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< Back Dr. Cemil AKTAN Spine Trauma Classifications Early systems such as Denis’ three-column model and Allen–Ferguson’s mechanism-based classification emphasized anatomical and mechanical concepts of instability. Over time, modern systems evolved to integrate neurological evaluation and clinical relevance, resulting in improved surgical decision-making. For cervical injuries, multiple region-specific classifications exist — including Anderson–Montesano for occipital condyle fractures, Traynelis for occipito–atlantal dislocation, Fielding–Hawkins for atlantoaxial rotatory fixation, and Anderson–D’Alonzo for odontoid fractures. In the thoracolumbar region, progression from Holdsworth’s two-column theory to Denis’ three-column model, followed by Magerl’s AO classification, established the foundation for contemporary systems. The Thoracolumbar Injury Classification and Severity Score (TLICS) and its evolution — the AO Spine Thoracolumbar Classification (AO TLS) — combine morphology, neurological status, and modifiers, guiding evidence-based operative versus nonoperative management. Spine Trauma Classifications 1-General Principles - The primary objective of spinal trauma classification systems is to provide a standardized framework that characterizes the severity, morphology, and stability of the injury, thereby guiding therapeutic decision-making and prognostication. -Spine trauma classification: Earlier systems (Denis, Allen–Ferguson) emphasized morphology alone, whereas modern frameworks (AO Spine-TLICS) integrate morphology, neurological status, and modifiers. -Contemporary classification systems incorporate neurologic status and mechanical stability, enhancing communication, prognostication, research, and treatment planning. 2-Cervical Spine -Upper Cervical Injuries : Composed of occiput, atlas (C1), and axis (C2), collectively called the craniocervical junction (CCJ). Occiput–C1: Provides 50% of cervical flexion–extension. C1–C2: Provides 50% of cervical rotation. Injury prevalence is bimodal, in children and adults >60 years. Pediatric: Predominantly motor vehicle accidents or pedestrian–vehicle collisions. Elderly: Most often due to falls. a)Occipital Condyle Fractures · The most widely used classification is the Anderson & Montesano system. Type I : Axial load; often comminuted; ligaments intact; unilateral stable, bilateral may be unstable (A). Type II : Extension of basioccipital fracture from direct blow; ligaments intact; usually stable (B). Type III : Alar ligament avulsion with medial fragment displacement into the foramen magnum; from forced rotation + lateral bending; potentially unstable (C). b) Occiput-Atlas dislocations · The most commonly employed classification system was described by Traynelis. Type I – Anterior displacement of the occiput on atlas. Type II – Longitudinal distraction; traction may worsen neurologic deficit. Type III – Posterior subluxation/dislocation. c) Atlas (C1) Fractures · Described by Jefferson (1921); it involves anterior & posterior arches (weakest C1 points). · 2–13% of cervical fractures; 25% of atlantoaxial injuries; mean age 30. · The most common motor vehicle accidents are caused by axial load drops. · Up to 50% with other cervical fractures—commonly dens, hangman’s, C2 teardrop, burst, or lateral mass fractures d) Atlantoaxial Subluxation and Dislocation · Fielding and Hawkins presented the most commonly used classification scheme. Type I – Pure rotation. Type II – Rotation + anterior displacement <3–5 mm → partial transverse ligament deficiency. Type III – Rotation + anterior displacement >5 mm → complete transverse ligament deficiency. Type IV – Rotation + posterior displacement. e) Transverse Ligament Injuries · Primary stabilizer of the atlantoaxial joint. · Disruption is irreparable; original strength and function cannot be restored. · Dickman Classification ( Dickman CA, Greene KA, Sonntag VK. Injuries involving the transverse atlantal ligament: classiication and treatment guidelines based upon experience with 39 injuries. Neurosurgery. 