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Is a calcaneal spur in the plantar fascia?

Discussion in 'General Issues and Discussion Forum' started by Craig Payne, Jul 12, 2005.

  1. Bruce Williams

    Bruce Williams Well-Known Member

    To all as Ignorant as I am, here is a google searched definition of Apoptosis

    For every cell, there is a time to live and a time to die.

    There are two ways in which cells die:
    They are killed by injurious agents.
    They are induced to commit suicide.

    Death by injury
    Cells that are damaged by injury, such as by
    mechanical damage
    exposure to toxic chemicals

    undergo a characteristic series of changes:
    They (and their organelles like mitochondria) swell (because the ability of the plasma membrane to control the passage of ions and water is disrupted).
    The cell contents leak out, leading to
    inflammation of surrounding tissues.

    :)
    Bruce
     
  2. Mart

    Mart Well-Known Member

    Just wanted to add my cents worth to this; Paul is your concern regarding effects of lidocaine related to reported concerns over use to tx active TrPs?

    If so I am not sure how it may be relevent to doing a series of ankle nerve blocks to perform foot surgery, I think this may explain this apparent confusion:confused:

    cheers

    Martin
     
  3. musmed

    musmed Active Member

    Bruce

    Your definitions are correct.

    Failure of apoptosis in neutrophils is now the recognised way leukaemias commence with help from bone fibroblasts (only announced on last sunday from Melbourne)

    In Achilles tendonitis it has been found those that have the tendonititis not only have a great increase in VEGF, increased vessel growth, Alpha TNF and others they also have failed apoptosos of the tenocytes.

    Now dare I mention tensegrity (yes I did) here is the intersting part.

    When a tenocyte is placed in growth medium it along like every other cell changes shape and becomes spherical. All cell when taken out of the body (read tensegrity) they become spherical.

    If tension is the 'command' word and when not in tension the tenocyte thinks it is under 'non-tension' ie compression.

    The cell becomes spherical and start to lay down type 1 Collagen along with primitive cartilage ie it thinks it is now a chondrocyte.

    Prof Khan is studying tendinitis and spontaneous rupture of the Achilles.

    What they are seeing is areas of necrosis (U/Sound holes) but also clusters of blue staining roundish cells that should be single tenocytes. These cells are presumed to be due to the failure of apoptosis.

    Now the use of 0.5% Lignocaine and 40% glucose placed subcutaneously in 6 by 0.5ml blebs, three each side of the tendon have profound outcomes in the resolution of this cursed problem.

    It is due to apoptosis of the chondrocytes and stopping of the process of the VEGF infiltration followed by angiogenesis. Glucose causes apoptosis of the new blood vessels.

    Hope that clears up what I am hinting at. All new and very exciting.

    Regards

    Paul C
     
  4. musmed

    musmed Active Member

    Mark

    Me thinks new information that is out there is scarring you.

    I suggest more reading and less visits to the "Yuendumu".

    Signing off

    Paul C
     
  5. Stanley

    Stanley Well-Known Member

    Paul,

    A tendon is a tension element, and cartilage is not a tension element. The tenocyte under tension acts as a tenocyte, and when it is not under compression acts as a chondrocyte. Why not just put the cells under continuous tension to make it act like it should?

    Regards,

    Stanley

    If the tenocyte under tension becomes a
     
  6. Stanley

    Stanley Well-Known Member

    Paul,

    A tendon is a tension element, and cartilage is not a tension element. The tenocyte under tension acts as a tenocyte, and when it is not under compression acts as a chondrocyte. Why not just put the cells under continuous tension to make it act like it should?

    Regards,

    Stanley
     
  7. musmed

    musmed Active Member

    Stanley

    From What Prof Khan said in the lectures that this is what they are aiming to do ut how is the question.

    Paul
     
  8. kevin miller

    kevin miller Active Member

    Hello all,

    I have been following this thread. It, like most of the simple initial questions, has blossomed (exploded?) into a debate.

    KK, I am not sure that everyone is clear on what you are saying. Perhaps you might back up a few posts, because earlier in the debate you made a very accurate statement that seems to have twisted somehow. You wrote that in your surgeries that it appeared that the fascia was just plantar to the spurs. After dissecting well over 100 feet in the past two years, I concur. I have never seen a spur originate from the plantar aponeurosis. They are all associated with the underlying musculature. I think what is missing is a biomechanical explanation of what is producing the traction which pulls the fibers of Sharpey free and allows osteocytes to “leak”. There is not enough room or time to go through an extended explanation, but briefly, this is the pattern that I have seen:

    People with the spurs have either pronation or worse that produces abduction of the Mets. I.e., they deviate laterally of their normal position, in line with the calcaneus. (To clarify, a line through the calcaneus, parallel to a flat substrate/floor, should be parallel to a similar line through the Mets. Don't quote me on this, but it was either Elftman or Manter that noted this over 50 years ago.)

