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< Back Clavicle Fractures Clavicle fractures are common shoulder injuries, especially in young active individuals, typically caused by a fall onto the shoulder or an outstretched hand. Overview 2–5% of all fractures, ~40% of shoulder girdle injuries Most common: middle third (~80%) Bimodal distribution: young active (sports, traffic) + elderly (falls) Mechanism: fall on shoulder, direct blow, FOOSH (less common) Clinical Presentation Local pain, swelling, tenderness Visible deformity or step-off in displaced cases Reduced shoulder motion due to pain Skin tenting → risk of open fracture Always check neurovascular status Imaging X-ray: AP + 15° cephalic tilt view (Zanca view) CT: distal (AC joint) or medial end (SC joint) fractures Classification Allman Classification I: Middle third (nearly %80) II: Distal third III: Medial third AO/OTA Classification (Clavicle, Distal) Type A – Nondisplaced, CC ligaments intact A1 : Extra-articular fracture A2 : Intra-articular fracture Typical management : Nonoperative Type B – Displaced, CC ligaments intact B1 : Extra-articular fracture B2 : Comminuted fracture Management : Can be treated nonoperatively or with surgery depending on symptoms and patient factors Type C – Displaced, CC ligaments disrupted C1 : Extra-articular fracture C2 : Intra-articular fracture Management : Operative fixation usually required Neer Classification (distal) : Type I Stable fracture pattern, usually managed non-operatively Fracture line lies lateral to the coracoclavicular (CC) ligaments Trapezoid and/or conoid ligament remains intact Type IIA Unstable injury, often requiring surgical fixation Fracture is medial to the CC ligaments with significant displacement of the medial fragment Conoid ligament preserved Trapezoid ligament intact Type IIB Unstable fracture, high risk of nonunion, usually surgical Fracture occurs between the CC ligaments Conoid ligament torn, trapezoid ligament intact Medial clavicle fragment displaced Type III Stable fracture, generally treated non-operatively Intra-articular extension into the acromioclavicular joint Both conoid and trapezoid ligaments intact Type IV Pediatric pattern, Salter-Harris type I physeal injury, usually stable Medial clavicle fragment displaced superiorly Periosteal sleeve avulsed from the inferior cortex Conoid and trapezoid ligaments intact Type V Unstable comminuted fracture, typically surgical Medial clavicle fragment displaced Inferior fragment remains attached to CC ligaments Conoid and trapezoid ligaments intact Robinson (Edinburgh) Classification: Considers location (medial, middle, distal), displacement, and comminution More comprehensive, useful for research/epidemiology Treatment Nonoperative Sling or figure-of-eight bandage Analgesia, early motion Indication: minimally displaced, <2 cm shortening Operative Indications Open fracture / threatened skin Neurovascular compromise 2 cm shortening or marked displacement Comminution in active/high-demand patients Symptomatic nonunion Techniques Plate fixation (superior or anteroinferior) Intramedullary devices (elastic nail, pin) for midshaft Distal: hook plate, locking plate, CC fixation Complications Nonunion (esp. distal, smokers, comminuted) Malunion (cosmetic, functional deficit) Hardware irritation, infection Rare: neurovascular injury Key Pearls Most middle-third fractures heal well nonoperatively Distal type II fractures = higher nonunion risk → surgery often indicated 2 cm shortening in young/active = consider fixation Look for associated injuries: ribs, pneumothorax, scapula clavicle-fractures Previous Next

< Back Dr. Ali Erkan YENIGUL Primary Bone Lymphoma A rare lymphoma subtype presenting primarily in bone, often mimicking other primary bone tumours. Epidemiology Accounts for 3–7% of all primary malignant bone tumors. About 5% of extranodal lymphomas , but <1% of all Non-Hodgkin lymphomas (NHL) . Predominantly affects 20–50 years , with male preponderance . Femur most common site (~29%), followed by tibia, pelvis, and spine . Rare presentations: solitary lesions in the skull. Etiology Mostly non-Hodgkin B-cell lymphomas (DLBCL commonest). Rarely T-cell variants. Genetic predisposition and viral infections (EBV) implicated. Classified as: Solitary bone site Multiple bone sites Bone + soft tissue lymphoma Clinical