Bone and Soft Tissue Pathology — MCQs

Bone and Soft Tissue Pathology Indian Medical PG Practice Questions and MCQs

Question 241: A 30-year-old man presents with a radiolucent lesion. Imaging reveals a hollow cavity without epithelial lining. What is the most probable diagnosis?

A. Aneurysmal bone cyst
B. Static bone cavity
C. Hemorrhagic bone cyst (Correct Answer)
D. Ameloblastoma

Explanation: ### Explanation The correct diagnosis is **Hemorrhagic Bone Cyst** (also known as Traumatic Bone Cyst or Simple Bone Cyst). **1. Why the correct answer is right:** A Hemorrhagic Bone Cyst is defined as a **pseudocyst** because it lacks a true epithelial lining. Pathologically, it presents as an empty or fluid-filled hollow cavity within the bone, often scalloping between the roots of teeth. The absence of an epithelial lining is the pathognomonic feature that distinguishes it from true cysts [2]. It is most commonly seen in the mandible of young adults. **2. Why the incorrect options are wrong:** * **Aneurysmal Bone Cyst (ABC):** While also a pseudocyst, ABC is characterized by blood-filled spaces separated by fibroblastic connective tissue containing multinucleated giant cells and osteoid [1]. It typically presents as an expansile, "soap-bubble" radiolucency, rather than a simple hollow cavity. * **Static Bone Cavity (Stafne Cyst):** This is a developmental depression on the lingual aspect of the mandible containing salivary gland tissue. It is located below the inferior alveolar canal and is not a "hollow" cavity in the surgical sense. * **Ameloblastoma:** This is a true neoplasm. Radiographically, it shows a multilocular ("honeycomb") appearance and histologically features odontogenic epithelium arranged in nests or plexiform patterns with peripheral palisading. **3. NEET-PG High-Yield Pearls:** * **Key Radiographic Sign:** "Scalloping" between the roots of teeth without causing root resorption or tooth displacement. * **Surgical Finding:** Upon surgical entry, the cavity is often found to be **empty** (void of tissue or fluid), which is a classic diagnostic clue. * **True Cyst vs. Pseudocyst:** Always check for the presence of an **epithelial lining** [2]. If absent, think of Hemorrhagic Bone Cyst or Aneurysmal Bone Cyst. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1206-1208. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Question 242: Lipoma most commonly becomes malignant at which site?

A. Subcutaneous
B. Subaponeurotic
C. Retroperitoneal (Correct Answer)
D. Intermuscular

Explanation: The correct answer is **Retroperitoneal**. **1. Why Retroperitoneal is correct:** While lipomas are the most common mesenchymal tumors, they are almost always benign [1]. However, the risk of malignancy (transformation into or being misdiagnosed as **Liposarcoma**) is significantly higher in deep-seated locations. Retroperitoneal "lipomatous" masses are notoriously aggressive [1]. In fact, most experts suggest that any large, deep-seated lipomatous tumor in the retroperitoneum should be considered a **Well-Differentiated Liposarcoma (WDL)** [1]. These tumors often harbor MDM2 gene amplifications, which are absent in benign subcutaneous lipomas [1]. **2. Why the other options are incorrect:** * **Subcutaneous (Option A):** This is the most common site for lipomas (e.g., on the back, neck, or proximal extremities) [1]. These are almost universally benign and have a negligible risk of malignant transformation. * **Subaponeurotic (Option B) & Intermuscular (Option C):** These are types of "Deep Lipomas." While they are deeper than subcutaneous ones, they are still predominantly benign. **3. Clinical Pearls for NEET-PG:** * **Most common soft tissue tumor in adults:** Lipoma [1]. * **Most common soft tissue sarcoma in adults:** Liposarcoma. * **Cytogenetics:** Liposarcomas (WDL/ALT) are associated with **MDM2 and CDK4 amplification** on chromosome 12q13-15 [1]. * **Histology:** The presence of **lipoblasts** (cells with indented nuclei by lipid vacuoles) is a hallmark of liposarcoma, though not always required for the diagnosis of the well-differentiated subtype [1]. * **Rule of Thumb:** A lipomatous mass >10 cm in the retroperitoneum is a Liposarcoma until proven otherwise. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1222-1223.

Question 243: Tennis racquet cells are characteristic of which of the following tumors?