1996;38:44-50.) Type I – Intrasubstance rupture. - IA : Midportion tear. - IB : Tear at periosteal insertion on atlas. Type II – Bony avulsion from C1 lateral mass. - IIA : Lateral mass comminuted. - IIB : Lateral mass intact. f) Fractures of the Odontoid · Mechanism: flexion → anterior displacement; extension → posterior displacement. · Anderson–D’Alonzo Classification Type I –Tip avulsion at alar ligament insertion; may accompany severe occipitocervical injury. Type II – Base/neck fracture at dens–C2 junction; poor healing from limited blood supply. Type III – Extends into C2 body; larger cancellous surface allows better healing than Type II. g) Hangman’s Fracture (Traumatic Spondylolisthesis of C2) Type I · Caused by hyperextension + axial load. · Bilateral pars fractures with <3 mm translation, no angulation. · Disc and anterior longitudinal ligament remain intact. · May be associated with C1 posterior arch or dens fractures. Type II & Variant · Type II: >3 mm translation + angulation; axial load + hyperextension → flexion; disc disruption ± C3 or C2 body fracture. · IIA: Marked angulation, ≤3 mm translation; flexion–distraction; disc & PLL disruption; traction widens disc space. Type III · Unstable; severe displacement/angulation with C2–C3 facet dislocation. Disc & PLL disruption, frequent neurologic injury. Mechanism: flexion–distraction → hyperextension. Lower Cervical Injuries 1- Subaxial (C3–C7) : ⅔ of all cervical injuries. · Spinal cord injury in 0.8–1.2% ; incidence is higher in >65 years, rare in children. · Male: female ≈ 2:1. · Mechanisms : Vehicle collisions (50%), falls (40%, especially elderly). 2- Throcal-Lomber injury Most common site of thoracic/lumbar injury; predominantly young males, high-energy trauma. Location : >50% between T11–L1; 30% between L2–L5. Mechanism : 50% motor vehicle accidents; 25% falls >6 ft (1.8 m). Neurologic injury : 20% complete, 15% incomplete. Associated injuries (>50% cases): fractures, head trauma, pulmonary, and intra-abdominal injuries. Noncontiguous spinal injuries : 5%, remote from the primary site. Classifications: a) Nicoll (1949) : Anterior wedge, lateral wedge, fracture–dislocation, isolated neural arch fractures. b) Holdsworth : Mechanism-based (flexion, flexion–rotation, extension, compression); introduced the two-column theory : i. Anterior column resists compression ii. PLC resists tension iii. Stable: wedge compression, compression burst (PLC intact) iv. Unstable: dislocations, extension/dislocations, rotational fracture–dislocations c) Denis Three-Column Model Introduced by Denis (1983) to classify spinal trauma and stability. Divides the spine into three anatomical columns: Anterior column → anterior longitudinal ligament + anterior two-thirds of vertebral body. Middle column → posterior one-third of vertebral body + posterior longitudinal ligament. Posterior column → facet joints + posterior ligamentous complex. Primary paradigm: based on the morphological extent of injury to bony and ligamentous structures. Widely adopted as a guide for trauma management; introduced the concept of instability. Mechanical instability: failure of ≥ 2 columns. Neurologic instability: deficit present (often mechanically unstable). Provided the foundation for subsequent classification systems. Three-column model validated in biomechanical cadaver studies; forms basis for modern classifications and treatment algorithms. d) Magerl Classification of Thoracolumbar Trauma (1994) Introduced by Magerl et al. (1994) ; focused on morphological assessment of osseous and ligamentous injury. Type A – Compression injuries · A1: Wedge compression (A1.1, A1.2, A1.3) · A2: Split fractures (A2.1, A2.2, A2.3) · A3: Burst fractures (A3.1, A3.2, A3.3) Type B – Distraction injuries · B1: Posterior tension band disruption, ligamentous (B1.1–B1.3) · B2: Posterior tension band + osseous disruption (B2.1–B2.3) · B3: Anterior tension band failure, hyperextension injuries (B3.1–B3.3) Type C – Rotational / Translational injuries · C1: Rotation with Type A pattern (C1.1–C1.3) · C2: Rotation with Type B pattern (C2.1–C2.3) · C3: Pure translational displacement (C3.1–C3.3) Each type is further divided into 3 groups , each group into 3 subtypes → >50 distinct injury patterns. Provided detailed morphological categorization but was criticized for excluding the neurological status of the patient. e) Thoracolumbar Injury Classification and Severity Score (TLICS, 2005) Developed by the Spine Trauma Study Group (2005) to standardize decision-making in thoracolumbar trauma. Designed as an algorithmic tool for surgical decision-making. Incorporates three major parameters: a. Injury morphology (compression, burst, translation/rotation, distraction) b. Integrity of the posterior ligamentous complex (PLC) c. Neurological status (intact, nerve root injury, incomplete SCI, complete SCI, cauda equina) Each parameter is assigned a weighted score → total score determines treatment pathway. · ≤3 points: Nonoperative management recommended · 4 points: Indeterminate (surgeon’s judgment) · ≥5 points: Surgical stabilization recommended Addressed limitations of purely morphological systems by integrating neurologic assessment. Demonstrated good interobserver reliability across both Orthopedic and Neurosurgery disciplines. f) Modified AO Spine Thoracolumbar Injury Classification (AO TLS) Developed to address limitations of TLICS, particularly indeterminate cases (scores 3–5), e.g., neurologically intact burst fractures with suspected PLC injury. Combines elements from Magerl (morphology) and TLICS (neurologic status, modifiers) . Core Components: a. Fracture morphology b. Neurologic status c. Modifiers (injury-specific/patient-specific) a) Fracture Morphology Type A – Compression injuries A0: Minor injury (transverse/spinous process fracture) A1: Wedge compression A2: Pincer fracture (endplates, no posterior wall) A3: Incomplete burst (without posterior wall involvement) A4: Complete burst (with posterior wall involvement) Type B – Tension-band injuries (no translation) B1: Osseous posterior tension band injury (e.g., Chance fracture) B2: Ligamentous posterior tension band injury B3: Anterior tension band failure (e.g., ankylosing spondylitis) Type C – Translational injuries Translation/distraction with complete disruption of spinal column Includes complete soft tissue hinge disruption even without visible listhesis b) Neurologic Status N0: Intact neurologic exam N1: Transient deficit, full recovery N2: Nerve root injury (weakness, radiculopathy) N3: Cauda equina / incomplete SCI N4: Complete SCI NX: Neurologic exam not assessable (e.g., intubated, sedated) c) Modifiers Modifiers were incorporated to account for variables that may influence surgical decision-making. These are categorized into injury-specific and patient-specific factors. M1 (Injury-specific): Indeterminate tension band injury (suspected on imaging) M2 (Patient-specific): Conditions complicating management (ankylosing spondylitis, DISH, osteoporosis, severe burns, etc.) If multiple patterns exist, classify by the highest injury type present. References 1. Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine (Phila Pa 1976). 1998;13:731–736. 2. Traynelis VC. Classification system of occiput–atlas dislocations. In: Rothman RH, Simeone FA, eds. The Spine. 7th ed. Philadelphia: Elsevier; 2018:1295. 3. Levine AM, Edwards CC. Fractures of the atlas. J Bone Joint Surg Am. 1991;73:680–691. 