Presentation Bone pain unrelieved by rest (most common). ~25% present with pathological fracture. Neurological symptoms if spine involved. Systemic symptoms : fever, weight loss, night sweats. Imaging X-ray: variable → from near-normal to lytic, mixed lytic-sclerotic, or permeative lesions ± soft tissue mass. MRI, PET-CT, CT : essential for marrow infiltration, extraosseous spread, treatment response. Differential diagnosis: osteomyelitis, multiple myeloma, metastasis . Pathology Diagnosis: biopsy + bone marrow aspiration . Histology: Diffuse large B-cell lymphoma (DLBCL) most frequent. IHC: CD20+, CD45+, LCA+ . “Small round blue cell” infiltration possible. Treatment Multidisciplinary approach : systemic chemotherapy + local radiotherapy. CHOP-like regimens (anthracyclines, cyclophosphamide) = mainstay. Chemotherapy alone effective for most lesions. Surgery : reserved for pathological fracture fixation or stabilization. References Beal K, Allen L, Yahalom J. Primary bone lymphoma: treatment results and prognostic factors with long-term follow-up of 82 patients. Cancer . 2006;106(12):2652-6. Jawad MU, Schneiderbauer MM, Min ES, Cheung MC, Koniaris LG, Scully SP. Primary lymphoma of bone in adult patients. Cancer . 2010;116(4):871-9. Messina C, Christie D, Zucca E, Gospodarowicz M, Ferreri AJM. Primary and secondary bone lymphomas. Cancer Treat Rev . 2015;41(3):235-46. Ramadan KM, Shenkier T, Sehn LH, Gascoyne RD, Connors JM. A clinicopathological retrospective study of 131 patients with primary bone lymphoma: a population-based study of successively treated cohorts from the British Columbia Cancer Agency. Ann Oncol . 2007;18(1):129-35. Fletcher CDM, Bridge JA, Hogendoorn P, Mertens F, eds. WHO Classification of Tumours of Soft Tissue and Bone . 5th ed. Lyon: IARC Press; 2020. Previous Next

< Back Dr. Savas CAMUR Revision Knee Arthroplasty Revision TKA is a complex reconstructive procedure performed to address implant failure due to infection, aseptic loosening, instability, periprosthetic fracture, or stiffness. Proper diagnosis requires a combination of clinical, radiographic, and laboratory evaluation to identify the cause of failure. Management aims to restore joint stability, mechanical alignment, and bone stock while minimizing complications. Modern evidence supports the use of modular stemmed and constrained implants to improve fixation, with either cemented or press-fit stems achieving comparable alignment outcomes. Prevention of periprosthetic joint infection (PJI) remains crucial, and intraosseous antibiotic prophylaxis provides superior local drug concentrations and lower infection rates compared to traditional intravenous administration. Etiology The most common causes of TKA failure include: Infection (PJI): The leading indication for early revision (<2 years). Aseptic loosening: The most frequent cause of late revision (>2 years). Instability: Secondary to ligament imbalance or component malposition. Periprosthetic fracture: Increasing with aging and multiple prior surgeries. Arthrofibrosis and extensor mechanism failure: Contribute to stiffness and poor function. Epidemiological data indicate that infection and aseptic loosening together account for over two-thirds of revision cases. Evaluation Clinical Assessment Pain pattern (activity-related vs. rest pain) helps distinguish mechanical failure from infection. Examine gait, alignment, range of motion, stability, and prior incisions. Assess swelling, warmth, and effusion for infection. Laboratory Work-Up ESR and CRP are first-line screening tools. Joint aspiration for cell count, differential, and culture confirms infection per MSIS criteria. Imaging Radiographs: Serial AP/lateral and long-leg standing films evaluate loosening, wear, and alignment. CT scan: Assesses component rotation, bone loss, and defect mapping. Bone scan: May support diagnosis when loosening or infection is unclear, though nonspecific. Surgical Management Preoperative Planning Meticulous evaluation of bone loss, ligament integrity, and soft-tissue envelope guides implant selection. Digital templating and long-leg alignment analysis are essential. Fixation Strategy Cemented vs. Press-Fit Stems: A 2025 multicenter study found that short-cemented stems (<75 mm) achieved mechanical alignment equivalent to long-cemented or press-fit stems, with greater intraoperative