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< 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

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< Back Dr. Serdar DEMIROZ Histologic Types of Soft Tissue Sarcoma Soft tissue sarcomas (STS) represent a diverse group of malignant mesenchymal tumors with distinct molecular, histologic, and clinical behaviours. Advances in cytogenetic and molecular diagnostics—notably the detection of recurrent translocations (e.g., t(X;18), t(12;16)) and gene amplifications (MDM2, CDK4)—have transformed diagnosis, replacing purely morphologic classification with a genotype-driven approach. Prognosis varies widely according to histologic grade, size, depth, and resectability, underscoring the importance of precise histopathologic and molecular diagnosis in both treatment planning and patient counselling. 1. Undifferentiated Pleomorphic Sarcoma (UPS) Overview Formerly known as Malignant Fibrous Histiocytoma (MFH) . Typically affects men > 50 years , often in proximal lower extremities , trunk , or retroperitoneum . Presents as a painless enlarging mass . Pathology Marked cellular pleomorphism and high mitotic activity . Areas of necrosis common. No specific genetic driver , making it a diagnosis of exclusion after ruling out other sarcoma subtypes. Treatment Wide excision with negative margins. Radiotherapy : routinely used pre- or postoperatively for local control. Chemotherapy : reserved for metastatic or high-risk cases; response modest. Prognosis Metastatic pattern: lungs > bone > liver . Lymph node involvement uncommon. Adverse prognostic features: large size, deep location, and lymphovascular invasion. 2.Liposarcomas Overview Second most common soft tissue sarcoma after UPS. Arises from adipocytic differentiation; MDM2 amplification is characteristic. MDM2 regulates p53 , and its amplification suggests dedifferentiation. Atypical lipomatous tumors / well-differentiated liposarcomas resemble adipose tissue both grossly and radiographically (fat-like on MRI). a.Dedifferentiated Liposarcoma (DDLS) May arise from pre-existing atypical lipomatous tumors or occur de novo . MRI: heterogeneous non-fatty areas adjacent to lipomatous regions. Histology: high-grade spindle cell component with MDM2 & CDK4 amplification. Retroperitoneal DDLS can reach massive size at presentation. Treatment: wide excision; radiotherapy used for extremity/trunk lesions, rarely in retroperitoneum. Chemotherapy response: poor; MDM2 and CDK4 targeted therapies under study. b. Myxoid Liposarcoma Affects adults aged 30–60 years . Characteristic t(12;16)(q13;p11) translocation → FUS-DDIT3 fusion. Round cell component indicates poor prognosis. Unique for metastasis beyond lungs → abdomen, pelvis, spine. Sensitive to radiotherapy and chemotherapy. c. Pleomorphic Liposarcoma Rarest and most aggressive form (5–10% of liposarcomas). Typically in patients >60 years . Histologic confirmation requires lipoblastic differentiation . Prognosis: poor; chemotherapy may provide modest benefit. 3.Synovial Sarcoma Overview Occurs in adolescents and young adults , typically near large joints (knee, ankle). Despite its name, does not arise from synovium . Histology: monophasic (spindle) or biphasic (spindle + epithelial). Cytogenetics: t(X;18)(p11.2;q11.2) → SS18-SSX1/SSX2 fusion. Mimics: epithelioid tumors or malignant peripheral nerve sheath tumors (MPNST). Treatment: wide resection + radiotherapy; highly chemosensitive . 4.Myxofibrosarcoma Overview Previously grouped with UPS; incidence ~0.1/100,000. Occurs in older adults (6th–8th decade). Predominantly in lower limbs , occasionally trunk or neck. Microscopic "tail sign" on MRI represents fascial spread. High local recurrence risk due to infiltrative margins. 5-year survival ~77%. Treatment: wide excision + radiotherapy; chemotherapy for advanced disease. 5.Clear Cell Sarcoma Overview Also known as malignant melanoma of soft tissue . Immunohistochemistry: HMB-45, Melan-A, S100 positive. t(12;22)(q13;q12) → EWSR1-ATF1 fusion in nearly all cases. May express BCL-2 . High potential for lymph node metastasis → consider sentinel node evaluation. Often indolent for years → frequent diagnostic delay and unplanned excision. 