OPBSMusculoskeletalBiomechanics
Must Know
- Tendon joins muscle to bone and transmits force. Ligament joins bone to bone and guides joint motion.
- Ligaments are the primary static stabilisers. Tendons add dynamic stability and secondary restraint.
- Hierarchy runs collagen triple helix, microfibril, fibril, fascicle, tendon.
- Endotenon binds fascicles. Epitenon wraps the whole tendon. Both carry vessels, lymphatics and nerves.
- Achilles has a paratenon. Flexor tendons have a synovial sheath for gliding.
- Small leucine-rich proteoglycans control fibril thickness and assembly. Decorin and biglycan are the commonest in tendon.
- Crimp is the microscopic wavy pattern of fibrils, straightened in the toe region of loading.
- Tenocytes make matrix, sense load and talk to each other through gap junctions.
- Intra-articular soft tissue injuries heal less well than extra-articular ones.
More on tendon function
- Hamstrings act as secondary restraint to anterior tibial translation in the ACL deficient knee.
Tendon Versus Ligament
| Feature | Tendon | Ligament |
|---|
| Water, share of wet weight | 50 to 60 percent | 60 to 70 percent |
| Collagen, share of dry weight | About 75 percent | About 80 percent |
| Type I share of collagen | 95 percent | About 90 percent |
| Type III collagen | Small amount | More than tendon |
| Fibre arrangement | Parallel, highly aligned | Interwoven, more cross-linked |
| Cells | Tenocytes, hypocellular | Fibroblasts, more metabolically active |
| Outer layer | Epitenon | Epiligament |
| Toe region | Shorter | Longer, fibres take longer to align |
- Ligament proteoglycans and elastin are each about 1 percent of dry weight.
More on composition
- Fibromodulin and lumican are class II SLRPs. Decorin and biglycan are class I.
- GAGs bind water and are thought to contribute to viscoelasticity, though some studies show no direct effect in ligament.
- Ligament also holds collagen types V, VI, XI and XIV.
- Ligament proteoglycan content varies with how much compressive load the ligament bears.
- Elastin returns ligament to its prestretched length after loading.
- ACL cells look chondroid and are less active than the elongated MCL cells.
- Ligament vessels come mainly from the epiligamentous plexus and are densest near insertions.
Junctions and Insertions
| Insertion | Structure | Where |
|---|
| Direct (fibrocartilaginous) | Four zones. Tendon or ligament, uncalcified fibrocartilage, calcified fibrocartilage, bone | High tensile load, rotator cuff. Commoner type |
| Indirect (fibrous) | Fibres blend with periosteum as Sharpey fibres | Tibial MCL, distal rectus femoris |
More on junctions and insertions
- At the myotendinous junction, staggered end sarcomeres send myofilament bundles straight onto collagen fibrils.
- Ligament cells are elongated in the midsubstance and rounded at the insertion.
Blood Supply and Nerves
- Tendon vessels enter through the paratenon or bony insertion, then run in the endotenon.
- Sheathed tendons receive vessels through vincula (mesotenon) and nutrition by synovial fluid diffusion.
- Watershed zones prone to rupture lie in supraspinatus, long head of biceps, Achilles and patellar tendons.
| Nerve ending | Behaviour | Site |
|---|
| Golgi organ | Steady state signal under prolonged large stimulus | Myotendinous region |
| Pacinian corpuscle | Sensitive, fast adapting | Myotendinous region |
| Ruffini ending | Sensitive, slow adapting | Myotendinous region |
| Free nerve ending | Nociception | Enthesis |
More on blood supply and nerves
- A tendon shares the nerve of its muscle.
- ACL deficient knees show reduced proprioception, linked to loss of mechanoreceptors.
Mechanics
| Curve | Type of property | Slope | Peak | Area under curve |
|---|
| Load versus elongation | Structural, whole construct | Stiffness | Ultimate load | Energy absorbed to failure |
| Stress versus strain | Material, normalised to area and length | Modulus | Tensile strength (and ultimate strain) | Strain energy density |
- Curve regions are toe (crimp recruitment, low slope), linear, then failure.
- Nonlinear anisotropy means properties change with load direction and load magnitude.
- Viscous behaviour dominates at low loads. Elastic behaviour dominates at high loads.
| Viscoelastic test | Held constant | What happens |
|---|
| Creep | Load | Elongation slowly increases |
| Stress relaxation | Elongation | Load falls over time |
| Hysteresis | Cyclic loading and unloading | Unloading curve differs, area between is energy lost |
| Cyclic load relaxation | Repeated cycles to set length | Peak load falls each cycle |
| Cyclic creep | Repeated stress | Deformation creeps up |
More on testing variables
- Tendon stiffness falls as temperature rises. Hydration also alters results.
- A high length to width (aspect) ratio limits grip slippage and stress concentration.
- Ligament tensile properties rise slightly with faster extension rates.
- Freezing ligament causes no significant change in structural or mechanical properties.
- Ligament results vary with test orientation of the bone ligament bone complex.