    Abduction of the Mets along with the associated decrease in radius of the medial arch curvature produces more tension on the medial tubercle of the calcaneus than the lateral side. The same physiology/mechanics that produces enthesopathies elsewhere in the body apply here. Fascial insertions are not where we see these, it is tendon insertion where they form. Certainly, there are a number of possible origins, other than the Plantar Ap., that fit the normal etiology.

    Regards to all,
    Kevin M
     
  9. Quasar

    Quasar Member

    [Check4SPAM] RE: URL Attempt

    There was some years ago a longitudinal study of heel spurs conducted by Steve Smith in Chicago the conclusion of which was that spurs were delayed healing microfractures due to stressing over time of the plantar calcaneal cortex. The spur is essentially the bone callus.
     
    Last edited by a moderator: Jun 11, 2009
  10. NewsBot

    NewsBot The Admin that posts the news.

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  11. NewsBot

    NewsBot The Admin that posts the news.

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    Calcaneal spurs: Examining etiology using prehistoric skeletal remains to understand present day heel pain.
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  17. Petcu Daniel

    Petcu Daniel Well-Known Member

    Yesterday I've read "(again) Eric Fuller's "The Windlass Mechanism of the Foot" where "high tension in the fascia could cause a periosteal lifting at its insertion on the calcaneus and bony healing could cause the growth of the spur that is seen in this location". If this is happening "less frequently, within the PF and at the insertion site of the short plantar ligament" how the windlass model will change the prescription of foot orthosis (as in the Eric's article "an increased supination moment from some other source" could be a solution) ?
    And if the "location is at "at the insertion sites of abductor digiti minimi and flexor digitorum brevis muscles", increasing the loading on lateral forefoot will lead to an increase of the tension in these muscles, isn't it ?
    Daniel
     
    Last edited: Jul 16, 2015
  18. drhunt1

    drhunt1 Well-Known Member

    I've read this thread with some interest. First, let me state that I probably perform more of these types of surgeries than anyone here in central California. The plantar exostoses is NOT part of the plantar fascia; it is directly above the origin. Further, the "spur" is not the source of the pain. Plantar heel pain, especially when the patient complains of severe pain when arising in the morning, or after they remain NWB during the day is due to periostitis...or inflammation of the periosteum at the origin of the plantar fascia. The "spur" is a secondary finding and a result of chronic traction of the plantar fascia on the periosteum. As we know, the periosteum is not only the nerve supply to the bone, it also has osteogenic cells, (osteoblasts) associated with it. This is not true plantar fasciitis, which effects runners typically and is symptomatic in the plantar aspect of the midfoot. The proper term for this malady would/could therefore be: Acute (or chronic) plantar calcaneal periostitis. I haven't removed the planter exostoses in decades, but rather just remove a ~2.5 cm portion of the plantar fascia from the origin. By removing the exostoses, one has to "denude" the bone of the periosteum, which only increases post-op pain symptoms as the body has to repair the periosteal deficit. By leaving the "spur" intact, it is more often then not that the patient states they felt less pain the day after surgery than the day before. Healing time is quicker as well.
     
  19. efuller

    efuller MVP

    In my article I cited a study that showed decreased tension in the fascia of cadavers with lateral wedging. In my article I presented my rationale for STJ pronation increasing the distance between the origin and insertion of the plantar fascia. The theoretical implication is that pronation of the STJ will tend to increase tension in the plantar fascia. Using the windlass model things that would decrease tension on the plantar fascia are increased lateral forefoot loading (= decreased medial forefoot loading) and increased supination moment of the STJ. The increased supination moment may not directly change foot position, but should slow the velocity of pronation. If the plantar fascia is stopping pronation, a lower pronation velocity would lead to a lower impulse (force x time) applied to the fascia. I've said it before, it is not the position of the joints, but the forces applied to the anatomical structures that is the cause of pathology.

    The orthotic prescription would depend on the source of pronation moment that is causing the STJ pronation. In some feet the source of the moment is the peroneal muscles and in other feet it is ground reaction force. I believe that the source of pronation moment is determined by STJ axis position. So, when you see a medially deviated STJ axis you should add supination moment with your orthotic prescription. (medial heel skive, inverted cast) When you see a lateral deviated STJ axis you should work on shift the weight to the lateral forefoot (which should reduce the peroneal activity and reduce tension in the fascia.)

    Eric
     
  20. Stanley

    Stanley Well-Known Member

    I agree that the plantar exostosis is not attached to the plantar fascia.
    I learned this in 1988 when visiting a student of mine who did minimal incision surgery. He showed me the spur and then he showed me the plantar fascia. Prior to that I just assumed they were connected and when I performed surgery, I assumed that I cut the plantar fascia while I was exposing the exostosis.

