Does rotation exist and what causes it?
There is a fierce debate on social media about laminitis. The arguments have become cloudy and confusing, with conflation of changes in phalangeal alignment and changes in distances between the dorsal wall and pedal bone and the subsequent hoof capsule deformations and between what happens and treatment during the acute and chronic phases. It seems the main bones of contention are around three main points. This review will outline the research and evidence to address these points. A review of treatment methods is not within the scope of this piece, it will focus on what happens during laminitis.
The three points that seem to be disputed are.
1. The distal phalanx doesn’t rotate during laminitis due to a breakdown of the suspensory apparatus (SADP)
2. The rotation is caused by farriery practices and not systemic inflammatory processes
3. If P3 rotation was down to systemic inflammatory processes, then it would ping back into its correct position.
To address these points, we need to start by analysing the research into the mechanisms of the laminal bond breakdown, known as suspensory apparatus of the distal phalanx (SADP) failure. This has been covered in previous articles on this website but here is a brief overview..
Laminitis can be broken down into phases; the developmental phase; the acute phase; and the chronic phase.
During the developmental phase, before clinical signs of pain, the horse or pony usually experiences a problem with one or more of the following organ systems: gastrointestinal, respiratory, reproductive, renal, endocrine, musculoskeletal, integumentary and immune. These issues, while visceral, result in dysfunction within the lamellar tissues of the feet leading to separation and disorganisation of lamellar anatomy. The mechanisms of these visceral dysfunctions reaching the lamellar tissues via the circulation, is still being studied, but there is a large body of literature on the effects on the SADP.
The main body of research suggests four main risk factors corresponding to four types of laminitis:
1) sepsis /SIRS (systemic inflammatory response syndrome) related laminitis.
2) endocrinopatic laminitis.
3) pasture-associated laminitis.
4) supporting limb laminitis, experimentally linked to hoof lamellar hypoxia.
While the causes may be different, the main failure in most of these cases is a break down of the connection between the basal epithelial cells in the epidermal lamellae to the underlying dermal lamellae at the basement membrane (BM) level. At the base, there is damage to the dermo-epidermal interface of the lamellae that causes failure of the attachment of epidermal lamellae, connected to the hoof wall, to the dermal lamellae, attached to the distal phalanx. Basically, lamellar separation, with failure of the attachment between the inner hoof wall and the distal phalanx (Figure 1).
Studies on a microscopic level into the changes in the cells point to lamellar cell stretching. The stretching that occurs is now regarded as a key early structural event and was noticeable at just 6 hours. This cellular stretching was accompanied and followed by evidence of an accelerated cell death-proliferation cycle. Microscopic lesions were located close to the hoof wall and included apoptosis, lamellar fusion, hyperplasia and partial replacement with aberrant keratin containing nucleated debris and proteinaceous lakes. So, there is a physical infill with keratin or proteinaceous fluid.
So, damage to the lamellae can cause the SADP to fail and the underlying third phalanx to separate from the wall. The space created is a lesion infilled with scar tissue. This is a culmination and summary of many studies agreeing that systemic issues affect the chemical processes in charge of the maintenance of the SADP on a microscopic level. The distal phalanx and hoof wall become detached from one another, the pedal bone displaces, and the laminal wedge is formed (Fig.2). This answers one question of why the pedal bone doesn’t ping back into its correct position, because the space it once filled it taken up with scar tissue.
The histopathology of laminitis clearly shows the major feature of acute laminitis is a progressive increase in the distance between the hoof wall and the distal phalanx. Initially this distance is tiny but rapidly progresses to a separation measurable radiographically.
Radiographically this is seen as an increase in the distance between the outer hoof wall and the upper surface of the distal phalanx known as, the hoof, distal phalangeal distance (HDPD). What’s vital in this debate to understand is that the HDPD is constant in normal horses. An increase in the HDPD only happens in laminitis!! This brings us to an important misunderstanding that seems to be part of the confusion.
