Sometimes linear cord like, sometimes broad and sheet like, tendons in the body vary in structure, macroscopically, at the microscopic level and at the level of the intracellular aparatus depending upon the particular setting in which they act. Tendons impart the force of contraction of a muscle to bone either to stabilize its position in space against an external force or to accelerate the bone through space. From the standpoint of the joint in the first case the motion of the joint is prevented by the neutralization of an external force the length of the muscle tendon unit remains relatively fixed or in the second case the motion of the joint is produced by shortening of the muscle-tendon unit with relaxation and relative lengthening of the antagonist muscles.
While the classic conception of a concentric contraction affecting flexion or extension of a joint provides a basic statement of the manner in which a muscle tendon unit functions, in the body the function is often more complex. It is the role of the muscle tendon unit to dampen impact forces to the skeleton and to modulate the motion by the allowance for eccentric contraction leading to smooth decelerations and the imparting of forces through a transfer of potential energy in the form of spring like elastic forces contained by the stretched muscle tendon units. The muscle contraction serves to maintain tension in the muscle tendon unit so that the transfer of kinetic and potential energy can occur. This biomechanically more complex arrangement is especially evident in the highly coordinated activities of running and throwing. Aging results in a less elastic structure within tendon leading to deteriorating performance in these activities after age 40. Tendinosis within the supraspinatus tendon is present in somewhat less than 1/3 or individuals under the age of forty with increasing frequency with age but still absent in 10% of 80 year olds thus the changes conflate with aging but may not be justifiably characterized as due to aging. Tendinosis is noted in a higher percentage of torn tendon samples than in intact tendons suggesting that this process does contribute to a vulnerability to injury. Inflammation as defined by the presence of neutrophils occurs at the sight of tendon rupture however they may be there in response to necrotic tenocytes and disrupted collagen. While submaximal strains may result in collagen disruption which stimulates an inflammatory response, the cytokine activity stimulated by the inflammatory response may further weaken the tendon leading to failure upon repeated strains prior to structurally competent remodeling.
Gait analysis reveals the perfect, or in the pathologic state the imperfect, balancing of floor reaction force vectors, as derived from force plate data, in relation to joint axis and just sufficient opposing torque, as derived from dynamic EMG data, imparted by the contracting muscle tendon unit such that the center of gravity can be advanced in an energy efficient manner. Feedback via stretch receptors (golgi organs) at the terminal ends of sensory neurons terminating mostly on the surface of tendons and especially at the musculotendinous junction provide the feedback to mediate these reflex contractions.
In the case of the elaborate programmed and learned activities such as these the proprioceptive function of the tendons provide for anticipatory reflexive contractions to occur whereby the joints are spared excessive forces. In this way the coordinated function of the muscle tendon unit protect the skeleton and the cartilage from damage. Joint architecture in conjunction with periarticular ligamentous structures are likewise evolved to enable motion while avoiding deleterious shear forces upon the cartilage which is durable in compression but prone to structural damage when exposed to shear. Joints act in series to permit a greater arc of overall motion while maintaining joint contact forces perpendicular to the opposing joint surfaces, thus allowing for the range of motion while remaining a mechanically sound environment compatible with the working material parameters of cartilage. The segmental structure of the spine and the serial structure of the wrist and ankle are examples.
Human movement evolves in patterns by which combinations of posture and gesture communicate intent and social relation augmenting or undermining verbal communication. The effect crosses cultural and even species barriers. Movement
Histology of tendons reveal columns of tenocytes elongated with oval nuclei in aligned with the linear pattern of collagen the concentric production of collagen extruded from the tenocyte and arrayed in the extracellular matrix resulting in the fascicle pattern observed. There are associated blood vessels and nerves a peritenon and epitenon with a slight fluid layer between in larger tendons. Bursae are frequently associated as in the shoulder and about the achillus tendon and hamstring insertion at the knee.
The smallest functional unit that we acknowledge is a fascicle consisting of collagen aligned end to end a quarter staggered array. Fibril diameters vary from 10 to 500 nm depending upon species and age. Fibrils are bundled to form fascicles which are surrounded by loose connective tissue endotenon through which course blood vessels lymphatics and nerves.
Tendon structure has variation in the size of fascicles and variations in the degree of crimp of the collagen within the matrix, a feature that serves ot dampen sudden strains and responsible for the toe region of the stress strain curve. The crimping straightens after which the stress strain curve becomes linear from about 2% strain to 4% strain after which bond slippage and finally failure begins to occur with gross failure at 8% strain on average. High strain rates and obliquity of strain increase the likelihood of failure. Tendons which typically handle higher sudden loading generally exhibit greater crimp angles. Some tendons notably the rotator cuff may be subject to compressive and shear forces which the structure must contend with. These tendons have more complex ultrastucture with some transverse and spiral patterned collagen fiber orientation. Muscle tendon units that cross more than one joint may be uniquely vulnerable by virtue of more complex patterns of mechanical stresses, the achilles tendon the hamstrings and the extensor carpi radialis brevis tendon are noteworthy in this regard.
