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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Progressive physical and biochemical damage to articular cartilage and subchondral bone accompanied by nonseptic inflammation of the synovial membrane and joint capsule.

Pathophysiology!!navigator!!

  • Abnormal forces, such as repetitive trauma, overwhelm the normal metabolic repair functions of the joint, leading to a net cartilage matrix loss and chondromalacia. Unchecked, this cycle creates further damage and loss of viscoelastic properties of the remaining cartilage
  • Capsulitis and synovitis result from biomechanical damage and are often part of the disease process of OA. The inflamed synovium contributes many inflammatory mediators and degradative enzymes (prostaglandins such as prostaglandin E2, cytokines such as interleukin 1, and matrix-degrading enzymes such as matrix metalloproteinases). The viscous shock-absorbing and lubricating synovial fluid, rich in hyaluronan, loses viscosity in this inflammatory milieu, reducing its protective abilities
  • The subchondral bone plate provides shock absorption. It remodels and becomes less compliant if repetitive trauma overwhelms its ability to heal microdamage normally. Remodeled stiffer subchondral bone offers less shock absorption to articular cartilage, further traumatizing it
  • In addition to cartilage thinning and joint capsule thickening, joint changes occur. Capsulitis can result in enthesophyte formation. Osteophytes are formed at the articular cartilage margins. These fibrocartilage-covered bony outgrowths can fracture, becoming osteochondral fragments (chip fractures). Loose articular fragments can increases the inflammatory process within the joint

Systems Affected!!navigator!!

Musculoskeletal—diarthrodial joints.

Genetics!!navigator!!

None elucidated.

Incidence/Prevalence!!navigator!!

Undefined lameness to joint disease is the most significant factor responsible for loss of racehorses’ performance.

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

  • Athletic horses
  • Repetitive training that overwhelms repair mechanisms, e.g. race training
  • All ages and both sexes

Signs!!navigator!!

General Comments

The hallmark of OA is articular cartilage degeneration, a process occurring in a tissue devoid of innervation. Lameness is attributed to the involvement of periarticular soft tissue structures. Pain originating from subchondral bone changes is controversial.

Historical Findings

  • Intra-articular fractures, previous septic arthritis, osteochondrosis, dislocation, or ligamentous damage are predisposing factors
  • Insidious OA-related lameness in low-motion joints (distal intertarsal, tarsometatarsal joints) possible. High-motion joints (fetlock) more likely to have acute-onset lameness
  • Lameness may decrease after rest period

Physical Examination Findings

  • Variable lameness (mild lameness during exercise to lameness at walk)
  • Lameness is rarely acute and severe in onset
  • Pain on flexion
  • Synovial effusion in high -motion joints
  • Acute synovitis, heat
  • Chronic OA joints—thickened joint capsule, reduced range of motion, ± crepitation, grossly thickened, ± palpable bony abnormalities

Causes!!navigator!!

Exact cause is unknown. It is a combination of traumatic events that involve the soft tissue, bone, and cartilage of diarthrodial joints.

Risk Factors!!navigator!!

  • Abnormal limb conformation that increases joint stress, collateral ligament strain, or weight-bearing (e.g. carpal varus, flexural tendon laxity, “back-at-the-knees”)
  • Intense high-speed and/or repetitive training

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Septic arthritis—ruled out with synovial fluid analysis
  • Young horses with joint effusion, osteochondrosis—ruled out with radiography

CBC/Biochemistry/Urinalysis!!navigator!!

For research purposes, urine excretion of various “joint markers.” Clinical application uncertain.

Other Laboratory Tests!!navigator!!

Joint viscosity may be reduced.

Imaging!!navigator!!

  • Radiology—mainstay of diagnosis. Good quality, standard 4 views per joint, ± other views (flexed lateral, “skyline”)
  • Radiographic changes include:
    • Narrowing or loss of joint space
    • Osteophyte formation or fragmentation
    • Periosteal bone proliferation
    • Subchondral bone sclerosis
    • Ankylosis possible
    • Osteolysis in distal intertarsal or tarsometatarsal joints
    • ±Additional diagnostics to determine clinical significance of radiologic OA
  • Nuclear scintigraphy—increased radiopharmaceutical uptake of joint and/or subchondral bone. Assesses metabolically active OA. Diagnostic of choice for subchondral bone changes
  • Diagnostic arthroscopy—direct visualization of joint, articular cartilage
  • MRI—pathologic changes in articular cartilage, subchondral bone, and periarticular soft tissue structures. High-field magnets preferred for cartilage assessment

Other Diagnostic Procedures!!navigator!!

Perineural and/or intra-articular anesthesia to localize joint pain causing lameness.

Pathologic Findings!!navigator!!

  • Articular cartilage thinning, erosion, fibrillation, and scoring
  • Osteophyte and enthesophyte formation
  • Reduced synovial fluid viscosity
  • Subchondral bone sclerosis

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

Reduce joint inflammation and facilitate restoration of joint homeostasis.

Appropriate Health Care!!navigator!!

  • Mainstay of treatment is early recognition and medical management
  • Numerous medications and combinations of medications are used. Decisions regarding treatment are multifactorial (specific joint, stage of OA, performance type, treatment costs, response to therapy, competition regulations regarding medications)
  • Cartilage resurfacing techniques are in advanced experimental stages and are available at certain university teaching hospitals for clinical cases. They may play a role in OA management in the future

Nursing Care!!navigator!!

