Before focusing on specific diseases affecting the joints, tendons, and ligaments, it helps to understand some basic anatomy.

The articulation between two bones is called a joint. The ends of healthy bones are covered in smooth articular cartilage. A joint capsule surrounds the joint and is comprised of a tough outer coat and thinner lining called the synovium or synovial membrane. The synovium produces synovial fluid that is viscous and slippery and lubricates the joint.

Trauma and/or infection can damage the articular cartilage, leaving it roughened or eroded. Inflammation of the synovium can result in excessive production of abnormal synovial fluid, resulting in obvious joint distention. Synovial fluid in diseased joints frequently loses some of its lubricating properties, leading to more wear and tear on articular cartilage, which leads to painful arthritis.

The outer portions of many joint capsules are thickened to form ligaments that attach bone-to-bone. When damaged, sprained, or torn, ligaments are slow to heal and often require prolonged periods of rest in addition to a variety of local therapies. Tendons connect muscle to bone and are also susceptible to a variety of injuries.

No matter what your pleasure horse does for a job – trail rides, local shows or just putzing around the pasture – he might develop arthritis at some point in his life. That’s because hard work isn’t the only contributor to these conditions; conformation faults also can predispose a horse to changes in the joints over time.

Arthritis describes inflammation of a joint and can involve the bones, articular cartilages, joint capsules, synovium, and synovial fluid. Long-term changes can include destruction of articular cartilage, bony proliferation, and decreased quality of synovial fluid. Arthritis resulting in damage to the articular cartilage is termed degenerative joint disease (DJD) or osteoarthritis.

Ringbone describes degenerative joint disease (osteoarthritis) and/or new bone formation that affects the coffin joint (low ringbone) or the pastern joint (high ringbone). Ringbone can be visible to the eye because of the bony changes that occur to the joint, forming a ring around it.

If your pleasure horse is starting to show signs of arthritis or joint pain, talk to your veterinarian about treatment options.

When osteoarthritis happens in one or more joints in the hock, it is sometimes termed bone spavin. Degenerative joint disease of the hock frequently results in bone spur formation between the small bones of the hock with loss of joint space and decreased movement between bones. Your veterinarian may diagnose these bony changes via radiographs.

Horses prone to bone spavin are usually ones that use their hocks hard, performing repetitive quick stops and sharp turns like in roping, barrel racing, reining or hunter/jumpers. Poor hock conformation can also predispose a horse to bone spavin and other inflammatory conditions of the hock.

Bog spavin describes noticeable fluid accumulation (excessive synovial fluid) within the hock joint and is often accompanied by heat and pain. There may or may not be any cartilage damage or bony changes associated with this condition.

If your horse becomes reluctant to use his hind legs properly, call your veterinarian for a lameness exam.

Sprains typically describe injury to a ligament. A “pulled suspensory” describes such trauma to the suspensory ligaments that extend along the backs of all four lower limbs. The most important course of treatment involves managing the pain and inflammation, along with controlled rest and rehabilitation under the direction of a veterinarian.

Equine Polysaccharide Storage Myopathy is a muscle disease that results in the accumulation of large amounts of polysaccharide (a class of carbohydrates such as glycogen) within skeletal muscle fibers. There are two recognized types of PSSM – Type 1 Polysaccharide Storage Myopathy (PSSM1) and Type 2 Polysaccharide Storage Myopathy (PSSM2).

PSSM1 is caused by a genetic mutation and is an inherited problem characterized by abnormal glycogen storage in skeletal muscle tissue. Breeds potentially affected by PSSM1 include horses with Quarter Horse bloodlines (Quarter Horses, American Paint Horses, Appaloosas) and draft breeds (Belgians, Percherons).

PSSM2 encompasses the other forms of PSSM, including PSSM-ER and myofibrillar myopathy (MFM), in horses that do not have the genetic mutation that causes PSSM1. PSSM-ER is most commonly diagnosed in Quarter Horse-related breeds and MFM is most commonly diagnosed in Warmblood breeds.

Clinical signs of EPSSM

• Horses with any of the types of PSSM described above may “tie up” repeatedly. Episodes of tying up may occur after light exercise or, in horses with PSSM1, without exercise.
  • Signs of tying up
    • Severe muscle pain
    • Stiff gait
    • Reluctance to move
    • Firm, swollen muscles (muscles of the rump, thigh and back are most commonly affected)

If your horse ties up, the best thing to do is to keep your horse quiet and call your veterinarian immediately. These tying-up episodes can be sporadic or can occur every time the horse is ridden. Draft breeds often experience more severe episodes leading to recumbency with inability to rise. Chronic cases tend to show generalized muscle wasting over the rump and hind limbs.

