< Back Dr. Serkan BAYRAM Endoprosthesis Endoprosthetic reconstruction is a cornerstone technique in musculoskeletal oncology, allowing immediate restoration of skeletal continuity and early mobilization after wide tumor resection. Modern modular megaprostheses, made of titanium or cobalt-chromium alloys, are designed for durability, functional recovery, and ease of revision. They are primarily indicated for periarticular or diaphyseal bone loss following tumor excision, failed fixation, or pathological fractures. Cemented fixation ensures immediate stability, while press-fit and porous-coated designs promote biological integration. Despite excellent limb salvage rates (>90%), complications such as infection, aseptic loosening, and mechanical failure remain challenges. Advances including silver-coated implants, expandable pediatric prostheses, and improved soft-tissue reattachment techniques continue to enhance long-term outcomes and quality of life for oncology patients. Definition An endoprosthesis is a modular metallic implant used to reconstruct bone and joint defects following wide resection of primary or metastatic musculoskeletal tumors. The aim is to achieve immediate structural stability , preserve limb function, and allow early mobilization, particularly in cases where biological reconstruction (allograft or autograft) is not feasible. Indications Segmental bone loss after tumor resection, particularly in the proximal humerus , distal femur , and proximal tibia . Periarticular destruction due to primary bone sarcomas (e.g., osteosarcoma, Ewing sarcoma) or metastatic disease. Reconstruction after pathological fractures or failed fixation in oncologic bone. Salvage after infection or mechanical failure of previous reconstruction. Design and Components Modern tumor prostheses are modular megaprostheses made from titanium or cobalt-chromium alloys, often with: Cemented or press-fit stems for fixation into the remaining diaphysis. Rotating hinge joints (knee and elbow) to reduce torque and wear. Porous-coated or hydroxyapatite collars to promote soft-tissue and bone integration. Expandable designs for skeletally immature patients, allowing non-invasive limb-length adjustment. Cemented fixation offers immediate stability, while cementless (press-fit) fixation supports long-term biological fixation and easier revision. Surgical Principles Wide oncologic margins are mandatory to minimize local recurrence. Preservation of neurovascular structures and soft-tissue coverage is essential. Stable fixation and restoration of limb length should be achieved intraoperatively. Reconstruction of muscle attachments (especially in proximal humerus and tibia) improves functional outcome. Prophylactic antibiotic cement or silver-coated implants are used to reduce infection risk in high-risk cases. Advantages Immediate load-bearing capability. Shorter operative time compared to biological reconstructions. Predictable early function and pain relief. Can be revised modularly if components wear or fracture. Complications Infection (5–15%); more common in immunocompromised or irradiated patients. Mechanical failure (loosening, stem breakage). Aseptic loosening due to stress shielding. Periprosthetic fracture and soft-tissue failure (e.g., extensor mechanism insufficiency). Outcomes and Prognosis Endoprosthetic reconstructions provide excellent pain relief and limb salvage rates exceeding 90% in modern series. Five-year implant survival is around 70–80% , depending on site and indication. Long-term durability is enhanced by improved modular designs, better fixation strategies, and multidisciplinary care. References Rizzo SE, Kenan S. Pathologic Fractures. StatPearls Publishing, 2025. Fields RC et al. Management of Pathological Fractures: Current Consensus. Knee Surg Sports Traumatol Arthrosc , 2024. Boussouar S et al. Tailored Approach for Appendicular Pathologic Fractures from Metastatic Bone Disease. Cancers (Basel) , 2022. Jeys L, Grimer R. Endoprosthetic Reconstruction After Tumor Resection. J Bone Joint Surg Br , 2019. Henderson ER et al. Failure Mode Classification for Tumor Endoprostheses: An International Consensus. Clin Orthop Relat Res , 2017. Quick Facts Feature Details Purpose Reconstruction of segmental bone or joint defects after tumor resection Main Indications Primary or metastatic bone tumors, failed fixation, post-infection salvage Common Sites Distal femur, proximal tibia, proximal humerus, proximal femur Design Type Modular or custom-made megaprostheses (cemented or press-fit fixation) Expandable Prostheses Used in skeletally immature patients to allow limb-length adjustment Key Materials Titanium, cobalt-chromium alloys, silver-coated or hydroxyapatite collars Advantages Immediate stability, early mobilization, predictable limb function Common Complications Infection (5–15%), aseptic loosening, mechanical failure, periprosthetic fracture Functional Outcome Limb salvage rate >90%; 5-year implant survival 70–80% Preferred in Large bone defects or periarticular resections where biological grafting is not feasible Previous Next

