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Disordered Physiology and Hoof Morphology - The Chicken and the Egg

The physiological effect of poor conformation and hoof morphology on the wider skeletal system of the horse is a highly complexed subject, as touched on by Simon Curtis (2002) the variations of both are limitless and therefore their physiological effects differ vastly, however we can apply the laws of physics to predict the predispositions of certain conformations.

Poor hoof conformation effects the musculoskeletal system and hoof morphologies are caused by conformation defects and both can be perpetuated by the lack of recognition, a limb with a deviation will cause the foot to distort over time, leading to the damaging of the internal structures, so we have a chicken and egg situation when it comes to whether hoof morphology influences the wider physiology or vice versa.

Even with an ideal conformation, hoof morphology will have a wider effect on the skeletal system, there are many papers that study the physiological effect of hoof morphology on the internal structures of the digit, Van Heel et al (2004) and Van Heel et al (2005) along with Moleman et al (2006) all describe how the centre of pressure (CoP) of the hoof moves caudally as the hoof grows putting more pressure on the navicular region and the deep digital flexor tendon. Wilson et al (1998) talks about medio lateral and dorso-palmer imbalances of the hoof on the wider skeletal system, he discussed how the CoP moved towards the higher side of the imbalance, this in turn puts uneven loading on structures higher up, predisposing to injury, these effects are exacerbated in poorly conformed horses.

Poor medio lateral hoof morphology effects the wider skeletal system by causing uneven loading of the limb, all structures on the high side suffer from compressive forces and the low side from strain.

Fig 1 shows side bone, the lateral cartilages are one of the structures effected by medio lateral imbalance, when the hoof lands, the high side will make contact first, taking most of the impact forces and then subsequently as shown in Wilson et al (1998) will continue to bear more load during the stride. This uneven loading will predispose to damage of ligaments and joints all the way up the limb, an example being splints (uneven loading of the metacarpal bones causing damage to the interosseous ligaments). Often the articular joints of the limb can be almost touching on the compressed side, when loaded this can cause damage to the articular cartilage as the bones collide, in some cases causing OCD as a chip of cartilage and/or bone is broken off and floats within the joint capsule, or the cartilage can suffer excessive wear on the load bearing side. Medio lateral imbalance will also cause the animal to change its stance to try and counter the imbalance, this can predispose the animal to muscular issues and changes in muscular development (Kilmartin 2014).

Fig 2. shows the environmental and biomechanical effects on hoof morphology. The hoof responds to the forces acting upon it. Courtesy of M. Caldwell

Fig 3. shows that poor hoof morphology is perpetuated by forces acting upon an imbalanced hoof. Courtesy of M. Caldwell

Poor mediolateral morphology can be caused by farriery (repeatedly trimming imbalanced) or by conformation, as discussed by Simon Curtis (1999) angular limb deformities are a route cause of poor medio lateral hoof morphology. He discusses how the horses hoof will morph according to the loads and stresses it is exposed to, this is expanded on in fig2 and Fig3. If the horse is base wide and has knock knees (carpal Valgus), it will have a hoof capsule that is distorted laterally so that it flares on the lateral wall, is upright or under-run medially and may have the medial bulb shunted proximally. Its action will dish, and it will probably land on the lateral hoof wall, smack down hard on the medial side during the weight bearing phase and breakover on the inside toe. If its uneven landing is severe it will be prone to corns and even quarter cracks. (Curtis 1999 Foal to race horse pg. 3)

Poor mediolateral imbalance can also predispose the horse to interference injury as the conformational defect effects limb flight. Fetlock Varus for example, as discussed by Curtis (1999) may cause the hoof to be upright laterally, flared medially and cause an axial movement in flight causing interference injuries with the opposing limb.

In the ideal conformation the loads and strains of the horse are evenly distributed throughout the hoof, this allows for a balanced hoof morphology as the forces acting upon the hoof are what is responsible for the hoof shape fig2.