flexibility and comparable hip-knee-ankle (HKA) anglesmain Stem choice: Short-cemented : ideal for controlled alignment correction and limited bone loss. Long-cemented : preferred for poor bone quality and extensive defects. Press-fit (hybrid) : used when strong diaphyseal engagement is achievable. Metaphyseal reconstruction: Metal augments, sleeves, or cones are indicated for AORI Type 2B–3 bone defects. Alignment Principles Mechanical alignment remains the gold standard, targeting neutral HKA (≈180°) and symmetric coronal balance. Femoral alignment is more variable than tibial, but both achieve acceptable mechanical restoration when stems are properly seated. Infection Prevention .Evidence supports intraosseous antibiotic prophylaxis , which delivers higher local antibiotic concentrations in bone and fat tissue and significantly reduces PJI risk compared with intravenous dosing (OR ≈ 0.26) without increased systemic complications. Complications Infection: 4–7% risk, higher than primary TKA. Neurovascular injury: Especially peroneal nerve during deformity correction. Wound complications: Optimize skin flaps, use negative-pressure dressings when indicated. Extensor mechanism disruption: Managed with allograft or mesh reconstruction. Residual pain or stiffness: Expect longer recovery compared to primary TKA. References Giabbani N, Innocenti M, Sangaletti R, et al. Coronal alignment in revision total knee arthroplasty: a comparison of cemented vs. press-fit stems for restoring mechanical axis. Arthroplasty Today. 2025;35:101863.main Lee S, Kang J, Moon Y, et al. Efficacy and safety of intraosseous versus intravenous antibiotic in primary and revision total joint arthroplasty: a systematic review and meta-analysis. Medicina. 2025;61(10):1750.medicina-61-01750-v2 [Additional supporting references from J Clin Med 2024 and J Arthroplasty 2025 can be appended for infection prevention and alignment optimization.] Type Indications Posterior-stabilized PCL deficiency Constrained condylar Collateral laxity, moderate instability Rotating hinge Global ligament deficiency, severe bone loss Megaprosthesis Salvage for massive defects or tumor resection 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

< Back Peripheral Nerve Structure and Function Peripheral Nerves Function: Connect CNS ↔ muscles, joints, tendons, skin; carry motor, sensory, autonomic fibers Neuron structure: Soma (nucleus), dendrites (input), axon (signal), synapse (communication) Axon: Diameter 0.2–20 μm; conduction ↑ with larger diameter & myelin Myelin: Lipid-protein sheath by Schwann cells → faster conduction, less energy Connective layers: Endoneurium (axon), perineurium (fascicle, barrier), epineurium (whole nerve + vessels) General Features Peripheral nerves connect the central nervous system with muscles, bones, joints, tendons, and skin. They play a role in both motor and sensory transmission. Voluntary movement, reflex activity, and sensory perception rely on the integrity of these structures. Basic Structure of the Neuron Cell body (soma): The metabolic center, containing the nucleus and organelles. Dendrites: Short extensions that receive inputs from other neurons. Axon: A single, long extension that propagates electrical signals to distant targets. The axon hillock is the site where the action potential is generated. Synapse: Specialized junction enabling communication between neurons. Axonal Structure Axon diameter ranges from 0.2–20 µm. The cytoplasm contains mitochondria and microtubules. Conduction velocity is determined by axonal diameter and myelination. Axon terminals form synaptic contacts with target cells. Myelin and Its Function Myelin is a multilayered lipid- and protein-rich sheath that insulates axons, increasing conduction velocity and reducing energy expenditure. In the peripheral nervous system, Schwann cells are responsible for myelin formation. Unmyelinated axons conduct impulses more slowly. Connective Tissue Layers Endoneurium: Surrounds individual axons. Perineurium: Encloses fascicles; contributes to the blood–nerve barrier. Epineurium: Envelops the entire nerve, containing blood vessels and lymphatics. Functional Properties Peripheral nerves contain both afferent (sensory) and efferent (motor) fibers. Afferent fibers: Transmit mechanical, thermal, and nociceptive stimuli. Efferent fibers: Control