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Effects of Subtalar Joint Axial Location on Midtarsal Joint Dorsiflexion Stiffness

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Kevin Kirby, Sep 28, 2014.

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    I have just finished a series of Precision Intricast newsletters on the subject of why a medially deviated subtalar joint (STJ) axis causes a decrease in midtarsal joint (MTJ) dorsiflexion stiffness (i.e. an increase in MTJ dorsiflexion compliance) and why a laterally deviated STJ axis causes an increase in MTJ stiffness. I have now lectured twice on this subject, both in Australia and at the California School of Podiatric Medicine in Oakland, and these concepts have been well-received.

    As many of us have been saying over the years, Elftman was wrong about the MTJ and it's "locking" mechanism (Elftman H: The transverse tarsal joint and its control. Clin. Orthop., 16:41-44, 1960). It is not, as has been taught in nearly podiatric medical school and every podiatric and orthopedic textbook over the past 50 years, a "crossing of the midtarsal joint axes" that are the cause of an increase in MTJ dorsiflexion stiffness with STJ supination and a "parallel nature of the midtarsal joint axes" that are the cause of an increase in MTJ dorsiflexion compliance.

    Rather, it is the increased dorsal-to-plantar cross-sectional thickness of the MTJ that causes the more supinated STJ, or laterally deviated STJ axis foot, to have increased MTJ dorsiflexion stiffness. In addition, it is the decreased dorsal-to-plantar cross-sectional thickness of the MTJ that causes the more pronated STJ, or medially deviated STJ axis foot, to have decreased MTJ dorsiflexion stiffness, or increased MTJ dorsiflexion compliance.

    In structural engineering, it is known that as the thickness of a wooden or steel beam is doubled, the bending stiffness of that beam does not double, but rather, it increases by a factor of 8. It is also known that as the thickness of a wooden or steel beam is halved, the bending stiffness of that beam does not become half of it's original value, it becomes one eighth of its original value. This is because the bending stiffness of a beam is determined by the cube of its cross-sectional thickness (i.e. it's cross-sectional thickness to the third power).

    In much the same way, the human foot's ability to resist dorsiflexion bending moments within the sagittal plane at the MTJ is largely dependent on the three- dimensional relationships of the talo-navicular joint to the calcaneo-cuboid joint which will change not only with rotational motions of the STJ, but will also change with changes in spatial locations of the STJ axis, since these changes in STJ rotational position and STJ axial location both affect the dorsal-to-plantar cross-sectional thickness of the MTJ.

    I believe that once these mechanical concepts are better comprehended, the important link between STJ rotational position,STJ spatial location and MTJ function will also be better understood In addition, I also believe, in time, these concepts will be supported by scientific research since they correlate exactly to my past three decades of observing the changes in MTJ function with changes in STJ axis spatial location during weightbearing activities.

    Here is one of the illustration I just recently made for my October 2014 Precision Intricast Newsletter titled "BIOMECHANICS OF FLATFOOT DEFORMITY – VOLUME IV". This illustration demonstrates the mechanical concepts mentioned above more clearly and, I believe, these concepts which tie STJ spatial location to MTJ function should eventually put Elftman's ill-conceived ideas of "crossing and parallel MTJ axes", which both the podiatry and orthopedic professions have accepted as gospel fact for the past half century, to rest on a permanent basis.
  2. The problem with this model as I see it is that we should observe a concomitant decrease in ab/ adduction stiffness across the MTJ as the STJ becomes more supinated because the cross-sectional area that resists these motions is reduced when the foot is supinated; conversely, we should see an increase in ab/ adduction stiffness across the MTJ as the STJ becomes more pronated since the cross-sectional area that resists these motions is increased with STJ pronation, yet this is not observed in-vivo. I've attached a slide from the presentation I gave last year in Zaragoza which I think illustrates this. Beam theory may go some way to help explain the mechanics of the midfoot, but it falls short of allowing a full understanding.

    Attached Files:

    • MTJ.pdf
      File size:
      307.3 KB
  3. I do see MTJ ab/adduction stiffness reduced with increased lateral deviation of STJ axis during manual examination of these feet clinically. During gait, however, since the MTJ ab/adduction moments are much less than the MTJ dorsiflexion moments (probably 10 times less, at least). Therefore, we should not expect the MTJ ab/adduction motion to be increased necessarily in these feet.

