Joint Management for Different Stages of Training
Thursday, December 1, 2004
By Rhonda Rathgeber, PhD, DVM

Dr. Rathgeber has a PhD in equine locomotion and anatomy, with a special interest in the forces of kinematics of equine gaits over different surfaces, and is a practicing veterinarian.

A joint is defined as being where 2 or more bones join as a single unit.  There are several types of joints in the body.

• Fibrous—as in the skull
• Cartilaginous—as between the sternum and ribs
• Synnovial—where 2 or more bones join to form a moveable articulation.  Because of this movement, there is the opportunity for damage.

The Synnovial joint consists of external supporting structures (skin, muscles, tendons and ligaments) which are important for joint congruity of movement, and critical to joint health because damage to them can lead to joint injury, as well as the joint capsule, synnovial fluid and joint cartilage.  It is only fairly recently that we have begun to understand the role the external supporting structures play in joint health—and how injuries to them can contribute to the disease we call arthritis or degenerative joint disease.

When there is damage to the support structures, there is a change in the normal movement patterns of the horse.  The first signs that we often see are heat, pain and swelling around the joint capsule.  The joint capsule is extensive—not overlying just the joint itself, but extending well beyond the actual joint space.  The joint capsule contains blood vessels which are a source of nutrition for the joint and a source of synnovial fluid.  The joint capsule provides joint stability, maintains range of motion, and synthesizes hyaluronic acid and synnovial fluid.

Normal synnovial fluid is clear and white, and has the consistency of egg whites.  It should NOT contain blood.  Its chief component is hyaluronic acid (HA), which is a long chain non-sulfated glucosaminoglycan (GAG) that is folded into a thick reticulum in the synnovial fluid.  It serves as a barrier to cells and larger molecules and is a boundary to cartilage.

The ARTICULAR CARTILAGE is only designed for the normal wear and tear.  We used to think it was for absorbing shock, but we now understand that its purpose is for spreading concussive forces across the joint.  It is a very thin layer.  Its health is the limiting factor, because it NEVER heals.  When it becomes injured, it is replaced with FIBROUS CARTILAGE which has different properties than articular (hyaline) cartilage.  The articular cartilage serves both for synnovial tissue lubrication and hydrostatic lubrication.  It has no direct blood supply and no nerve supply, and is nourished solely by the synnovial fluid.  (The pain that is felt from cartilage injury actually is from the underlying subchondral bone).  If a limb loses range of motion, either due to injury (or being placed in a cast), there is deterioration and flaking of the articular cartilage.  For this reason, passive range of motion is recommended as much as possible now for all types of injuries, and complete immobilization is avoided except in extreme cases).

When external force compresses the articular cartilage, it squeezes water (synnovial fluid) out, and when the force is removed, healthy clean water (synnovial fluid) returns.  This movement and activity is needed for joint health.  The orientation of the fibers allows for the shock distribution in the collagen of the articular cartilage.

The SUBCHONDRAL BONE is the structure that ultimately absorbs shock.  It also provides some nutrients for the articular cartilage.  It is present beneath the articular cartilage in every joint with synnovial fluid and is considered part of the joint.  It is a myth that the cartilage absorbs shock.  In actuality, it transmit shock to the subchondral bone, which is constantly in a state of remodeling and repair.  If the damage exceeds the rate of repair, then damage to the subchondral bone is the end-stage process, and arthritis occurs.

Traumatic Joint Disease is the result of either repeated (more common) or a single episode of injury.

A normal joint requires:

1. Freedom of movement: Casting for 6 weeks will cause cartilage defects.
2. Mechanical stability to prevent physiological abnormal forces from acting on the joint.
3. Equitable distribution of force: poor conformation, incorrect shoeing, angular limb deformities, and poor feet will all contribute to the development of defects.

Trauma results in soft tissue injury, with subsequent inflammation, resulting in synnovitis and capsulitis.  This leads to the release of inflammatory mediators, which are vasodilators, that cause a cascade of events.  White blood cells in the joint release enzymes that are part of a normal self-defense mechanism that leads to repair and wound healing, but in the joint, that can get out of control far too easily and become hard to reverse.  That leads to prostaglandin formation and pain potentiation.  This is the step where Aspirin, Bute and other anti-inflammatories work to greater or lesser effect.  The prostaglandin formation causes chemotaxis, and cells are drawn to the area to engulf microbes, dead tissue, etc., and we see heat, pain, swelling, redness and loss of function.

This synnovial insult leads to direct damage to the articular cartilage and chondrocytes, so that there is increased degration and decreased repair of articular cartilage, with subsequent development of osteoarthritis.

The most common cause of Degenerative Joint Disease is a traumatic synnovitis secondary to “use trauma” from everyday events.  The egg white consistency synnovial fluid becomes more watery, inflammatory mediators are released, chondrocyte function decreases, articular cartilage damage begins with the development of frayed pieces that float in the synnovial fluid, further increasing the number of inflammatory mediators and accelerating the process.  When full thickness loss has been reached, the articular cartilage is replaced by fibrocartilage, which is less resilient than articular cartilage and cannot distribute force as efficiently, leading to damage to the subchondral bone.

When the subchondral bone is damaged, microfractures occur beneath the cartilage surface, and repair results in formation of osteophytes and sclerosis of the subchondral bone.  Additionally, if the subchondral bone does not repair properly, chips may occur.

The pain due to osteoarthritis is a LATE OCCURRENCE, and due to either joint capsule distension or subchondral microfractures.  It does not occur in the earlier stages of articular damage.