muscle contraction and glandular secretion. Autonomic fibers are also carried within peripheral nerves. Clinical Relevance Peripheral nerve injuries result in motor and sensory deficits. Their regenerative capacity is limited, although axonal elongation is possible. Demyelination decreases conduction velocity and represents a fundamental pathophysiological mechanism in neuropathies. Peripheral Nerve System Injury: Diagnosis and Management Mechanisms of Injury Peripheral nerve injuries may result from trauma, surgical interventions, tumors, metabolic disorders, or inflammatory processes. Following injury, endoneurial and epineurial permeability increases, leading to edema. Distal to the lesion, Wallerian degeneration occurs: macrophages clear myelin debris while Schwann cells support regeneration. Classifications Seddon classification: Neurapraxia: Conduction block with intact axons; recovery occurs within weeks. Axonotmesis: Axonal disruption with preserved connective tissue sheaths; regeneration is possible. Neurotmesis: Complete transection of both axons and connective sheaths; spontaneous recovery is poor, requiring surgical repair. Sunderland classification: Five grades, ranging from Grade I (neurapraxia) to Grade V (complete transection), offering more detailed prognostic information. Clinical Presentation Motor deficits, sensory loss, and diminished reflexes are typical. Muscle atrophy and trophic skin changes may develop. Autonomic involvement can result in abnormal sweating and circulatory disturbances. Pain may be acute or chronic. Diagnostic Methods Clinical examination is the first step, assessing motor strength, sensory distribution, and reflexes. Nerve conduction studies (NCS): Assess conduction velocity and amplitude. Electromyography (EMG): Detects denervation and reinnervation. Imaging: Ultrasound and MR neurography visualize nerve continuity and compression sites. Treatment Approaches Conservative management: Indicated in neurapraxia and mild axonotmesis; includes rest, anti-inflammatory therapy, physiotherapy, and splinting. Regeneration is monitored over time. Surgical repair: Required for neurotmesis and high-grade Sunderland injuries. Techniques include epineural or perineural suturing. For large defects, nerve grafting or nerve transfers are performed; microsurgical techniques improve outcomes. Rehabilitation: Aims to preserve muscle strength, maintain joint mobility, and support functional recovery. Regeneration and Recovery Axonal regrowth occurs at a rate of ~1–3 mm/day. Schwann cells enhance conduction by remyelination. Recovery depends on injury severity, timing of repair, and rehabilitation. Children generally exhibit faster recovery than adults. Complications Aberrant axonal sprouting may lead to neuroma formation. Persistent sensory and motor deficits can result in long-term disability. Chronic pain syndromes and muscle atrophy negatively impact quality of life. Conclusion Early diagnosis and appropriate treatment are critical for functional outcomes in peripheral nerve injuries. Classification systems, diagnostic tools, and surgical techniques guide clinical decision-making, while comprehensive rehabilitation is essential for long-term success. 1. Zhang K, Guo J, Zhang Y, Chen B, Du X. Innovations in peripheral nerve regeneration: biomaterials, growth factors, and cell therapy. Front Neurosci . 2024;18:1594435. doi:10.3389/fnins.2025.1594435 2. Liu X, Li X, Zhang T, Xu W, Guan Y, Li X, et al. Electrical stimulation accelerates Wallerian degeneration and promotes nerve regeneration after sciatic nerve injury. Glia . 2023;71(3):758–774. doi:10.1002/glia.24309 Previous Next

< Back Classifications A SA trauma-classifications Previous Next

< Back Developmental Dysplasia of Hip (DDH) developmental-dysplasia-of-hip-ddh Previous Next

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< Back Physeal Anatomy & Physiology physeal-anatomy-physiology Previous Next

