Dense fibrous tissues, which include tendons, ligaments, and joint capsules, are also subjected to age-related changes. Although alterations in these tissues received less attention than those in skeletal muscle or articular cartilage, serious impairment can develop in aged individuals as a result of age-dependent changes in fibrous structures.
Tendons are tough yet flexible connective tissue bands that attach muscle to skeletal structures. Bundles of collagen that are held together by a layer of loose connective tissue are the main components of tendons. These dense tissue straps are well-suited as transducers, enabling the force of a muscle to be exerted at a distance from the muscle itself. Tendons possess typical tensile properties—the forces applied to a tendon may be more than five times body weight.
It has been proposed that tendons lose their elasticity and slowly become stiffer and more brittle as a result of age. Moreover, the blood supply that nourishes the tendon was also reported to diminish with age and may cause a decrease in vascular perfusion (Brewer, 1979; Rathbun et al., 1970). These alterations may lead to spontaneous or low-energy ruptures of mostly the rotator cuff of the shoulder, the long head of the biceps brachii, the posterior tibial tendon, patellar tendon, and the Achilles tendon (Brewer, 1979; Burkhead, 1990; Jahss, 1991).
Taking a closer look at structural, mechanical, or cellular age-related changes in tendons, Birch and coworkers reported that there exist differences in structural changes in different tendons. In some tendons aging resulted in a significant increase in collagen-linked fluorescence and a decrease in cellularity, whereas in other tendons high levels of type III collagen were found as a function of age (Birch et al., 1999). These findings are supported by x-ray data on human tendons, demonstrating age-related changes in collagen packing (Naresh et al., 1992). Furthermore, in human supraspi-natus tendons there was a significant decrease in total glycosaminoglycan, chondroitin sulphate, and dermatan sulphate concentration with age (Riley et al., 1994). These differences in macromolecular composition and aging may contribute to a tendon specific degeneration.
However, Goodman et al. suggested that tenocytes, which become differentiated at an early age, respond to cyclical strain and transforming growth factor-^ stimulation, and preserve their tendon specific response, but increasing age had only little effect on tenocytes (Goodman et al., 2004). Regarding age-related changes in biomechanical properties, no difference in tensile strength between mature and old tendons was found, suggesting a high compliance of tendons during aging (Nakagawa et al., 1996). Additionally, the tensile and viscoelastic properties of the patellar tendon differed minimally between younger and older ages (Johnson et al., 1994).
Age-related changes in tendon composition may contribute to degeneration of this tissue. Otherwise, the impact of age on mechanical properties seems to be only minimal. This could depend on an above-average physical training status in some individuals, since it has been reported that strength training in old age, at least partly, can reverse the deteriorating effect of aging on tendon properties and function (Maganaris et al., 2004).
Ligaments, which are structurally quite similar to tendons, but appear to have more elastic fibers, attach adjacent bones to one another and maintain them at their correct anatomical positions during movement. They also provide structural support around joint capsules and at sites where bones make contact with other bones. Ligaments have dynamic characteristics, since they respond to exercise or immobilization by altering their tensile strength and are capable of repair after injury.
As seen in tendon tissue, mechanical properties of ligaments may undergo changes with increasing age, such as the deterioration of tensile properties. The structural characteristics of ligament-bone complexes show a progressive decline in tensile stiffness and ultimately lead to failure with increasing age (Woo et al., 1991). Similar results were reported for human lumbar posterior spinal ligaments, where a significant correlation with a decrease in the mechanical strength and increasing age was found (Iida et al., 2002).
A recent light and electron microscopic study revealed ultrastructural differences in the posterior cruciate ligaments, that is, a decrease in collagen fiber diameter and increase in collagen fibril concentration, with aging (Sargon et al., 2004). These data paralleled previously published work on age-related changes of collagen fibrils in human anterior cruciate ligament and Achilles tendon (Strocchi et al., 1991; Strocchi et al., 1996).
When ligament tissue was tested upon alterations in the content of matrix components, an age-dependent decrease in elastin and collagen metabolism was obvious (Osakabe et al., 2001). Moreover, age-related changes of elements were investigated, showing an increase in calcium and magnesium, although iron levels were reduced in the tested ligaments (Tohno et al., 1999; Utsumi et al., 2005).
Given the age-related changes occurring in ligaments affecting mechanical properties, we would expect a quite high incidence of ligament injuries with aging. In particular, since aging ligament cells synthesize lower amounts of elastin and collagen, that may contribute to a decline in mechanical properties and consecutively to an increased risk of injury with advancing age. However, the ability to respond to growth factor stimulation is not lost in aged ligament fibroblasts (Deie et al., 1997), which may uphold matrix remodeling to such a degree to sufficiently withstand mechanical stress even in older individuals. Besides, an overall reduction in physical activity with increasing age may further prevent injuries to this tissue.
The joint capsule resembles a sac-like envelope that forms a sleeve around the synovial joint and encloses its cavity. The joint capsule is a dense fibrous connective tissue that is attached to the bones via specialized attachment zones at the end of each involved bone. It seals the joint space, provides passive stability by limiting movements, provides active stability via its proprioceptive nerve endings, and may form articular surfaces for the joint. It varies in thickness according to the stresses to which it is subject, is locally thickened to form capsular ligaments, and may also incorporate tendons.
Nevertheless, some authors doubt the existence of a joint capsule as a defined structure, since it may be regarded as a basketwork of the surrounding ligaments and tendons appearing to form a fibrous capsule.
Little is known about age-related changes in joint capsules. In addition, detailed biomechanical trials of age-dependent alterations in joint capsules have not been reported to the best of our knowledge.
Investigations in knee and finger joint capsules showed that the attachments to bone contain fibro-cartilage that is rich in type II collagen and glycosami-noglycans. The attachment changes with age as type II collagen spreads into the capsular ligament or tendon (Benjamin et al., 1991). With mechanical loading parts of the capsule adapt by forming fibrocartilaginous tissue by accumulating cartilage-like glycosaminoglycans and type II collagen. Such regions can be found especially in aged material (Benjamin et al., 1991).
Since the joint capsule contains tendinous and liga-mentous structures, the similarity between these tissues suggests that their mechanical properties may also deteriorate with age (Buckwalter et al., 1993).
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