Fig 3 helps to explain how poor hoof morphology is perpetuated by poor conformation and other environmental influences, as discussed by Curtis (2002) form follows function, this poor morphology is likely caused by poor conformation and then the cycle is perpetuated due to the mechanical function of the hoof being compromised.

The effect that distal limb deformities can have on the loading forces imposed on the hoof capsule is demonstrated in fig.4. the blue line indicating the direction of the centre of force descending the limb. As stated by T. Stashak (2002) base narrow conformation causes the horse to bear more weight on the outside of the foot and a base wide horse causes the foot to bear more weight medially, these imbalances will inherently cause poor hoof morphology.

Fig.4 Lower limb deformations, craniocaudal conformations. Table shows deviations from the ideal in lower limb craniocaudal conformation. Picture courtesy of Veteriankey.com

Poor medio lateral balance can also give rise to sheared heels as discussed by T. Stashak (2002) as one heel is repeatedly subjected to more load. Sheared heels can then lead to other predispositions such as chronic heel soreness, hoof cracks in the bars or quarters and deep thrush in the central sulcus as the frog essentially splits in half.

Poor dorso-palmer hoof balance (DPHB) is a major cause of lameness in sports horses, Witte (2014) discussed how DPHB has a direct effect on the centre of pressure (CoP) within the hoof and the lever arms of the toe and deep digital flexor tendon (DDFT), a horse with long toes and low heels or a broken back hoof pastern axis (BBHPA) will have a long lever between the point of rotation and the tip of the toe, this requires an increase force from the DDFT to initiate breakover, this subjects the DDFT and the whole navicular area to increased load and strain predisposing them to injury. T. Witte statements are backed up by Van Heel et al (2004) Van Heel et al (2005) and Moleman et at (2006) who all discuss the movement of the CoP in relation to hoof morphology.

Fig 5. Shows a “flat” long toe, low heel foot, poor hoof morphology, remedial farriery has corrected the HPA, but the cause of the hoof morphology can have many parts to the equation.

Fig 5 shows an x-ray of poor DPHB, you can clearly see a BBHPA, the DDFT is already under strain due to the increased angle in the distal interphalangeal joint.


Fig 6 shows the change in angle between the pastern and hoof caused by low week heels and a long toe, this shows a possible Negative palmer angle discussed later in this article.

As well as the predispositions with the navicular structures and the DDFT, studies have shown that poor DPHB can affect the wider skeletal system, T. Anderson et al (2004) touched on this by stating that the HPA had a relationship with Carpal and Tarsal effusion in race horses. An earlier study by O. Balch (2001) goes into some depth as to the predispositions of poor DPHB, he stated that underrun heels may not be a direct cause of musculoskeletal disease but strongly predisposes the musculoskeletal system to injury. Horn tubules in the part of the heel that is underrun are folded, this reduces their resistance to compression, the heels bear increased concussion due to simultaneous reduction in ground surface area and dorsal shift in location. The dorsal shift of ground–contact surface causes hyperextension in the joints of the digit, this increases tensile forces on the palmar aspect of the distal limb and increases compression loading on the dorsal surface of the distal limb.

The wider effects of poor hoof morphology are also discussed by Kilmartin (2014) who states that the distortion of the hoof can cause the muscles higher up to over exert and even predispose the thoracic spine to injury. Kilmartin (2014) went into depth explaining that hoof morphologies cause physiological adaptations within the horse leading to muscular pathologies, he stated, as an example, “Looking at the sole of the hoof the medial wall is higher than the lateral wall. In these cases, the Transverse, Ascending, and Descending Pectoral muscles are working along with the Subscapularis and Brachiocephalic to keep the fore limb under the body. These horses again consistently show pain or reactivity over the cartilage of the scapula. There is no pain or flinching at all after correct adjustment and permanent resolution with levelling hoof trim.” (Kilmartin 2014 Equine Orthopaedic Balance pg. 4)