< Back Dr. Özcan KAYA He was born in 1983. Following his pre-undergraduate studies, he began his medical education at Istanbul University's Istanbul Faculty of Medicine in 2001 and earned his MD in 2007. He completed his residency at Istanbul University's Istanbul Faculty of Medicine and became an Orthopedics and Traumatology Specialist in 2013. During his residency, he served as a spine surgery observer at Thomas Jefferson University & Rothmann Institute, one of the leading spine clinics in the United States, examining patients and participating in surgeries. He continues to practise at Istanbul Biruni Hospital. For more info, visit https://drozcankaya.com.tr/ Spine ozcankaya.md@gmail.com Previous Next

< Back Regional Flaps regional-flaps Previous Next

< Back Scaphoid Fractures scaphoid-fractures Previous Next

< Back Dr. Hakan ESKARA University of Health Sciences, Istanbul, Sancaktepe City Prof. Dr. Ilhan Varank Health Application and Research Center Oncologic Orthopaedics, Sports Medicine hakaneskara@gmail.com Previous Next

Arthroplasty General Principles Indications for Arthroplasty Implant Designs & Materials Preoperative Planning Periprosthetic Joint Infection Postoperative Rehabilitation Hip Arthroplasty Total Hip Arthroplasty (THA) Hip Approaches Revision Hip Arthroplasty Periprosthetic Hip Fractures Dislocation & Instability Knee Arthroplasty Total Knee Arthroplasty (TKA) Knee Approaches Unicompartmental Knee Arthroplasty (UKA) Revision Knee Arthroplasty Ligament Balancing in TKA Patellofemoral Arthroplasty Special Considerations Robotic Assisted UKA Robotic Assisted TKA Robotic Assisted THA Myths and in Arthroplasty

