Navicular Disease

Navicular Disease

Navicular Disease is a soundness problem in horses, more accurately called "navicular syndrome" as opposed to "disease." It most commonly describes an inflammation or degeneration of the navicular bone and its surrounding tissues, usually on the front feet. It can lead to significant and even disabling lameness.


Description of the Navicular Area

Knowledge of equine forelimb anatomy is especially useful for understanding navicular syndrome. The navicular bone (or distal sesamoid) lies behind the coffin bone and under the small pastern bone. The deep digital flexor (DDF) tendon runs down the back of the cannon and soft tissue in that area and under the navicular bone before attaching to the back of the coffin bone. The DDF tendon flexes the coffin joint, and the navicular bone acts as a fulcrum that the DDF tendon runs over.

The navicular bone is supported by several ligaments above, below, and on the side. One of these ligaments is the impar ligament, which attaches the navicular bone to the coffin bone (distal phalanx). Cartilage lies between the navicular bone and the coffin joint, as well as between the navicular bone and the DDF tendon. The navicular bursa - a small sac that protects the DDF and navicular bone from abrasion as the tendon slides over the area - lies between the navicular bone and the DDF tendon.[1]

Causes and Contributing Factors of Navicular Syndrome

There is no single known cause of Navicular Syndrome, although many theories. The two most important factors in Navicular Syndrome are:

Compression of the navicular bone under the DDF tendon and the back of the small pastern bone. Repeated compression in this area can cause cartilage degeneration, with the cartilage flattening and gradually becoming less springy and shock absorbing. The cartilage may also begin to erode. Cartilage degeneration is common in navicular horses, usually along the flexor surface. This finding, and the associated biochemical changes, have led some researchers to conclude that there are elements in navicular disease common to osteoarthritis, and to suggest similar therapeutic regimes.[2]

Cartilage erosion may progress to the point that the bone underneath will become exposed. With the cartilage no longer present to protect it, the navicular bursa and DDF tendon may become damaged by the constant rubbing against the navicular bone. Navicular bursitis (inflammation of the navicular bursa) may occur, even if cartilage damage is not severe. This is probably due to the friction between the navicular bone and the DDF tendon from compression.

Constant compression can also increase the bone density directly under the cartilage surfaces, especially on the flexor side. This actually tends to make the bone more brittle, and thus more likely to break.

Tension placed on the ligaments that support the navicular bone. Some experts believe that the degenerative process begins with excess tension placed on these ligaments. Excess tension causes strain and inflammation. Inflammation from strain of the impar ligament can decrease blood flow to and from the navicular bone, as the major blood vessels supplying the bone run up and down this area. If the ligament continues to be strained, it can thicken and permanently reduce blood flow to the navicular bone.

Because veins are more easily compressed than arteries, blood flow to the bone would be less obstructed than blood flow from the bone. This would cause a build up of pressure within the navicular bone. The navicular bone, in response to both the increased pressure and overall decreased blood supply, would absorb mineral from its center.

Excess tension can also cause exostoses where the ligaments attach to the navicular bone, giving the bone a "canoe" shape. If tension is extreme, the ligaments may actually tear.

Toe-First Landing

Recent research has found correlations between "toe-first landing" of the hooves and navicular problems, due to excessive strain put on the deep digital flexor tendon, as a consequence of misalignment of the lower joints.[citation needed] Toe-first landing, usually seen as a consequence of navicular disease, may actually be a cause or at least a contributing factor to the onset of tendon inflammation and bone modifications.

Toe-first landing is often caused by frog and heel overtrimming, long toes, and/or poor shoeing.

Contributing Factors


Certain conformational defects may contribute to Navicular Syndrome, especially defects that promote concussion. These include upright pasterns, small feet, narrow and upright feet, significant downhill build (commonly seen in American Quarter Horses), and long toes with low heels (commonly seen in Thoroughbreds).

The long toe, low heel conformation places constant stress on the navicular bone, even as the horse is standing. Upright feet increase concussion, especially in the heel region of the hoof where the navicular bone is located. Excess concussion cannot be absorbed as well by the structures designed to do so (the frog, heels, and digital cushion), and so more impact is transmitted to the structures within the foot.

Poor hoof shape is usually inherited, although poor shoeing and trimming can contribute to these shapes.

With the long toe, low heel conformation can come contracted heels (narrowing of the heel) which further compresses the navicular bone along with sheared heels adding more stress to the tendons and navicular bones.


