< Back Dr. İlkay TOSUN What the Pathologist Needs Accurate pathological diagnosis is the cornerstone of musculoskeletal tumor management. Even the most advanced imaging cannot replace high-quality, representative tissue and precise clinical context. The pathologist’s ability to deliver an accurate diagnosis depends not only on tissue quality but also on the quality of information provided by the surgeon. Effective communication between the surgical, radiologic, and pathology teams is therefore essential. Essential Clinical Information When submitting a biopsy or resection specimen, the following details must be clearly documented on the pathology request form and discussed, ideally in a multidisciplinary setting: Patient demographics: Age, sex, and relevant medical history (especially prior malignancy or radiation). Clinical presentation: Duration of symptoms, pain, swelling, growth rate, trauma history. Anatomical location: Specific bone, side (right/left), and compartment (intramedullary, cortical, soft-tissue). Radiologic findings: Summary of MRI, CT, and X-ray features (matrix pattern, cortical involvement, soft-tissue extension). Suspected diagnosis or differential diagnosis: To guide appropriate sampling and staining. Previous procedures: Any prior biopsy, curettage, or surgery must be mentioned, as they may alter histologic appearance. Tissue Handling and Labelling Mark orientation: Use sutures or ink to identify margins and anatomical orientation. Avoid crush or cautery artifact: Handle tissue gently to preserve architecture. Separate samples: If both soft-tissue and bone are present, send them in separate containers. Include imaging correlation: Providing printed or digital images helps the pathologist select representative areas for sectioning. Communication During Intraoperative Consultation In frozen-section or intraoperative evaluation, the pathologist must be informed of: The surgical goal (diagnosis confirmation vs. margin assessment). The area of interest (solid vs. necrotic, viable vs. cystic). Whether margin evaluation is required, and from which site. Surgeons should ensure timely specimen delivery to prevent desiccation or thermal artifact. The pathologist’s main intraoperative contribution is to confirm tissue adequacy and margin status , rather than to provide an immediate tumor type. Accurate diagnosis relies on a combination of clinical, radiologic, and histologic data — emphasizing the importance of multidisciplinary tumor board discussions. Frozen Section Limitations Frozen section (intraoperative consultation) is not suitable for diagnosing bone and soft-tissue tumors. Soft-tissue tumors are inherently heterogeneous , and frozen sections may not reflect the entire lesion. Bone tumors require decalcification for accurate evaluation, which is a time-dependent process and cannot be performed during frozen examination. Therefore, definitive diagnosis should not be expected from frozen sections in musculoskeletal oncology. However, frozen sections may be useful for assessing surgical margins , especially in wide resections or recurrent cases. Sampling and Biopsy Considerations Small or limited biopsies (e.g., tru-cut or core biopsies ) may not always provide a definitive diagnosis because large tumors are often heterogeneous. Extensive sampling is essential — ideally at least one tissue block per centimetre of tumor diameter — to capture representative areas, including viable, necrotic, and atypical regions. Close coordination between the surgeon and pathologist ensures correct orientation, adequate fixation, and avoidance of crush artefacts. Common Challenges Non-representative sampling: Necrotic or hemorrhagic areas yield non-diagnostic results. Lack of clinical context: Leads to misclassification (e.g., distinguishing infection from neoplasm). Improper fixation: Inadequate formalin volume (should be 10× tissue volume) affects morphology. Delayed transport: Causes autolysis and RNA degradation, limiting molecular studies. Key Points The pathologist needs context as much as tissue — imaging findings, clinical suspicion, and surgical notes are indispensable. Always coordinate with pathology before biopsy for specimen handling and ancillary test planning. Representative, well-oriented, and fresh tissue improves diagnostic accuracy. Successful diagnosis in MSK oncology is a team process , not a laboratory event. References Mankin HJ, Hornicek FJ. Diagnosis, Classification, and Management of Bone Tumors: The Importance of Multidisciplinary Communication. J Am Acad Orthop Surg. 2017;25(8):540–551. Bridge JA, et al. Molecular Diagnostics of Bone and Soft Tissue Tumors: Evolving Role in Classification and Therapeutics. Mod Pathol. 2020;33(S1):27–44. O’Donnell P, Tirabosco R, Saifuddin A. What the Pathologist Needs from the Radiologist in Bone Tumour Diagnosis. Skeletal Radiol. 2018;47(10):1321–1332. Fletcher CDM, et al. WHO Classification of Soft Tissue and Bone Tumours, 5th Edition. IARC Press, 2020. 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 Body Mass Index > 40 Is Not Correlated With Early Complications in Patients Undergoing Primary Total Joint Arthroplasty at an Ambulatory Surgical Center Retrospective study of 2,367 patients undergoing primary total hip or knee arthroplasty (THA/TKA) at an ambulatory surgical center. Patients were stratified by BMI groups (normal, overweight, obesity classes I–III including ≥40). Outcomes assessed: early (24h) and 1–90 day complications, perioperative times, PACU course, and pain scores. 🧠 Key Points Complication rates at 24h and 1–90 days were not significantly different across BMI groups, including BMI ≥40. Operative and pre-op times were longer in higher BMI patients, but PACU discharge was earlier . Pain scores before discharge were higher in obesity groups, but without increased adverse events. Estimated blood loss was similar across BMI groups. Conclusion: With proper preoperative optimization, BMI ≥40 should not be an exclusion criterion for outpatient TJA; outcomes are comparable to lower BMI patients. The Journal of Arthroplasty (2025) doi.org/10.1016/j.arth.2025.08.065 Previous Next