4. Fielding JW, Hawkins RJ. Atlanto-axial rotatory fixation (fixed rotatory subluxation of the atlanto-axial joint). J Bone Joint Surg Am. 1977;59:37–44. 5. Zadnik PL, Sciubba DM. Anatomy, Cervical Spine. In: Papadakos PJ, Gestring ML (eds). Encyclopedia of Trauma Care. Berlin, Heidelberg: Springer; 2015. doi:10.1007/978-3-642-29613-0_577 . 6. Dickman CA, Greene KA, Sonntag VK. Injuries involving the transverse atlantal ligament: classification and treatment guidelines based upon experience with 39 injuries. Neurosurgery. 1996;38:44–50. 7. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56:1663–1674. 8. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037. 9. Caron T, Bransford R, Nguyen Q, et al. Spine fractures in patients with ankylosing spinal disorders. Spine. 2010;35(11):E458–E464. 10. Hasler RM, Exadaktylos AK, Bouamra O, et al. Epidemiology and predictors of cervical spine injury in adult major trauma patients: a multicenter cohort study. J Trauma Acute Care Surg. 2012;72(4):975–981. 11. Nicoll EA. Fractures of the dorso-lumbar spine. J Bone Joint Surg Br. 1949;31:376–394. 12. Holdsworth F. Fractures, dislocations, and fracture-dislocations of the spine. J Bone Joint Surg Am. 1963;45:6–20. 13. Denis F. The three-column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine (Phila Pa 1976). 1983;8(8):817–831. 14. Magerl F, Aebi M, Gertzbein SD, Harms J, Nazarian S. A comprehensive classification of thoracic and lumbar injuries. Eur Spine J. 1994;3(4):184–201. 15. Patel AA, Whang PG, Brodke DS, et al. Evaluation of two novel thoracolumbar trauma classification systems. Indian J Orthop. 2007;41(4):322–326. 16. AO Spine Knowledge Forum Trauma. AO Spine Textbook: Comprehensive Overview on Surgical Management of the Spine. AO Foundation; 2020. 17. Rothman RH, Simeone FA. The Spine. 7th ed. Philadelphia: Elsevier; 2018. Previous Next

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< Back Alper DUNKI Cellular and Molecular Biology, Immunology and Genetics Terminology Spot Knowledge The nucleus stores DNA; nucleolus produces ribosomes. Defects cause syndromes with skeletal anomalies. Mitochondria are key for ATP; dysfunction leads to neuromuscular and metabolic disease. Lysosomes degrade waste; defects → storage disorders (e.g., Tay-Sachs). ECM (collagen, GAGs, proteoglycans) provides structural support and lubrication. Stem cells : mesenchymal stem cells can differentiate into osteoblasts and chondrocytes. Cellular Structures and Functions Nucleus & Nucleolus: Store genetic material, produce ribosomes. Syndromes: Bloom, Treacher Collins, Rothmund-Thomson. Cytoplasm: Site of metabolism. Mitochondria: ATP production, signaling. Mutations → neuromuscular disease, diabetes, deafness. Golgi apparatus: Packages proteins/hormones; linked to secretion disorders. Lysosomes: Waste degradation; lysosomal storage diseases (Tay-Sachs, Gaucher). Endoplasmic Reticulum: Protein & lipid synthesis. Ribosomes: Protein synthesis; ribosomopathies. .Cytoskeleton: Shape, motility; defects → cardiomyopathy, genetic deafness1. Cellular and Molecular Biolo… Extracellular Matrix (ECM) Provides scaffolding for tissues. Components: Collagen (main structural protein), GAGs , fibronectin , laminin . .GAGs + proteoglycans → cushioning, lubrication1. Cellular and Molecular Biolo… Intracellular Signal Transduction Mediated via receptors: GPCRs, ion channels, tyrosine kinases. Second messengers: cAMP, Ca²⁺. .Control gene expression and cellular responses1. Cellular and Molecular Biolo… DNA & Genetics DNA: Double-stranded, stores genetic info. Genes: Exons (coding) + introns (non-coding). Promoters/Enhancers: Regulate expression. Mutations: Basis of inherited disease (Down, DiGeorge). Mitochondrial DNA: Maternal inheritance. .SNPs & Epigenetics: Variation and environment-driven expression1. Cellular and Molecular Biolo… RNA Biology mRNA: Protein coding. miRNA: Gene