We must re-define, or rather change the lay language used to describe what happens in laminitis to the pedal bone (P3). Using the phrase a change in hoof-distal phalanx distance (HDPD) is more appropriate than the term rotation. Rotation of P3 happens all the time, it rotates around its axis with normal locomotion and with changes to heel to toe height ratios of the hoof capsule. For instance, in normal trimming. We also have different orientations of P3 with differently conformed digits and can even have a broken forward P3 in club feet (Figure 3-4).
The progression at the late stages of the acute phase into the chronic laminitic phase is defined by the development of radiographic evidence of P3 displacement relative to the hoof capsule. This point is of course disputed as existing, with capsule manipulation being blamed for changes in radiographic presentation. However, with recent advances in digital radiography systems we have improved visualisation of the soft tissue layers of the digit, and this helps us to clarify and redefine what we mean by P3 displacement in laminitis and whether it can be caused by the farrier. The implications for the arguments pointed out in the introduction are obvious.
Specifically, two distinct layers of the hoof wall can be visualised, a superficial (radiopaque) layer consisting of the stratum externum and stratum medium and a deeper ‘hoof lucent zone’ consisting of stratum internum (the lamellae) and dermis parietis (the sublamellar dermis). This ‘lamellar lucent zone’ (LLZ) corresponds with the lamellae and sublamellar dermis on magnetic resonance imaging (MRI); and can be reliably measured radiographically with appropriate post-acquisition windowing and manipulation. Furthermore, LLZ measurements, unlike measurements from the outer hoof wall, are not affected by hoof wall trimming!!!
Therefore, increases in the LLZ correspond with the physical changes in the lamellae and sublamellar dermis, increased HDPD, that occur in the late stages of acute laminitis. Research has clearly shown significant increases in dorsal LLZ measurements in lateromedial radiographs of horses with acute and subacute laminitis compared with a healthy control group (Figure 4)!!!
Farriery, while having the ability to make changes to the orientation of P3 and therefore PA can not affect LLZ width or affect changes in the relationship between P3 and the dorsal wall. These paragraphs clearly demonstrate that an increase in HDPD occurs because of systemic, visceral issues in the horse causing a breakdown of the SADP. Horses have normal radiographs that show an increased HDPD after a laminitic attack (Figure 5). Farriery does not cause laminitic rotation. If high heels created rotation, then we would see an increase in the HDPD in all upright and club feet, which we simply do not.
Unfortunately, it seems evidence like figure 5 is limited, possibly since horses aren’t generally radiographed unless they are lame and is certainly an area for further research. This does show a potential failure of the industry in the monitoring and documentation of changes to the hoof capsule. Which is of course a re-occuring message from the author and the reason behind the creation of HoofmApp. The author will look to compile some cases. However, the vast number of radiographs that exist from non-laminitic horses showing a constant HDPD, and the findings of the study above, can be accepted as a strong indicator that “laminitic rotation” occurs after an acute laminitic event.
This review puts the ball firmly back into the court of those who would present the three statements in the introduction, the substantial body of research and evidence agrees and therefore the proof that is it not correct is their responsibility.
See Appendix 1 for a critical appraisal of arguments.
However, applying critical thinking it would be logical to the author that there is one point that warrants further research. Does keeping feet trimmed to the hard sole around the entire periphery stop an increase in HDPD from occurring?
In the author’s opinion this point should be the message the alternative theorists should be presenting, rather than disputing robust science and blaming professionals for systemic disease.
It is possible that feet trimmed to the hard sole around the entire periphery do not rotate due to the bone column being supported through direct and constant contact through the frog, caudal hoof structures and entire sole, as this is the focus of post attack treatment by those competent in laminitic hoof care treatment.
The healthy barefoot is not completely dependent on the laminae for support. The arch of the sole and outer sole callus is designed to support some load. However, many domesticated shod horses lack a functional sole and probably depend more on the laminar interface for support. The sole is often suspended off the ground, disengaged from weight bearing, atrophied, or sometimes even intentionally and radically trimmed out to form a convex contour. There could be some truth in when this “domestic” foot is affected by laminitis, mechanical collapse of the foot is more readily incurred.
