Arthritis and DJD: An Overview

Arthritis in Horses

  by Robert N. Oglesby DVM

Introduction

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Arthritis is often a misunderstood term. Arthritis simply means "inflammation in the joint". But the cause and the course of the inflammation and even which part of the joint is inflamed differs from case to case. Arthritis can be an acute reversible situation such as you might see in blunt trauma to a joint or a chronic progressive disease which cannot be cured. It may involve just the surrounding soft tissue like the joint capsule or collateral ligaments or all the tissues including the cartilage that lines the bones that make up the joint. The cause of the inflammation can be trauma, infection, abnormal growth of the cartilage, or reactions to medications.

What most equestrians mean when they use the word arthritis is the chronic progressive form so often seen in the joints of horses. This form of arthritis is called osteoarthritis or degenerative joint disease (DJD) and includes the diseases of bone spavin and ringbone. DJD is an appropriate term because once it begins the degeneration is progressive. Though progressive and a cure beyond our capabilities at this time, many horses with DJD can still perform at some level with appropriate management and therapy. This article discusses how DJD starts, diagnosis, treatment and prognosis of osteoarthritis or DJD in horses. Links are provided to articles on specific forms of arthritis and therapies used in the treatment of arthritis.

How DJD Develops

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It is fair to say that you and your horse are developing DJD in every joint at this very moment. Joints are traumatized every day. Running, trotting, even walking or perhaps standing in one position too long all introduce small amounts of trauma to the tissues of the joint's parts, the synovial membrane, the cartilage and it's underlying bone. Like any tissue they respond with inflammation and repair. If the trauma is not too great the repair is close to 100%. But if the trauma is severe the damage may not be completely repairable or may take time. These areas of incomplete repair are initially still functional but now not as strong and more sensitive to the ongoing trauma and responds with greater inflammation. The areas of incomplete repair worsen and in permanent damage can occur setting up a cycle of damage and inflammation that results in ongoing deterioration.

At this point the structural integrity of the joint is so poor that no matter what is done the degeneration has become progressive and DJD has set up. When this occurs depends on many factors. A single severe acute traumatic episode may bring on DJD, but for most horses DJD develops insidiously over time do to repetitive small traumas. The harder the work is without adequate periods of rest the faster this accrued damage occurs. Skeletal deformities can exacerbate the trauma. Depending on conditions it may take several years or several decades, but eventually joints will wear out and DJD established.
arthritis

In what is the largest best controlled study of DJD in horses, risk factors were assessed in 420 horses of a single breed that was sired by 17 different sires. This study may have significance to other forms of arthritis so bear studying. The risk factors associated with radiographic signs of DJD in the hock:
  • age
  • tarsal angle
  • birthplace
Factors not associated with the prevalence of hind limb lameness and/or radiographic signs of DJD in the distal tarsus training intensity:
  • applied training intensity (surprisingly)
  • the use of a professional or amateur trainer
  • the temperament
  • front limb action

The rate of culling due to bone spavin in Icelandic horses: Survival analysis

In a field survey, 614 healthy and sound Icelandic horses in the age range of 6-12 year (mean age 7.9 year), and in use for riding were examined radiographically and clinically for OA in the distal tarsal joints, to estimate the prevalence and clinical relevance of the disease in the riding horse population, to evaluate the effect of potential (environmental and intrinsic) risk factors and to estimate the heritability of the disease. Radiographic signs of OA in the distal tarsal joints (RS) were found in 30.3% of the horses and hindlimb lameness after flexion test of the tarsus was found in 32.4%. There was a significant correlation between the two diagnostic methods and 16.4% of the horses had both of RS and lameness after flexion test.

The survival culling rate of the horses in the five following years was significantly affected by RS and horses with the combination of RS and a positive flexion test had the poorest prognosis. A survival analysis was used to compare the culling rate of Icelandic horses due to the presence of radiographic and clinical signs of bone spavin. A follow-up study of 508 horses from the survey five years earlier was performed. In the original survey 46% of the horses had radiographic signs of bone spavin (RS) and/or lameness after flexion test of the tarsus. The horse owners were interviewed by telephone. The owners were asked if the horses were still used for riding and if not, they were regarded as culled. The owners were then asked when and why the horses were culled. During the 5 years, 98 horses had been culled, 151 had been withdrawn (sold or selected for breeding) and 259 were still used for riding. Hind limb lameness (HLL) was the most common reason for culling (42 horses). The rate of culling was low in all groups up to the age of 11 years, when it rose to about 5% a year for horses with RS about twice the rate of without RS. The risk of culling (prognostic value) was highest for the combination of RS with lameness after flexion test, next highest for RS and lowest for lameness after flexion test as the only finding. It was concluded that bone spavin affects the duration of use of Icelandic horses and is the most common cause of culling due to disease of riding horses in the age range of 7-17years

The prevalence of RS was strongly correlated to age and tarsal angle (increased as the tarsal angle decreased). The birthplace was also significantly associated with RS, and considered to be an indirect genetic effect. The prevalence of lameness after flexion test was not influenced by age but a significant effect of sire was established. The prevalence was higher for horses that were broken to saddle late (6 year or older) and for horses that had not participated in a stud show. The heritability of age-at-onset of RS, reflecting the predisposition for OA, was estimated to be 0.33 and a similar figure was found for the heritability of lameness after flexion test.

It was concluded that bone spavin is a common disease in Icelandic horses affecting their durability, although often subclinically manifested. The high prevalence of histological findings in the young horses (1-4 year) and radiographical findings in the 6-12 year old horses demonstrated a progressive nature of the disease although the progression may be slow. The initiation of the disease was unrelated to the use of the horses for riding and workload was not found to effect the development of the disease negatively. The medium high heritability together with the association to the tarsal angle and the radiographic pattern of uneven distribution of load in the CD joint, strongly indicate that poor tarsal conformation or architecture of the distal tarsal joints is the main etiological factor of the disease.

Symptoms

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