Ligament and Joint Capsule
Ligaments of the joint capsule are made of up to 80% collagen with up to 5% elastic fibers (Akeson, 1987). The inner synovial membrane of the joint capsule is made of a loose connective tissue membrane that covers the entire capsule except for the weight-bearing bony articular surfaces. The inner synovial membrane is elastic to prevent the pinching of local tissue during joint movement. It also contains synoviocytes and a capillary network which produce the synovial fluid that lubricates the joint and the ligaments as well as provides nutrition to the weight-bearing cartilage cells, labrum, and menisci. The flow of synovial fluid is aided by movement so the lack of joint motion over a long period of time can compromise the tissues within the joint capsule (Akeson, 1987). Type A synoviocytes resemble macrophages and phagocytes. The type B synoviocytes consist of fibroblasts which produce hyaluronan and other proteins (Hügle, 2016). Hyaluronan ensures constant synovial fluid volume during exercise (Levick, 1995). The synoviocytes do not possess a basal layer or cell-cell junctions compared with typical cells. This allows for the exchange of fluid between the synovium, blood and lymphatic vessels (Hügle, 2016).
The joint capsule and adjacent ligaments facilitate, restrain and stabilize articular joint motion. When excess stress occurs across the joint capsule, secondary dynamic muscular stabilizers are recruited which feel as a muscle strain or muscle spasms (Akeson, 1987). The joint capsule is made up of an outer fibrous cuff of collagen oriented in a crisscross weave pattern, which limits the gliding of individual fibers. The fibers are aligned and recruited in the direction of their load. This allows for large displacement without force transmission until the fibers are straight and able to tighten at the attachment points (Akeson, 1987). Thickened capsular ligaments at sites of greater stress such as the anterior cruciate ligament of the knee further stabilize the joint. The load-deformation curve of ligaments has three regions. The first region demonstrates the straightening of crimp as more fibers are recruited to act against the increasing displacement. The second region demonstrates the full recruitment of all the fibers. The third region demonstrates failure and disruption of the fibers (Akeson, 1987).
In animal studies, muscle atrophy and fatty infiltration begin two weeks after joint immobilization. Adhesions also begin to develop between the connective tissue and cartilage surfaces. The cartilage surfaces that are in contact begin to demonstrate thinning at 30 days and ulcerations at 60 days. Fibrovascular proliferation begins to erode the subchondral bone after 60 days of immobilization. There is also disorganization of parallel fibrils and osteoclastic changes at the bony attachments with generalized osteoporosis, increased turnover of the matrix (Akeson, 1987). Persistent and potentially reversible bone remodeling then takes place which is represented as early degenerative changes of the joint (Anetzberger, 2014). It usually takes twice as long as the original period of immobility to regain full mobilization but cartilage changes continue to persist (Enneking, 1972, Evans, 1960).
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