< Back Complex Limb Salvage complex-limb-salvage Previous Next

< Back Alper DUNKI Skeletal Muscle Spot Knowledge Structure Motor unit = motor neuron + innervated fibers Sarcomere = contractile unit (actin + myosin) Membranes: Sarcolemma, T-tubule, SR → form “triad” for excitation–contraction coupling Connective layers: Endomysium, perimysium, epimysium Neuromuscular Transmission ACh release at NMJ → depolarization → Ca²⁺ release → contraction Drugs: Non-depolarizing blockers → receptor antagonists Depolarizing (succinylcholine) → persistent depolarization AChE inhibitors → prolong transmission Disorder: Myasthenia gravis → ↓ ACh receptors Contraction Twitch → summation → tetanus Contraction types: isotonic, isokinetic, isometric Eccentric > concentric in force (but ↑ injury risk) Force ∝ cross-sectional area + fiber length + pennation angle Fiber Types Type I: Slow, oxidative, fatigue-resistant Type IIA: Intermediate Type IIB: Fast, glycolytic, fatigue-prone Training shifts capacity (endurance ↑ mitochondria, oxidative enzymes) Energetics Phosphagen system → ATP + creatine phosphate (seconds) Anaerobic glycolysis → lactate (20–120 sec) Aerobic metabolism → Krebs + oxidative phosphorylation (long-term, efficient) Injury & Repair Repair: Macrophages + cytokines → activate satellite cells Limitations: Fibrosis may impair full recovery Clinical: DOMS = 24–72h after eccentric work Strains = at myotendinous junction Lacerations → scar tissue Denervation → fibrillation potentials (2–4 weeks), ↑ ACh sensitivity Immobilization Leads to rapid atrophy, loss of strength Atrophy worse in slack position Muscles in stretch add sarcomeres but still ↓ cross-sectional area Skeletal Muscle: Structure, Function, Energetics, Injury, and Repair General Information Skeletal muscles are innervated by the peripheral nervous system. They provide voluntary movement of the axial and appendicular skeleton. A motor unit consists of a single motor neuron and the muscle fibers it innervates. Hierarchical Structure of Muscle A muscle fiber is a multinucleated, highly specialized cell. The contractile unit is the sarcomere. Sarcomeres are aligned in series to form myofibrils. Mechanical coupling between myofibrils is provided by intermediate filaments. Each fiber is surrounded by endomysium, fascicles by perimysium, and the whole muscle by epimysium. Membrane Systems The T-tubule system originates as invaginations of the sarcolemma and transmits excitation to myofibrils. The sarcoplasmic reticulum stores, releases, and reuptakes calcium. The T-tubule and two adjacent terminal cisternae form the “triad” structure. This arrangement enables rapid and synchronized activation of contraction. Composition and Organization of the Sarcomere The thick filament is myosin; the thin filament is actin. Tropomyosin covers myosin-binding sites on actin in the resting state. Upon calcium binding, the troponin complex induces a conformational shift of tropomyosin, initiating actin–myosin interaction. The A band (actin + myosin), I band (actin), H band (myosin), and Z line create the typical striation pattern. During contraction, the sarcomere shortens; filament lengths remain constant, but overlap increases. Neuromuscular Junction (NMJ) and Transmission Each muscle fiber is activated by a single motor endplate. Acetylcholine (ACh) is released from the presynaptic terminal, activates postsynaptic receptors, and generates an action potential. The impulse propagates via the T-tubule/SR network. ACh is rapidly degraded by acetylcholinesterase. Transmission can be modulated pharmacologically: – Non-depolarizing agents competitively block receptors. – Depolarizing agents (succinylcholine) cause persistent depolarization. – AChE inhibitors prolong transmission by preventing ACh degradation. Myasthenia gravis is characterized by a reduction in postsynaptic ACh receptors. Mechanical Responses of Muscle A single stimulus produces a “twitch” response. Repeated stimuli lead to temporal summation and tetanus. Force is proportional to the physiological cross-sectional area; fiber length and pennation angle are also determinants. Types of contraction: isotonic, isokinetic, isometric; concentric (shortening) and eccentric (lengthening) behaviors occur. According to the force–velocity relationship, eccentric contraction produces the greatest tension and carries higher risk of injury. Fiber Types and Performance Type I fibers are slow, oxidative, and fatigue-resistant. Type IIA fibers display intermediate properties. Type IIB fibers are fast, glycolytic, and fatigue rapidly. Training can modify distribution and oxidative capacity; endurance training increases mitochondrial content and oxidative enzyme activity. Energy Systems Skeletal muscle contraction is fueled by three main pathways: Phosphagen system: Provides very short-term, anaerobic energy via ATP and creatine phosphate. Anaerobic glycolysis: Produces lactate from glucose, supporting 20–120 seconds of high-intensity activity. Aerobic metabolism: Krebs cycle and oxidative phosphorylation yield high ATP output; fat and protein substrates can also be utilized. Endurance training enhances oxidative efficiency and promotes fat utilization. Muscle Injury and Repair Repair is mediated by cytokines released from neutrophils, monocytes/macrophages, fibroblasts, and endothelial cells. Necrotic fibers are cleared by macrophages. The source of regeneration is satellite cells , which are activated upon injury. Concurrent fibrosis can limit full functional recovery. Delayed-onset muscle soreness (DOMS) arises 24–72 hours after eccentric loading; edema and increased intramuscular pressure are implicated. Contusions involve hematoma, inflammation, and variable regeneration; myositis ossificans may develop within 2–4 weeks. Muscle strains typically occur at the myotendinous junction in muscles crossing two joints; incomplete tears show early inflammation and force reduction with recovery within a week (experimental data). Complete ruptures present with contour deformity. Healing after laceration usually results in scar tissue; regeneration and reinnervation are limited. Denervation manifests within 2–4 weeks with fibrillation potentials and increased ACh sensitivity. Immobilization and Disuse Rapid atrophy, loss of strength, and increased fatigability occur. Myofibrillar loss is the main cellular finding. The length at which the muscle is immobilized is important: atrophy is greater in a slack position (e.g., quadriceps in knee extension). Muscles held under stretch add new sarcomeres, partially compensating for atrophy, although cross-sectional area continues to decrease. Clinical Implications Selection of anesthetics and neuromuscular blockers is based on NMJ physiology. Eccentric loading should be appropriately dosed in rehabilitation. Early and adequate loading supports mitochondrial and oxidative adaptations. Timing of inflammation and duration of immobilization are critical in limiting fibrosis and optimizing satellite cell response after injury. Summary This overview presents the cellular and mechanical foundations of skeletal muscle, its energy utilization, adaptive responses, and the dynamics of injury and repair in relation to clinical decision-making. References 1. Jin JB, Zhao D, Wu H, et al. Metabolic and molecular regulation in skeletal muscle function and regeneration. Front Cell Dev Biol . .doi:10.3389/fcell.2025.1651553 2. Yeowell GJ, Dunbar PJ, Carré MJ, Tarsuslugil A, Mason PH, Hennessey P. Molecular mechanisms of muscle wasting in muscle disuse, denervation, and chronic disease. J Cachexia Sarcopenia Muscle . 2023;14(3):799–815. doi:10.1002/jcsm.13098 3. Brorson J, Lin L, Wang J, et al. Complementing muscle regeneration—fibro-adipogenic progenitor and macrophage-mediated repair of elderly human skeletal muscle. Nat Commun . 2025;16:5233. doi:10.1038/s41467-025-60627-2 Previous Next