Diagnosis

Early diagnosis optimizes a successful outcome. A diagnosis of EPSSM is confirmed through genetic testing of hair root samples (PSSM1) and/or evaluation of appropriate muscle biopsies (PSSM2). Affected horses also may have abnormally elevated blood levels of muscle enzymes following even light exercise.

Management of horses with EPSSM

There is no cure for EPSSM of any type, but in many horses the signs can be managed. After a veterinary evaluation and diagnosis, management of a horse with EPSSM focuses on adjusting the diet and implementing a controlled exercise program.

• Affected horses benefit from diets that minimize carbohydrates. If additional calories are needed to maintain a healthy bodyweight, they should come from fat
• With these guidelines in mind, you should remove high-carbohydrate sweet feeds and molasses from your horse’s diet
• High-quality forages (alfalfa and alfalfa/grass mix) are essential dietary components
• Prolonged periods of stall rest should be avoided and replaced with daily turn out
• When exercising, it helps to warm up and cool down at a walk for 15 minutes each

Resources: For further information regarding Equine Polysaccharide Storage Myopathy go to: Kentucky Equine Research (KER.com)

HYPP is a condition that causes intermittent abnormal muscle function. It is caused by a genetic defect resulting in unbalanced sodium and potassium concentrations within muscle cells. The word “Hyperkalemic” in this condition’s name refers to elevated potassium levels in the blood. HYPP is an autosomal dominant trait, which means only one gene copy inherited from either the mare or the stallion is required for the offspring to be affected. Individuals inheriting two copies of the gene are more severely affected. This genetic defect is observed in Quarter Horses and related breeds, such as Paints and Appaloosas, that have the Quarter Horse stallion Impressive in their pedigree.

Clinical Signs of an HYPP episode (affected horses are normal between episodes)

• Generalized muscle weakness and trembling
• Intermittent twitching and muscle tremors
• Elevation and/or twitching of the third eyelid
• Difficulty eating, swallowing, and even breathing
• Sudden collapse
• Occasionally death can occur

Diagnosis and treatment

Genetic testing of hair roots or a blood sample will determine a horse’s HYPP status. The goal for treating HYPP episodes is to stimulate insulin secretion, which promotes reuptake of potassium into the cells. Insulin secretion is stimulated by administration of carbohydrate (sugar). For mild episodes, prompt oral treatment with an easily absorbed source of carbohydrate (ex. oats or light Karo syrup) can be beneficial. A veterinarian needs to attend to horses experiencing moderate or severe HYPP episodes. The veterinarian will administer IV fluid therapy with dextrose and calcium to return the sodium and potassium levels to more normal levels as quickly as possible.

Horses with HYPP should have their potassium intake limited to help prevent clinical episodes of muscle twitching and collapse. Grass or oat hay is preferable to legume hay (such as alfalfa), which tends to be much higher in potassium. Hays can vary in potassium content based not only on forage type, but also on stage of maturity, rainfall, and application of fertilizer. To reduce unwanted fluctuations in insulin concentrations that can, in turn, affect potassium levels, grain meals should be offered as two or three small meals per day rather than one large meal. Soybean meal and oil, as well as molasses, contain high levels of potassium and should be avoided.  Beet pulp, on the other hand, is low in potassium and can be safely added to the diet as a source of fermentable fiber. Fasting can also precipitate HYPP attacks and should be avoided. For horses that experience frequent HYPP episodes it can be beneficial to treat them with acetazolamide daily to help decrease their overall potassium levels. Acetazolamide is a diuretic that promotes potassium loss in the urine.

Before you buy

Before purchasing a horse with Impressive bloodlines, ask the seller for a genetic test confirming HYPP status. There is no such thing as an “asymptomatic” H/H or N/H horse. Some horses won’t show symptoms until their teens, and then may be severely affected on their first episode. You can never know for sure when the disease will strike.

• H/H: This status means that a horse carries a double copy of the HYPP gene and will pass at least one copy of the gene and the disease to 100 percent of its offspring.
• N/H: This status means that the horse carries one normal gene and one HYPP gene. Statistically an N/H horse will pass the gene and the disease to 50 percent of its offspring when bred to a N/N or non-Impressive bred horse. N/H to N/H crosses will statistically result in 25 percent N/N progeny, 50 percent N/H progeny, and 25 percent H/H progeny.
• N/N: This status means that the horse carries two normal genes. It does not have the disease, nor can it pass the disease on.