    I partly agree with the spur is not the source of the pain. If you read the MRI reports, sometimes you will find bone marrow edema. This does not always resolve with corticosteroids. Removal of the spur will allow the fluid within the bone to drain out.

    Regards,
    Stanley
     
  21. Petcu Daniel

    Petcu Daniel Well-Known Member

    And, if the location is at "at the insertion sites of abductor digiti minimi and flexor digitorum brevis muscles" ?
    Daniel
     
  22. efuller

    efuller MVP

    Then, the windlass model of the first ray is not relevant. It is interesting to think about whether the muscles can develop enough tension to cause an enthesiopathy. Is it just the passive structures or can you have problems at the origin/insertion caused by muscle tension.

    Sarafian described 3 slips of the plantar fascia. As I recall there was some variation in the lateral slip. I don't remember the percentages off the top of my head. High lateral column bending moments would tend to increase tension in the lateral slip. An orthotic that shifted the load from the 5th metatarsal head to the shaft of the metatarsal would reduce the lateral forefoot bending moment. In tissue stress, you just model the tissue and think about how to reduce load on it.

    Eric
     
  23. drhunt1

    drhunt1 Well-Known Member

    There are two slips to the plantar fascia...the medial and the lateral band, (and a central band for the nit pickers).

    http://media-cache-ec0.pinimg.com/736x/c6/2c/89/c62c8969ca027321a2ceb1f3df6a9706.jpg

    If excessive traction is produced by the medial slip, eg., from over elongation of the medial column, then I have no idea how a lateral valgus extension would address this problem. A valgus wedge should actually increase medial load, not decrease it, and thus impart greater GRF to this structure. Simple OTC arch supports can be quite effective in treating this problem for the majority of patients.
     
  24. Petcu Daniel

    Petcu Daniel Well-Known Member

    Kogler's article could give some explanations: http://www.researchgate.net/publica..._wedges_on_loading_of_the_plantar_aponeurosis
    Daniel
     
  25. Petcu Daniel

    Petcu Daniel Well-Known Member

    Are you thinking at the reducing of the moment arm of the ground reaction force to the origin of the muscles (or the site of the spur )?
    Thanks,
    Daniel
     
    Last edited: Jul 18, 2015
  26. efuller

    efuller MVP

    I'm thinking of reducing the moment arm acting on the lateral column. If you shift ground reactive force from the fifth met head to the fifth met shaft, ground reaction force will have a shorter lever arm to dorsiflex the forefoot on the rearfoot. The plantar structures, including the muscles you mentioned, will need less tension to prevent dorsiflexion of the forefoot on the rearfoot.

    Eric
     
  27. efuller

    efuller MVP

    This is a good example of what can go wrong when you look at position as opposed forces. You have to understand the cause of "elongation of the medial column.h" Actually the medial column does not even have to lengthen. Ground reaction force on the first metatarsal head will attempt to dorsiflex the metatarsal. The plantar fascia is one of the anatomical structures that will resist that dorsiflexion. The greater the force on the first metatarsal head, the greater the force there will be in the plantar fascia.

    When you look at pressure plots of feet at rest, you will see some feet that have a lot more force under the medial forefoot when compared to the lateral forefoot. John Weed used to describe part of his exam where he would try and run his fingers under both the medial and lateral part of the foot to assess for this difference in load. In those feet that have little load under the lateral forefoot a valgus wedge can increase the load under the lateral forefoot. If you increase the load on the lateral forefoot, it must decrease somewhere else. The total force on the foot is body weight. The force on the heel, medial forefoot, and lateral forefoot have to add up to body weight. So, when medial forefoot force decreases, tension in the platnar fascia will decrease.

    This is what was seen in this article Kogler GF, Solomonidis SE, Paul JP The influence of medial and lateral wedges on the loading of the plantar aponeurosis. Proceedings from the IXth World Congress of the International Society of Prosthetics and Orthotics. Amsterdam: International Society of Prosthetics and Orthotics.

    Eric
     
  28. NewsBot

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  29. drhunt1

    drhunt1 Well-Known Member

    Thanks, Daniel...but the problem with the article, at least in my view, is that Kogler doesn't describe what type of feet he's addressing. To make a blanket statement that medial or lateral additions do this or that, without describing the type of foot that the patient had prior to these additions is not complete. I have successfully treated plantar fasciitis with medial forefoot extensions on a number of patients...but acoording to Kogler, I should've made them worse.
     
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    This is good:

    The plantar calcaneal spur: a review of anatomy, histology, etiology and key associations
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  34. Should be a must read by all
     
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