed during the healing of a fractured bone. The plural version was calluses.
As a verb, to callus means to produce or cause thickening of the tissues. Inflected forms of the intransitive verb would be callused, callusing, and calluses. Callous meantime is not a noun but an adjective meaning unfeeling and insensitive. When used to describe callus it means skin that has hardened and thickened. The term callous can also be used as a verb to describe the pathological processes involved in producing callus (es). The intransitive, inflective version of the verb being calloused, callousing, and callouses. All meaning to make or become callus. So as a footnote to this piece allow me to demonstrate correct usage. Do not confuse the adjective callous, as in
"Years of dealing with self centered, self opinionated, patients with self inflicted injuries has left me callous, with the thought of the callus(es) and corns on the soles of their feet."
Also, do not confuse the verb callous, which means “to make or become callous,” with the verb callus “to form or develop hard skin.”
There is quite a lot known about the biochemical control of epithelial rates and epithelial growth factors. The research is based in the area of neoplasms and there heas never been done, to the best of my knowledge, studies on on simple hyperkeratosis in humans. I am not conversant with dyskeratosis and parakeratosis however but I would suspect skin conditons like psoarisis have volumes of research. Wound epithelielisation would also contain reference to epithelial growth factors.
As far as I understand Bullough's Chaoline theory is still held as plausable. Much of the early research was done on rat's tails and more recently hairless mice.
Bulloch predates EGF albeithe wason the right lines.
The chaoline theory relates to an inverse rule where depending on the quantity of "chaoline" ( an emzyme?) in the blood will determine the epithelial growth. High concentration low epithelial growth and vice versa. The chaoline was tissue specific.
The chaoline theory relates to an inverse rule where depending on the quantity of "chaoline" ( an enzyme?) in the blood will determine the epithelial growth. High concentration low epithelial growth and vice versa. The chaoline was tissue specific.
At the risk of appearing monumentally dim (or even dumb), where can I reference Bullough’s research - and if “chaoline” has been demonstrated to be tissue specific and act in the manner you suggest, has there been any in vivo study to determine whether it can be introduced artificially into the tissues to influence cell proliferation?
I think this is a reference to Jarret's book Biochemistry and Physiology of the Skin Vol 2. New York and Oxford: Oxford University Press, 1983: 1255-95.
You should get a reference to Bullough's work there.
Jarret makes reference to an epithelial growth factor but had not isolated it by the time he published the book. They were working with interferon at the time (on cancer) and all he would say when we had a chat the EGF was likely to act in a similar manner.
Much water has passed under the bridge since then and thereis now much more know about epithelialisation. Try this site as an introduction.
Are Corns "Curable"?
Linear Mode