Whether healthy bare feet are less likely to “rotate” is plausible and perhaps should be considered as a hoof care industry. Of course, research is required, if someone could find an ethical method to do so. It would also have to be researched as to whether this practice would enable other hoof balance parameters to be maintained for longevity of working career. How would this practice affect phalangeal alignment and the subsequent loads on the flexor structures for instance. Consideration of the practicality of this practice within different domestic settings would also be required as hoof health is not simply a factor of the trim, but diet, movement, terrain, environment etc etc. A strong and healthy barefoot is possible within certain environments and management practices, and indeed trimming protocols, however all of those remain a luxury in most domestic settings and therefore laminitic changes in the hoof will remain a reality.
Before we conclude, it may be worth suggesting some reasons behind the thought process behind the three points, although as stated this article will not go into treatment.
Growth rate of the heels increases in chronic laminitis, meaning trimming cycles should focus on trimming down the heels to maintain PA. This is agreed, although perhaps not understood by some practitioners. When horses with laminitis are presented to those of alternate theories, it would be logical assumptions that at least in some cases.
1. The previous hoof care has either been less than ideal, and/or
2. The horse will be due or overdue for trimming/shoeing, and/or
3. The previous hoof care practitioner/vet didn’t either know, or didn’t explain the need for feed and management changes.
When the horses go to the care of the alternate care providers, they therefore have high heels, but correlation does not mean cause! What the alternate care providers obviously do well, to achieve their apparent success is, yes trim the heels down, but deal with the cause of the systemic inflammation and provide an environment for healing to take place. Another point of which they should be focusing their teaching on!
Now regarding their treatment method and not removing toe leverage, this comes under treatment and is not going to be covered in this review except to express, that with an open mind, it may be possible that due to the fact these horses are going through a rehabilitation period, addressing inflammatory pathogenesis, maintaining solar support, trimming down heels and changing management regime are probably far more important than removing toe leverage in a non-performing horse.
If these hoof care providers would refrain from trying to discredit established science and focused on objectively quantifying the factors in their apparent success, the industry could benefit from new research.
In conclusion, it is abundantly clear that an increased HDPD, which defines the term rotation in the context of laminitis, is a result of the effects of the systemic syndrome laminitis on the SADP. The argument is therefore not about whether “rotation” occurs and whether it’s the hoof care professionals’ fault, but rather whether having a foot trimmed around its entire periphery to the hard sole mitigates laminitic rotation. This then creates more questions as to this trimming methods practicability within different domestic settings and environments, and a much wider debate about domestic management as a whole.
This is the discussion and research that should be occurring, which would be much more in the interests of the horse!
Appendix 1
Critical appraisal of arguments
Credit to Natasha Sunderland for this comment on FB
This statement (made by the professors of the points made in the introduction) makes bold claims challenging traditional hoof care science, but several points raise questions that warrant closer examination:
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1. Lack of Published Scientific Evidence
The post dismisses peer-reviewed research as flawed but doesn’t provide its own peer-reviewed studies to support its claims. While real-world results are important, they must be subjected to scientific scrutiny through controlled studies, repeatability, and objective measurements.
Potential hole: If "hundreds of horses" have been successfully rehabbed using this method, why hasn't the data been formally published for peer review? Without standardized research, anecdotal evidence—even if compelling—does not necessarily disprove existing theories.
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2. Strawman Argument Against "Dead Hoof" Studies
The claim that hoof research is mostly based on studies of "dead hooves" oversimplifies and misrepresents modern equine science. While cadaver studies have limitations, many studies use live horses, motion analysis, force plates, and radiographs to assess hoof mechanics dynamically.
Potential hole: If mainstream research is flawed due to reliance on cadaver studies, why not reference specific studies and provide counter-evidence from live hoof studies? The claim needs to be substantiated with examples.
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3. Contradictory Claims About the DDFT (Deep Digital Flexor Tendon)
The post repeatedly insists that there was “absolutely no pull from the DDFT” during or after Wex’s rehabilitation, yet also claims that P3 rotation was resolved by lowering the heels.
This is contradictory because:
The DDFT directly affects P3’s positioning. Lowering the heels decreases the palmar angle and reduces strain on the DDFT.
If heel height was a problem initially, then logically, there must have been some DDFT tension before adjustment.
Potential hole: If there was no DDFT involvement, then what was keeping P3 in its incorrect rotated position in the first place?