regulation. .rRNA: Part of ribosome, diagnostic use in bacteria1. Cellular and Molecular Biolo… Gene Expression & Protein Synthesis Transcription: DNA → RNA. Translation: RNA → protein. Transcription factors (RUNX2, SOX9, PPAR-γ) regulate bone and cartilage differentiation. .Post-translational modifications: glycosylation, phosphorylation1. Cellular and Molecular Biolo… Molecular Biology & Protein Techniques FISH, CGH: Detect chromosomal abnormalities. Flow cytometry: Cell surface antigens. PCR/RT-PCR: Gene amplification. Blotting (Northern/Southern): Nucleic acid analysis. Microarray: Gene expression profiles. Recombinant DNA: Produces proteins (e.g., BMP-2, IL-6 inhibitors). .Immunohistochemistry, ELISA, Western blot: Protein detection/quantification1. Cellular and Molecular Biolo… Immunology Innate immunity: Fast, nonspecific. Adaptive immunity: Antigen-specific, memory formation. Humoral: B-cell mediated. Cellular: T-cell mediated. .Inflammation in connective tissue → osteoclastogenesis → bone resorption1. Cellular and Molecular Biolo… Stem Cells Adult stem cells: Self-renewal & tissue repair. Mesenchymal stem cells: Differentiate into bone, cartilage. Embryonic stem cells: Pluripotent, rejection risk. .Induced pluripotent stem cells: Reprogrammed somatic cells with pluripotency1. Cellular and Molecular Biolo… Organelle Function Clinical Relevance Nucleus Stores DNA Cancer karyotyping, mitotic abnormalities Nucleolus Ribosome synthesis Bloom, Treacher Collins, Rothmund-Thomson Mitochondria ATP production Neuromuscular disease, diabetes, deafness Lysosome Waste degradation Tay-Sachs, Gaucher, Niemann-Pick Golgi Apparatus Protein packaging Secretion disorders Endoplasmic Reticulum Protein/lipid synthesis Liver & muscle diseases Ribosomes Protein synthesis Ribosomopathies, macrocytic anemia Cytoskeleton Shape & motility Cardiomyopathy, hearing loss References Valls AF, et al. Nat Rev Mol Cell Biol . 2022. Krajnik B, et al. Front Cell Dev Biol . 2020. Levoin N, et al. Front Cell Dev Biol . 2020. .Meng F, et al. Trends Cell Biol . 20241. Cellular and Molecular Biolo… Previous Next

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< Back Ligament Balancing in TKA • The basic aim is to get both extension and flexion gaps rectangular, equal and balanced. This balanced tension is important for implant stability and long-term survival. • Two popular knee replacement techniques currently practiced are: “measured resection” which depends on tibial and femoral bone cuts through resection guide and “balanced resection” which depends on optimising ligament tensioning. Both affect ligament balancing during the operation. • A stepwise approach for sequential ligament releases, according to the type of deformity, is essential to good outcomes. Balancing Coronal Plane Varus knee: Medial side is tight and lateral side is loose. Medial releases 1) Removal of osteophytes / Deep MCL release 2) Release posteromedial corner subperiostally 3) Medial tibial reduction osteotomy 4) Release semimembranous 5) Superficial MCL release · Pie crusting technique · Release anterior part if it is tight in flexion, posterior part if it is tight in extension 6) Complete superficial MCL release subperiosteally from the tibia. · CCK / Constrained prosthesis has to be used. Lateral tightening · Use a thicker polietilen to fill up the gap and medial release to make the stretched lateral ligaments taut. · Proximal fibula osteotomy and advancing it distally to tighten the LCL. Valgus knee: · Lateral femoral condyle is hypoplastic · The distal femoral cut should be made less valgus (3ᵒ) to avoid residual valgus deformity. · To avoid the distal femur cut in internal rotation, the trans-epicondylar axis should be referenced instead of the posterior condylar line. Lateral releases (debatable) · The lateral collateral ligament is a stabilizing structure