Poor DPHB can be high heel low toe, this conformation can cause increased strain on the suspensory and the extensor tendons and can subject the digit and limb to increased concussive forces, it is important with this conformation to understand the root cause of the morphology as sometimes veterinary treatment may be necessary to re-establish balance, it can have different causes, one being flexural deformities (S. Adams 2000). As discussed by T. Shashak (2002) this conformation could predispose the horse to injuries associated with the increased strain on the structures stated above. Pyramidal distortion, extensor process fracture and low ring bone are mentioned as predispositions of the gait of high heeled conformation. Ball (2001) discussed the conformations that can cause navicular, he clearly stated that poor conformation, causing poor hoof morphology predisposes the horse to navicular syndrome. he stated that as well as low heels or BBHPA being a cause for reasons stated previously, a broken forward hoof pastern axis (BFHPA) also predisposes to this syndrome.

Skeletel asymmetry is a natural part of biological variation, and these variations will influence hoof morphology, high – low hoof conformation is a common issue seen by farriers, this conformation is caused by skeletal variation or inury, Watson et al (2003) showed 76% of thoroughbred racehorses to have a larger right third metacarpal and hinted at asymmetries having an effect on coordination and balance and Pearce et al (2005) questioned whether common femoral asymmetrys were congenital or acquired through workload, studies of the hoof found that uneven hooves could be attributed to foal grazing habits producing laterality, Van Heel et al (2006) found 50% of foals to have a preferred side to load while feeding which directly caused them to develop uneven feet and loading patterns, Hobbs et al (2018) then went on to measure the effect of this conformation on the musculoskeletal system, showing that the asymmetric propulsive forces directly effected the centre of mass balance and predisposed the horse to orthopaedic injury, this is the perfect example of conformation causing hoof morphology that causes a predisposition to pathology. Another common conformation-pathology cycle is that of negative palmer angle (NPA) of hind hooves (Fig 7) and spinal/hind end pathology, the question being does spinal pathology cause the animal to stand under to avoid pain which then excessively loads the heels causing crushing and creating the NPA or does the NPA and stance cause the spinal pathology.

Fig.7 Negative Palmer Angle in a hind hoof.

Mansmann et al (2010) discussed the stood under stance of horses with long toe low heeled hind feet, it stated that this hoof conformation caused gluteal pain and bringing the breakover back alleviated this, however this could be debated as breakover is seen as a fore limb mechanical process and this method doesn’t address the NPA, the increased comfort could be down to the temporary improvement in HPA by the trimming down of the toe, the length of the shoe at the heels and the reduction of work load of the DDFT. Many studies have shown that differences in the fore and hind hoof angle have direct effects on both static and dynamic biomechanical forces of the proximal limb, but in the hind particularly it is still debated whether the associated hind limb and spinal pathologies are the cause or effect, Pezzanite et al (2019) studied this relationship and found that the majority of horses with hind limb pathology did have a NPA, O’Grady et al (2018) expressed how conformational hoof defects predispose to a different string of pathologies in front then the hind due to the different biomechanical function of the fore and hind limbs, the fore limb being primarily weight bearing and the hind being the propulsive engine, it also outlined the vast improvements that farriery intervention could provide in the alleviation of a NPA, but in all these studies the chicken and egg question remained unanswered.

Fig 8. Stood under stance with a NPA hoof, this horse has gluteal discomfort but which came first?

As well as the musculoskeletal/hoof morphology relationship there is also a systemic/hoof relationship, diet has a direct effect on the quality of the hoof but one systemic disease stands out as having effects on hoof morphology.

Laminitis causes poor hoof morphology by retarding growth to the front part of the hoof Curtis (2002) in acute cases it causes a dislocation of the distal phalanx in relation to the hoof wall. Curtis (2002) went into some depth as to how the wider physiological system of the horse causes this disease of the foot, stating that there are 4 theoretical pre-cursers to what is eventually seen in the hoof, Vascular theory, toxic theory, metabolic theory and mechanical theory.