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4. Misrepresentation of Long Toe Biomechanics
The post argues that Wex improved despite having a “long toe”, challenging the idea that a long toe causes excessive lever forces and worsens rotation. However, biomechanical principles suggest that a long toe increases breakover stress, which can contribute to further hoof pathology.
Potential hole: The post doesn’t explain why Wex’s case contradicts established biomechanics. Was there compensatory loading elsewhere? What about the effect on the suspensory apparatus? The reasoning isn’t fully explored.
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5. Ignoring Other Potential Factors in Recovery
The post strongly dismisses the role of diet and management in Wex’s recovery, claiming that trimming was the primary factor. However, research and experience suggest that systemic factors like diet, turnout, movement, and overall metabolic health play major roles in hoof rehabilitation.
Potential hole: Could Wex have improved due to a combination of factors, including movement, circulation, and systemic health, rather than trimming alone? A well-rounded discussion would acknowledge these variables.
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6. Exaggerated Critique of Conventional Hoof Care
The claim that conventional hoof care methods lead to “more pathology, more suffering, and more unnecessary euthanasia” is an overstatement. While hoof care practices evolve over time, mainstream farriery and barefoot methods have rehabilitated countless horses successfully.
Potential hole: Where is the data showing that conventional methods systematically fail in comparison to this alternative approach? Blanket statements discrediting an entire industry require strong evidence.
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7. Possible Logical Fallacy – False Dichotomy
The post presents a false dichotomy, implying that people must either:
1. Accept this new approach as the truth.
2. Be blindly following outdated, flawed science.
Hoof care is not black and white. Many professionals incorporate both traditional research and real-world adaptations to optimize their trimming approach.
Potential hole: Why frame it as an either-or scenario? Could there be a middle ground where different methods work for different horses?
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Conclusion
This post brings up valuable points about the importance of real-world evidence, but it has several weaknesses:
1. It dismisses peer-reviewed science without providing its own published research.
2. It misrepresents mainstream hoof research, ignoring live-horse studies.
3. It contradicts itself regarding DDFT involvement.
4. It oversimplifies long-toe mechanics without addressing biomechanical consequences.
5. It ignores the role of diet and management in rehab.
6. It exaggerates the failure of conventional methods.
7. It presents a false dichotomy instead of acknowledging the complexity of hoof care.
To strengthen these claims, the author should provide objective data, controlled case studies, and biomechanical analysis rather than relying on anecdotal observations. If this method is truly superior, it should withstand scientific scrutiny.
References
References are too numerous to list but these are some profound ones..
Eades. S,C. 2010, Overview of Current Laminitis Research, Veterinary Clinics: Equine Practice, Volume 26, Issue 1, 51 - 63
Marcato, P. S. and Perillo, A. (2020) ‘Equine laminitis. New insights into the pathogeneMarcato, P. S., & Perillo, A. (2020). Equine laminitis. New insights into the pathogenesis. A review. Large Animal Review, 26(6), 353–363.sis. A review’, Large Animal Review, 26(6), pp. 353–363.
Lykkjen, S., Stenbakk, L.K. and Holmøy, I.H., 2023. Prevalence and risk factors for laminitis within the Norwegian pony breed Nordlandshest/Lyngshest. Acta Veterinaria Scandinavica, 65(1), p.22.
Menzies‐Gow, N., 2018. Laminitis in horses. In Practice, 40(9), pp.411-419.
Pollitt, C. C. (2008) ‘Equine laminitis : current concepts’, Rural Industries Research and Development Corporation, (08/062), pp. xii–100.
Skelton, G. et al. (2024) ‘Evaluation of digital radiographic measurements for the diagnosis of acute laminitis’, Equine Veterinary Journal, (May), pp. 1–12. doi: 10.1111/evj.14436.
Morrison. S, 2010, Chronic Laminitis: Foot Management, Veterinary Clinics: Equine Practice, Volume 26, Issue 2, 425 – 446
SHETA, E., 2002. EFFECT OF CHRONIC LAMINITIS ON THE HOOF HORN GROWTH IN ARABIAN HORSES. Veterinary Medical Journal (Giza), 50(3).
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