    I think that you, Simon, along with Eric Fuller and myself have all talked about these types of mechanisms over the years. I first talked about it about 20 years ago with Michael Burns, DPM, and he said he had heard it called "midtarsal joint stacking". I think that it is about time these ideas were published as a possible alternative theory for the clinical observation of increased sagittal plane dorsiflexion motion of the forefoot on the rearfoot in more severe flatfeet versus the more commonly accepted notion of making the "axes of motion" of the talo-navicular and calcaneo-cuboid joints more "parallel". Dorsal-to-plantar MTJ cross-sectional thickness makes so much better mechanical sense than "crossing of MTJ axes" that it needs to be published. Don't you agree?
  4. I tend to agree that these ideas need to be discussed and that the old skewing of axes doesn't provide a good enough model, I just think there is more to the problem than cross-sectional area. If it were all about cross-sectional area, then the forefoot should be much less likely to abduct on the rearfoot in association with a "flat-foot", yet we all see that "too many toes" sign because of the plastic set in the spring ligament which occurs with medial deviation of the talar head- so ligamentous restraining has to be considered too.

    Good discussion.:drinks
  5. blinda

    blinda MVP

    `thumbs up`:drinks
  6. I was just thinking that same thing, that MTJ dorsiflexion stiffness is probably dependent more on the dorsal-to-plantar distance from the plantar aponeurosis (if it is still intact) to the dorsal aspect of the talo-navicular joint than only being dependent on the cross-sectional dorsal-to-plantar thickness of the TNJ and CCJ themselves.

    Sounds like a good potential paper.
  7. From Mcpoil and Hunt p. 27 physical therapy of the foot and ankle 2nd edition:
    "Benink... Examined vertical displacement of the tibia and found that normal subtalar alignment resulted in a height change of almost 4mm in a specimen that was external rotated from 0-30 degrees. The low profile foot showed an increase of almost 10mm in height, whereas the high profile foot showed no change. Novick and Kelly measured the vertical height in 21 subjects and found an increased height of greater than 4.8mm in the centre of the ankle joint when excessively pronated subjects wore orthotics... This increase was only partially explained by the thickness of the orthoses."

    Some evidence then that rearfoot position alters the vertical cross-sectional area at the rearfoot. Moreover, perhaps a glimpse at the magnitudes involved.

    Hope this helps.
  8. rdp1210

    rdp1210 Active Member


    You'll remember that in 1975, Milton Wille, PhD Mechanical Engineering, challenged Mert Root on the Elftman concept. He set up a device, and he met twice with Root et al. to show them on 2 freshly amputated specimens that that Elftman concept was wrong. This held up production of volume 2 of Root's work for 2 years; as a result the copyright is 1977 instead of 1975. If you have any questions about the accuracy of these events, please contact Bill Orien. Root removed the term "osseous locking" in referring to the precise Elftman concept, and instead referred to some type of soft tissue locking mechanism, which was never defined.

    As to your claim about the ROM of the MTJ in relation to the STJA location, I can't say whether you are right or wrong. But I do hope that you are preparing a research paper documenting this idea. Just as in my comments to Dennis Shavelson, I will say to you, I am going to be very interested on how you measure the forefoot to rearfoot range of motion NWB. In fact I will challenge all who read this, that the next major breakthrough in understanding the biomechanics of the normal-vs.-abnormal foot will come after we have a proven methodology of measuring the available ROM of the forefoot to the rearfoot in-vivo.

    Your idea about the thickness of the MTJ, though, seems to be almost a corollary of the Elftman concept. The motion is occurring across a joint. Your precept about the bending moment of inertia of a solid body is questionable when trying to apply it to two solid bodies joined together by soft tissues. It would seem that the only application the important area moment of inertia concept would be if you are talking about the thickness of the ligamentous constraints limiting the motion of the joints. Otherwise you are talking about two bones hitting each other limiting the ROM. So in summary, the number of lectures you've given is immaterial to the argument, I think you're mixing apples and oranges to come up with an explanation of an undocumented phenomenon.

    I'm not going to debate your theory beyond what I've said above until we have some data to support your claim that the ROM of the MTJ is indeed correlated to the STJA location. Once we have that data, then the next problem will be to determine if the limitation in the ROM is due to adaptation of the flexibility of the ligaments, e.g. crosslinking due to lack of stretching or whether the engineering principle you're quoting really enters into the equation significantly. Please understand, I utlize the area moment of inertia daily in my practice in both understanding injury as well as in making adjustments to my therapies. BTW, have you also considered the idea that it is harder to bend an object that has a small radius of curvature vs. an object that has a large radius of curvature?

    Best wishes,

  9. Please explain to me, Daryl, where in Elftman's paper he talked about the dorsal-to-plantar cross sectional thickness affecting the dorsiflexion stiffness of the midtarsal joint. To me, you are comparing apples to oranges, by saying these ideas I have presented are "a corollary of the Elftman concept".

