madman
Super Moderator
Tendon: Principles of Healing and Repair (2022)
Christian Chartier, MD, Hassan ElHawary, MD, MSc Aslan Baradaran, MD, MSc Joshua Vorstenbosch, MD, PhD, FRCSC Liqin Xu, MD, MSc, FRCSC Johnny Ionut Efanov, MD, PhD, FRCSC
Abstract
Tendon stores, releases, and dissipates energy to efficiently transmit contractile forces from muscle to bone. Tendon injury is exceedingly common, with the spectrum ranging from chronic tendinopathy to acute tendon rupture. Tendon generally develops according to three main steps: collagen fibrillogenesis, linear growth, and lateral growth. In the setting of injury, it also repairs and regenerates in three overlapping steps (inflammation, proliferation, and remodeling) with tendon-specific durations. Acute injury to the flexor and extensor tendons of the hand is of particular clinical importance to plastic surgeons, with tendon-specific treatment guided by the general principle of minimum protective immobilization followed by hand therapy to overcome potential adhesions. Thorough knowledge of the underlying biomechanical principles of tendon healing is required to provide optimal care to patients presenting with a tendon injury.
Tendon has chiefly a mechanical part to play at the intersection of muscle and bone, directly transmitting contractile forces while dissolving stress that would otherwise concentrate should muscle interface directly with bone.1,2 It stores, releases, and dissipates energy to efficiently maintain the joint-loading cycle while protecting adjacent tissues.1 Nonetheless, tendinous injuries are exceedingly common, with 50% of musculoskeletal injuries recorded in the United States involving tendinous or ligamentous injury and 10% of people (50% of runners) experiencing Achilles tendinopathy by age of 45.1,3 While tendon rupture usually corresponds to an acute incident, evidence suggests that chronic degenerative changes are usually present and contribute to the rupture.4 Thus, it is crucial to consider tendon healing in the context of its development, and regeneration, and of the histologic changes that reflect its long-term degeneration.
*Tendon Anatomy and Classification
*Epidemiology of Tendon Injury
*Development and Structure of Healthy Tendon
*Acute and Chronic Changes in Tendon Injury
While extreme exercise, concomitant loading, aging, and oxidative stress are recognized as physical and biological factors that engender tendinopathy, the exact pathogenesis of tendinopathy is poorly defined. For years, the accepted model of tendinopathy was one of tendinitis or inflammation. More recent histopathological studies have identified tendinosis (chronic degeneration), as the culprit in most cases of tendinopathy.26–30 It is responsible for the symptoms of pain, decreased strength, and impairment in activities of daily living commonly attributed to tendinitis. The affected region in tendinosis exhibits structural and cellular changes relative to unaffected tissue. While a healthy tendon is characterized by parallel, wavy, clearly defined bundles of collagen, diseased tissue is recognizable by its lack of alignment or demarcation between neighboring bundles and its increased diameter.31 On a cellular level, tendinosis is characterized by neovascularization, hypercellularity, and atypical fibroblast proliferation.32 Tenocytes capable of producing collagen change shape, with their nuclei exhibiting signs of fibrocartilaginous metaplasia.33,34 Biomechanically, tendinosis predisposes tendons to rupture.4
Similar features have been observed in the senescent tendon. Aging decreases tenoblast volume and plasmalemmal surface density increases the nucleus-to-cytoplasm ratio and suppresses protein synthesis.1 Collectively, these features contribute to decreased collagen turnover, characterized by thicker collagen fibers with greater variability in fiber diameter. The activity of lysol oxidase, an enzyme essential for collagen production, decreases, which in turn increases nonreducible collagen cross-linking.1,35 Biomechanically, this impedes the capacity to withstand loading and increases stiffness.1
In the setting of acute intrasynovial flexor tendon injury, disruption of the tissue surrounding the lacerated tendon compound the severity of the injury. Leakage of synovial fluid from within the digital sheath causes tendon starvation, slowing the repair process. This occurs through absolute synovial fluid loss, but also through disruption of the pressure distribution crucial to the process of imbibition by which the tendon gets most of its nutrients.36 It follows logically that injury to the tendon blood supply itself also hinders tendon healing in the acute setting. Importantly, as surgical apposition of the two ends of an injured tendon remains the gold standard for tendon injury treatment, one must be mindful to limit intraoperative trauma, which is additive to the severity of the original injury.
A common nontraumatic pathology of hand tendons is proliferative extensor tenosynovitis of the wrist, a condition well-documented in patients diagnosed with rheumatoid arthritis. It is characterized by pain and limited range of motion localizing to the fourth extensor compartment and can lead to tendon rupture.37 In the context of rheumatoid arthritis, the proliferation is due to synovial tissue hypertrophy, inflammation, and fluid production. Histologically, the pathology infiltrates the tendon properly and exhibits fibrinous adhesions, a feature also observed in tendon healing from acute or chronic traumatic injury.37
*Repair and Regeneration
*Practical Approach for Surgeons
Conclusion
Tendon injury is an exceedingly common presentation to emergency departments, making it one of the conditions most frequently treated by plastic surgeons. Factors such as age, mechanism of injury, time to repair, and physical exam findings play critical roles in determining the optimal method of management and postoperative rehabilitation. Hand surgeon familiarity with the subtleties of tendon healing is thus essential to ensure favorable long-term outcomes.