While poor trimming, shoe selection, or inappropriate shoe attachment are well-known causes of lameness,[3] research[4] suggests that shoeing itself can increase the incidence of navicular disease in horses[5][6][7]. In nature, a horse's hoof is designed to expand and contract as the horse moves. This expanding and contracting acts as an auxiliary blood pump, and aids the circulation of blood to the lower extremities. When the inflexible metal shoe is attached to the hoof, the hoof can no longer work as designed, and blood flow is inhibited.[7] Barefoot trimmers have stated that this results in the hoof becoming numb, and may eventually alter the physiology of the hoof. However, this is based on indirect evidence obtained from cadaver limbs.[8]

Although navicular disease is fairly common in the modern day domesticated horse, it is virtually non-existent in wild horse populations. [9] However, evidence of navicular degeneration is well established in the fossil record of early horses.[10]


Working on steep hills, galloping, and jumping all contribute to Navicular Syndrome, as they place greater stress on the DDF tendons, and may cause overextension of the pastern and coffin joints.

Regular exercise on hard or irregular ground increases concussion on the hoof, thus increasing the risk of Navicular Syndrome.

It is possible that standing can increase the chance of navicular disease (such as a horse that spends most of the day in a stall with little turnout, usually seen in racehorses and some show horses). This is because blood flow to the hoof decreases when the horse is not in motion. The horse is also constantly applying pressure to the navicular bones (which is intermittent as the horse moves).

Body weight

Horses with a high weight-to-foot-size ratio may have an increased chance of exhibiting symptoms of Navicular Syndrome, since the relative load on the foot increases. This might explain why Navicular Syndrome is seen more frequently in Thoroughbreds, American Quarter Horses, and Warmbloods as opposed to ponies and Arabians.[11]


Heel pain is very common in horses with Navicular Syndrome. Lameness may begin as mild and intermittent, and progress to severe lameness. This may be due to strain and inflammation of the ligaments supporting the navicular bone, reduced blood flow and increased pressure within the hoof, damage to the navicular bursa or DDF tendon, or from cartilage erosion.

Affected horses display a "tiptoe" gait - trying to walk on the toes due to heel pain. They may stumble frequently. The lameness may switch from one leg to another, and may not be consistent. Lameness usually occurs in both front feet, although one foot may be more sore than the other.

Lameness is usually mild (1-2 on a scale of 5). It can be made worse when the horse is worked on a hard surface or on a circle.

After several months of pain, the feet may begin to change shape, especially the foot that has been experiencing the most pain, which tends to become more upright and narrow.

Treatment and Prognosis for Navicular Syndrome

No single treatment works for all cases, probably because there is no single cause for all Navicular Syndrome cases. The degenerative changes are usually quite advanced by the time the horse is consistently lame, and these changes are believed non-reversible. At this time, it is best to manage the condition and focus on alleviating the pain and slowing the progression of the degeneration.


Putting the foot into proper neurological and biomechanical balance is crucial. Often Navicular horses have long toes and underrun heels with very little inner wall depth or strength. Exposing the horse to proper stimulus to improve hoof form and structure is also vital.

Hoof Care

The issue of hoof care is subject to great debate. Corrective shoeing can be beneficial to horses suffering from navicular disease, although sometimes the effects are only temporary. Others believe that removing the shoes altogether is the best way to manage navicular disease, as it allows increased circulation to the hoof.[8] People from both sides agree, proper hoof shape and angle are an important long-term management plan for a horse with navicular disease. As with laminitis, each horse may respond differently to a given technique, so the farrier, owner, and veterinarian should work as a team to formulate a plan and to adapt if the initial plan is not effective.

People who choose to treat navicular disease through shoeing will sometimes use a shoe designed to lift and support the heels.[12] This can sometimes be accomplished with a flat shoe and trimming alone. Wedge pads or wedged shoes are often used, but can amplify heel-related problems if present.[13] Another strategy is to use a bar type shoe. Often, an egg-bar shoe[14], or straight bar shoe.[12] Some horses will also benefit from shoes that change the breakover of their foot (like a rolled toe). With or without shoes, the hoof must be trimmed in such a way as to restore the balance and angle that may have been lost. Horses with long toe-low heel conformation need careful trimming to counter this. Horses with upright feet may need their heels lowered and a shoe that will allow their heels to spread. Early intervention is key; in one study, shoeing was successful in 97% of horses treated within ten months of the onset of signs, while only 54% of horses lame for over a year responded.[15]