< Back Metacarpal Fractures metacarpal-fractures Previous Next

< Back Dr. Ahmet Müçteba YILDIRIM Enchondroma Overview • Enchondroma is a benign hyaline cartilage tumor, accounting for 20-25% of benign bone tumors. • It arises from residual cartilage cells that fail to undergo necrosis after physeal growth. • Can be solitary or multiple (Ollier’s disease, Maffucci syndrome). Clinical Presentation Often asymptomatic, detected incidentally (except in hand lesions). Hand enchondromas: Pain due to bone expansion, cortical thinning, or microfractures. Long bone enchondromas with pain: Rule out first intra-articular pathologies, atypical cartilage tumor or chondrosarcoma Radiographic Features Enchondromas are typically incidental, well-defined intramedullary lesions smaller than 5 cm. They appear lytic with a narrow transition zone and smooth margins. Characteristic “rings-and-arcs” chondroid calcifications may be present, though lesions in the hands and feet often remain purely lytic. Mild endosteal scalloping or slight expansion can occur, but cortical breakthrough, periosteal reaction, or soft-tissue mass should not be seen. These lesions usually arise in the metaphysis, reflecting their origin from the growth plate; an epiphyseal cartilaginous lesion should raise concern for chondrosarcoma. Plain Radiograph and CT Enchondromas usually present as small (<5 cm), intramedullary, lytic lesions with non-aggressive characteristics such as: · well-defined margins and a narrow transition zone · possible “rings and arcs” calcification reflecting a chondroid matrix · in the hands and feet, frequently purely lytic without visible matrix mineralization · occasional mild expansion and endosteal scalloping · absence of cortical breakthrough unless secondary to a pathological fracture MRI Findings MRI best demonstrates lesion extent and confirms the intramedullary, lobulated nature of enchondromas. T1-weighted: intermediate to low signal with internal low-signal foci corresponding to calcified cartilage. T2-weighted: sharply defined high signal due to water-rich cartilage, with “rings-and-arcs” low-signal areas. Post-contrast (T1 + Gd): peripheral or septal enhancement following the lobulated contours. No surrounding bone-marrow or soft-tissue edema is expected. However, enhancement patterns may occasionally resemble those of low-grade chondrosarcoma, so correlation with clinical and radiographic features is essential. Associated Syndromes Ollier’s disease: Multiple enchondromas, unilateral, 20-50% malignant transformation risk. Lesions are generally unilateral. Short stature, limb length discrepancy, and angular deformities in bones and joints are commonly seen. Maffucci syndrome: Enchondromas + soft tissue hemangiomas; higher malignancy risk than Ollier’s. Due to phleboliths, hemangiomas are also detected on X-rays. Common Sites Hands (40-65%): Proximal phalanges > metacarpals > middle phalanges. Long bones: Femur, humerus, tibia (metaphyseal). Rare in carpal/tarsal bones or distal phalanges. Imaging Features X-ray: Hands: Lytic, sclerotic rim, bone expansion, cortical thinning, calcification is not usually seen. Long bones: Metaphyseal, indistinct margins, endosteal scalloping, matrix calcification. CT: Evaluates calcification and cortical integrity. MRI: Assesses soft tissue extension, peritumoral edema, contrast enhancement (for differential diagnosis) and fat entrapment. PET-CT: Useful for enchondromatosis/pelvic lesions Biopsy Not routine; reserved for atypical features (e.g., pain, growth, or imaging suspicious for chondrosarcoma). Target less calcified, fat entrapment and heterogeneous areas on MRI. Biopsy tract should align with potential surgical incision. Treatment Asymptomatic, small (<4 cm), stable lesions: Annual monitoring.(BACTIP Protocole* : Birmingham Atypical Cartilage Tumor Imaging Protocol) Surgical indications: Pain, growth on follow-up, or pathologic fracture risk. Techniques: Intralesional curettage + adjuvant + bone-filler (PMMA/graft) ± fixation (fracture risk in lower extremities). Hand lesions: Curettage alone/ Curettage and bone filler (PMMA/Graft) Differential Diagnosis Atypical Cartilage Tumor (ACT): WHO 2020 reclassified grade I chondrosarcomas in extremities as ACT (no metastasis risk but can recur). Suspect if pain, size >4 cm, generalized endosteal scalloping. Chondrosarcoma: Cortical destruction, soft tissue involvement, axial skeleton location. Type Tumor Length Endosteal Scalloping Management 1a <4 cm None Discharge 1b <4 cm Focal Follow-up in 3 years; refer to oncology or discharge based on changes 1c <4 cm Generalized Immediate oncology referral 2a ≥4 cm None Follow-up in 3 years; refer to oncology or discharge based on changes 2b ≥4 cm Focal Follow-up at 1 & 3 years; refer to oncology or discharge 2c ≥4 cm Generalized Immediate oncology referral 3 any size Aggressive features Immediate oncology referral The Birmingham Atypical Cartilage Tumor Imaging Protocol (BACTIB) classification CT and MRI images of the distal femur demonstrate a well-defined intramedullary chondroid lesion with characteristic rings-and-arcs calcifications on CT, consistent with enchondral matrix mineralization. On MRI, the lesion shows intermediate to low signal on T1-weighted and high signal on T2-weighted sequences with internal low-signal foci corresponding to calcified cartilage. There is no cortical destruction, periosteal reaction, or soft-tissue extension, supporting the diagnosis of a benign enchondroma. Previous Next