6.Angiosarcoma Overview Usually affects elderly (>60 years) ; commonly involves skin and superficial tissues . Highly aggressive, often multifocal. Markers: CD31, CD34, ERG positive. May respond to Pazopanib (VEGFR inhibitor) or PD-1 immunotherapy . Treatment: wide excision; reconstruction often needed. Prognosis: poor due to early dissemination. 7.Kaposi Sarcoma Overview Vascular endothelial tumor with four clinical types: Classic (Mediterranean/Eastern European) Endemic (African, often in children) Iatrogenic (post-immunosuppression) AIDS-related Associated with HHV-8 infection . Presents as violaceous plaques, nodules, or macules—commonly on lower limbs. May mimic vascular insufficiency or venous stasis. Secondary malignancies (e.g., Non-Hodgkin lymphoma) in up to one-third. Treatment: depends on type and extent—surgery, radiotherapy, or chemotherapy. 8.Epithelioid Sarcoma Overview Most common soft tissue sarcoma of the hand and forearm . Occurs in patients <40 years . Often slow-growing and misdiagnosed as a benign fibrous lesion. Radiographs: may show calcification or cortical erosion. High recurrence and pulmonary metastasis risk . INI1 (SMARCB1) loss is characteristic. Treatment: wide excision + radiotherapy. Prognosis: generally poor. 9.Dermatofibrosarcoma Protuberans (DFSP) Overview Low-grade dermal fibroblastic tumor (~1% of soft tissue sarcomas). Common in young adults , often on trunk and proximal limbs . t(17;22) → COL1A1–PDGFB fusion. May show fibrosarcomatous transformation (high grade). Treatment: wide local excision or Mohs surgery . Imatinib effective for unresectable or metastatic disease. 10.Extraskeletal Ewing Sarcoma Overview Rare; affects thigh and gluteal regions . Rapidly enlarging painful mass. Cytogenetics: t(11;22)(q24;q12) → EWS-FLI1 fusion. Treatment: multimodal—chemotherapy + surgery ± radiotherapy. Prognosis: better than skeletal form if localized. 11.Extraskeletal Osteosarcoma Overview Extremely rare (<1% of STS), usually in older adults . Produces osteoid matrix visible as calcifications on X-ray . Histology: malignant cells producing osteoid without bone involvement. Treatment: surgical excision ± radiotherapy; chemotherapy poorly effective. Prognosis: generally poor. 12. Extraskeletal Myxoid Chondrosarcoma Overview Occurs in older adults, typically lower extremities . Radiographs: calcifications suggest chondroid origin, though no true cartilage present. t(9;22)(q22;q12) or t(9;17)(q22;q11) translocations. Indolent growth , but high recurrence and metastasis (~50%). Treatment: wide excision + radiotherapy; limited chemo response. 13.Alveolar Soft Part Sarcoma Overview Affects young women (<30 years) ; usually thigh or gluteal region . Histology: alveolar architecture; t(X;17)(p11;q25) translocation. Slow-growing but aggressive , with frequent metastases. Treatment: surgery + radiotherapy ± chemotherapy. Requires long-term surveillance. 14.Leiomyosarcoma Overview Smooth muscle–derived malignant tumor. Predominantly affects retroperitoneum and abdomen , less often extremities. Venous origin (e.g., IVC) indicates poorer prognosis. Markers: SMA, desmin, h-caldesmon positive. Treatment: wide excision + radiotherapy. Metastatic in ~20% at diagnosis; chemotherapy has limited role. 15.Rhabdomyosarcoma Overview Most common STS in children ; originates from skeletal muscle precursors. Subtypes: embryonal, alveolar, pleomorphic. t(2;13) translocation typical of alveolar type. Embryonal form common <5 years; small round blue cell morphology. Lymph node metastasis relatively frequent. Treatment: multimodal (chemotherapy + surgery + radiotherapy). Adults respond poorly to chemotherapy. 16.Malignant Peripheral Nerve Sheath Tumor (MPNST) Overview Often develops in patients with Neurofibromatosis type 1 (NF1) . Transformation of pre-existing neurofibroma suspected. Pain and rapid growth in a known neurofibroma are classic warning signs. Imaging: PET-CT may help detect malignant transformation. Histology: high-grade spindle tumor, S-100 positive in ~50%. Prognosis: poor; 5-year survival 30–40%. Treatment: wide resection + radiotherapy; chemotherapy limited benefit. References: WHO Classification of Soft Tissue and Bone Tumours, 5th Edition. IARC: Lyon, 2020. Casali PG, Abecassis N, Bauer S, et al. Soft tissue and visceral sarcomas: ESMO–EURACAN–GENTURIS Clinical Practice Guidelines. Ann Oncol. 