Advocates of barefoot trimming cite recent studies which show that removing the shoes can help alleviate the symptoms of navicular disease, and in some cases, reverse some of the damage done to the hoof.[16] Because navicular disease can be caused, or at least exacerbated by shoeing, removing the cause is the first step in this strategy toward the management of pain in the animal.[8] Successive carefully applied trims help to restore the natural angle and shape of the hoof, while walking helps to stimulate circulation to the hoof.[16] It is not uncommon to find horses whose navicular disease is completely manageable through corrective barefoot trimming. [8] However, this may require a transition period lasting from weeks to years where the horse may remain lame,[9] or may never become sound[17][18],[19]

If there is significant degeneration in the bone, a flexor cortex cyst, adhesions to the deep digital flexor tendon, or avulsion fractures, relief is typically incomplete no matter what foot care technique is used.[20]


Horses with Navicular Syndrome need a work schedule that is less intense. Their fitness can be maintained by slow long-distance work or swimming, as opposed to being worked at high speeds, up steep hills, on hard surfaces, irregular terrain, or deep footing. Reducing the frequency of jumping is also important.


Vasodilators: improve the blood flow into the vessels of hoof. Examples include isoxsuprine (currently unavailable in the UK) and pentoxifylline.

Anticoagulants: Also to improve blood flow. The use of warfarin has been proposed, but the extensive monitoring required makes it unsuitable in most cases.

Anti-Inflammatory Drugs: used to treat the pain, can help the lameness resolve sometimes if shoeing and training changes are made. Include NSAIDs, corticosteriods, and other joint medications. The use of intramuscular glycosaminoglycans has been shown to decrease pain in horses with navicular disease, but this effect wanes after discontinuation of therapy.[21] Additionally, oral glycosaminoglycans also may have a similar effect.[22]

Bisphosphonates can be useful in cases where bone remodeling is causing pain.[23]

There is evidence that Gallium Nitrate may also have a beneficial effect. Gallium is extremely anti-inflammtory and it has effects superior to bisphonates. It has been studied in a 100 horse research trial with the abstract reading: Navicular disease, also termed navicular syndrome or caudal heel syndrome, in horses cause much foot pain and lameness. Classical treatments often do not provide satisfactory results and the horse remains lame and occasionally the horse must be euthanized. Little is known of the etiology of navicular disease. A hypothesis was advanced that gallium nitrate, a compound reported to have anti-inflammatory, anti-bacterial, anti-hypercalcemic and anti-bone-resorptive activity, would be a safe and effective treatment for navicular syndrome. Horses diagnosed with navicular syndrome, and non-responsive to classical treatments were treated orally with 500 cc of a one percent gallium nitrate (1.36 grams elemental gallium/day) aqueous solution. Treatment reduced mean pain scores fifty percent within 14 days, as measured using a five point scale of observed lameness. Mean pain scores for the second two-week period were statistically lower than the mean pain scores of the first two-week period (p < 0.0001). Complete soundness was achieved in 33 out of 83 horses in less than 28 days, with 24 out of the remaining 50 horses showing improvement in that period, for a total of 57 (69%) horses becoming better. None were worsened and none were euthanized. Most horses remained sound long after treatment ended. No side effects, toxicity or sequela were reported. Oral gallium nitrate is an alternative treatment for navicular syndrome that appears much more effective than classical treatments, and it may, upon favorable replication of these results, become a first-line treatment for navicular syndrome. Future trials and field use of gallium nitrate to treat navicular syndrome in horses should follow a continuous dosage protocol, not the two-week on / two-week off protocol described here. [24]


Palmar Digital Neurectomy (or "nerving" or "denerving") is not without adverse side effects and should therefore be used as a last resort. In this procedure, the palmar digital nerves are severed, so the horse loses sensation in the back of the foot. This procedure should only be performed if it will eliminate the lameness associated with navicular syndrome, and only after all other options have been explored. The procedure is usually performed on both front feet. Complications can include infection of the wound, continuation of the lameness (if the nerves regrow or if small branches of the nerves are not removed), neuromas, and rupture of the deep digital flexor tendon. After the neurectomy, if the horse becomes injured in the area the injury may go undetected for a long period of time, which risks the animal's health. Due to this, the feet should be cleaned and inspected regularly. Neurectomy tends to lower the market value of a horse, and may even make the horse ineligible for competition. Neurectomy is controversial. It is best to speak to your vet if you consider it as an option. The most common misconception about "nerving" a horse is that it will permanently solve the lameness/pain issue. In fact, though the time periods vary based on the individual horse and surgical method utilized, these nerves will often regenerate and return sensation to the afflicted heel region within two to three years.

