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< Back Anticoagulants Anticoagulants are medications that prevent clot formation. They are essential in orthopaedics for thromboprophylaxis, especially after surgery. Common Anticoagulants in Orthopaedics: Low Molecular Weight Heparin (LMWH): Enoxaparin Direct Oral Anticoagulants (DOACs): Rivaroxaban, Apixaban, Dabigatran Unfractionated Heparin Warfarin (less common due to monitoring needs) Indications in Orthopaedics: Prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE) after joint replacement or major trauma Management of patients with a history of thromboembolism Atrial fibrillation with orthopaedic comorbidities Key Considerations: Start prophylaxis 6–12 hours after surgery (depending on bleeding risk) Continue for at least 10–14 days, sometimes up to 35 days in hip replacement Adjust dosing for renal function Monitor for signs of bleeding (wound hematoma, prolonged bleeding) Contraindications: Active bleeding Severe bleeding risk (e.g., recent CNS surgery) Coagulopathy Bridging and Reversal: Reversal agents: Protamine (heparin), Vitamin K (warfarin), Idarucizumab (dabigatran) Bridging required with LMWH in warfarin patients undergoing surgery Previous Next

< Back Dr. Alper DUNKI Pigmented Villonodular Synovitis Pigmented Villonodular Synovitis (PVNS), also known as tenosynovial giant cell tumor (diffuse type), is a benign but locally aggressive proliferative disorder of the synovium, tendon sheaths, and bursae. It is characterized by hemosiderin deposition, multinucleated giant cells, and synovial villous nodular overgrowth. Although histologically benign, PVNS can cause significant joint destruction if untreated. Epidemiology Incidence: approximately 1.8 cases per million per year . Most common in adults aged 30–50 years . Slight female predominance. Knee is affected in about 75% of cases, followed by hip, ankle, and shoulder. Pathophysiology Thought to arise from clonal neoplastic proliferation of synovial cells driven by CSF1 gene overexpression due to a t(1;2)(p13;q37) translocation. Overproduction of colony-stimulating factor 1 (CSF1) recruits macrophages and giant cells, leading to synovial hyperplasia and hemosiderin deposition . Classified into two forms:Localized (Nodular) PVNS – affects tendon sheaths, often in the hand or foot. Diffuse PVNS – involves entire synovial lining of large joints, most commonly the knee or hip. Clinical Presentation Gradual joint swelling , pain , and stiffness over months or years. Recurrent hemarthrosis (bloody effusion) is a classic finding. Mechanical symptoms (locking or catching) in large joints due to nodular tissue. In advanced disease, cartilage erosion and secondary osteoarthritis may occur. Imaging Features Radiographs: Often normal in early stages. Later show periarticular bone erosions with preserved joint space. MRI (gold standard): Diffuse synovial thickening with low signal intensity on both T1 and T2 (due to hemosiderin). “Blooming artifact ” on gradient-echo sequences is characteristic. Contrast enhancement demonstrates active synovial proliferation. CT Scan: Useful to assess bone erosion and subchondral involvement . Histopathology Synovial villi and nodules composed of mononuclear histiocyte-like cells , multinucleated giant cells , foam cells , and hemosiderin deposits . Mitotic activity is present but without atypia or malignant features. Differential Diagnosis Condition Distinguishing Feature Rheumatoid arthritis : Bilateral, symmetric, elevated serologic markers Hemophilic arthropathy : History of bleeding disorder, absence of proliferative nodules Synovial chondromatosis : Cartilaginous nodules visible on imaging Synovial sarcoma : Malignant histology, soft-tissue mass, calcifications Treatment The mainstay of treatment is complete synovectomy , with the goal of eradicating diseased synovium while preserving joint function. 1. Surgical Management Arthroscopic synovectomy – preferred for localized or accessible diffuse disease. Open synovectomy – required for extensive or extra-articular extension. Combined approach (open + arthroscopic) may reduce recurrence in the knee. Joint replacement (arthroplasty) indicated in end-stage degenerative joints. 