Perhaps there is no diagnosis more dreaded by horse owners than one of laminitis – also commonly referred to as “founder”. An inflammation of the laminae of the hoof wall, laminitis is a very painful condition that can have varying degrees of severity. The onset of signs can be slow and subtle or acute and severe.

In the most severe cases, the laminae are so inflamed that the third phalanx (also known as the coffin bone), that is supported by these structures, rotates, and can penetrate the bottom of the sole. Horses with this severe type of laminitis experience extreme pain and spend the majority of their time lying down. Due to their poor quality of life and poor prognosis for return to comfort, these horses are often humanely euthanized. Cases of laminitis that are not as severe can often be treated and managed with appropriate management of predisposing conditions (like PPID and/or Equine Metabolic Syndrome), a proper diet, and corrective shoeing.

Signs of Acute Laminitis

• Lameness, accentuated when a horse is turned in circles; shifting weight when standing
• Heat in the feet and increased digital pulses in the arteries supplying blood to the feet
• Pain in the toe area when hoof testers are applied
• Reluctant or hesitant gait
• Standing with the front feet stretched out in front to alleviate pressure on the toes and the hind feet positioned underneath the horse to support their weight
• Swollen coronary bands with possible clefting

Signs of Chronic laminitis

• Rings in the hoof wall that become wider as they are followed from toe to heel
• Bruised soles
• Widened white line with blood pockets and/or recurrent foot abscesses
• Dropped soles or flat feet
• Dished hooves, resulting from the heels growing faster than the rest of the hoof
• Intermittent episodes of acute laminitis can occur in horses affected with chronic laminitis

Researchers are still working to discover how and why laminitis happens, but we do know several risk factors:

Risk Factors for Laminitis

• Carbohydrate overload (ex. horse gets into the feed bin or too much time on lush green grass or clover)
• Mechanical overload (ex. a horse with an injury such as a fracture will bear more weight on the uninjured leg, thus predisposing it to laminitis)
• Certain endocrine or metabolic disease conditions, such as PPID (formerly known as Equine Cushing’s Disease) or Equine Metabolic Syndrome (EMS)
• Severe, systemic bacterial illnesses (ex. septic metritis in a post-partum mare or a horse with Potomac Horse Fever diarrhea) that result in release of toxins into the blood stream

If you are concerned about laminitis, talk with your veterinarian right away as early intervention is the best chance for a positive outcome. Therapy for laminitis can vary, but includes pain medication, anti-inflammatory drugs, and proper foot support. Icing the affected feet is an effective therapy during the acute stages of laminitis. Chronic cases of laminitis require teamwork between your veterinarian and farrier (sometimes one and the same individual!) to provide proper trimming and shoeing as indicated by radiographs and clinical signs.

Senior horses (15 years or older) can be at an increased risk of developing laminitis due to endocrine imbalances such as PPID (formerly known as Equine Cushing’s disease) or Equine Metabolic Syndrome.

Maintaining a proper body condition score and having routine veterinary examinations play an integral role in helping to prevent laminitis.

To many horse owners, equine navicular syndrome is one of the top lower limb lameness concerns. The condition references a very small bone in the foot, the navicular bone, but the disease packs a mighty punch in terms of the lameness it can cause.

Navicular syndrome is now known as just one of the causes of heel pain in the horse and can be difficult to diagnose, manage, and treat. Thanks to more sophisticated diagnostics, like MRI, horse owners and veterinarians now have an enhanced ability to see what structures in the lower limb are affected, but making an accurate diagnosis as to the cause of a horse’s lameness can still be challenging. Management and treatment therapies also remain limited.

The navicular bone is a small bone that lies within the hoof and is surrounded by the deep digital flexor tendon, multiple small ligaments, and the navicular bursa. The bone-tendon-bursa interface is a synovial structure, so the bone is ideally covered with synovial fluid that acts as lubrication and helps in its function.

The bone’s function is to act as a fulcrum point over which the deep digital flexor tendon passes before inserting on the distal phalanx or coffin bone (the bone within the foot). The coffin joint is the joint formed by the coffin bone and the short pastern bone. The coffin joint, and subsequently the navicular bone due to its anatomical relation, are integral players in the shock absorption of the limb. The term navicular syndrome encompasses any lameness associated with the navicular bone, its synovial structures, or supporting soft tissues structures such as the deep digital flexor tendon and surrounding ligaments.

Diagnosis and treatment

MRI is the diagnostic modality of choice for horses with signs of heel pain. With an MRI, your veterinarian can view images of all the structures in the foot and lower limb and formulate a more accurate diagnosis, treatment plan, and prognosis.