< Back Alper DUNKI Skeletal Development Spot Knowledge Bone formation occurs via intramembranous and endochondral ossification . The growth plate has three main zones: resting, proliferative, hypertrophic . The hypertrophic zone is the weakest and most prone to injury. Hormones, vitamins, and mechanical loading directly regulate growth plate activity. Cartilage and Bone Development Intramembranous ossification: Osteoblasts form osteoid matrix directly → skull, clavicle, scapula, pelvis. Endochondral ossification: Responsible for growth plate activity and fracture healing; osteoid deposited on cartilage. Embryonic timeline: Week 4: limb buds form Week 6: mesenchymal cells → chondrocytes Week 7: hypertrophy & matrix calcification Week 8: vascular invasion → primary ossification center Growth Plate Structure Resting zone: Few cells, rich in type II collagen. Proliferative zone: Main site of cell division, irregular collagen fibrils, matrix vesicles. Hypertrophic zone: Weakest layer, cells enlarge, mineralization begins. Metaphysis: Removes mineralized cartilage, remodels trabecular bone. Ranvier’s groove & LaCroix’s ring: Provide mechanical support. Biochemistry & Mineralization Oxygen usage: Resting: low oxygen Proliferative: aerobic metabolism Hypertrophic: anaerobic glycolysis Mineralization: Initiated by matrix vesicles and type X collagen; driven by mitochondrial calcium release. Matrix remodeling: MMPs activated by IL-1 and plasmin. Hormonal & Nutritional Regulation Thyroxine (T4): Stimulates DNA synthesis, collagen production. PTH: Increases mitosis and proteoglycan synthesis in epiphyseal chondrocytes. Calcitonin: Accelerates calcification. Glucocorticoids: Excess → suppress proliferation and growth. Androgens: Enhance mineralization. GH & IGF-1: Regulate proliferation across all zones. Vitamin D: Promotes proliferation (absent in hypertrophic zone). Vitamin A: Deficiency → impaired maturation; excess → weak bone. Vitamin C: Essential for collagen synthesis. Biomechanics & Growth Plate Injury Hueter–Volkmann Law: Increased mechanical load → slowed growth. Early muscle contractions affect endochondral ossification. Interface between metaphysis and proliferative zone adapts to stress. Pathological Conditions Genetic Disorders: Type II collagen defects → Kniest, Stickler syndromes Type X collagen defects → Schmid-type metaphyseal chondrodysplasia Sulfate transporter defects → diastrophic dysplasia Mucopolysaccharidoses → GAG accumulation Hypophosphatasia → defective matrix calcification Environmental: Infections at metaphysis (bacteria in vascular sinusoids → abscess) Radiation suppresses growth (longitudinal > transverse impact) Nutritional: Rickets: Vitamin D/mineral deficiency → impaired calcification Scurvy: Vitamin C deficiency → defective collagen synthesis (Frankel’s line radiographically) References Vélez-Reyes GL, et al. Developmental Dynamics . 20212. Skeletal Development OR Cai R, et al. Front Cell Dev Biol . 20232. Skeletal Development OR Tomatsu S, et al. Bone . 20202. Skeletal Development OR Previous Next

< Back Tibial Osteotomies tibial-osteotomies Previous Next

< Back Nerve Injuries (Median, Ulnar, Radial) nerve-injuries-hand Previous Next

< Back Pediatric Trauma C A pediatric-trauma Previous Next

< Back Distal Femoral Osteotomy (DFO) distal-femoral-osteotomy Previous Next

< Back Toe Deformities (Claw, Hammer, Mallet Toes) toe-deformities Previous Next

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