    If you don't like my theory, Daryl, then please provide us with an alternative theory. In other words, what is your explanation as to why feet with lower dorsal-to-plantar thickness at the MTJ are the ones that always show the most dorsiflexion of the forefoot on the rearfoot during gait (i.e. rocker bottom flatfoot)?
  10. rdp1210

    rdp1210 Active Member

    As I noted, Kevin, I'm not going to debate a reason for a phenomenon that has no proof of existence. Please provide your reference for:

    1) feet that have increased dorsal-plantar thickness have in-vivo less ROM of the MTJ than feet with decreased dorsal-plantar thickness

    2) that there is a correlation between STJ axis location and foot thicknes, or with MTJ ROM.

    If we have the references, then we can start to talk about reasons.

    If you want, I can submit the mathematics of change in angle traversed of a chord crossing a given distance with two different starting radii of curvature, given the same 10% stretching of the chord. That's pretty straight forward. Should be an interesting differentiation.


  11. efuller

    efuller MVP

    HI all,

    Some quick thoughts. Elftman did not discuss beam theory and his lining up of the axes should no longer be taught. Axes are imaginary lines and imaginary lines cannot limit motion.

    The MTJ stacking is a nice term. I've called it the joist effect and I am sure that others have other names for it. The "stacking" (positioning the talar head more on top of the calcaneus) will increase the height between talonavicular joint and the plantar fascia and this is quite plausible explanation for an increase in rigidity.

    The height is one factor in rtidity. The shape of the joints surfaces is another factor in rigidity. The calcaneal cuboid joint is one of the most variable in shape in the human body. Some calcanei have a bone shelf that juts out over the top of the cuboid. On lateral x-ray this will make the cc joint look more like an "s" that a flat joint. I've also heard it described as the anteater sign where the anterior aspect of the calcaneus looks like the nose of an anteater sniffing the navicular. It is a sign of tarsal coalition, so you will tend to see it in rigid feet.

  12. So, Daryl, when Mert Root proposed that in order to be "normal" the foot must have a heel that is perpendicular, a forefoot that is perpendicular to the rearfoot, etc etc, with not a shred of research evidence to back up or support his claims over the past four decades since he proposed them, did you ever say to Dr. Root while he was alive:

    "Mert, I'm not going to debate a reason for a phenomenon that has no proof of existence."

    You have been tenaciously holding onto and supporting and debating in defense of Dr. Root's many theories for decades even though is no research evidence that the various measurements he proposed are predictive either of foot and lower extremity function or predictive of foot and lower extremity function.

    However, now, with me, you tell me that you're "not going to debate a reason for a phenomenon that has no proof of existence." This seems as rather odd to me. On one hand, you are very willing to defend one person's theories even though there is absolutely no support within the research literature that his theories are true. Then, on the other hand, when someone else (who isn't Mert Root) proposes a theoretically coherent and biologically plausible theory you tell them that you won't debate them because there is "no proof of existence". Does this makes sense to you? It doesn't to me.

    No, Daryl, what I propose is what is called "a theory". Like all theories, my theory serves as a possible explanation of observable phenomena, and are either going to be supported or refuted by future research. My explanation is not only biologically plausible but it is also theoretically coherent and makes perfect sense from a biomechanics and engineering standpoint. Eric Fuller and Simon Spooner also have used very similar descriptions of the midtarsal joint as the one I propose. Will you not debate them either until they have "proof of existence" that "midtarsal joint stacking", "midtarsal joint beam theory", "midtarsal joint joist theory" or what ever you want to call it, has indeed been researched sufficiently for you to therefore declare that there is now "proof of existence"?

    In other words, am I correct in understanding that what you are saying that no one has a right to propose a theory for why certain events occur if that theory has no proof of existence, even though it is theoretically coherent, biologically plausible and makes sense using our known laws of physics and engineering?
  13. Back to the plot.......

    These guys consider tarsal stacking as significant in inhibiting midfoot motion (see p.161 paragraph 3), they reference Close and Inman's 1967 paper on the subtalar joint- I have that paper at work so can check what they actually said tomorrow, or one of my colleagues might pop it up here to save some time?
    http://shiftleft.com/mirrors/www.hp...ker/papers/Pedal Mechanics and Bipedalism.pdf

    In paragraph 4 they talk about the twisted plate model of MacConaill and Basmajian- I know I don't have that paper. If you read through the rest of the linked paper and ignore the whacky axis crossing bits, they clearly believe that tarsal stacking is significiant in increasing midfoot stiffness.

    Now that we have some references can we enter into a debate?
  14. rdp1210

    rdp1210 Active Member

    Back up a little here, Kevin in your allegations: I published in 1983 a paper in which I was interested in seeing if the forefoot to rearfoot relationship did increase in eversion and whether it was a linear increase. I had posed the question to John Weed when I was a student, and he had an opinion that it was linear, but had no data. If you read the paper you'll see that I published the data on all in-vivo subjects. The STJ neutral was not calculated, it was measured using a goniometer that Gary Lucin in 1977 had shown to be reliable. You can view the data yourself. We found the testing population average to have 1.5 degrees subtalar joint varus, and to have 1.5 degrees of forefoot valgus. This was a very homogenous genetic population (no non-majority ethnic members in the data set). This value was statistically not different from what Mert was saying existed. The paper confirmed the phenomenon of what Mert was saying. I did not discuss why it should be so, or whether it should be so. The paper did not compare function and availability of ROM. Haven't seen anyone rebut the 1983 paper, though by today's standards 30 years later I recognize multiple weaknesses in the paper.