< Back Dr. Erhan OKAY Synovial Sarcoma Synovial sarcoma is a high-grade malignant soft tissue tumor primarily affecting the extremities of young adults. Diagnosis requires MRI, histopathology, and molecular confirmation of the SS18–SSX fusion gene. Treatment is multidisciplinary, centered on complete surgical excision with limb preservation when feasible, combined with perioperative radiotherapy and chemotherapy for large, deep, or high-risk lesions. Prognosis depends on tumor size, depth, margin status, and recurrence, with lung metastasis being the most common pattern of spread. Long-term surveillance is essential due to the potential for late metastatic relapse. Epidemiology Synovial sarcoma is a high-grade soft tissue sarcoma predominantly affecting adolescents and young adults , most commonly arising in the extremities , especially the lower limbs. The median age at diagnosis is in the 30s, with a slight male predominance . Diagnostic delays are common, with up to 35% of cases initially undergoing unplanned excision before referral to specialized centers (Broida 2024). The lungs are the most frequent site of metastasis (≈70%), followed by bone (10–20%) and lymph nodes (17%) (Wu 2017). Diagnosis & Imaging Diagnosis relies on a combination of MRI, histopathology, and molecular testing . Core needle biopsy with immunohistochemistry and fusion testing (SS18–SSX) should be performed at a sarcoma center before any surgery. MRI is the modality of choice for local staging (size, depth, neurovascular or bony involvement). Triple sign (mixed high, intermediate, low signal on T2) is a typical imaging feature. Chest CT is essential for staging due to pulmonary metastasis risk. PET-CT can help assess treatment response or recurrence. Pathology Histologically, synovial sarcoma presents as monophasic, biphasic, or poorly differentiated forms, the latter associated with worse prognosis. Immunoprofile: Bcl-2 , EMA , and TLE1 are commonly positive (Li 2024). Molecular confirmation via SS18–SSX gene fusion testing is diagnostic, particularly when morphology or IHC is inconclusive (Amary 2007). Treatment Overview Optimal management requires multimodal therapy within a specialized multidisciplinary team . Surgery : Complete (R0) resection with limb preservation is the cornerstone of treatment. Limb salvage is feasible in >60% of cases, and negative margin status strongly predicts local control and survival (Sharma 2024). Radiotherapy : Indicated for residual disease or high recurrence risk. Preoperative RT (≈50 Gy) followed by R0/R1 resection improves local control (Gingrich 2020). Surgery is typically scheduled 3–4 weeks post-RT . Chemotherapy : Neoadjuvant anthracycline–ifosfamide regimens are used for large, deep, or borderline-resectable tumors. Adjuvant chemotherapy is considered for high-risk patients and systemic disease. Prognosis Prognosis depends on tumor size, depth, margin status, bone invasion, mitotic count , and recurrence . Adverse factors include tumor >5 cm, deep location, positive margins, axial site, and local relapse (Song 2017, Broida 2024). Late metastases (>5 years) are not uncommon; therefore, long-term surveillance is essential. Early re-excision with negative margins and appropriate perioperative therapy significantly improves metastasis-free and disease-specific survival . References Broida SE, Arguello AM, Sullivan MH, et al. Unplanned Excision of Synovial Sarcoma: Factors Associated with Recurrence and Survival. Cancers (Basel). 2024;16(18):3157. doi:10.3390/cancers16183157 Wu Y, Bi W, Han G, Jia J, Xu M. Influence of Neoadjuvant Chemotherapy on Prognosis of Patients with Synovial Sarcoma. World J Surg Oncol. 2017;15(1):101. doi:10.1186/s12957-017-1165-9 Li C, Krasniqi F, Donners R, et al. Synovial Sarcoma: The Misdiagnosed Sarcoma. EFORT Open Rev. 2024;9(3):190–201. doi:10.1530/EOR-23-0193 Amary MF, Berisha F, Bernardi Fdel C, et al. Detection of SS18–SSX Fusion Transcripts in Formalin-Fixed Paraffin-Embedded Neoplasms: Analysis of Conventional RT-PCR, qRT-PCR, and FISH as Diagnostic Tools. Mod Pathol. 2007;20(4):482–496. doi:10.1038/modpathol.3800761 Sharma J, Deo SVS, Kumar S, et al. Clinicopathological Profile and Survival Outcomes in Patients with Localised Extremity Synovial Sarcomas. Clin Oncol (R Coll Radiol). 2024;36(4):e97–e104. doi:10.1016/j.clon.2024.01.018 Gingrich AA, Marrufo AS, Liu Y, et al. Radiotherapy is Associated With Improved Survival in Patients With Synovial Sarcoma Undergoing Surgery: A National Cancer Database Analysis. J Surg Res. 2020;255:378–387. doi:10.1016/j.jss.2020.05.075 Song S, Park J, Kim HJ, et al. Effects of Adjuvant Radiotherapy in Patients With Synovial Sarcoma. Am J Clin Oncol. 2017;40(3):306–311. doi:10.1097/COC.0000000000000148 Previous Next