Equis ISSN 2398-2977
Musculoskeletal: osteoarthritis (joint disease)
Synonym(s): Degenerative joint disease, DJD, OA, Arthritis
Contributor(s): David Moll, Vetstream Ltd, Chris Whitton, Laura Quiney
Print off the Owner factsheets on Caring for the older horse and Osteoarthritis - the facts to give to your clients.
- Cause: progressive, degenerative disease of articular cartilage with a number of potential causes and factors including trauma, age, conformation, joint instability or previous joint disease.
- Signs: pain causing lameness or stiffness, may be worse after a period of rest, eg stabling, joint distension, pericapsular fibrosis, reduced range of motion of affected joint(s), crepitus, secondary (disuse) muscle atropy.
- Diagnosis: physical examination, gait evaluation, diagnostic analgesia, diagnostic imaging, arthroscopy, synovial fluid analysis. Diagnosis of clinical significance should not be made based on the results if radiographic examination only.
- Treatment: exercise and management modification, medication (biological agents, corticosteroids), nutritional supplementation, neutraceuticals, non-steroidal anti-inflammatory drugs, surgical, chemical or surgical ankyloses.
- Prognosis: varied.
- A chronic non-inflammatory disorder of diarthrodial joints involving alteration to the normal structure (degeneration and loss) and function of articular cartilage, with periarticular osteophyte formation and joint effusion.
- Osteoarthritis (OA) is an active disease process with a regenerative component, so degenerative joint disease (DJD) is probably a misnomer.
- Typically classified as primary or secondary, but increasing number of etiologic factors are being identified, making idiopathic or primary OA rare.
- Osteoarthritis is not always clinically relevant. This may depend on a variety of factors including age, workload, psychological factors (motivation), other disease, hereditary and biomechanical factors.
- See also:
- Mechanical forces/trauma - supraphysiological events (abnormal forces), or repeated physiological events, ie normal exercise, wear and tear.
- Abnormal articular environment:
- Abnormal forces:
- Incomplete ossification of the small tarsal bones as a foal → crush-type injury.
- Delayed endochondral ossification of epiphysis or cuboidal bone hypoplasia.
- Malalignment due to valgus or varus deformities in foals Musculoskeletal: angular deformity, over at the knee conformation , toe-in or toe-out conformation.
- Poor joint (limb) stability - poor muscular support, collateral ligament laxity/injury.
- Increased weightbearing to protect injured contralateral limb.
- Regardless of inciting causes, the common endpoint is cartilage degeneration.
- Several hypothesized mechanisms:
- Most popular hypothesis: repetitive loading → damage to cartilage matrix or cells → proteolytic enzyme released from chondrocytes → cartilage fibrillation.
- High motion joints → repetitive loading → fatigue failure of subchondral bone → loss of cartilage support → erosion of overlying cartilage. Therefore racing/training/competing → increased risk of developing OA.
- Synovial inflammation due to direct trauma or cartilage and bone fragments → release of cytokines, proteinases from synoviocytes → metalloproteinase released from chondrocytes → proteoglycan depletion.
- Low motion joints → stationary area of maximal weight bearing → cartilage and subchondral bone under greater load → focal excess weight bearing → necrosis - due to direct trauma or retained cartilage cores → full thickness articular cartilage erosions, subchondral sclerosis (see distal intertarsal and tarsometatarsal joint disease Tarsus: osteoarthritis (bone spavin)).
The normal joint
- Articular joint consists of two articulating bones, joint capsule (outer fibrous layer and inner synovial membrane), joint cavity containing synovial fluid, articular cartilage overlying the subchondral bone, collateral ligaments, other periarticular soft tissues.
- 1-4 layers of synoviocytes (synovial intima) contiguous with synovial fluid in the joint space, and blood vessels in the subsynovial stroma.
- Synoviocytes secrete hyaluronan and collagen (and smaller proportions of other macromolecules).
- Facilities exchange of waste products and nutrients between synovial fluid (sole source of nutrition to adult cartilage) and bloodstream.
- A plasma diasylate - contains hyaluronic acid (important soft tissue lubricant), plasma electrolytes, and proteins (mainly small molecular weight).
- Allows near frictionless movement of joints.
- Composed of water (70-80%) > collagen > proteoglycans > chondrocytes.
- Chondrocytes (synthesize collagen and proteoglycans) in an extracellular matrix (ECM), primarily made up of type II collagen.
- Matrix proteoglycans are glycosaminoglycan (GAGs) are embedded within ECM; predominantly glycosaminoglycans called chondroitin 4 and 6, and keratan sulfate; proportion of chondroitin 6 increases with age.