    Now interestingly enough, in 1992 I published a paper with in-vivo measurements that corroborated your theory that there was a STJ axis. Or at least the paper showed that within clinical measurment techniques we couldn't prove that it wasn't rotating around a single axis. Of course you published a paper with Spooner about 14 years later that also showed my argument about being able to treat the STJ axis as being fixed relative to the talus, which would mean that in CKC we are dealing with a moving axis. Because of my independent corroboration, people can have more faith in your STJ axis theory.

    I didn't realize that you were proposing a theory about ROM of the midfoot in relationship to STJA or to midfoot thickness. It certainly wasn't presented in your posting as only a theory. You stated the observation as fact and then went on to theorize why it should be so. I still believe your reasoning to be very weak based purely on area moment of inertia of a solid body. I see your argument as being the same as arguing whether a 1" thick steak or a 2" steak is stiffer. Actually Eric has a little better argument with his stacking ideas. I'll try to get to the mathematics later today of elongation of a cord with angular changes of the arc it crosses. The differential of this will tell the story.

    So the question still remains: Is the phenomenon you describe true? You say it is, but have others also found this to be true? I haven't really noticed it, but then again I haven't been looking for it. For me to debate something I haven't noticed, would be careless indeed (I've had a lot of experience trying tonotice if Root ideas are valid -- some are and some I've modified). And if the phenomenon is being observed by others, how are we going to prove it exists? If the phenomenon is true is the relationship causal or not?

    So let's forget Mert Root, this is not an argument about him, his theories, or either of our past relationships with him. The simple fact is that you made a statement about the ROM of the MTJ, and its direct relationship to 1) the thickness of the forefoot and/or 2) the location of the STJ axis. Are you theorizing that the phenomenon does exists and that it should exist?

    Take care,

  15. rdp1210

    rdp1210 Active Member

    Simon, I have the paper and will be quoting from it in a new paper I'm polishing off. If you want it, send me your personal email and I'll send it.

    Take care,

  16. If you send it to skspooner@blueyonder.co.uk

    Thanks Daryl.

    BTW I think we need to think less of this problem as a beam of say oak and more like a beam of plywood in which each of the laminas within the ply are different materials.
  17. I'm sorry that I gave a very condensed version of my theory here. I have actually written four recent newsletters on this subject where I go into much greater detail on the subject.

    Actually Simon Spooner, Eric Fuller and I have all been saying the same thing about midtarsal joint "stacking" or MTJ "beam effect" causing the increase in sagittal plane dorsiflexion MTJ stiffness seen with STJ supination and a decrease in MTJ dorsiflexion stiffness seen with STJ pronation. I simply added the concept that STJ axis spatial location will also affect the sagittal plane dorsiflexion MTJ stiffness due to the change in 3D orientation of the TNJ to the CCJ seen with different STJ axis locations.

    This is a theory based on my observations over the last 30 years of looking at STJ axis location and MTJ function and correlating that to weightbearing function of the foot. It is a theory, nothing more, nothing less. However, at least to me, it is a much better theory than Elftman's theory that was included in Root et al's books and some other orthopedic textbooks, who also presented Elftman's theories "as fact" as you stated above.

    Do you have a better theory as to why we see changes in MTJ dorsiflexion motion during gait that seem to dependent on the morphology of the foot?
  18. Finite element analysis (FEA) would probably be the best way of solving this problem, including the load-deformation characteristics of the plantar ligaments into the FEA equations. FEA should very nicely show how it is the vertical distance from the plantar ligaments and plantar fascia, including their elastic modulus and thickness, to the TNJ, that would most effectively predict dorsiflexion stiffness of the MTJ.

    Anything is better than Elftman's "crossing and parallel" imaginary MTJ axes that Root et al and many other orthopedic authors have been presenting as fact in their textbooks over the last four decades as to why the MTJ "locks", etc.:craig::bang:
  19. Yeah, I appreciate that and checked through the finite element papers earlier to see if anyone had looked at this; unfortunately not so far. My FEA modelling/ software is simply not up to this because the model foot has to be reconstructed from CT scans and have input material characteristics which I just don't have the computing power to do.

    I can probably build a jig to test some of these ideas in-vivo though.