2. Adjuvant Therapies External beam radiotherapy (EBRT) or radiosynovectomy (Yttrium-90) can reduce recurrence after incomplete resection. Targeted therapy: CSF1 receptor inhibitors (e.g., Pexidartinib ) are effective for unresectable or recurrent cases. Prognosis Localized PVNS: recurrence <10%. Diffuse PVNS: recurrence 20–50%, often within 2 years. Delayed diagnosis or incomplete excision can lead to joint destruction requiring arthroplasty. Metastasis is exceptionally rare. Key Points PVNS is a benign but destructive synovial tumor driven by CSF1 overexpression . MRI blooming artifact is a key diagnostic feature. Complete synovectomy remains the gold standard treatment. Targeted CSF1 inhibitors offer new hope for recurrent or unresectable cases. Localized PVNS → Arthroscopic excision gives excellent outcomes with minimal recurrence. Diffuse PVNS → Combined synovectomy ± adjuvant therapy provides better local control. CSF1R inhibitors (e.g., Pexidartinib ) are now first-line for unresectable or recurrent diffuse PVNS. References Mastboom MJL, et al. Diffuse-Type Tenosynovial Giant Cell Tumor: Current Concepts and Future Perspectives. Nat Rev Rheumatol. 2021;17(6):363–376. Cassier PA, et al. CSF1R Inhibition with Pexidartinib in Tenosynovial Giant Cell Tumor. N Engl J Med. 2019;379(4):341–350. van der Heijden L, et al. Pigmented Villonodular Synovitis: A Review of Current Management Strategies. J Am Acad Orthop Surg. 2020;28(15)–e673. Mollon B, et al. Arthroscopic vs. Open Synovectomy in PVNS: A Meta-Analysis. J Bone Joint Surg Am. 2015;97(6):522–534. Murphey MD, et al. Imaging of Pigmented Villonodular Synovitis and Tenosynovial Giant Cell Tumor. Radiographics. 2008;28(5):1493–1518. MRI Findings Summary Table Feature Description Diagnostic Value Synovial Thickening Diffuse or nodular proliferation of synovium lining the joint capsule Seen in both localized and diffuse PVNS Signal Intensity (T1) Iso- to hypointense relative to muscle Hemosiderin deposition lowers T1 signal Signal Intensity (T2) Predominantly low due to hemosiderin, sometimes mixed with high areas (fibrosis vs inflammation) “Dark on T2” pattern is characteristic Blooming Artifact Signal drop on gradient-echo (GRE) sequences caused by magnetic susceptibility of hemosiderin Pathognomonic for PVNS Contrast Enhancement Strong enhancement of synovial tissue, absent in cystic or necrotic areas Reflects active disease Bone Involvement Cortical erosion, pressure remodeling, subchondral cysts Indicates chronic or advanced disease Extra-Articular Extension Seen in diffuse type (knee, hip, ankle) Helps determine need for open approach Joint Effusion Usually minimal to moderate, occasionally hemorrhagic Supports diagnosis but non-specific Radiograph and sagittal MRI images of the knee show diffuse synovial thickening with low-to-intermediate signal intensity and heterogeneous enhancement after contrast administration. Subchondral erosions and mild bone marrow edema are present. Findings are consistent with diffuse-type tenosynovial giant cell tumor (pigmented villonodular synovitis). Pigmented villonodular synovitis Tendon sheath tumor pathology Previous Next

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< Back Dr. Ali Erkan YENIGUL He completed his residency at Marmara University. He currently works at Uludağ University's Orthopedics and Traumatology Clinic. Oncologic Orthopaedics alierkanyenigul@hotmail.com Previous Next

Spine General Principles Anatomy & Biomechanics Stability Principles Neurologic Assessment Spine Trauma Classifications Imaging Cervical Spine Occipital-Cervical Injuries Atlantoaxial Injuries (C1-C2) Odontoid Fractures Hangman’s Fracture Subaxial Cervical Spine Fractures Facet Dislocations Cervical Myelopathy Cervical Radiculopathy Thoracolumbar Spine Thoracic Spine Fractures Lumbar Spine Fractures Chance Fractures Burst Fractures Compression Fractures Flexion-Distraction Injuries Sacral Fractures Lumbar Disc Herniation Lumbar Spinal Stenosis Degenerative Spondylolisthesis Thoracolumbar Burst Fractures Adult Isthmic Spondylolisthesis Special Considerations Ankylosing Spondylitis & DISH Fractures Osteoporotic Spine Fractures Pediatric Spine Trauma Spinal Cord Injury Management Timing of Surgery Adult Spinal Deformity Adolescent Idiopathic Scoliosis Pediatric Spondylolysis & Spondylolisthesis Congenital Scoliosis Spinal Cord Monitoring Adult Pyogenic Vertebral Osteomyelitis

