Trauma General Principles 1.Polytrauma Evaluation 2.ATLS & Resuscitation 3.Compartment Syndrome 4. Crush Syndrome 5. Open Fracture Management Upper Extremity 1. Clavicle Fractures 2. Proximal Humerus 3. Humeral Shaft 4. Supracondylar (Peds) 5. Elbow Injuries 6. Forearm (Monteggia, Galeazzi) 7. Distal Radius/Ulna 8. Scaphoid 9. Hand & Fingers Lower Extremity 1. Pelvic Ring 2. Acetabular Fracture 3. Hip Fractures 4 .Femoral Shaft 5. Tibial Plateau 6. Tibial Shaft 7. Ankle Fractures 8. Calcaneus 9. Talus 10. Foot & Toes Special Considerations 1. Pediatric Trauma 2. Geriatric Patterns 3. Classifications 4. Surgical Timing 5. Damage Control

< Back Alper DUNKI Bone and Joint Biology Bone Functions: Support, mineral homeostasis, marrow housing Bone Types: Long (endochondral), flat (intramembranous) Macrostructure: Cortical → dense, load-bearing Trabecular → porous, marrow-rich, weak in osteoporosis Cells: Osteoblasts (matrix formation, Runx2, osterix) Osteocytes (mechanosensors, RANKL secretion) Osteoclasts (resorption, RANKL/M-CSF, inhibited by OPG) Matrix: Mineral (HA, TCP) + collagen (type I) + growth factors (BMP, TGF-β, IGF) Bone Homeostasis: Balance of formation/resorption → disrupted in osteoporosis, osteopetrosis Fracture Healing: Primary → direct, stable fixation Secondary → hematoma, callus, endochondral ossification, remodelling Therapies: Bisphosphonates, PTH (intermittent), anti-RANKL, calcitonin Synovial Joint: Cavity, capsule, cartilage, synovium (Type A & B cells), synovial fluid (HA, lubricin); proprioception (A fibers), pain (C fibers). Non-Synovial Joints: Symphysis (fibrocartilage, e.g. pubic symphysis) Synchondrosis (cartilage-only, e.g. costal, cranial base) Syndesmosis (fibrous, e.g. distal tibiofibular) Bone Functions: Provides mechanical support, regulates mineral homeostasis, harbors bone marrow elements. Types: Long bones: Formed via endochondral ossification from a cartilage model. Flat bones: Formed via intramembranous ossification directly from mesenchymal tissue. Anatomy: Diaphysis: Cortical bone tube enclosing the medullary canal with trabecular bone; surfaces consist of periosteum and endosteum. Metaphysis: Transition zone between epiphysis and diaphysis; composed of loose trabecular bone. Epiphysis: Articular end containing subchondral bone and the growth plate. Vascular and neural supply: Neurovascular bundles enter through the periosteum and run within Haversian and Volkmann canals. Inner two-thirds of cortical bone are supplied by the nutrient artery, while the outer one-third is nourished by periosteal vessels. Macrostructure: Cortical bone: Dense, load-bearing; serves as boundary in metaphysis/epiphysis. Trabecular bone: Porous, marrow-containing; architecture compromised in osteoporosis. Microstructure: Woven bone: Primary bone, irregular collagen alignment. Lamellar bone: Secondary bone, organized structure. Lacunar–canalicular system: Provides osteocyte interconnections. Extracellular matrix: Mineral (60–70%): Hydroxyapatite, tricalcium phosphate; provides compressive strength and mineral reservoir. Organic (20–25%): 90% type I collagen, other collagens, adhesive proteins (fibronectin, vitronectin), matrix proteins, proteoglycans, growth factors (BMP, TGF-β, IGF). Cells: Osteoblasts: Synthesize bone matrix, regulate osteoclasts; differentiation via Runx2 and osterix. Osteocytes: Mechanosensors, secrete RANKL, maintain bone homeostasis. Osteoclasts: Multinucleated, perform bone resorption; activated by RANKL and M-CSF, inhibited by OPG. Bone homeostasis: Maintained by the balance of osteoblast and osteoclast activity. Renewal occurs via Howship’s lacunae in trabecular bone and osteons in cortical bone. Disease and treatment: Remodeling impaired in conditions like osteoporosis and osteopetrosis . Therapies: Bisphosphonates, intermittent PTH, anti-RANKL agents, calcitonin. Fracture healing: Primary healing: Direct bone formation under stable fixation. Secondary healing: Hematoma, inflammation, cartilage callus, endochondral ossification, and remodeling. Growth factors (BMP, TGF-β, IGF) and angiogenesis play critical roles. 2. Synovial Joint Structure: Joint cavity, articular cartilage, capsule, ligaments, tendons. Development: Arises from mesenchymal condensation; apoptosis within interzone forms the cavity. Components: Articular cartilage: Provides low-friction motion. Ligaments: Provide stability. Capsule: Encloses the joint. Synovium: Contains type A cells (macrophage-like) and type B cells (fibroblast-like, producing hyaluronan); provides nutrition and synovial fluid. Synovial fluid: Plasma ultrafiltrate rich in hyaluronic acid and lubricin. Innervation: Type A fibers (proprioception). Type C fibers (pain). Function: Enables wide range of motion between bones with minimal friction. 3. Non-Synovial Joints Types: Symphysis: Fibrocartilaginous disc between bones (e.g., intervertebral disc, pubic symphysis); stability, load transfer, limited mobility. Synchondrosis: Cartilage-covered joint surfaces without synovium; limited motion (e.g., sternomanubrial, costal cartilage, cranial base). Syndesmosis: Fibrous connection without cartilage interface; limited movement (e.g., distal tibiofibular joint). 1. Parini P, Canalis E, Schilling T. Bone remodeling: an operational process ensuring survival and function. Bone Res . 2022;10:8. doi:10.1038/s41413-022-00219-8 2. Sims NA, Gooi JH. Current perspectives on the multiple roles of osteoclasts. J Mol Endocrinol . 2024 Previous Next