    BTW, Salathe employed beam theory to model metatarsal bending here: http://www-k12.atmos.washington.edu/~salathe/papers/full/Salathe_1989.pdf and here: http://www.atmos.washington.edu/~salathe/papers/full/Salathe_1986b.pdf but perhaps the answers to some of our question lie in here: http://www.sciencedirect.com/science/article/pii/S0268003303002572 or here: http://www.sciencedirect.com/science/article/pii/S0268003301000110 or maybe even here: http://www.jbiomech.com/article/0021-9290(90)90165-Y/abstract But it's probably in here: http://fai.sagepub.com/content/21/3/216.abstract all of which I don't have the full text accesses to.
  20. Those look like good references, Simon. This will give me a start in seeing what others have done more recently on this subject that has "no proof of existence".;)
  21. A question if I may

    In Kevins pictures the compliance of the Plantar fascia may effect the MTJ dorsiflexion stiffnes as well, so a medially deviated STJ axis may still have a high dorsiflexion stiffness if the Plantar fascia has increased stiffiness?

    right or ?

    also Plantar Fasciosis would add to the thickness of the midfoot beam, and thus increasing MTJ dorsiflexion stiffness ?

    Just working through the ideas
  22. Lab Guy

    Lab Guy Well-Known Member

    From my current understanding of what Kevin and others have written, with a medially deviated STJ axis, your unlikely to see resupination of the foot in terminal stance and there will be a delay in the activation of the windlass. This will lead to a decrease in the cross sectional thickness of the MTJ as it is not "stacked".

    The GRF has the mechanical advantage to produce an external dorsiflexion moment on the rearfoot due to long distance from the center of pressure and STJ axis. This results in a pronation moment through the MTJ resulting in a decreased cross sectional thickness of the MTJ which then results in less stiffness of the MTJ to resist the GRF in stance.

    I would say the causative factor is not the plantarfascia but the location of the STJ axis. Clinically, when I see a medially deviated STJ axis, the patient has either a flexible pes planus or a rigid pes planus. Either way, the foreoot is dorsiflexed to its end range of motion in midstance and terminal stance which is also being exacerbated by the eccentric contraction of the soleus.

    I also think that Plantar Fasciosis would decrease rather than increase the MTJ DF stiffness due to the collagen being strained beyond the elastic limit due to the high tensile stress within the fascia resisting the tension from lowering of the medial longitudinal arch.

  23. Rob Kidd

    Rob Kidd Well-Known Member

    I have problems with this. Sure I recognise the gross simplicity of Elftman's lines, but you seem to take the view that tarsal stacking and Elftman's lines are mutually exclusive. I argue that they are not; both are clear, concise and valid concepts. The human talar head undergoes a torsion far more than any other primate, which in itself give vertical thickness to the beam that you allude to. It also gives credibility to Elftman's lines.
  24. efuller

    efuller MVP

    There is no credibility in Elftman's lines. Elftman's lines are allegedly axes of rotations. An axis of rotation is an imaginary line that describes the motion that has occurred. It is not the existence of a hinge. There is a misguided concept out there that joints must move around an axis of rotation that you find in a book. For the midtarsal joint, you can create an infinite number of lines (axes of rotation). The two axes that Elftman found "with the eye of a connoisseur" are two possible lines, but there are more.

    I could stop there, but imaginary lines cannot limit motion. Compression of bony surfaces and tension in ligaments can limit motion. The midtarsal joint has an envelope of motion. As you move the distal part relative to the proximal part in any direction you can get some motion and when the ligaments become tight the motion will be resisted.

    It is long past time to put Elftman to rest.

  25. rdp1210

    rdp1210 Active Member

    I am glad that you clarified that you are expressing a theory based on anecdotal observations. I can accept that you are using only anecdotal subjective observations. That is where all good research starts. I have not personally made these observations, therefore I cannot comment yet about whether I agree or disagree with the observations. What would be really nice now is if you and others could actually gather and collect in-vivo measurement data and share this with the world. Once everyone has this measurement data then we can all participate in sorting out causality and other relationships.

    I am a little confused by your insistence that Root continued to perpetuate the Elftman concept in his volume 2. I have related the story, because I am the next closest living eye witness (Bill Orien is the first) of the events that brought Mert to realize that Elftman was wrong in 1975. They spent 2 years revising volume 2 to remove all of the terms "osseous locking" (referring to Elftman's mechanism) and replacing it with terms indicating soft tissue restraing. Please note the following quotation from page 80 of Root's volume 2:

    "Osseous restraint of motion at the midtarsal joint is not independent of soft tissue tension like it is at the subtalar joint. Loading forces at the midtarsal joint are oblique to the ground rather than vertical to the ground as they are at the subtalar joint. Therefore, weight supported by the foot produces compression and tension forces at the midtarsal joint. ligaments or muscles must resist the tension forces at the midtarsal joint, and, in sod doing, they increase the compression forces upon the midtarsal joint."​
    So does this sound like Root et al believed the Elftman hypothesis?