Christian Chartier, MD, Hassan ElHawary, MD, MSc Aslan Baradaran, MD, MSc Joshua Vorstenbosch, MD, PhD, FRCSC Liqin Xu, MD, MSc, FRCSC Johnny Ionut Efanov, MD, PhD, FRCSC
Abstract
Tendon stores, releases, and dissipates energy to efficiently transmit contractile forces from muscle to bone. Tendon injury is exceedingly common, with the spectrum ranging from chronic tendinopathy to acute tendon rupture. Tendon generally develops according to three main steps: collagen fibrillogenesis, linear growth, and lateral growth. In the setting of injury, it also repairs and regenerates in three overlapping steps (inflammation, proliferation, and remodeling) with tendon-specific durations. Acute injury to the flexor and extensor tendons of the hand is of particular clinical importance to plastic surgeons, with tendon-specific treatment guided by the general principle of minimum protective immobilization followed by hand therapy to overcome potential adhesions. Thorough knowledge of the underlying biomechanical principles of tendon healing is required to provide optimal care to patients presenting with a tendon injury.
Tendon has chiefly a mechanical part to play at the intersection of muscle and bone, directly transmitting contractile forces while dissolving stress that would otherwise concentrate should muscle interface directly with bone.1,2 It stores, releases, and dissipates energy to efficiently maintain the joint-loading cycle while protecting adjacent tissues.1 Nonetheless, tendinous injuries are exceedingly common, with 50% of musculoskeletal injuries recorded in the United States involving tendinous or ligamentous injury and 10% of people (50% of runners) experiencing Achilles tendinopathy by age of 45.1,3 While tendon rupture usually corresponds to an acute incident, evidence suggests that chronic degenerative changes are usually present and contribute to the rupture.4 Thus, it is crucial to consider tendon healing in the context of its development, and regeneration, and of the histologic changes that reflect its long-term degeneration.
*Tendon Anatomy and Classification
*Epidemiology of Tendon Injury
*Development and Structure of Healthy Tendon
*Acute and Chronic Changes in Tendon Injury
While extreme exercise, concomitant loading, aging, and oxidative stress are recognized as physical and biological factors that engender tendinopathy, the exact pathogenesis of tendinopathy is poorly defined. For years, the accepted model of tendinopathy was one of tendinitis or inflammation. More recent histopathological studies have identified tendinosis (chronic degeneration), as the culprit in most cases of tendinopathy.26–30 It is responsible for the symptoms of pain, decreased strength, and impairment in activities of daily living commonly attributed to tendinitis. The affected region in tendinosis exhibits structural and cellular changes relative to unaffected tissue. While a healthy tendon is characterized by parallel, wavy, clearly defined bundles of collagen, diseased tissue is recognizable by its lack of alignment or demarcation between neighboring bundles and its increased diameter.31 On a cellular level, tendinosis is characterized by neovascularization, hypercellularity, and atypical fibroblast proliferation.32 Tenocytes capable of producing collagen change shape, with their nuclei exhibiting signs of fibrocartilaginous metaplasia.33,34 Biomechanically, tendinosis predisposes tendons to rupture.4
Similar features have been observed in the senescent tendon. Aging decreases tenoblast volume and plasmalemmal surface density increases the nucleus-to-cytoplasm ratio and suppresses protein synthesis.1 Collectively, these features contribute to decreased collagen turnover, characterized by thicker collagen fibers with greater variability in fiber diameter. The activity of lysol oxidase, an enzyme essential for collagen production, decreases, which in turn increases nonreducible collagen cross-linking.1,35 Biomechanically, this impedes the capacity to withstand loading and increases stiffness.1
In the setting of acute intrasynovial flexor tendon injury, disruption of the tissue surrounding the lacerated tendon compound the severity of the injury. Leakage of synovial fluid from within the digital sheath causes tendon starvation, slowing the repair process. This occurs through absolute synovial fluid loss, but also through disruption of the pressure distribution crucial to the process of imbibition by which the tendon gets most of its nutrients.36 It follows logically that injury to the tendon blood supply itself also hinders tendon healing in the acute setting. Importantly, as surgical apposition of the two ends of an injured tendon remains the gold standard for tendon injury treatment, one must be mindful to limit intraoperative trauma, which is additive to the severity of the original injury.
A common nontraumatic pathology of hand tendons is proliferative extensor tenosynovitis of the wrist, a condition well-documented in patients diagnosed with rheumatoid arthritis. It is characterized by pain and limited range of motion localizing to the fourth extensor compartment and can lead to tendon rupture.37 In the context of rheumatoid arthritis, the proliferation is due to synovial tissue hypertrophy, inflammation, and fluid production. Histologically, the pathology infiltrates the tendon properly and exhibits fibrinous adhesions, a feature also observed in tendon healing from acute or chronic traumatic injury.37
*Repair and Regeneration
*Practical Approach for Surgeons
Conclusion
Tendon injury is an exceedingly common presentation to emergency departments, making it one of the conditions most frequently treated by plastic surgeons. Factors such as age, mechanism of injury, time to repair, and physical exam findings play critical roles in determining the optimal method of management and postoperative rehabilitation. Hand surgeon familiarity with the subtleties of tendon healing is thus essential to ensure favorable long-term outcomes.