Treatment options vary. Corrective shoeing, non-steroidal anti-inflammatory drugs, steroid and/or hyaluronic acid (lubricant) injections into the navicular bursa or coffin joint, vasodilation drugs (such as isoxsuprine), bisphosphonates, acupuncture and a variety of oral joint health supplements have been used to medically manage the disease. Talk to your veterinarian for more information.

Navicular disease is highly studied due to its complexity and lack of accurate information regarding its cause and pathology. Veterinarians hope that a better long-term prognosis exists for horses in the future.

Formerly known as “Equine Cushing’s Disease”, Pituitary Pars Intermedia Dysfunction (PPID), is a commonly encountered endocrine disease in older horses. It is a slowly progressive degenerative disease of the hypothalamus, a portion of the brain that influences the pituitary gland. The disease results in an increased amount of ACTH and other substances that have health consequences for the horse.

Clinical signs of PPID

• Long hair coat, patchy shedding, retained guard hairs
• Topline muscle loss
• Chronic infections
• Exercise intolerance
• Abnormal sweating
• Laminitis
• Drinking a lot of water, urinating a lot

Diagnostic testing

Based on your horse’s age and clinical signs your veterinarian may recommend either a baseline ACTH test or a TRH stimulation test to screen your horse for PPID. A baseline ACTH test simply requires a one-time blood sample from your horse. A TRH stimulation test requires drawing an initial blood sample, administering TRH intravenously, then drawing another blood sample 10 minutes later. Time of year can alter the results as it is normal for all horses’ ACTH to be higher in the fall (July-November). It is not recommended to perform TRH stimulation tests between July and November because results have not been validated for that time of year.

Treatment

There is no cure for PPID, but clinical signs and, importantly, laminitis risk can be decreased with daily pergolide treatment. Prascend^® is an FDA-approved tablet that contains pergolide and is easy to administer once a day. Since PPID is a progressive disease, it is important to work with your veterinarian to monitor your horse’s clinical signs and ACTH levels over time. Your horse’s Prascend dose may need to be increased over time.

Equine Metabolic Syndrome describes a group of risk factors associated with an increased risk of laminitis and other health problems. Horses with EMS have abnormal insulin regulation and are typically breeds at higher risk of being overweight – sometimes termed “easy keepers”. The syndrome is characterized by regional adiposity (fat deposits in certain places on the body, like the crest of the neck), insulin resistance (similar to type-II diabetes in humans), and a propensity for recurrent bouts of laminitis that often occur following ingestion of forages and feeds containing high amounts of non-structural carbohydrates (NSC).

Signs Horse is Predisposed to EMS

• Easy keeper
• Unusual fat deposits in the neck (i.e., cresty neck), behind the shoulders, and around the tail head. This unique distribution of fat deposits is referred to as “regional adiposity”
• Commonly affected breeds: Ponies, Arabians, American Saddlebreds, Morgans, Paso Finos, Andalusians, Miniature Horses, and Warmbloods
• Genetics and environment/diet are contributing factors.

Insulin resistance is a state in which insulin is not as effective as it should be, and glucose is not being taken up by the target cells at a normal rate relative to the level of insulin present. Recurrent bouts of laminitis, abnormal glucose metabolism, and increased fat deposition are the results.

Eating too much and exercising too little also play a role in the development of EMS. Your veterinarian can help identify EMS with a thorough physical examination coupled with endocrine testing to measure glucose and insulin concentrations in the blood. A percentage of horses with PPID also have abnormal insulin sensitivity so testing for PPID may also be indicated (see above for more information).

Treatment

Therapy includes weight loss for obese horses, changes in diet, and an increase in exercise if/when the horse is sound enough for increased activity. Medical therapy and foot care appropriate for laminitis may also be indicated. If your horse has risk factors for EMS, but does not have abnormal insulin sensitivity, focus on prevention measures that include weight management and restricting the intake of certain carbohydrates.

• Restrict or eliminate pasture access, especially when grasses are likely to contain high amounts of water-soluble carbohydrates (WSC). Conditions favoring high WSC include springtime when pastures become lush, in the fall particularly when nighttime temperatures are low and there is a lot of sun during the day, and early winter after the first frosts. Horses can be kept in dry lots or intake can be limited using a grazing muzzle.
• Provide a diet based on grass hay to limit the intake of WSC and non-structural carbohydrates (NSC). Have your hay analyzed and feed hays with a low sugar and starch content. Soaking hay in water prior to feeding can help leach out the WSC making some hays safer to feed to a horse with EMS.
• If a horse has been diagnosed with both PPID and EMS it is important to treat the PPID, as described above, to help control PPID-related insulin dysregulation.