Navicular Suspensory Desmotomy: The ligaments supporting the navicular bone are severed. This makes the navicular bone more mobile, and thus reduces the tension of the other ligaments. It is successful about half the time.


The prognosis for a horse with Navicular Syndrome is guarded. Many times the horse does not return to its former level of competition. Others are retired. Eventually all horses with Navicular Syndrome will need to lessen the strenuousness of their work, but, with proper management, a horse with Navicular Syndrome can remain useful for some time.


  1. ^ U Missouri Extension
  2. ^ Viitanen M, Bird J, Smith R, Tulamo RM, May SA, "Biochemical characterisation of navicular hyaline cartilage, navicular fibrocartilage and the deep digital flexor tendon in horses with navicular disease.", Res Vet Sci. 2003 Oct;75(2):113-20
  3. ^ Parks A (2003) "Horseshoes and Shoeing", in Ross, Dyson "Diagnosis and Management of Lameness in the Horse, pp.262-271, ISBN 0-7216-8342-8
  4. ^ New Methods For The Treatment Of Navicular Disease
  5. ^ Todays Horse - Navicular Syndrome
  6. ^
  7. ^ a b Laminitis, Navicular Syndrome, Coffin Bone Penetration - Natural Hoof Care, Maple Plain, Minnesota
  8. ^ a b c d Horse Shoeing Pathological Effects, Lameness Treatment Hoof Care, Maple Plain, Minnesota
  9. ^ a b Back to Basics Natural Hoof Care
  10. ^ Turn your head and roar: can diagnosing disease in fossils shed light on modern maladies? - evidence of diseases in dinosaurs that are similar to those found in humans and other animals today - Cover Story | Science News | Find Articles at
  11. ^ Equine Podiatry | Dr. Stephen O'Grady, veterinarians, farriers, books, articles
  12. ^ a b O'Grady, S (2006)"Strategies For Shoeing the Horse with Palmar Foot Pain", AAEP Proceedings, 52(209-217)
  13. ^ Rogers, Back (2003) "Wedge and eggbar shoes change the pressure distribution under the hoof of the forelimb in the square standing horse." Journal of Equine Veterinary Science 23(306-309)
  14. ^ Ostblom et al. (1984), "Navicular bone disease: results of treatment using egg-bar shoeing technique", Equine Veterinary Journal, 16(203)
  15. ^ Turner (1986) "Shoeing Principles for the management of navicular disease", Journal of the American Veterinary Medical Association 189(298-300)
  16. ^ a b Natural Hoof - Articles
  17. ^ No Shoes?
  18. ^ Some horses need shoeing, some don't
  19. ^ Equine Podiatry | Dr. Stephen O'Grady, veterinarians, farriers, books, articles
  20. ^ Dyson S (2003) "Treatment and Prognosis of Horses with Navicular Disease" In Ross M, Dyson S, Diagnosis and Management of Lameness in the Horse 299-304, Saunders ISBN 0-7216-8342-8
  21. ^ Crissman et al. (1993) "Evaluation of polysulfated glycosaminoglycan for treatment of navicular disease", Proceedings of the American Association of Equine Practitioners Convention pp.219-220
  22. ^ Dr Reid Hanson, Auburn University, cited in Proceedings of the World Equine Veterinary Association Congress 1997. See [1]
  23. ^ Tiludronate as a new therapeutic agent in the treatment of navicular disease [Equine Vet J. 2003] - PubMed Result
  24. ^ Oral Gallium Nitrate Restores Soundness in Horses with Navicular Disease - A Pilot Study


  • King, Christine & Mansmann, Richard, VMD, PhD. Equine Lameness. Copyright Equine Research (1997). (p. 610-626).
  • PT Colahan, IG Mayhew, AM Merrit & JN Moore Manual of Equine Medicine and Surgery Copyright Mosby Inc (1999). (p. 402-407).
  • RJ Rose & DR Hodgson Manual of Equine Practice Copyright WB Saunders (2000). (p. 126-128).
  • Viitanen M, Bird J, Smith R, Tulamo RM, May SA, "Biochemical characterisation of navicular hyaline cartilage, navicular fibrocartilage and the deep digital flexor tendon in horses with navicular disease.", Res Vet Sci. 2003 Oct;75(2):113-20
  • Dr Reid Hanson, Auburn University, cited in Proceedings of the World Equine Veterinary Association Congress 1997. See [2]

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