< Back Compartment Syndrome Reconstruction compartment-syndrome-reconstruction Previous Next

< Back Hip Arthroscopy Previous Next

< Back Dr. Enes KANAY He was born in 1985 in Istanbul. After completing his secondary education at Pertevniyal Anatolian High School, he began his medical training at Istanbul University Cerrahpaşa Faculty of Medicine and graduated in 2009. He completed his Orthopedics and Traumatology residency at Istanbul Training and Research Hospital in 2016. He served in various hospitals, including Batman Kozluk State Hospital, Beykoz State Hospital, and Istanbul Medeniyet University Göztepe Süleyman Yalçın City Hospital. Since 2024, he has been working at Acıbadem Ataşehir Hospital. Dr. Kanay has authored numerous national and international publications and conference presentations, with a special interest in orthopedic oncology, joint arthroplasty, and complex reconstructive surgeries. He continues his clinical and academic work with Prof. Dr. Korhan Özkan in the field of orthopedic oncology. https://www.acibadem.com.tr/doktor/enes-kanay/ Orthopaedic Oncology eneskanay@gmail.com Previous Next

< Back Dr.Bengül SERARSLAN YAĞCIOĞLU Education & Training Radiation Oncology, Specialist (M.D.) Istanbul Northern Anatolian Public Hospitals Association, Umraniye Training and Research Hospital Nov 2014 – Present Residency in Radiation Oncology Istanbul University, Institute of Oncology Aug 2009 – Aug 2015 General Practitioner Istanbul Beykoz Soguksu Clinic Oct 2008 – Jan 2009 Doctor of Medicine (M.D.) Çanakkale Onsekiz Mart University, Faculty of Medicine (Education carried out at Istanbul University Cerrahpaşa Medical Faculty) 2002 – 2008 Abitur & High School Education Istanbul High School Selected Publications & Presentations Mantle Planning via Multileaf Collimator – 9th National Radiation Oncology Congress, Antalya (2010) Effects of Volume Changes in Seroma on Dose Distribution in Whole Breast RT – 9th National Radiation Oncology Congress (2010) Non-Small Cell Lung Cancer: Case Report – 5th National Thoracic Oncology Congress, Istanbul (2010) Bilateral Breast Autoamputation Due to Metachronous Breast Cancer – 9th Radiation Oncology Congress (2010), 19th National Cancer Congress (2011) Osteosarcoma of Maxillary Sinus: Case Report – 19th National Cancer Congress, Antalya (2011) Concurrent Chemotherapy and Prolonged RT Time in Cervical Cancer – 19th National Cancer Congress (2011) Our Stereotactic RT Experience in Primary & Metastatic Lung Cancer – National Lung Congress, Kapadokya (2013) Evaluation of Pulmonary Toxicity after Breast Cancer Postop RT – 21st National Cancer Congress, Antalya (2015, Oral) Multiple oral/poster contributions at ESTRO (2012) , World Congress of Brachytherapy (2012) , and Turkish National Oncology Meetings. Radiation Oncologist bengulser@yahoo.com Previous Next

