Through neurologic, orthopedic, metabolic, and other diseases, veterinary patients frequently have reduced weight-bearing and use of limbs.1 Disuse, the state of not being used, is a broad label that describes tissue’s low mechanical load or mechanical unloading when not used enough.2 Immobilization is a term that describes a limb that is maintained in a fixed position by splints, casts, or external fixation.1 Rehabilitation of veterinary patients with acute or chronic neurologic or orthopedic conditions counteracts the effects of disuse and immobilization. It does this by applying controlled challenges to tissues to improve strength, conditioning, and function.1
Six tissues most affected by disuse and immobilization:
- Articular cartilage covers the ends of long bones and is composed of chondrocytes, extracellular matrix, and water. Chondrocytes are cells found in healthy cartilage and are responsible for cartilage formation. The extracellular matrix consists of collagen, proteoglycans, and water. Collagen is the main structural protein found in skin and other connective tissues, whereas proteoglycans is a compound composed of a protein bonded to glycosaminoglycan groups. The presence of proteoglycans in connective tissue provides hydration and swelling pressure enabling tissue to withstand compressional forces. In contrast, water comprises 65-85% of total cartilage weight.1 Articular cartilage is avascular (lacks blood vessels), aneural (lacks nervous tissue), and alymphatic (lacks lymphatic vessels and lymph nodes) (1). Weight-bearing results in a synovial fluid “pumping mechanism” that facilitates the transfer of nutrients and waste exchange by diffusion from the cartilage surface. During loading, water is forced out of articular cartilage, and some water weeps onto the articular surface, allowing hydrostatic lubrication.1 When the load ceases, water is reabsorbed. With rapid loading, cartilage is stiffer because water distributes more slowly, resulting in less cartilage compression. Cartilage is more compliant with slow loading because there is additional time for fluid movement to the cartilage surface.1
- The joint capsule consists of an outer fibrous layer (also membrane) and an inner synovial layer. It surrounds a synovial joint, a joint found between bones that move against each other such as a shoulder, hip, elbow, or stifle (or knee). Through contracture, immobilization affects the joint capsule. The cause of joint capsule contracture may be associated with the proliferation of myofibroblasts, the predominant cell type present in granulation tissue of contracting wounds and fibrocontractive diseases.3 This process may also include collagen and growth factors, a substance required to stimulate growth in living cells.2
- Skeletal muscle is connected to the skeleton to form part of the mechanical system. It allows movement of the limbs and other body parts and is a critical tissue in maintaining functional ability and contributing to health status.2 Plasticity is a characteristic that allows skeletal muscle to change and adapt depending on the stimuli placed upon it.4 Muscle plasticity is the ability of a given muscle to alter its structural and functional properties in accordance with the environmental conditions imposed on it. Increases in mechanical load and increasing workload will stimulate muscle hypertrophy, the enlargement of the muscle due to an increase in cell size. In contrast, removing mechanical load can lead to muscle atrophy.4 Atrophy, the process in which body tissue wastes away, primarily due to the degeneration of cells, occurs with disuse. This process plays a role in some of the adverse effects of aging resulting from a progressive reduction of physical activity.1 The most vulnerable muscles to disuse atrophy are the postural muscles that contain a relatively large proportion of slow muscle fibers and cross a single joint.5 In contrast, muscles that are not used as postural muscles are least susceptible to atrophy, cross multiple joints, and are predominantly composed of fast muscle fibers.5
- Tendons consist primarily of type one collagen that forms parallel fibers that permit the movement of bones by connecting muscles to bones.1 They are a flexible but inelastic cord of strong fibrous collagen tissue that can also attach muscles to structures such as the eyeball. With disuse, there is an inverse decline in structural material properties of tendons. Immobilization of a joint can deteriorate the mechanical properties of tendons. In this process, there is a reduction in their cross-sectional area, with differences occurring in the speed of deterioration among tissues with the mobilization of the joints that they cross.6
- Ligaments also consist primarily of type one collagen, connecting bone to bone and giving joints such as stifles (or knees), ankles, and elbows support while limiting movement. Studies have suggested that ligaments are not metabolically inert structures, and the effects of disuse and immobilization through stress deprivation rapidly reduce the mechanical properties of the ligaments.1 Importantly, one portion of a ligament may be taut at a particular joint position while another is relaxed. Because of this, certain joint positions may need to be avoided to reduce stress so that a ligament can heal.1
- Bone is a rigid body tissue that consists of organic and inorganic components. It provides structural support for the mechanical action of soft tissues and protects soft organs. In addition, bone protects specialized tissue such as the blood-forming system and acts as a mineral reservoir. Studies have shown that young dogs tend to lose bone more quickly following immobilization than older animals, even though older dogs may have less bone mass.1 The degree of bone loss increases with the length of immobilization, with the rate of loss slowing as the time of the mobilization increases. Bone loss is more significant in the more distal weight-bearing bones than in proximal minimally weight-bearing bones.1
References
- Millis, D. L., & Levine, D. (2014). Canine rehabilitation and physical therapy (2nd ed.). Saunders, Cop.
- Brooks, N. E., & Myburgh, K. H. (2014). Skeletal muscle wasting with disuse atrophy is multi-dimensional: the response and interaction of myonuclei, satellite cells and signaling pathways. Frontiers in Physiology, 5. https://doi.org/10.3389/fphys.2014.00099.
- Tomasek, J. J., Gabbiani, G., Hinz, B., Chaponnier, C., & Brown, R. A. (2002). Myofibroblasts and mechano-regulation of connective tissue remodelling. Nature Reviews Molecular Cell Biology, 3(5), 349–363. https://doi.org/10.1038/nrm809
- GOLDBERG, A. L., ETLINGER, J. D., GOLDSPINK, D. F., & JABLECKI, C. (1975). Mechanism of work-induced hypertrophy of skeletal muscle. Medicine and Science in Sports and Exercise, 7(3), 185???198. https://doi.org/10.1249/00005768-197500730-00016
- Lieber, R. L., Fridëan, J. O., Hargens, A. R., Danzig, L. A., & Gershuni, D. H. (1988). Differential response of the dog quadriceps muscle to external skeletal fixation of the knee. Muscle & Nerve, 11(3), 193–201. https://doi.org/10.1002/mus.880110302
- Yasuda, K., & Hayashi, K. (1999). Changes in biomechanical properties of tendons and ligaments from joint disuse. Osteoarthritis and Cartilage, 7(1), 122–129. https://doi.org/10.1053/joca.1998.0167