Equine joints must provide the solidity, sturdiness and mobility needed to move a horse quickly and easily while simultaneously serving the antithetical purpose of bearing the enormous stresses generated by such movement.
Primary components of the joint structure include ARTICULAR CARTILAGE, ARTICULAR (or JOINT) CAPSULE, SYNOVIAL MEMBRANE and SYNOVIAL FLUID.
Articular cartilage is a vital contributor to the maintenance of normal joint function and integrity. It must satisfy very demanding requisites with regard to elasticity, compression resistance and friction reduction in order to perform its role effectively.
Cartilage is devoid of blood vessels and nerves, and can therefore be compressed to absorb mechanical stress and transfer it to diffusely-innervated underlying bone tissue... all without causing pain or vascular injury. Moreover, the smooth and congruent nature of the cartilage minimizes friction during movement of articular tissues.
Fundamental constituents of the cartilage matrix include collagen, glycosaminoglycans (chondroitin sulfates, keratan sulfates and sodium hyaluronate) and water. These elements are arranged in a way that lends cartilage tissue greater elasticity and compression resistance.
Glycosaminoglycans, submerged in an aqueous medium, are anchored at one end to protein chains within the cartilage matrix, thereby forming proteoglycans. On the cartilage surface, glycosaminoglycans have mutually-repelling negative electric charges that give proteoglycan its characteristic cotton bud-like shape.
Like glycosaminoglycans, proteoglycans are mutually-repellent and provide the cartilaginous structure with extraordinary properties of elasticity and compression resistance.
Collagen fibers make up 50% of cartilage's dry substance and are generated by chrondrocytes (cartilage cells). They are responsible for cartilage nutrition in addition to furnishing the tissue with considerable traction resistance.
As you might expect, synthesis of collagen decelerates as horses age. Consequently, the ability of cartilage to self-regenerate and self-repair also diminishes with age.
Chondrocytes, which are submerged in an amorphous matrix devoid of blood and lymph vessels, do not receive any direct nutrition from blood. They compensate via hydraulic capture of nutritional elements from synovial fluid: Cartilage compression under weightbearing load expels the synovial liquid and banishes catabolites; cartilage expansion when the load is reduced results in the absorption of new synovial fluid that is rich in nutrients. Of course this mechanism requires properties of elasticity that only intact/ healthy cartilage possesses.
The articular capsule, constituted by well-innervated and vascularized connective tissue, completely encompasses the joint. Its inner surface is lined with a synovial membrane, which is rich in capillaries and nerve terminations and scattered with macrophagic and fibrinoid synoviocytes.
The inner surface of the articular capsule is coated by synoviocytes
The synovial membrane is responsible for maintaining joint homeostasis through phagocytosis and the production of highly-viscous SYNOVIAL FLUID.
Synovial fluid is composed of high-molecular-weight sodium hyaluronate and plasma derivatives (water, glucose, amino acids and electrolytes). It is responsible for providing lubrication and shock absorption within the articular structure.
Synovial fluid must be highly-viscous and elastic in order to perform its role effectively.
The denser and heavier the molecular chains of sodium hyaluronate, the greater the lubricating and protective-power of synovial fluid. Without this lubricating element, the articular surfaces would encounter great resistance as they slide over one another. Injury to articular tissues as a consequence of excessive friction and/or compression would ensue, thereby precipitating arthritis.
NORMAL JOINT PHYSIOLOGY
With the exception of cartilage, all joint tissues are well-vascularized and directly fed by the surrounding blood vessels.
The biochemical equilibrium of the intrarticular environment is constantly regulated by the synovial membrane, synovial fluid and articular cartilage. Alteration of any one of these elements inevitably compromises the physiologic status of the others.
Together, the synovial membrane and synovial fluid form the BLOOD-SYNOVIAL BARRIER which is a sophisticated, dynamic system that regulates articular flows to and from the joint.
SYNOVIOCYTES, which are anchored to the interior of the articular capsule by thin elastic strands, stretch into the articular cavity where they perform an essential phagocytic function.
In normal physiologic conditions, synovial fluid is highly-viscous and effectively fills gaps between the synoviocytes. By doing so, the fluid forms a biological filter that selects against circulating inflammatory cells (leukocytes) but remains permeable to substances destined for chondrocyte nutrition (such as glucose, electrolytes and amino acids) and to catabolites (articular waste products) as they are purged into the bloodstream. The viscous nature of synovial fluid to owed to one of its essential constituents: HYALURONATE (also known as Hyaluronic Acid or HA).
By preventing inflammatory cells from entering the articular cavity, the blood-synovial barrier protects articular tissues from the degradative effects of their enzymes (known primarily as lysozymes). The blood-synovial barrier therefore constitutes the first line of defense against the deleterious effects associated with leukocyte invasion (joint inflammation) and is considered to be the most fundamental element in preventing osteoarthritis.
As a consequence of the inflammation associated joint injury and/or instability, vascular alterations within the joint capsule allow activated macrophages to invade the articular cavity. The presence of these cells within the synovium promotes the degradation of sodium hyaluronate (HA), an essential component responsible for maintaining adequate synovial fluid viscosity. As HA is downgraded to a lower-molecular-weight polymer, synovial fluid viscosity is reduced along with its ability to contribute to blood-synovial barrier function.
And so the cycle of degenerative joint disease begins....
Please click HERE to review JOINT PATHOPHYSIOLOGY in detail.
Please click HERE to review the basics of DEGENERATIVE JOINT DISEASE in the horse.