2022;33(12):1348–1365. NCCN Clinical Practice Guidelines in Oncology: Soft Tissue Sarcoma, Version 2.2025. National Comprehensive Cancer Network, 2025. Fletcher CDM, Bridge JA, Hogendoorn PCW, Mertens F. WHO Classification of Tumours of Soft Tissue and Bone. 4th ed. IARC, Lyon, 2013. Thway K, Fisher C. Histopathology and molecular genetics of soft tissue sarcomas. Histopathology. 2015;67(1):51–70. Italiano A, Toulmonde M, Stoeckle E, et al. Clinical outcome of dedifferentiated liposarcoma: a retrospective study of 418 patients. Ann Oncol. 2012;23(6):1601–1608. Antonescu CR. The role of genetic testing in soft tissue sarcomas. Histopathology. 2014;64(1):26–38. Miettinen M, Fanburg-Smith JC, Virolainen M, et al. Epithelioid sarcoma: an immunohistochemical and clinicopathologic study of 112 cases. Am J Surg Pathol. 1999;23(1):41–50. Stacchiotti S, Van Tine BA. Synovial sarcoma: current concepts and future perspectives. J Clin Oncol. 2018;36(2):180–187. Gronchi A, Miah AB, Dei Tos AP, et al. Soft tissue sarcoma: ESMO–EURACAN–GENTURIS guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2021;32(11):1348–1365. Widemann BC, Italiano A. Biology and management of malignant peripheral nerve sheath tumor. Neuro Oncol. 2018;20(6):763–773. Thway K, Jones RL, Noujaim J, et al. Myxofibrosarcoma: pathology, genetics, and management. Histopathology. 2014;64(1):49–64. Sirvent N, Maire G, Pedeutour F. Chromosome translocations in dermatofibrosarcoma protuberans. Hum Pathol. 2003;34(12):1293–1301. Doyle LA. Sarcoma immunohistochemistry update: diagnostic utility and molecular correlates. Histopathology. 2014;64(1):12–38. Davis EJ, Chugh R, Zhao L, et al. Angiosarcoma: outcomes and prognostic factors in a series of 119 patients. Ann Oncol. 2014;25(10):2245–2251. Lin O, Hameed M, Healey JH, et al. Extraskeletal osteosarcoma: clinicopathologic analysis of 20 cases. Am J Surg Pathol. 2003;27(12):1510–1517. Meis-Kindblom JM, Bergh P, Gunterberg B, Kindblom LG. Extraskeletal myxoid chondrosarcoma: a reappraisal of the clinical, morphologic, and immunohistochemical features. Am J Surg Pathol. 1999;23(6):636–650. Rhabdomyosarcoma pathology Previous Next

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< Back Dr. Osman Emre Aycan Aneurysmal Bone Cyst (ABC) Aneurysmal bone cyst (ABC) is a benign but locally aggressive, expansile osteolytic lesion composed of blood-filled cavities separated by fibrous septa. It primarily affects children and young adults, typically in the first two decades of life, with no clear sex predilection. Although non-malignant, it can cause significant pain, swelling, and pathological fractures due to rapid growth and cortical thinning. Epidemiology Accounts for approximately 1–2% of all primary bone tumors . Most common sites: long bones (femur, tibia, humerus) and posterior elements of the spine . Less frequently seen in the pelvis, clavicle, or small bones of the hands and feet. Pathophysiology The exact etiology remains unclear, but two forms are recognized: Primary ABC – arises de novo, often associated with a translocation involving the USP6 gene (17p13) , leading to osteolytic activity and vascular proliferation. Secondary ABC – develops in association with another lesion such as giant cell tumor, chondroblastoma, osteoblastoma, or fibrous dysplasia . The lesion consists of multiple blood-filled spaces without endothelial lining , separated by septa containing fibroblasts, osteoclast-type giant cells, and reactive bone. Clinical Presentation Progressive pain, swelling, and restricted motion near the affected site. Palpable mass may be present. Pathologic fracture is a common first presentation in long bones. Neurological deficits can occur when lesions arise in the spine due to canal compression. Imaging Features Radiographs: Expansile, lytic lesion with “blow-out” or balloon-like appearance . Thin cortical shell and possible septations. May show fluid–fluid levels if internal hemorrhage is present. MRI: Multiple fluid–fluid levels due to different blood degradation stages. Surrounding bone marrow edema and soft tissue extension are possible. Contrast enhancement in septa but not in cystic cavities. CT: Useful for cortical evaluation and surgical planning. Histopathology Multiple cystic spaces filled with blood, lacking endothelial lining . Septa contain fibroblasts, osteoid tissue, and multinucleated