by Richard Dunivant - X-rays submitted by James Garfinkel, DVM

Published in the December 2000 Issue of Anvil Magazine

Image: Right front foot

Recently, a client presented a new horse described as being "gimpy in both front feet, especially after hard exercise." When I pulled the shoes I found the sole had been excessively trimmed. Heel corns had begun to develop from axial redirection of the shoe branches by a farrier who erroneously stated "this would prevent the horse from overreaching." Sole bruising was present inside the white line where the inside of the shoe web had exerted excessive pressure on the sole. The front gait was choppy and the horse frequently stumbled and forged as a result. The horse, a barrel racer, was subjected to constant concussion on hard, rocky surfaces, but the clients were unable to say how long these conditions had been present. Initially I thought that foot bruising from improper shoeing, overzealous trimming of the sole, and the pain from the developing corns were responsible. I hoped the horse would improve with time and proper shoeing. Six weeks later, the corns were almost obsolete, no visible signs of hemorrhage in the epidermal tissues were present, but the horse remained persistently lame without improvement in both front feet. He reacted strongly to hoof testers by pulling away. I instructed these clients to have their veterinarian do a workup on the horse for pedal osteitis, which was later confirmed.

Image: Right front foot

A second horse presented with a history of recurrent, intermittent episodes of front right lameness and frequent right front subsolar abscesses that required drainage. The horse was utilized as a hunter and, when obtaining a history, the owners stated he had sustained a penetrating injury to the frog three years ago when hunting in the field. The horse presented with symptoms of a subsolar abscess. Close inspection of the foot, however, revealed a small drainage tract from the old area of injury. Once again the veterinarian was called to x-ray for pedal osteitis. When a diagnosis of septic pedal osteitis was made, the horse was referred to the large animal clinic at a nearby university for surgical debridement of infected bone and soft tissues. After an eight-month convalescence, he returned to normal athletic functioning.

What is pedal osteitis? Why does its symptoms present so differently and often so vaguely?

Pedal osteitis is defined as an inflammatory disorder of the coffin bone that is characterized by either diffuse or focal radiolucent changes and new bone formation. (See Editor's Note at the end of this article.) The disorder is a result of persistent inflammation in the foot. Since the coffin bone does not have a medulla (bone marrow), the bone inflammatory process is labeled osteitis as opposed to osteomyelitis. The disorder is more commonly seen in front limbs since 60 percent of the horse's weight is distributed there, but it can affect the hind feet as well. Involvement can be unilateral or bilateral depending on the cause. There are two types of pedal osteitis: nonseptic and septic. Causes of the entity are varied - it can occur as a primary or secondary condition. Treatment is often aimed at correcting the underlying condition that caused its development.

Image: Right front foot


Primary nonseptic pedal osteitis typically results from severe or chronic sole bruising sustained from repeated concussion during exercise on hard surfaces. Secondary nonseptic pedal osteitis can be the result of conformation faults or improper farrier work that have caused uneven weight bearing on the sole. Hoof testers elicit positive responses between the sole and wall in diffuse or localized areas. Lameness can vary in degrees of severity and is often exacerbated after exercise or shortly after trimming or shoeing. Sole bruising may not always be apparent, since foot opacity can prevent immediate visibility until the hemorrhage spreads into the epidermis distally and becomes apparent to the eye. Most of the time, chronic bruising is visible on the solar surface and horn hemorrhage can appear stippled because of the tubular and intertubular horn pattern.

Radiographic changes are required to make a true diagnosis of both types of pedal osteitis. Bone demineralization that occurs in this disorder can often be difficult to detect in field x-rays, since numerous variables can affect a radiographic image, such as amperage and distance from the machine. Multiple x-rays are often required. Typically, bone demineralization will occur around the toe margin and irregular bone formation is seen along the solar margin or the dorsal (top) surface of P3. The fibrous membrane that covers bones except at joint surfaces is called the periosteum. It contains numerous blood vessels and an inner layer of connective tissue cells which act as osteoblasts (bone-forming cells) when the bone is injured or subjected to persistent long-term inflammation. This periosteal proliferation appears on x-ray as irregular bone surfaces. When viewed laterally, an irregular bone projection extending downward toward the heel region is often seen. Other radiographic changes include widened vascular channels or passages known as nutrient foramina. Severe cases of demineralization can weaken the bone margins and cause fractures of the coffin bone. X-ray alone should never be used to make the diagnosis of pedal osteitis, since there is a small percentage of asymptomatic horses that show similar changes. Palmar digital nerve blocks are also used to make a diagnosis. The entire foot may need to be blocked if the dorsal bone surface is involved. Thermography is a helpful adjunct when radiographic findings are inconclusive and will show chronic inflammatory processes existing in the hoof.

Image: Left front foot

Once a diagnosis is made, optimally, the veterinarian and farrier will work together to come up with a shoeing regimen/prescription. For example, the veterinarian may prescribe nonsteroidal anti-inflammatory agents (NSAIDS), and, while consulting with the farrier for his/her input, they will arrive at a shoeing regimen that will vary according to the needs of the animal. Severe or chronic sole bruising must be minimized. I always recommend an aluminum shoe since aluminum absorbs more concussion than steel. It is sole concussion that initiates the inflammatory process responsible for bone demineralization and periosteal proliferation. These horses also benefit from the use of sole-toughening agents such as a combination of iodine and formaldehyde in a 1:1 solution concentration. Commercial products like Durasole can be employed by the farrier and client.