Vascular theory describes how vasoconstriction within the digit causes ischaemia to the sensitive laminae, in turn causing a break down in the bond between sensitive and horny laminae and a subsequent tearing away of the dorsal wall (Hood et al 1993). Pollitt & Daradka (1998) and Johnson et al (1998) discussed the breakdown of the connective tissue of the base membrane caused by the activation of matrix metalloproteases (MMPs) as the root cause of laminitis. Metabolic theory says that the breakdown of the base layer is due to metabolism (Curtis 2002). Mechanical theory states that laminitis can be induced by repeated trauma to the laminae (Curtis 2002).

Regardless of the cause of laminitis, it very often causes a chronic hoof morphology (Curtis 2002) the hoof grows a poor DPHB, the heels grow high and the toe tears away forming a laminal wedge.

Fig.9The hoof morphology of chronic laminitis.

Due to the poor hoof morphology caused by laminitis other structures become affected. As stated above some structures are directly affected by the causes of laminitis, these being the laminae and the dorsal wall and heels, subsequent to these effects, Curtis (2002) listed some other structures that become affected: Due to the pull of the DDFT and the breakdown of the laminal bond the pedal bone often rotates with the toe pointing toward the sole, solar bruising and prolapse of the sole can occur in the area directly below the distal fringe of the pedal bone, in chronic cases the bone can remodel itself due to the un natural pressures forced on it. Sand cracks can form due to the curve in the wall and lead to abscesses, abscesses can become frequent in the heels as they become overloaded and underrun. It can also be quite common in sinker cases for the bone column to sink within the hoof capsule medio-laterally imbalanced, caused by one side of the hoof sinking more than the other, this then predisposes the animal to poor medio lateral predispositions as discussed earlier.


It can be clearly seen that the relationship between hoof morphology and the physiological musculoskeletal systems of the equine is not linear and this review only touches the surface of the complexities of it. Disordered anatomy has an influence on hoof morphology and hoof morphology, whether poor, or simply normal growth between shoeing/trimming periods, predisposes anatomy and physiology to increased or imbalanced load/strain injury. Any deviation from the ideal in conformation has a direct effect on the morphology of the hoof and poor hoof morphology whether medio-laterally or dorso-palmer has a direct effect on the anatomy of not only the digit but the entire horse. Other physiological systems can also affect hoof morphology, including the circulatory and digestive systems especially in the case of laminitis. In order to really answer the chicken and egg question long term longitudinal studies would have to be performed to watch the process unfold, even then you would probably get instances of chickens laying eggs and eggs hatching chickens, but one thing that can be taken from this is that farriers must look up, ask questions of what conformation is in front of them and be a pro-active part of a larger team of professionals that understand the important and vital relationship between the hoof and the horse.

Stay tuned to the Equine Documentalist for further reading into some of the relationships discussed above or book a lecture on Pro-active farriery. Farriery consultation also available.


Adams, S.B. (2000) ‘Management of congenital and acquired limb deformities.’ Proc. Am. Ass. Equine Practnrs, Vol. 46. pp. 117-125

S. Curtis (2002) Corrective farriery: A text book of remedial farriery Newmarket: Newmarket Farrier Consultancy p.106

Stashak, T. (2002) Adams lameness in horses: Fifth edition. Baltimore

Anderson, T, et al (2004) ‘The role of conformation in musculoskeletal problems in the racing Thoroughbred.’ Equine Veterinary Journal, Equine vet. J. Vol. 36, No. 7, pp. 571-575

van HEEL, M.C.V et al (2004) ‘Dynamic pressure measurements for the detailed study of hoof balance: the effect of trimming” Equine Veterinary Journal, Vol. 36, No. 8, pp. 778-782

van HEEL, M.C.V. et al (2005) ‘Changes in location of centre of pressure and hoof-unrollment pattern in relation to an 8-week shoeing interval in the horse.’ Equine Veterinary journal, Vol. 37, No. 6, pp. 536-540