giant cells. No malignant cells are present. Differential Diagnosis Lesion Distinguishing Features Telangiectatic Osteosarcoma Malignant cells, atypia, and osteoid production Giant Cell Tumor (GCT) Occurs after skeletal maturity, lacks fluid–fluid levels Chondroblastoma Epiphyseal location, presence of calcifications Fibrous Dysplasia Ground-glass matrix, lacks hemorrhagic cavities Simple Bone Cyst Single cavity, no septations, usually in metaphysis Treatment Management depends on lesion size, location, and aggressiveness: Extended curettage and high-speed burring – mainstay for most cases. Adjuvant therapies to reduce recurrence:Argon beam coagulation, phenol, or liquid nitrogen. Filling of cavity with bone graft or bone cement . Selective arterial embolization (SAE) – used for spinal or pelvic lesions or as preoperative adjunct. Percutaneous sclerotherapy (e.g., doxycycline or polidocanol) is increasingly used as a minimally invasive alternative. En bloc resection reserved for recurrent or inaccessible lesions. Prognosis Recurrence rate: 10–30%, usually within the first two years post-treatment. Risk factors for recurrence include younger age , open physes , and incomplete excision . Long-term prognosis is excellent with appropriate treatment; malignant transformation is exceedingly rare. Key Points ABC is a benign, vascular, expansile bone lesion with locally destructive potential. USP6 translocation confirms diagnosis in ambiguous cases. Fluid–fluid levels on MRI are suggestive but not pathognomonic. Minimally invasive approaches (e.g., sclerotherapy, embolization ) show recurrence rates comparable to surgery in recent studies. Extended curettage with adjuvant remains the gold standard for accessible lesions in long bones. Recurrent cases may benefit from a combined strategy (embolization → curettage → bone graft). References Oliveira AM et al. USP6 Gene Rearrangement in Aneurysmal Bone Cyst. Am J Pathol. 2021;191(7):1210–1220. Mascard E, Gomez-Brouchet A, Lambot K. Aneurysmal Bone Cyst: Clinical and Therapeutic Update. Orthop Traumatol Surg Res. 2015;101(1 Suppl)–S19. Park HY et al. Treatment of Aneurysmal Bone Cysts: A Review of Current Concepts. J Bone Joint Surg Am. 2020;102(4):280–289. Rastogi S et al. Percutaneous Doxycycline Sclerotherapy in Aneurysmal Bone Cyst. J Orthop Surg. 2019;27(3):2309499019878422. Rapp TB et al. Aneurysmal Bone Cyst: A Review of Pathophysiology and Current Management. J Am Acad Orthop Surg. 2012;20(4):233–241. Treatment Modality Description / Technique Recurrence Rate Advantages Limitations / Complications Extended Curettage + Adjuvant (Phenol / Argon / Cryotherapy) Thorough curettage of lesion cavity with mechanical and chemical adjuvant use 10–25% Effective local control, joint preservation Risk of growth plate injury or fracture Curettage + Bone Graft / Bone Cement Filling Cavity filled after curettage to provide stability 15–20% Restores bone strength, simple procedure Possible graft resorption, infection En Bloc Resection Complete excision with margin of healthy bone <10% Lowest recurrence rate Loss of function, reconstructive need Selective Arterial Embolization (SAE) Preoperative or definitive occlusion of feeding vessels 10–20% Minimally invasive, useful in spine/pelvis Risk of incomplete occlusion, recurrence Percutaneous Sclerotherapy (Doxycycline / Polidocanol) Chemical ablation via multiple percutaneous injections 5–15% Outpatient, minimal morbidity, excellent cosmetic results Requires multiple sessions, rare skin necrosis Radiotherapy (rarely used) Reserved for inoperable or recurrent cases Variable (~20%) Non-surgical alternative Radiation-induced sarcoma risk, growth disturbance Treatment Options and Recurrence Rates in Aneurysmal Bone Cyst (ABC) Axial and coronal MRI images of the sacrum demonstrate an expansile, multiloculated cystic lesion centered at the S1 level. The lesion shows multiple fluid–fluid levels with low-to-intermediate signal on T1-weighted, high signal on T2-weighted images, and thin peripheral and septal enhancement after gadolinium administration. Imaging features are characteristic of a benign aneurysmal bone cyst without evidence of solid enhancement or soft-tissue invasion. 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

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