< Back Osteoporotic Spine Fractures Osteoporotic Spine Fractures Previous Next

< Back Dr. Hakan ESKARA Soft Tissue Tumor Classification The WHO introduced the classification of soft tissue and bone tumors (fifth edition) in 2020. The new WHO classification of soft tissue and bone tumors, introduced in 2020 (fifth edition), has made significant improvements in classification and introduced many new diagnoses. Histologic Subtypes of Soft Tissue Sarcomas 1. Undifferentiated Pleomorphic Sarcoma (UPS) Previously Malignant Fibrous Histiocytoma (MFH) . High-grade pleomorphic tumor without identifiable line of differentiation. Common sites: thigh, buttock, shoulder girdle, retroperitoneum . Aggressive local behaviour; lung metastases common. Treatment: wide excision ± radiotherapy; chemotherapy in selected cases. 2. Malignant Peripheral Nerve Sheath Tumor (MPNST) Originates from peripheral nerves or pre-existing neurofibromas . Strongly associated with Neurofibromatosis type 1 (NF1) . Rapidly enlarging deep-seated mass along nerve pathways. S-100 and SOX10 positive in subset. Prognosis: poor; 5-year survival <50%. 3. Synovial Sarcoma Typically affects young adults (15–40 years) , often around large joints (especially knee, ankle). Despite name, does not arise from synovium . t(X;18)(p11;q11) translocation → SYT-SSX fusion. Histology: biphasic (epithelial + spindle cell) or monophasic. Treatment: surgery + radiotherapy ± chemo (if high-grade or metastatic). 4. Liposarcoma Most common soft tissue sarcoma in adults. Occurs in thigh and retroperitoneum . Subtypes: Well-differentiated (low grade, local recurrence) Myxoid/round cell (t(12;16), intermediate grade) Pleomorphic (high grade, aggressive) Treatment: wide excision; radiotherapy for high-grade disease. 5. Rhabdomyosarcoma Skeletal muscle–derived tumor; most common STS in children. Subtypes: embryonal, alveolar, pleomorphic. Markers: desmin, myogenin, MyoD1. Treatment: multimodal — surgery + radiotherapy + chemotherapy. 6. Fibrosarcoma Malignant spindle-cell tumor producing collagen . Often arises in deep soft tissues of extremities or trunk . Histology: herringbone pattern. Management: wide excision ± radiotherapy. Recurrence common; metastasis via hematogenous route. 7. Leiomyosarcoma Originates from smooth muscle cells (vessels, uterus, GI tract, soft tissue). Common in retroperitoneum and large veins . Markers: SMA, desmin, h-caldesmon positive. Prognosis: size and grade dependent. 8. Epithelioid Sarcoma Occurs in young adults , often distal upper extremities (hand, forearm). Mimics granulomatous or epithelial lesions. Loss of INI1 (SMARCB1) expression diagnostic. Tendency for local recurrence and lymphatic spread. 9. Angiosarcoma Malignant endothelial tumor. May arise spontaneously or post-radiation . Common sites: skin (scalp/face of elderly), breast, liver . CD31, CD34, ERG positive. Highly aggressive, poor prognosis. 