    In a recent personal email from Bill Orien to myself, dated Sept 19, 2014, Bill made the following statement which I will share with all.

    "I've been listening to old tapes of lectures we gave . Several by Mert and John and several by all three of us. I have not found a specific reference to the locking mechanism of the MTJ. I do remember, the Mert did not like the term "locking" and preferred compression as the correct term. John and I liked locking since it was a better visualization of the method of maintaining propulsive stability at the MJP in the propulsive period."​

    Some of your ideas are indeed interesting. It is time people start looking at area and polar moments of inertia in the foot. It is nice to see that more people are interested in the intersegmental kinematics and kinetics of the foot instead of only looking at the rearfoot to leg relationship. I will look forward to your future publications on the subject.

    Best wishes,

  26. Daryl,

    Please look at the paragraph before the one you quoted (on page 80 of Normal and Abnormal). Does this paragraph sound like Root et al didn't believe in Elftman's hypothesis?

    Nowhere within this section on "The Midtarsal Joint Restraining Mechanism" in Normal and Abnormal on page 80 does Root et al state that he disagrees with Elftman. However, the term midtarsal joint "locking"and that the MTJ "locks" is repeated quite a few times on that page. However, I will give you that Root and colleagues do discuss compression and tension coupling at the MTJ as a method of achieving "osseous restraint".

    In addition, on page 67 of the Compendium, there is a whole diagram titled "Axial Locking of the Midtarsal Joint" graphically demonstrating Elftman's concepts. Whether Root approved this illustration or it was Sgarlato who approved it, I do not know.

    One thing I do know, is that we need more research and better theoretical papers on this subject.:drinks
  27. Rob:

    I agree with Eric.

    Careful reading of Elftman's original paper shows he determined his imaginary "midtarsal joint axes" simply by looking at the joint surfaces with "the eye of a connoisseur".

    Elftman did absolutely no kinematic studies of the midtarsal joint.

    Elftman did absolutely no kinetic studies of the midtarsal joint.

    He looked at some foot bones, dreamed up some imaginary lines on the joint surfaces that did not exist, and made up some dreamy story about how parallel axes allowed more motion and more oblique axes allowed less motion and then, somehow, got someone to publish his ideas with cool looking illustrations.

    And you call this Elftman's concepts clear, concise and valid? It certainly isn't clear, concise, valid or even theoretically coherent to me. Motion determines joint axes. Joint axes don't determine joint motion. Imaginary joint axes dreamed up by looking at the shape of joints don't determine the equilibrium of internal versus external forces and moments that allow joint stability to occur within the human foot and lower extremity.

    I believe it is a travesty that this sort of "biomechanical nonsense" is still being taught today in most, if not all, the podiatric medical schools around the world to this day, especially the level of biomechanics and engineering knowledge we have in this day and age.
  28. Rob Kidd

    Rob Kidd Well-Known Member

    To both Kevin and Eric, I recognise totally the ridiculous naivety of Elftman's lines and eye of the connoisseur. All I am saying is that one cannot deny that a subtalar supinated foot has a lesser ROM at the midtarsal (oblique - I do not accept a long) axis, and a greater ROM in a subtalar pronated state. I feel it was made far too big a deal of in yesteryear, but it will not go away. I would be a silly mistake to try and attach some variety of linear or even quadratic function to rates of change in ROM from one position to the other. Many authors have picked up on the extreme talar head torsion in humans and not in other primates, and relate this to the decrease ROM (though to be fair, the one coming to mind was about Neandertals - same difference). That is, There would not be a restraining mechanism in its absence.

    None of my thoughts in any way detract from the tarsal stacking that you comment on, and that I made small mention of in my PhD thesis 25 years ago. I still maintain that they are not mutually exclusive - but do note my comments about Elftman's naivety. Also please note that I refer to midtarsal joint movement as the navicular and cuboid moving in concert, not as separate entities. Rob
    Last edited: Oct 1, 2014
  29. rdp1210

    rdp1210 Active Member

    I don't know why you are so bent on pigeon-holing Root into one belief. I know that you were there in 1994, at the first Weed Seminar, when Root spoke a little, and he made some comments that he really was afraid of putting anything in writing, because from then on people would never allow him to change his mind. It is true that in 1971, when the compendium was published, Root was square-behind Elftman. However in 1975 Elftman was proved wrong to Root, when it was clearly demonstrated by Milt Wille that only ligamentous tension held the MTJ together, that it had nothing to do with STJ position. I believe that Kiteoka has also demonstrated similar findings. In his 1977 text, Root has to give way to Wille, but is having some difficulty doing so, so we can see him somewhat straddling the fence. But I can assure you that by 1977, Mert knew that it was ligaments, not articular shape limiting ROM of the MTJ. I'm not defending all of Root's ideas, only that you fairly represent his ideas, and allow him to progress in his ideas through the years.