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< Back Alper DUNKI Articular Cartilage: Structure, Components, and Clinical Relevance Overview Spot Knowledge – Articular Cartilage Composition: 95% ECM (water, collagen, proteoglycans), 5% chondrocytes Water: 65–80%, enables load-bearing, nutrient transport Collagen: >50% dry weight, mainly type II (90–95%); tensile strength Proteoglycans: 10–15% dry weight; aggrecan + GAGs provide compressive resilience Zones: Superficial (parallel collagen, friction reduction) Transitional (irregular, load distribution) Deep (vertical, compressive strength) Calcified (anchors to bone) Functions: Low-friction motion, load distribution, joint stability, resistance to forces Clinical relevance: Limited healing (avascular) Water/collagen/PG imbalance → osteoarthritis Collagen II & X defects → chondrodysplasias PG loss → elasticity ↓, cartilage breakdown Articular Cartilage: Structure, Components, and Clinical Relevance Overview Articular cartilage is composed predominantly of extracellular matrix (ECM, ~95%) and a small number of chondrocytes (~5%). Chondrocytes maintain ECM homeostasis throughout life. The main components of ECM are water, collagen, and proteoglycans. Water Water accounts for 65–80% of cartilage. It is 80% in the superficial zone and 65% in the deep zone. Water plays a critical role in load-bearing by deforming in response to compression. Its movement through ECM pores, along with frictional resistance and pressurization, provides high load-bearing capacity. Facilitates the transport of nutrients and metabolites. Alterations in water content affect permeability, stiffness, and elastic modulus. Collagen Collagen constitutes more than 50% of the dry weight and 10–20% of the wet weight. Provides tensile and shear strength. Type II collagen accounts for 90–95% of the total. Minor collagens include types V, VI, IX, X, and XI. Type VI: increases in early osteoarthritis. Type X: produced by hypertrophic chondrocytes during endochondral ossification; associated with calcification. The unique amino acid composition (glycine, proline, hydroxyproline, hydroxylysine) forms a triple-helix structure. Covalent cross-links between fibrils enhance durability. Defects in collagen type II and X can lead to achondroplasia, spondyloepiphyseal dysplasia, Kniest dysplasia, and metaphyseal chondrodysplasia. Proteoglycans Proteoglycans constitute 10–15% of dry weight and provide compressive strength. Synthesized by chondrocytes and secreted into the ECM. Contain glycosaminoglycans (GAGs) composed of repeating disaccharides: chondroitin sulfate and keratan sulfate. Chondroitin sulfate decreases with age, keratan sulfate increases. The most important proteoglycan is aggrecan, which consists of a long protein core with GAG side chains. Aggrecan molecules aggregate with hyaluronic acid and link proteins, imparting resilience to the matrix. Interact with collagen fibrils to form a robust network. Zones Histologically, articular cartilage is organized into four zones: Superficial zone: Collagen fibers are aligned parallel; reduces friction. Transitional zone: Fibers are irregular; distributes load. Deep zone: Fibers are vertically aligned; provides high compressive strength. Calcified zone: Anchors cartilage to bone. Functions Provides low-friction joint motion. Distributes loads and contributes to joint stability. Resists compressive and tensile forces. Maintains nutrient transport and metabolic homeostasis. Clinical Relevance Cartilage is avascular, with limited intrinsic healing capacity. Alterations in water, collagen, and proteoglycan content are associated with degenerative disorders such as osteoarthritis. Defects in type II and X collagen result in genetic chondrodysplasias. Loss of proteoglycans leads to reduced elasticity and cartilage breakdown. Reference 1. Guo L, Li P, Rong X, Wei X. Key roles of the superficial zone in articular cartilage physiology, pathology, and regeneration. Inflamm Regen . 2024;44:21. doi:10.1186/s41232-022-00202-0 2. Alcaide-Ruggiero L, Cugat R, Domínguez JM. Proteoglycans in Articular Cartilage and Their Contribution to Chondral Injury and Repair Mechanisms. Int J Mol Sci . 2023;24(14):11472. doi:10.3390/ijms241411472 3. Karpiński R, Szczodry M, Zawadzki G. Articular Cartilage: Structure, Biomechanics, and the Potential of Regenerative Medicine. Appl Sci . 2025;15(12):6896. doi:10.3390/app15126896 Previous Next