in flexion and extension, and has rotational and varus stabilizing effects. · The popliteus tendon complex also has passive varus stabilizing effects in flexion and extension, but has a more prominent role in external rotational stabilization of the tibia on the femur. · The posterolateral corner has primary stabilizing effects in extension, but also is effective in flexion. · The iliotibial band contributes to lateral knee stability when knee is extended, but when the knee is flexed to 90°, it is parallel to the joint surface, and cannot stabilize the knee to varus stress. 1) Removal of osteophytes 2) Posterolateral capsule 3) Iliotibial band (release must be performed only when contraction is present in extension.) 4) Popliteus tendon (if tight in flexion) 5) Lateral collateral ligament (stabilizing structure both in flexion and in extension.) 6) Lateral head of gastrocnemius muscle at femoral origin (if only tight in flexion) Medial tightening · Advance the MCL more proximally from the femoral origin with bone block · Advance the MCL more distally from tibial side and fix it with staple or screw · Suturing the MCL onto itself Balancing Sagital Plane · İf gap problem is symetric adjust tibia Tibial cut affects both flexion and extension gap · İf gap problem is asymetric adjust femur Distal femoral cut affects extension gap Posterior femoral cut affects flexion gap Rotation of the femoral component influences the flexion gap balancing! Posterior release order 1) Posterior femoral & tibial osteophytes 2) Posterior capsule 3) Additional resection of distal femur 4) Gastronemius muscles (medial and lateral) The addition of a PCL release for a PS knee increases the flexion gap. Treatment strategy for sagittal balance problem 1)Tight in extension and flexion Problem - Did not cut enough tibia Solution - Cut more proximal tibia 2)Loose in extension and flexion Problem - Cut too much tibia Solution 1. Use thicker poly insert 2. Add metal augments to tibial tray 3)Tight in flexion / Balanced in extension Common in CR / PCL tightness - Limited flexion - Anterior lift off of tibial tray Problem: - Insufficient posterior femoral cut - Scarred and too tight PCL - No posterior slope in tibial cut Solution: 1. Resect posterior osteophytes / release posterior capsule 2. Release / excise PCL 3. Recut tibia with increased slope 4. Resection of more bone from the posterior condyle by reducing the size of the femoral component 4)Loose in flexion / Balanced in extension Problem: - Cut too much posterior femur Solution: 1.Upsize femoral component 2.Recut distal femur, convert to symmetric gap problem and increase poly 5)Tight in extension / Balanced in flexion Problem: - Insufficient distal femoral cut - Tight posterior capsule Solution: 1. Release posterior capsule / osteophytes 2. Cut more distal femur 6)Loose in extension / Balance in flexion Problem: Cut too much distal femur. Solution: 1) Augment distal femur 2) Downsize femur, convert to symmetric gap problem and increase poly References · Whiteside LA. New York: Springer; 2004. Ligament balancing in total knee arthroplasty: an instructional manual · Babazadeh S, Stoney JD, Lim K, Choong PF. The relevance of ligament balancing in total knee arthroplasty: how important is it? A systematic review of the literature. Orthop Rev (Pavia). 2009 Oct 10;1(2):e26. doi: 10.4081/or.2009.e26. PMID: 21808688; PMCID: PMC3143981. · Matsuda S, Ito H. Ligament balancing in total knee arthroplasty-Medial stabilizing technique. Asia Pac J Sports Med Arthrosc Rehabil Technol. 2015 Aug 7;2(4):108-113. doi: 10.1016/j.asmart.2015.07.002. PMID: 29264249; PMCID: PMC5730662. · Basics in Hip and Knee Arthroplasty, 1e, Shrinand V. Vaidya Copyright c 2015, by Reed Elsevier India Pvt. Ltd. All rights reserved. ISBN: 978-81-312-4005-2 Previous Next

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