In an effort to minimize the forces of weight bearing on the sole, I have seen egg bar shoes prescribed with a sole trimmed to achieve a deep concave surface. The egg bar shoe's ability to extend weight behind the heels moves the center of weight bearing forward, allowing even distribution around the hoof capsule. However, egg bar shoes can lever the toe by allowing the heels to sink, and often exacerbate the symptoms of pedal osteitis. Trimming a sole to achieve a deep concave surface is not always possible on thin- soled horses or those that have been excessively pared out. Initially, I prefer the use of an aluminum straight bar shoe (which will not apply added leverage at the heel) along with a rolled or rockered toe, full pads (leather, Luwex, etc.) and sole packing of your choice. I do not recommend silicone since it can cause too much sole pressure if not applied correctly. My choices are Equi-Thane or Grand Circuit sole packing material because they allow even distribution of the material. Later, the shoe can be changed to a 1/4" x 1/2" aluminum shoe with a pad. The use of a wide web shoe may cause excessive sole pressure inside the white line. Grand Circuit aluminum stabilizers are another choice for providing sole protection and will minimize concussion on the sole. They can be riveted to an aluminum shoe for long-term use and do not increase chances of thrush development. Often, other types of corrective shoeing must be utilized to treat conformation deformities or coffin bone fractures that may be an underlying cause.


Septic pedal osteitis is caused by a pathogen that infects the soft tissue of the foot and extends into the coffin bone. Causes of septic pedal osteitis include a penetrating injury to the soft tissue, subsolar abscess, untreated white line disease, laminitis, infected corns or any long-standing soft tissue infection of the hoof. The infection can involve the coffin bone, sole structure, laminae and the hoof wall. Symptoms include drainage from the foot - often in the form of a tract leading directly to and from the coffin bone.

X-ray changes that are specific to the septic form of pedal osteitis show isolated areas of avascular bone that have become necrotic and have separated from the coffin bone known as sequestrums. These necrotic pieces can be designated as a primary sequestra (if the piece is entirely detached), secondary (if it's still loosely attached) and tertiary (if still attached by remaining in place). X-rays will also reveal bone density loss at the laminar attachments. MRI scans can be used to detect adjacent soft-tissue infection.

Treatment for septic pedal osteitis often involves surgical debridement under neural block or general anesthesia to drain purulent exudate, remove sequestra, and curettage of infected or necrotic bone and tissue. Up to one-fourth of the coffin bone can be removed without permanent long-term effects. The wound is initially treated with antibiotic-soaked gauze, waterproof bandages and daily wound cleansing with antibiotic irrigation. Often oral antibiotics and anti-inflammatory agents are prescribed. Areas of white line disease may be resected concurrently. After granulation tissue covers the coffin bone (usually in 7 to 10 days), the farrier can make a hospital plate to cover the area, provide relief from any sole pressure and allow observation and treatment of the foot. Selection of the type of plate depends on the size of the area needing to be treated and the skill of the farrier. Sole-hardening agents can be applied once granulation tissue is level with the sole as directed by the veterinarian. Recovery from septic pedal osteitis may require a lengthy convalescence, but the prognosis is excellent unless the underlying cause is laminitis.

With proper diagnosis, early detection, and a combination of medical and farrier techniques, pedal osteitis can be resolved and most horses returned to athletic function. Quite often these horses have other substantial underlying causes that must be resolved, making the treatment plan specific to the individual horse and a challenge to the skills of the farrier.

Editor's Note: This article was sent to James Garfinkel, DVM, of Shingle Springs, CA, for review. In regard to Mr. Dunivant's statement, "Pedal osteitis is defined as an inflammatory disorder of the coffin bone that is characterized by either diffuse of focal radiolucent changes and new bone formation," Dr. Garfinkel replies: "Clinically, we rarely see new bone growth, or regrowth of bone. In my experiences, once I have diagnosed pedal osteitis with bone resorption, I can radiograph that horse several years later and the lesion has not changed, unless the condition has flared up, and further bone degeneration has occurred. The same applies to coffin bone fractures; they heal with a fibrous union, but radiographically, they look the same in the years to come."


Gaughn, EM, Rendando VT, Ducharme NG: Surgical Treatment of Septic Pedal Osteitis in Horses: Nine Cases (1980-1987), J Am. Vet. Med. Assoc. 1989;195(8);1131- 1134.

Moyer WA: Traumatic Pedal Osteitis (TPO) in Racehorses. Radiographic Changes in the Distal Phalanges of Quarter Horses with Lower Leg Lameness. J Am Vet Radiology Society 1978;19:60-64.

Moyer WA, Colahan PT, Mayhew IG, Merritt AM, Moore JN: Pedal Osteitis: Equine Medicine and Surgery, 4th edition, Goleta, CA: American Veterinarian Publications 1991; pp.1340-1341.

Moyer WA: Traumatic Pedal Osteitis (TPO) in Racehorses. Annu. Proc. AAEP 1989, 34:417-419.OSTEITIS by Richard Dunivant  X-rays submitted by James Garfinkel, DVM

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