Concise orthopaedic education for residents and specialists, including surgical guides, core topics, and case-based learning." Where Orthopedic Minds Meet & Share OrthoRico is a modern orthopedic education platform designed for residents and specialists, offering evidence-based content, case-based learning, and step-by-step illustrated surgical guides. Why OrthoRico ? Learning and growing in orthopedics should be collaborative, visual, and accessible. OrthoRico is a non-commercial, academic platform created by and for orthopedic professionals. Whether you're a resident preparing for exams or a surgeon looking for clear visual guidance, OrthoRico offers: Evidence-based summaries of core orthopedic topics Step-by-step illustrated surgical procedures Real clinical cases and exam-style questions A growing community of orthopedic minds sharing knowledge Everything is peer-driven. Free. And focused on practical learning. Explore Our Sections Core Orthopedic Topics Each topic aims to provide concise information and key points about the subject, serving as a guide for orthopedic assistants and specialists. Read More Surgical Guides This section offers step-by-step surgical techniques, providing detailed instructions and insights for orthopedic procedures. Read More Literature Updates This section provides the latest research, studies, and reviews in the field of orthopaedics. Stay informed with the most recent advancements and evidence-based practices. Read More Contributors & Acknowledgements This section highlights the valuable contributions of authors, researchers, and professionals who have shared their expertise to enhance the content. Read More This Week’s Highlights Optimal Tightrope Positioning for Adequate Syndesmotic Stabilization in Simulated Syndesmotic Injuries Alignment Techniques in Total Knee Arthroplasty Short-term contemporary outcomes for staged versus primary lower limb amputation in diabetic foot disease Mirels' Score for Upper Limb Metastatic Lesions: Do We Need a Different Cutoff for Recommending Prophylactic Fixation? Working With the Best Associates & Partners

< Back Toddler’s Fracture (Tibia) toddlers-fracture Previous Next

< Back Optimal Tightrope Positioning for Adequate Syndesmotic Stabilization in Simulated Syndesmotic Injuries Use of syndesmotic suture button fixation has gained in popularity for treating an injury to the tibiofibular syndesmosis. Biomechanical fixation stability with suture button device (TightRope; Arthrex, Naples, FL) placed at 4 distances from the tibiotalar joint line (0.5, 1.5, 2.5, and 3.5 cm) and 3 trajectories (anterior, medial, and posterior) were studied using cadaveric lower extremities with created syndesmotic injuries. Fixation placed at 0.5 or 1.5 cm from the joint line in medial or posterior trajectories resulted in the lowest increases in fibular rotation. More proximal or anterior placements led to increased fibular motion and decreased rotational stability. 🧠 Key Points Syndesmotic suture button placement 0.5–1.5 cm from the joint line provides the most rotationally stable fixation. Medial and posterior trajectories are more stable than anterior placements. Proximal placements beyond 1.5 cm increase fibular motion and reduce stability. Ankle width changes were minimal but increased slightly with anterior or proximal placement. Biomechanical cadaveric testing simulates in vivo weightbearing and rotational loads. Foot & Ankle Orthopaedics (2025) DOI: 10.1177/24730114251342243 Previous Next

< Back DISH (Diffuse Idiopathic Skeletal Hyperostosis) Previous Next