The symptoms of DJD are changes in performance, abnormal stance and locomotion, heat/pain/swelling, and lameness.  Radiographic changes are even later findings.  For a lameness exam, watch the horse in motion, and with flexion tests.  Look for swelling, heat, pain on flexion, and pain on palpation.  Diagnostic blocks may also be helpful

Other diagnostic methods:

• Radiography: cartilage damage is NOT visible
• U/S: underused for diagnostic joint injury
• Synnovial Fluid Analysis—looking for appearance, consistency, protein, WBC count, and HA content.  Generally not done unless already going into the joint to block.
• Gait analysis
• Infrared thermography
• MRI
• CT
• Scintigraphy (bone scan)

Ultimate Gold Standard Test is the Diagnostic Arthroscopy.

The treatment objective for DJD is to stop/reduce the inflammatory process, relieve pain and return the horse to function.  Rest is rarely enough by itself.  Bandaging can help by supporting the external support structures.  Immobilization may also help to a point.  Medications also help.

Physical Therapy:

• Cold hydrotherapy for acute inflammation
• Heat for chronic nflammation
• Support wraps
• Liniments, braces, tighteners
• Poultices
• Hand walking (next best thing to passive range-of-motion)
• Therapeutic U/S, LASER, E-STIM)
• Passive flexion of joints

Hydrotherapy can be either by the direct application of cold water or by swimming.  Note that swimming does not maintain joint tone and will not maintain competition fitness.

High energy shock wave therapy is now also being used, and appears to be much better for chronic problems than for acute.  Accupuncture has also been used.

Therapeutic Arthroscopy has improved results by decreasing trauma and scarring, decreasing osteochondral fragments, stabiling intra-articular fractures, and joint lavage.

Medications:

• Adequan: Related to the HA in the cartilage, and can be given into the joint or IM.  Has been used in humans since 1959.  Contains a lot of sulfur.  Has anti-inflammatory properties, and stimulates HA production in the joint regardless of route of administration.  Rapidly absorbed IM, reaching peak levels in the blood in 20 – 30 minutes, in the synnovium in 2 hours and in the cartilage in 24 – 48 hours!  Therapeutic levels persist 96 hours.  Recommended dosing is every 4 days for treatment.  Levels are 30% higher in inflamed joints, used as a substrate for cartilage repair, and also blocks the action of deleterious enzymes in joints that destroy the cartilage matrix and thin the synnovial fluid.

1. Therapeutic: every 4 days for 7 treatments
2. Preventive: no clear protocol.  Best may be every 4 days on periodic basis.  One study done on yearlings giving it every 4 days every other month showed dramatic reduction in OCD lesions.
3. Blinded study comparing compounded generics to Adequan showed that the generics were much less effective in treating induced cartilage lesions (as measured by lameness scores and healing).

• NaHyaluronate (Legend, Hyvisc).  Wide body distribution, major joint fluid component, keeps “bad stuff” out and inhibits inflammation, plus stimulates HA production.  Can be used in combination with Adequan.  It will improve joint fluid, matrix and reduce inflammation and pain.  Can be given intravenously or intra-articularly, with virtually no reactivity.  NON-sulfated GAG that helps to restore the function of the HA lost due to inflammation.  Its effects last much longer than the drugs actual presence.  The IV form is preferred when treating multiple joints, or unable to localize the joint, for post-surgical patients, with a non-cooperative horse, or when there is concern the joint may be infected.  There is no evidence that it is incorporated into the cartilage matrix or that there are benefits to the cartilage matrix.
• Corticosteroids: These are the most potent drugs we have available for treating inflammation.  They can be used alone or with HA.  They act by inhibiting phospholipase at the beginning of the inflammatory cascade, and are usually given intra-articularly.  They are valuable if used judiciously.  The literature does not support their use as being dangerous.
• Oral glucosamines, other nutriceuticals: have not gone through an approval process, nor has there been a study of the efficacy, safety, or stability or are there quality controls in place.  Furthermore, manufacturers cannot legally make “medicinal claims.”  In fact, 70% when tested did not match their labels (and were tested at an independent laboratory)!  There are many different sources, and many different molecules.  They are thought to be the “building block” in oral form of the protein needed to repair/maintain joints.  However, to be effective, they must be absorbed, must go into the joint, and must then be utilized by the joint.  There is no placebo effect in the horse—so the must actually work to do any good.
  • Chondroitin Sulfate: is a very large molecule.  0 – 30% is absorbed in the HORSE (because they have a different GI tract than humans and dogs).  There is some relatively good evidence that it is NOT absorbed intact, and there is scant evidence for efficacy.
  • MSM: has anti-inflammatory properties that may be responsible for the improvement seen clinically with some of the nutriceuticals.  Oral cousin to DMSO.  No good data to support use in OA, however.

• Cosequin:  Has studies that show improved lameness scores in navicular syndrome.
• Corta-flex:  Did gait analysis studies using an objective program that showed an improved gait on their product.

• All of the products appear to be safe, but they are not usually used as the sole source of the agents.  The results usually take 2 – 8 weeks.

• Non-steroidal Anti-Inflammatories: provide short term relief of pain.  Have potential side effects of blood coagulopathies, ulcers (both gastrointestinal and oral), renal damage, and decreased proteoglycan synthesis.  The newest is SURPASS, a topical cream.
• DMSO: is a topical anti-inflammatory that also acts as a carrier. Benefits/role not clearly documented.

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