10. Dermatofibrosarcoma Protuberans (DFSP) Low-grade, locally aggressive tumor of dermal fibroblastic origin . t(17;22) → COL1A1–PDGFB fusion. Slow-growing plaque or nodule on trunk or proximal extremities . Treatment: wide local excision or Mohs surgery . Recurrence common, metastasis rare. References: Coindre JM. Histologic classification of soft tissue sarcomas (update and perspectives). Histopathology. 2014;64(1):51–70. Fletcher CDM, Bridge JA, Hogendoorn PCW, Mertens F. WHO Classification of Tumours of Soft Tissue and Bone, 5th Edition (2020). Coindre JM, Terrier P, Guillou L, et al. Predictive value of grade for metastasis development in the main histologic types of adult soft tissue sarcomas. Cancer. 2001;91(10):1914–1926. Chibon F. The genetics of soft tissue sarcoma: from normal mesenchymal cells to malignant sarcomas. Nat Rev Cancer. 2013;13(8):545–558. Jo VY, Fletcher CDM. WHO classification updates on soft tissue and bone tumours. Histopathology. 2014;64(1):38–49. Widemann BC, Italiano A. Biology and management of malignant peripheral nerve sheath tumor. Neuro Oncol. 2018;20(6):763–773. Helman LJ, Meltzer P. Mechanisms of sarcoma development. Nat Rev Cancer. 2003;3(9):685–694. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors. 7th ed. Philadelphia: Elsevier, 2020. Thway K, Fisher C. Leiomyosarcoma: recent advances and diagnostic approach. Histopathology. 2015;67(5):701–711. Sirvent N, Maire G, Pedeutour F. Chromosome translocations in dermatofibrosarcoma protuberans. Hum Pathol. 2003;34(12):1293–1301. Soft Tissue Tumor Classification Group Benign Intermediate (Local Agressive) Malignant Adipocytic Lipoma, Lipomatosis, Angiolipoma, Hibernoma vb. Atypical lipomatous tumor Well-diff. liposarcoma, Dediff. liposarcoma, Myxoid liposarcoma vb. Fibroblastic / Myofibroblastic Nodular fasciitis, Elastofibroma, Fibroma of tendon sheath vb. Palmar/Plantar fibromatosis, Desmoid-type fibromatosis, Dermatofibrosarcoma protuberans vb. Fibrosarcoma NOS, Myxofibrosarcoma, Sclerosing epithelioid fibrosarcoma vb. Fibrohistiocytic Tenosynovial giant cell tumor Plexiform fibrohistiocytic tumor, Giant cell tumor of soft parts Malignant tenosynovial giant cell tumor Vascular Synovial hemangioma, Epithelioid hemangioma, Lymphangioma vb. Kaposiform hemangioendothelioma, Retiform hemangioendothelioma, Kaposi sarcoma vb. Epithelioid hemangioendothelioma, Angiosarcoma Pericytic Glomus tumor NOS, Myopericytoma, Angioleiomyoma — Malignant glomus tumor Skeletal muscle Rhabdomyoma — Rhabdomyosarcoma (Embryonal, Alveolar, Pleomorphic, Spindle cell vb.) Chondro-osseous Chondroma — Extraskeletal osteosarcoma Peripheral nerve sheath Schwannoma, Neurofibroma, Perineurioma, Granular cell tumor vb. — Malignant peripheral nerve sheath tumor, Melanotic variant vb. Uncertain differentiation Myxoma, Angiomyolipoma vb. Haemosiderotic fibrolipomatous tumor, Atypical fibroxanthoma vb. Synovial sarcoma, Epithelioid sarcoma, Clear cell sarcoma, Undifferentiated sarcomas vb. Undifferentiated small round cell — — Ewing sarcoma, CIC-rearranged sarcoma, Sarcoma with BCOR alterations Intraosseos Lipoma Ochronosis pathology Previous Next