    The biggest mistake that Root et al. made was not publishing the experiments they did with Wille on the ligamentous support of the MTJ.

    Now lets look at the arguments about area moment of inertia and also the stacking ideas. Unfortunately I have a difficult time visualizing exactly how the stacking mechanism works without diagrams and/or pictures, so maybe Eric would be so kind as to provide such. However you have not addressed how ligament tightness affects the MTJ ROM. I would like to propose to you two scenarios and ask you to explain each scenario:

    Scenario #1: You have two feet, one with a dorsal-plantar thickness of 3" and one with a thickness of 5". If I read you correctly, you are going to say that the 5" foot has less MTJ motion than the 3" foot. You are then going to arthroscopically cut the all the plantar ligaments without disturbing the muscle attachments. After transecting all the plantar ligaments, the thickness of the two feet are their original thickness. Will the 5" foot still have less motion in the MTJ than the 3" foot? (Right now this is a thought experiment, but it could be turned into a real experiment)

    Scenario #2: You have two feet, one in which the navicular is above the cuboid, making it a thicker foot dorsal to plantar, but thinner medial to lateral. You have the second foot, same cross sectional area across the midfoot, but with the navicular lying more medial to the cuboid, so that the medial-lateral distance is greater than the first and the dorsal-plantar disance is less than the first. Is it your argument that the second foot will have less transverse plane motion across the MTJ than the first? Why or why not.

    I do agree with you that midfoot motion research is the greatest need in the realm of foot biomechanics.

    Best wishes,

  30. I was just quoting right out of his book, Daryl. I don't know how quoting out of his book is "pigeon-holing Root into one belief". You were the one that picked the paragraph out of the book that followed the one that included Elftman's reference. Why didn't you include the paragraph that I did that showed that clearly showed that Root talked about Elftman's reference without every saying he disagreed with Root? As you said to me, he presented is as "truth". You are the one who seem to defend Mert Root to the extreme. Therefore, I feel the need to suggest an alternative view just to keep things real for everyone following along.
  31. rdp1210

    rdp1210 Active Member

    I think it's time to let Mert Root go. I think you and I are going to have to agree to disagree about who the real Root was and what he believed. Your interpretation of the paragraph you quoted is very different than mine, (kind of like two different preachers reading the same verse). And the discussion was never about Mert in the first place. I knew in 1976, when I entered podiatry school, that "osseous locking of the midtarsal joint" was dead. I had spent many hours in 1975 and 1976 listening to Dr. Wille discuss the error of the osseous locking, while I watched him writing chapter 2 for Root. (I didn't know at that time who Elftman was). Now on the other hand you spent much more time with John Weed than I ever did; did you find him teaching you during your residency that Elftman was correct?

    So let's return to your original premise, that the area moment of inertia across the midfoot is what limits the ROM of the MTJ. Is that a correct statement of your premise? If not, please correct me and tell us what the correct statement is.

    If I have correctly stated your premise, what are your answers to thought experiment 1 and 2 that I proposed?


    PS: I am working on some drawings right now to give you another hypothesis for your observations about ROM of the MTJ, based on the twisted plate theory.

  32. OK, I was looking at the jig I built to measure supination resistance at work today and think I can modify it / use some of the components to measure forefoot dorsiflexion stiffness with varying degrees of frontal plane positioning of the rearfoot.

    I've attached a rough sketch, the forefoot will be clamped in a material testing machine ensuring that it remains parallel to the supporting surface and that only the vertical component is measured- basically load/ deformation about the medio- lateral MTJ reference axis. The rearfoot will be on a platform enabling angular change in the frontal plane, I'll probably clamp the heel to this too- it'll make more sense when I've built it and take some photo's. I'll clamp an angle finder to the calcaneus too like I did with the supination resistance work since we know the angle of the surface and the change in the angle of the calc are two different things; might need to build an STJ axis locator too, if we are interested in this as well.

    Couple of questions: at what level of the foot do you want the force gauge clamped to the forefoot? I was thinking just proximal to the metatarsophalangeal joints- Obviously we can't isolate the TNJ and CCJ here and will capture displacement occuring at the other joints proximal to these to the level of the clamp. Also going to need to "lock" the ankle somehow too, so that we don't get dorsiflexion occuring at the reafoot- any thoughts on how to achieve this?

    I'll get data from as many subjects as I can, but don't expect this to ever get published because due to the ludicrous ethical approval system in this country the fact that I don't work for a University nor the NHS means that I shall not be able to gain the ethical approval required for journal publication.