- Nutrition provided by synovial fluid, depends on capillary flow to synovial membrane; nutrients diffuse through cartilage matrix to chondrocytes.
- When the joint is loaded, fluid is squeezed out of the articular cartilage, thereby aiding lubrication during joint loading. When unladed, the GAGs facilitate fluid to be reabsorbed.
- Gross appearance - fibrillation, partial or full thickness erosions, eburnation, wear lines.
- Histologic appearance - superficial fibrillation, vertical cleft formation, chondroma formation, chrondrocyte necrosis and/or cloning and full thickness loss of articular cartilage.
- Biochemically - loss of glycosaminoglycans (GAGs), increased water content in cartilage due to collagen degeneration.
- Pathophysiology - breakdown of normal cartilage homeostasis → chondrocyte switches to a net catabolic state → attempts to replace deficit by increasing matrix metabolism → damage to collagen network results in continued loss of proteoglycans.
- Repair process:
- Intrinsic repair - mitotic activity of chondrocytes → increased production of extracellular matrix (limited).
- Matrix flow - centripetal flow of cartilage from edges of defect (limited).
- Extrinsic repair - classic repair in vascularized tissue - hematoma organizes defect → pleuripotential mesenchymal cells invade → fibroblasts → vascular fibrous repair tissue → increase in cellularity → becomes fibrocartilage with mainly type I collagen - not mechanically resilient.
- Factors affecting cartilage healing:
- Depth of defect - partial thickness defects cannot heal; but remaining original cartilage is probably mechanically superior to repair tissue; full thickness defects have potential to repair by extrinsic repair.
- Size of defect - smaller heal better than large.
- Location of defect - non-weightbearing regions heal better/repair tissue better able to withstand mechanical loads; defects next to the synovium can heal with fibrous adhesions to synovial membrane.
- Age of individual - young heal better than old.
- If inciting trauma continues, rate of damage may exceed rate of healing.
Synovial membrane and joint capsule
- Synoviocytes can release cytokines, prostaglandins and matrix metalloproteinasas (MMPs) which have been implicated in cartilage degeneration.
- Periarticular fibrosis - thickening of the joint capsule with chronic arthritis.
- Reduced concentration of hyaluronan in synovial fluid → decreased viscosity.
- Periarticular osteophyte formation in OA occurs as new bone growth at the margins of articular cartilage (theory: in an attempt to increase joint stability) and increased bone density in the subchondral bone marrow spaces immediately adjacent to injury (trabecular bone densification).
- Late stage/advanced OA - subchondral bone densification, subchondral bone lysis and defects, fragmentation, ankylosis.
- Cytokines - cellular peptide messengers (eg IL-1 and TNF-alpha) associated with the stimulation of matrix degradation; IL-1 (alpha and beta) mainly from monocyte/macrophage system also chondrocytes and fibroblasts - it can induce cartilage degradation and/or suppress proteoglycan metabolism - elevated levels in synovial fluid obtained from equine joint disease.
- Growth factors - cellular peptide messengers associated with stimulation of matrix production; fibroblast growth factor (FGF), transforming growth factor (TGF) and insulin-like growth factors (IGF); play significant anabolic role in cartilage homeostasis and therefore probably important mediator in pathogenesis and reparative phases of OA.
- Prostaglandins - product of arachdonic acid cascade produced by chondrocytes, cells of synovial membrane and white blood cells in response to cytokines such as IL-1; cause pain and other signs of inflammation and suppress proteoglycan synthesis; cause release of matrix degrading enzymes; elevated levels in synovial fluids from equine OA.
- Proteolytic enzymes:
- Cause loss of articular cartilage extracellular matrix (ECM) → inability to withstand repeated loading → cartilage fibrillation and erosive lesions.
- Matrix metalloproteinases (MMPs) - growing group of zinc-dependent endopeptidases; prime effectors of articular cartilage degeneration; increased in pathologic articular tissues and synovial fluid of horses.
- Serum proteinases - plasminogen activator and plasmin implicated in articular cartilage degradation.
- Cysteine and aspartic proteinases (cathepsins) present in articular cartilage but probably do not have a primary role in OA.
- Common cause of chronic lameness in horses.
- Significant effect of animal welfare and the equine industry.
- Believed to be most common in the aged horse population but can be seen in horses of all ages. Studies have indicated a prevalence of:
- 13.9% of horses in the UK.
- 33% of racehorses <3 years of age.
- 97% of aged horses (>30 years old).
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