While the majority of forces are in line tension the structures of muscle tendon units vary with resultant differences in excursion which appear to match the role the muscle tendon unit plays with multipennate and unipennate pattern which favor a priority upon power or excursion. Tendons transmit tension forces through a matrix composed predominantly of type I collagen (95%, very small amounts of elastin which is capable of 200% strain to failure as opposed to collagen in with a 8% strain typically results in failure. Type III collagen is seen in healed tendons, its presence in normal tendon represents a minor contribution under normal conditions. Proteoglycan is present and is felt to play a larger role in compressive forces where present. The subtleties of the composition vary through the body in a manner commensurate with the varying function of tendons. Lower extremity tendons involved in running and shoulder tendons involved in throwing have compositions with more elastin. Tendons involved in grasp and fine motor function are stiffer with more extensive cross linking of type I collagen. Distinctions in ultastructure are also noted with smaller fascicles in flexor tendons and larger fascicles in weight bearing tendons
The potential strength of a muscle contraction is proportional to the cross sectional area of the muscle. This strength of contraction can be made to vary with training and disuse and the atrophy or the hypertrophy of the muscle may be readily observed over a matter of days or weeks. The tendon, too, will respond to physiologic stress and lack of use thus as a living structure it thrives on regular mechanical strains to order itself. Adaptive change and functional reserve are facilitated by gradual transitions whereas sudden changes especially unanticipated high strain rate loading or sudden changes in the frequency of loading, like a new weekend project taken on by a white collar worker, can lead to injury. Indeed daily injury and mechanical stresses trigger adaptive remodeling by tendon modulating rates of cell proliferation and apoptosis in keeping with changing mechanical demands resulting in periodic renewal of tendon cellular structure and material composition. The mechanism and degree of adaptive changes occurring in tendons in response to conditioning remain ill defined. Likewise the presumed mechanism of chronic tendinosis leading to attritional failure as a consequence of a remodeling process out of step with demand remains a matter of speculation.
Tendon can withstand up to 1000 Kilograms per square centimeter, and at times appears to be subject of forces as within the achilles tendon during running which at 12 times body weight exceed the ultimate tensile strength of the tendon. The muscle tendon unit is protected by reflex relaxation of the muscle at higher strains.
Tendon displays viscoelastic properties consistent with the organic polymeric structure of its constituent type I collagen. Viscoelasticity is defined by such behaviors as increasing strain with sustained stress (creep) and decreasing stress at constant strain (stress relaxation), properties which one can appreciate in the process of conducting a stretching regimen. Another viscoelastic property is an increase in apparent stiffness at higher strain rates, which will also tend to mean a lower ultimate tensile strength and failure at a lower % strain at higher strain rate. These material properties also play a role under cyclic loading whereby phase lag (hysteresis) will contribute to the dissipation of mechanical energy. Atomic force microscopy of collagen structure suggests that its inherent mechanical strength is partly explained by the cross linking and hydrogen bonding between the triple helical strands of collagen which function as sacrificial bonds which break thus absorbing load and then rapidly reform.
It is hypothesized that repeated submaximal strains can result in an altered balance of proliferation and programmed cell death (apoptosis). Nuclear fragmentation characteristic of apoptosis is observed in tendinosis of the rotator cuff. Tendon remodeling which pushes the limit of its capacity to keep up results in a tendon structure that may be weaker and thus more readily prone to failure at a lower percent strain or at a lower strain rate than would otherwise be required. Lipoid and mucinous degeneration are both noted in tendon.
While many systemic factors come in to play one common thread may be a common influence upon the local blood flow to portions of certain tendons. Hypoxia with overuse may result in anoxic injury, reperfusion injury due to reactive oxygen species is suggested by the finding of enzymes in tenocytes that function to neutralize the toxic effect of reactive oxygen species. Watershed areas are implicated in the suprapinatus and achilles tendons. It is in keeping with the pruning effect of smoking on small blood vessels that the lack of colleral supply in these watershed areas may come into play.
It is debated whether the findings of fibroangioblastic change associated with tendinosis is in keeping with this hypothesis or not. The seemingly contradictory proliferation of blood vessels may reflect an attempt to overcome a previous phase of dysvascularity. It is also unknown whether apoptosis represents a primary pathologic process such as occurs in some forms of musculodystrophy or alzheimers or whether this process is secondary to some other pathology representing a normal remodeling process in response to that injury.
Ultimately it is the resident cell population of tenocytes that maintain the functional integrity of the matrix which provides the mechanical properties of the tendon although in cases of tendon laceration, both an intrinsic and extrinsic repair potential comes into play.