< Back Soft Tissue Assessment soft-tissue-assessment Previous Next

< Back Dr. Savas CAMUR Dislocation & Instability Despite advances in implant design, surgical technique, and perioperative protocols, instability continues to challenge both surgeons and patients.Hip dislocation remains one of the most feared complications following total hip arthroplasty (THA), associated with higher morbidity, increased healthcare costs, and up to 25% of all revision procedures. Hip Dislocations and Instability after Arthroplasty Incidence and Timing Reported incidence ranges from 0.2% to 10% globally, with large modern registries showing ~2.3% dislocation rate within 2 years after primary THA. Half of dislocations (≈52%) occur in the first 3 months , and >80% within 2 years postoperatively. Recurrent instability is common — 57% of patients with an initial dislocation experience recurrence, and 11% have ≥5 events , often necessitating revision surgery. Etiopathogenesis and Risk Factors Patient Factors Age <65 years and female sex are independent risk factors. Obesity (BMI >30) and high comorbidity burden (Elixhauser index ≥3) correlate with higher dislocation rates. Neuromuscular disorders, cognitive decline , and inflammatory arthropathy increase postoperative instability risk. Surgical Factors Posterior approach historically carried higher risk, yet modern evidence shows no difference in dislocation rates between posterior, lateral, or anterior approaches when soft tissue repair is adequate. Component positioning remains crucial — excessive cup anteversion, inclination >45°, or combined offset malalignment significantly increase instability. Femoral head size: larger diameters (≥36 mm) reduce dislocation risk by improving impingement-free motion arcs. Implant-Related Factors Cemented fixation and metal-on-poly or metal-on-metal bearings are associated with higher instability compared to ceramic-on-poly. Dual-mobility cups have emerged as effective solutions for high-risk patients. Hip Precautions and Rehabilitation Recent systematic reviews found no statistical difference between restricted vs unrestricted postoperative protocols (2.2% vs 2.0% dislocation rates). ➡️ Early mobilization and functional recovery improve patient satisfaction without increasing risk.Traditional precautions — avoiding >90° flexion, adduction, and internal rotation — have not been shown to reduce dislocation risk following posterior-approach THA. Mechanisms of Instability Soft-tissue insufficiency (capsular laxity, abductor deficiency). Component malalignment (excessive anteversion/retroversion). Impingement (bony or prosthetic). Head–neck ratio mismatch or short offset . Neurologic or proprioceptive deficits. Management Algorithm Initial episode: Closed reduction under sedation → radiographic assessment for component positioning and fracture. Activity modification + physiotherapy. Recurrent dislocation: CT-based evaluation of implant orientation. Consider dual-mobility constructs, constrained liners , or component revision when malposition or soft-tissue insufficiency confirmed. Chronic instability: Multidisciplinary approach — surgical correction of malalignment, soft-tissue reconstruction, or revision arthroplasty. Prevention Principles Accurate component positioning is the strongest modifiable factor. Repair posterior capsule and short external rotators when using posterior approach. Assess combined anteversion intraoperatively. Use larger heads (≥36 mm) to increase jump distance. Consider dual mobility or constrained liners in high-risk or revision cases. 💡 Soft-tissue balance and version alignment matter more than approach choice. Postoperative Protocols Traditional restrictions (avoiding >90° flexion, adduction, or internal rotation) do not significantly reduce dislocation rates . Modern rehabilitation emphasizes: Early mobilization Functional independence Education on safe movement patterns Diagnosis and Evaluation Radiographs: confirm reduction, component orientation, or periprosthetic fracture. CT scan: assess anteversion, inclination, and bone coverage. MRI (metal-artifact reduction): evaluate soft-tissue or abductor insufficiency. Clinical Pearls Most dislocations occur early — meticulous soft-tissue repair and orientation are more impactful than postoperative restrictions. Dual mobility or constrained liners should be considered for revision cases or high-risk primary THAs . Dynamic stability testing intraoperatively (flexion, rotation, extension) predicts postoperative behavior better than static visual assessment. . References Gillinov SM et al. Incidence, Timing, and Predictors of Hip Dislocation After Primary THA for OA. J Am Acad Orthop Surg. 2022;30:1047–1053. Crompton J, Osagie-Clouard L, Patel A. Do Hip Precautions After Posterior-Approach THA Affect Dislocation Rates? Acta Orthop. 2020;91:687–692. Dargel J et al. Surgical approach and risk of dislocation. Clin Orthop Relat Res. 2014. Peters RM et al. Effect of reduced hip precautions on dislocation and function after THA. Bone Joint J. 2019. Previous Next

< Back Dr. Ahmet SALDUZ Education Clinical Fellow – Orthopaedic Oncology , University of Iowa, USA — 2020–2021 Research Fellow – Orthopaedic Oncology , Mayo Clinic, Rochester, MN, USA — 2014–2015 Observer – Arthroplasty (Joint Replacement Surgery) , Hospital for Special Surgery, New York, USA — 2010 Orthopaedics & Traumatology Residency , Istanbul University, Istanbul Faculty of Medicine — 2004–2010 Doctor of Medicine (M.D.) , Istanbul University, Istanbul Faculty of Medicine — 1998–2004 Professional Experience Associate Professor , Department of Orthopaedics & Traumatology, Istanbul University, Istanbul Faculty of Medicine — 2012–Present https://www.birunihastanesi.com.tr/doktorlar/prof-dr-ahmet-salduz Previous Next

< Back Gait Analysis in Foot & Ankle gait-analysis-foot-ankle Previous Next