- Erector spinae tendon modulus is an order of magnitude higher than rotator cuff tendon.
- Teres major transfer for massive cuff tears works better when its proprioception is preserved.
Biological Factors
- Exercise raises tendon modulus and ligament strength and stiffness. Immobilisation lowers them.
- Immature ligaments fail by avulsion through open physes. Mature and older ones fail in midsubstance.
- Ligament stiffness, ultimate load and energy to failure rise until skeletal maturity, then fall with ageing.
- Females tear the ACL 2 to 8 times more often, partly from greater dynamic valgus.
- Oestrogen does not alter ligament mechanics. Excess relaxin weakens the ACL.
- Immobilisation causes osteoclastic resorption at insertions, which never fully recover after remobilisation.
More on tendon risk factors
- Older age raises tendon injury rates. Diabetes, hypercholesterolaemia and kidney disease degrade tendon.
Injury
- Tendinosis has replaced tendinitis because true inflammation is absent.
- Tendinosis histology shows disorganised collagen, more matrix, more tenocytes and neovascularisation.
- Direct ruptures come from penetrating trauma, commonest in upper limb flexor tendons.
- Indirect ruptures are commoner, occur in predisposed tendon, and follow eccentric contraction.
- Ligament sprain grade I overstretches fibres, grade II partly tears them, grade III ruptures completely.
- ACL and MCL share load. Loss of one raises force in the other.
More on injury patterns
- Chronic tendon injury shows rounded cells, more cellularity, poor collagen order and weaker mechanics.
- ACL anteromedial bundle resists anterior translation. Posterolateral bundle resists rotation in extension.
Healing and Repair
| Phase | Timing | Main events |
|---|
| Inflammation | First days | Haematoma, macrophages, tenocyte migration, type III collagen begins |
| Proliferation | Within a few days | High cellularity, peak type III collagen, scar like tissue |
| Remodelling | From about 6 weeks | Fewer cells and vessels, fibres realign, type I collagen dominates |
- Healed tendon and ligament are scar, mechanically inferior to native tissue.
- Extrinsic healing (cells from outside) is the main source of adhesions. Intrinsic healing uses cells within the tendon.
- Adhesions are worst in sheathed tendons such as flexor zone II.
- Immobilisation protects the repair but stiffens. Early motion aids gliding but risks the repair.
- Stiffness can rise while modulus falls if cross-sectional area grows. More tissue, poorer quality.
- Complete ligament tears heal poorly because the ends retract. Small gaps can bridge.
- Isolated MCL tears do well nonoperatively with early controlled motion.
- Intrasynovial tissue (ACL) is reconstructed. Extrasynovial tissue (rotator cuff) is repaired directly.
- Common ACL grafts are bone patellar tendon bone and semitendinosus or gracilis, autograft or allograft.
More on healing, grafts and tissue engineering
- Scaffolds need biocompatibility and high porosity for cell ingrowth.
- Resorbable synthetics include PLGA and silk. Nonresorbable ones include carbon and PTFE.
- Augmentation options include growth factors (TGF-β, PDGF, FGF), mesenchymal stem cells, fibroblasts, gene therapy and mechanical stimulation.
- No tendon or ligament engineering method is in routine clinical use. Skin substitutes such as Integra are FDA approved.
- Growth factors, hyaluronic acid, PRP and prolotherapy for ligament healing lack clear evidence.
- Chronic rotator cuff tears show muscle fatty degeneration and atrophy, which limit repair success.
- Healing ligament shows more types III and V collagen and more vessels.
- Grafts elongate under cyclic loading, losing initial stability.
- Xenografts have no current clinical use in tendon or ligament reconstruction.
Numbers to Remember
- Healed ligament. 30 to 50 percent of native tissue quality.
- Remodelling onset. About 6 weeks after injury.
- Return to sport after ACL injury. 65 percent reach preinjury level, 38 percent stay there for years.
Memory Aids
- Creep keeps the load, relaxation keeps the length. Whatever is held fixed, the other variable drifts.
- Structural is the Whole, material is the Matter. Stiffness and load for the whole, modulus and stress for the matter.
Exam Traps
- Ligament has less total collagen and more type III collagen than tendon.
- Direct insertions are the commoner type and suit high tensile load. Sharpey fibres mark indirect insertions.
- Free nerve endings cluster at the enthesis. Mechanoreceptors sit at the myotendinous region.
- A rise in stiffness alone does not prove better repair quality.
- Freezing does not change ligament mechanical properties.
- Adhesions come mainly from the extrinsic healing mechanism.
Related pages. Tendinopathy, Platelet Rich Plasma
Source
Counihan MM, Soslowsky LJ. Tendons and Ligaments. In. Aaron RK, editor. Orthopaedic Basic Science. Foundations of Clinical Practice. 5th ed. Philadelphia, Wolters Kluwer, 2021.
Practise Type X questions on this topic
Reviewed by Professor Phong Tran, Head of Orthopaedic Surgery, Western Health. Last updated 17 October 2026.
