Ligament
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Ligament
FIG. 1.44 Tendon and ligament architecture.
From Brinker MR, Miller MD: Fundamentals of orthopaedics,
Philadelphia, 1999, Saunders, p 15.
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Characteristics
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Originates and inserts on bone
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Stabilizes joints and prevents displacement of bones
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Contains mechanoreceptors and nerve endings that facilitate joint proprioception
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Like tendon, displays viscoelastic behavior
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Structure and composition
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Composition
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Similar to that of tendon
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Water: 60%–70% of total weight
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Collagen: 80% of dry weight
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90% type I collagen; also types III, V, VI, XI, and XIV collagen
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More collagen type I is seen at the origin and insertion, with collagen III seen midsubstance.
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Elastin (1% dry weight)
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Proteoglycans (1% dry weight)—function in water retention and contribute to viscoelastic behavior
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Fibroblast
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Primary cell, oriented longitudinally
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Functions to synthesize ECM, collagen, and proteoglycans
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Epiligament
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Similar to that in epitenon; carries the neurovascular and lymphatic supply of tendons
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Compared with tendon
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Less total collagen but more type III collagen
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More proteoglycans and therefore more water
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Less organized collagen fibers that are more highly cross-linked and intertwined
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“Uniform microvascularity”—receives supply at insertion site by the epiligamentous plexus
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Insertion
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Similar to that of tendon
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Direct (fibrocartilaginous) insertion
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Four layers: tendon, fibrocartilage, mineralized fibrocartilage, and bone
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More common
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Deep fibers attach at 90-degree angles
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Injury
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Indirect
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Superficial fibers insert into the periosteum and deep fibers insert into bone via Sharpey fibers (perforating calcified collagen fibers).
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Healing
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Knee and ankle ligaments are most commonly injured
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Ligaments do not plastically deform.
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They “break, not bend.”
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Midsubstance ligament tears are common in adults.
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Avulsion injuries are more common in children.
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Typically occurs between unmineralized and mineralized fibrocartilage layers
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Increased number of collagen fibers but
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Fewer mature cross-links (45% of normal at 1 year)
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Decrease in mass and diameter
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Three phases, as in bone
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Inflammatory—early acute mediators (PMNs and then macrophages), with production of type III collagen and growth factors
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Proliferative—around 1–3 weeks, with replacement of type
III collagen by type I collagen (Think of macrophages as weakening the structure—weakest point.)
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Remodeling and maturation
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Factors that impair ligament healing
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Intraarticular ligamentous injury
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Old age, smoking, NSAID use
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Diabetes mellitus
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Alcohol use
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Local injection of corticosteroids
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Factors that improve ligament healing experimentally
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Extraarticular ligamentous injury
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Compromised immunity
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IL-10 (antiinflammatory)
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IL-1 receptor antagonists
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Mesenchymal stem cells
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Scaffolds (such as collagen–platelet-rich plasma hydrogels)
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Neuropeptides
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Calcitonin gene–related peptide
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Immobilization
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Adversely affects ligament strength: elastic modulus decreases
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In rabbits, breaking strength reduced dramatically (66%) after 9 weeks of immobilization.
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Effects reverse slowly upon remobilization.
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Prolonged immobilization disrupts collagen structure, which may not return to normal within insertion sites.
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Exercise
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Improves mechanical and structural properties
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Increases strength, stiffness, and failure load
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