    Clearly this experiment may or may not show change in forefoot dorsiflexion stiffness with change in rearfoot position, but it won't tell us if any change is due to the moment of area, and/ or not due to some other mechanism, I'm not sure how you could isolate one from another? Perhaps (and I'm only thinking outloud here) if we meaure the dorso-plantar thickness of the midfoot in the different positions and we know the Young's modulus of bone can we then calculate what the stiffness should be if the load/deformation were purely due to the second moment of area and then look at how far away from this value we see with in-vivo measures? Just thinking.;)

    Attached Files:

    • jig.jpg
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  33. My understanding of the "twisted plate theory" or "lamina pedis" is that it is based on the same premise of second moment of area. ie. the "untwisting" of the plate with rearfoot pronation results in a smaller cross-sectional area, while the increased "twisting" results in a greater cross-sectional area. I don't see how this is any different from what is being proposed, but look forward to your explanation, Daryl.

    If we are talking about the lamina pedis it might be worth reviewing Lewis http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1233206/pdf/janat00236-0162.pdf

    And our previous discussion of "wring theory" here: http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=82910 As memory serves, I did not think that this so called "Wring theory" diverged much from, nor added much to the "lamina pedis model" presented by MacConeill and Basmajian; although, as previously stated, I no longer have access to a copy of the book in which this originally appeared so I am working from memory and the discussion of the lamina pedis which exists in Sarrafian's anatomy text. Yet, Saraffian is a bit confusing as he asserts that the midfoot is stiffer with rearfoot pronation as this provides close-packing?
  34. Thanks for that explanation, Rob. I agree with you. I just feel we need a more physics based explanation for the changes in midtarsal joint dorsiflexion stiffness seen clinically from one foot to the other than the explanation provided by Elftman over a half century ago.
  35. Question: do we see changes in midtarsal joint dorsiflexion stiffness from one foot to another clinically, or do we just see differences in loading which result in differences in deformation? Salathe's modelling suggests changes in rearfoot position will result in variation in the position and magnitude of the forefoot dorsiflexion moment, this in isolation will result in varying degrees of forefoot displacement on the rearfoot even if the actual stiffness of the midfoot joints, i.e. the load/ deformation characteristics of the joints themselves, are constant.
  36. Simon:

    This doesn't make sense clinically with what I see. I see patients with very low medial arch heights and medially deviated STJ axes have increased forefoot dorsiflexion on the rearfoot during late midstance and propulsion. I also see higher medial arch height feet with laterally deviated STJ axes having a relatively "stiff feet" with little forefoot dorsiflexion motion on the rearfoot during late midstance and propulsion. In both of these feet, the dorsiflexion moment should remain relatively constant assuming equal body mass and walking speed, but the forefoot dorsiflexion stiffness probably is quite different between these two extremes of foot structure.
  37. "A three-dimensional biomechanical model was used to calculate the mechanical response of the foot to a load of 683 Newtons with the subtalar joint in the neutral posi- tion, at five degrees of pronation, and at five degrees of supination. Pronation causes the forefoot to evert, increasing the load borne by the first metatarsal. This results in a 47% increase in the moment about the talon- avicular joint and a 58% increase in the moment about the navicular-medial cuneiform joint. Subtalar joint supina- tion causes the forefoot to invert and results in a 55% increase in the moment about the calcaneal-cuboid joint." http://fai.sagepub.com/content/21/3/216

    So if we have two feet at mid stance with identical midfoot stiffness but one foot is 5 degrees pronated at the rearfoot and one foot is 5 supinated a the rearfoot we should see different loading being applied to the two feet, this will result in the two feet deforming differently under loading despite having identical stiffness. The pronated foot with its increased moment acting on the medial column will show greater medial longitudinal arch flattening than the supinated foot; the supinated foot with its greater moment acting on the lateral column will show less displacement of the medial longitudinal arch. Isn't this what we see clinically?
  38. Now that I read what was said in the paper, I agree with it. Supination of the STJ will cause increased loading of the CCJ and STJ pronation will cause increased loading of the TNJ. I have written about this effect in relationship to dorsal midfoot interosseous compression syndrome (DMICS) in that medial DMICS is more likely to occur in feet with medially deviated STJ axes and lateral DMICS is more likely to occur in feet with laterally deviated STJ axes. However, the total MTJ (both TNJ and CCJ) dorsiflexion load probably doesn't significantly change with STJ pronation and supination.
  39. So does the relative distribution of dorsiflexion load applied to the CCJ and TNJ respectively impact upon the net forefoot dorsiflexion displacement given that each of these joints have their own individual dorsiflexion stiffness?
  40. I would say that is an affirmative.

    In addition, since the medial column should have less dorsiflexion stiffness than the lateral column (due to its greater number of joints), equal plantar loads on the medial forefoot and lateral forefoot metatarsal heads(combined with the increased moment arm of the longer medial than lateral metatarsals), will result in increased medial column dorsiflexion than lateral column dorsiflexion for these equal plantar metatarsal head loads.

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