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DEGENERATIVE JOINT DISEASE (DJD)

Equine Joints

Degenerative Joint Disease (DJD), often referred to as osteoarthritis, is an extremely common cause of lameness in performance horses. The average barn accommodates several horses (at least) that are suffering from sore joints.

This article highlights the fundamentals of DJD. Links to articles detailing treatment for joint disease are also provided.

I. TYPES OF JOINTS

There are three basic types of joints in the horse. These are classified according to their relative range-of-motion (mobility).

Synarthroses are immovable joints.

Amphiarthroses move slightly.

Diarthroses are movable joints.

Most of the joints in the equine limb are of the diarthrodial type and tend to be the ones we implicate as potential causes of equine lameness. Accordingly, we will limit this discussion to disease affecting the diarthrodial (aka synovial) joints of the horse.

Normal Joint Components

II. JOINT STRUCTURES

The synovial or diarthrodial joint is comprised of:

• Articulating surfaces of bone (called subchondral bone)

• A layer of cartilage (overlying the subchondral bone)

• A fibrous joint capsule

• Synovium (consisting of synovial membrane and fluid)

• Associated supporting ligaments

The combination of a smooth cartilage surface and thick synovial fluid provides a low-friction environment through which the articulating surfaces can move freely and independently of each other.

Normal Joint Components

Primary components of the joint structure include ARTICULAR CARTILAGE, ARTICULAR (or JOINT) CAPSULE, SYNOVIAL MEMBRANE and SYNOVIAL FLUID.

III. WHAT MAKES SYNOVIAL FLUID SO THICK AND SLIPPERY?

The horse's synovial membrane and synovial fluid contain a large molecule called hyaluronan. Hyaluronan is the primary component of synovial fluid which gives it its thick and slippery characteristics. Since minimizing friction is critical to normal joint function, the ample presence of normal hyaluronan within a joint is very important. Lack of hyaluronan within synovial fluid increases friction associated with the synovial membrane and articular surfaces, therefore predisposing cartilage to excessive wear and erosion.

HA Molecule

IV. WHAT CAUSES JOINT INFLAMMATION (ARTHRITIS)?

Joint inflammation is a consequence of joint injury and/or instability. Instability can occur as a result of compromise of the supporting structures of the joint (such as the collateral ligaments), loss of articular cartilage (as may occur in osteochondrosis), overuse, and/or increased age.

Click HERE to review joint pathophysiology in detail.

V. WHAT CAUSES JOINT PAIN?

The majority of the nerve endings lie within the fibrous capsule, underlying (subchondral) bone, and supporting ligaments of the joint. The attachments sites of the ligaments to bone are especially sensitive. By contrast, there is very little sensitivity in the cartilage and synovium.

Appropriately, the primary sources of joint pain are:

Synovial effusion: increased fluid within the joint resulting in distension/stretching of the fibrous capsule

Capsulitis: fibrosis (scarring) of the joint capsule

Osteochondritis: inflammation within the subchondral bone

Desmitis: inflammation associated with the supporting ligaments of the joint and/or their osseous (bony) attachment sites

Eliminating excess synovial fluid, inflammation within the fibrous capsule, subchondral bone pain and supporting ligament pathology will usually produce a comfortable joint.

VI. HOW DOES DEGENERATIVE JOINT DISEASE (DJD) OCCUR?

The degenerative cycle is initiated as a result of joint instability and/or injury. Inflammation of the synovial membrane (i.e. synovitis) occurs secondary to the insult.

We should consider what happens when there's an increased number of inflammatory cells within a diarthrodial joint:

• Their presence increases the hydrostatic pressure within the joint; this results in an influx of fluid and ensuing joint distension (effusion).

• They release catabolic enzymes (lysozymes) and other chemical mediators into the joint which hasten degradation of both the hyaluronate molecule and cartilage.

In summary, the increased hydrostatic pressure results in the influx of fluid into the joint (synovial effusion), distension (stretching) of the joint capsule, and pain. The enzymes released by the inflammatory cells degrade hyaluronan (the molecule that is involved in normal lubrication of the joint) as well as the cartilage layer. Compromise and eventual erosion of the cartilage layer results in loss of articular congruency, which in turn increases joint instability.

Interestingly, the presence of pain itself also accentuates the activity and release of harmful mediators into the joint. This further intensifies the inflammatory reaction, as well as its deleterious consequences.

And so the cycle continues...

Normal Joint Components

VII. HOW DO WE TREAT DEGENERATIVE JOINT DISEASE (DJD)?

In order for our treatment strategy to be successful, it must be directed at the following:

• Maximizing joint stability

• Minimizing trauma to the joint

• Minimizing synovitis (joint inflammation)

• Minimizing synovial effusion (excessive joint fluid)

• Minimizing fibrosis of the joint capsule (which occurs as a result of chronic inflammation)

• Normalizing the joint environment (i.e. maximizing the amount of normal hyaluronate within the synovium)

• Minimizing pain

Currently, we have no consistently effective way of stabilizing most diarthrodial joints without compromising their function and range of motion. Decreasing the challenge (i.e. the degree of extension/flexion) to the joints can often be achieved through corrective shoeing, however some degree of instability will usually persist. Surgery can be effective at improving joint stability and decreasing trauma in cases that involve developmental orthopedic lesions (such as osteochondrosis, OCD, subchondral cysts) and some types of fractures.

For the most part, however, we must rely on therapies designed to reduce inflammation, alleviate pain, and reestablish normal synovial integrity. These medications are referred to as arthrotherapies, and include both systemic and local forms.

Click HERE to review systemic arthrotherapeutic options for your arthritic horse.

Click HERE to review local arthrotherapeutic options for your arthritic horse.

Click HERE to review common treatment options for your arthritic horse.