  • Local cryotherapy (ice, cold water) during acute inflammation and joint swelling
  • Postoperatively—passive motion (flexion) may be used

Activity!!navigator!!

  • Reduce activity
  • In well-trained horses, swimming (maintains cardiovascular fitness while sparing the joints). This is not a substitute and should be carefully considered and integrated into a horse's program by experienced professionals.

Diet!!navigator!!

Diets for prevention of osteochondrosis, a predisposing factor for OA.

Client Education!!navigator!!

Condition is progress. Periodic lameness, performance assessment after diagnosis. Judicious use of intra-articular corticosteroids.

Surgical Considerations!!navigator!!

  • Arthroscopy—visualization of joint, osteochondral fragment(s) removal, removal of damaged cartilage, subchondral bone forage
  • In end-stage OA, surgical arthrodesis

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Systemic NSAIDs—phenylbutazone (2.2 mg/kg every 12–24 h) or flunixin meglumine (0.5 mg/kg every 12–24 h). Daily oral phenylbutazone can be used long term. Side effects include gastric ulceration, right dorsal colitis, and renal papillary necrosis
  • Intra-articular HA—10–20 mg of high molecular weight (>1 × 106 Daltons)
  • IV HA—40 mg daily every 14–28 days, as needed
  • Polysulfated glycosaminoglycan (500 mg IM every 4 days for 7 treatments) or sodium hyaluronate (40 mg IV every 7 days for 3 treatments)
  • Intra-articular corticosteroids—methylprednisolone acetate (20–60 mg/joint), triamcinolone (3–18 mg/joint), betamethasone sulfate (3–18 mg/joint). They are powerful anti-inflammatory agents but have dose-dependent deleterious effects on articular cartilage. Judicial use recommended. In high-motion joints, short- to medium-acting drug (betamethasone, triamcinolone). In low-motion joints, longer acting drug (methylprednisolone acetate)
  • Corticosteroids and HA are often injected intra-articularly simultaneously
  • Autologous conditioned serum (or interleukin receptor antagonist protein)—3–6 mL/joint every 7 days for 3 or 4 treatments

Contraindications!!navigator!!

  • Do not use NSAIDs in dehydrated horses
  • In horses with laminitis, intra-articular corticosteroids may exacerbate laminitis

Precautions!!navigator!!

  • Strict aseptic technique should be used for all joint injections
  • ±125 mg of amikacin sulfate added with intra-articular injection(s)
  • Patient sedation and adequate restraint are critical for successful injection
  • NSAID therapy and rest after joint injection
  • ±Joints are bandaged after intra-articular medication
  • Frequent, repeated use of intra-articular corticosteroid(s) can cause cartilage damage

Alternative Drugs!!navigator!!

Oral nutraceuticals that contain chondroitin sulfate and glucosamine are marketed. There is limited to no objective evidence to suggest efficacy for equine OA.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • After intra-articular injection, monitor for increased lameness, joint inflammation, and/or joint sepsis
  • Periodic lameness and radiographic evaluations to assess progression of OA

Possible Complications!!navigator!!

  • “Joint flare” (transient joint inflammation and effusion) after intra-articular injections should be distinguished from iatrogenic joint sepsis and treated with ice and NSAID therapy. The use of high-quality HA can reduce this chance
  • Corticosteroids can cause laminitis
  • Do not use compounded products intra-articularly

Expected Course and Prognosis!!navigator!!

  • In general, OA is progressive. Continued exercise, athletics, intra-articular corticosteroids exacerbate disease
  • Prognosis is extremely variable and depends on the location and severity of OA, use of the horse, and duration of clinical signs. Mild OA in low-motion joint(s)—with therapy, good athletic prognosis for years. Severe OA in high-motion joint(s)—poor prognosis for athletics, ± arthrodesis for breeding and/or retirement

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Zoonotic Potential!!navigator!!

None

Pregnancy/Fertility/Breeding!!navigator!!

N/A

Synonyms!!navigator!!

  • Osteoarthrosis
  • Degenerative joint disease
  • Arthritis

Abbreviations!!navigator!!

  • HA = hyaluronic acid
  • MRI = magnetic resonance imaging
  • NSAID = nonsteroidal anti-inflammatory drug
  • OA = osteoarthritis

Suggested Reading ⬆ ⬇

Caron JP. Osteoarthritis. In: Ross MW, Dyson SJ, eds. Diagnosis and Management of Lameness in the Horse, 2e. St. Louis, MO: Elsevier Saunders, 2011:655–667.

Frisbie DD. Synovial joint biology and pathobiology. In: Auer JA, Stick JA, eds. Equine Surgery, 4e. St. Louis, MO: WB Saunders, 2012:1096–1113.

McIlwraith CW. Traumatic arthritis and posttraumatic osteoarthritis in the horse. In: McIlwraith CW, Frisbie DD, Kawcak CP, van Weeren PR, eds. Joint Disease in the Horse, 2e. St. Louis, MO: Elsevier, 2016:33–48.

Author(s) ⬆

Author: José M. García-López

Consulting Editor: Elizabeth J. Davidson

Acknowledgment: The author and editor acknowledge the prior contribution of Emma Adam.