A. Rhabdomyoma
B. Rhabdomyosarcoma (Correct Answer)
C. Histiocytoma
D. Eosinophilic granuloma

Explanation: ### Explanation **Correct Answer: B. Rhabdomyosarcoma** The characteristic **"tennis racquet cells"** refer to **rhabdomyoblasts**, which are the diagnostic hallmark of Rhabdomyosarcoma (RMS). These cells are primitive mesenchymal cells showing skeletal muscle differentiation [1]. They possess an eccentric nucleus and an elongated, tapering cytoplasmic tail (tadpole or racquet shape) filled with eosinophilic cytoplasm. In well-differentiated areas, these cells may even show visible cross-striations under light microscopy. While RMS is the most common soft tissue sarcoma in children, the "embryonal" subtype (including Sarcoma Botryoides) is most frequently associated with these morphological variants [1]. **Analysis of Incorrect Options:** * **A. Rhabdomyoma:** While this is a benign tumor of skeletal muscle, it typically presents with "spider cells" (cells with large glycogen vacuoles and radial cytoplasmic strands) rather than the classic elongated racquet-shaped rhabdomyoblasts seen in malignancy. * **C. Histiocytoma:** Fibrous histiocytomas are characterized by a "storiform" or cartwheel growth pattern of spindle cells, not racquet cells. * **D. Eosinophilic Granuloma:** This is a form of Langerhans Cell Histiocytosis (LCH). While it features **Birbeck granules** (which look like tennis racquets under **Electron Microscopy**), the *cells* themselves are not racquet-shaped under light microscopy [2]. This is a common point of confusion in exams. **NEET-PG High-Yield Pearls:** * **Light Microscopy:** "Tennis racquet **cells**" = Rhabdomyosarcoma. * **Electron Microscopy:** "Tennis racquet **organelles**" (Birbeck granules) = Langerhans Cell Histiocytosis [2]. * **IHC Marker:** Desmin, Myogenin, and MyoD1 are the most specific markers for Rhabdomyosarcoma [1]. * **Sarcoma Botryoides:** A variant of embryonal RMS found in hollow organs (vagina/bladder) characterized by a "cluster of grapes" appearance and a subepithelial **Cambium layer** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 630.

Question 244: A 40-year-old woman has severe, disabling rheumatoid arthritis. Rheumatoid factor is positive. What would a biopsy of the synovium of her knee most likely reveal?

A. A nearly normal synovium with scattered inflammatory cells
B. A non-proliferative synovitis with abscess formation
C. A non-proliferative synovitis with many neutrophils
D. A proliferative synovitis with many lymphocytes, macrophages, and plasma cells (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. A proliferative synovitis with many lymphocytes, macrophages, and plasma cells** The hallmark of **Rheumatoid Arthritis (RA)** is a chronic, autoimmune-mediated inflammatory process [3]. The underlying pathophysiology involves a Type IV hypersensitivity reaction where T-cells (specifically Th1 and Th17) release cytokines (IFN-γ, IL-17) that activate macrophages and B-cells [2]. This leads to the characteristic histological finding: **Chronic Proliferative Synovitis**. The synovium undergoes marked hyperplasia (becoming thick and frond-like) and is heavily infiltrated by chronic inflammatory cells, namely **lymphocytes, plasma cells, and macrophages** [1]. These cells often organize into lymphoid follicles (Allison-Ghormley bodies) [2]. This thickened, inflamed vascular granulation tissue is known as **Pannus**, which eventually erodes the underlying articular cartilage and bone [1]. **Why the other options are incorrect:** * **Option A:** RA is a destructive, chronic disease; a "nearly normal" synovium would not be seen in a patient with severe, disabling symptoms. * **Option B & C:** Abscesses and a predominance of neutrophils are characteristic of **Septic Arthritis** (acute bacterial infection), not the chronic autoimmune process of RA [1]. While some neutrophils may be present in the synovial fluid during an acute flare, the synovial *tissue* biopsy is dominated by mononuclear cells. ### NEET-PG High-Yield Pearls: * **Pannus:** The pathognomonic feature of RA; it consists of proliferating synovial cells, inflammatory cells, granulation tissue, and fibroblasts [1]. * **Rice Bodies:** Fibrinous nodules shed into the joint space from the surface of the synovium. * **Rheumatoid Factor (RF):** An IgM autoantibody directed against the Fc portion of self-IgG. * **Anti-CCP (Cyclic Citrullinated Peptide):** The most specific serological marker for RA [2]. * **Joint Involvement:** Typically involves small joints of hands (MCP, PIP) and feet; characteristically **spares the DIP joints** [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 676-677. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1214.

Question 245: The prognosis of rhabdomyosarcoma is likely to be poor if the site of the tumour is:

A. Orbit
B. Extremity (Correct Answer)
C. Paratesticular
D. Urinary bladder

Explanation: **Explanation:** The prognosis of Rhabdomyosarcoma (RMS) is determined by several factors, including histological subtype, age, and, most importantly, the **anatomic site of origin**. [1] **1. Why "Extremity" is the correct answer:** Tumors arising in the **extremities** are associated with a **poor prognosis**. [1] This is primarily because extremity RMS is frequently of the **Alveolar subtype**, which is more aggressive and carries a higher risk of early lymph node and distant metastasis compared to the embryonal subtype. Additionally, these sites often allow the tumor to grow significantly before detection, leading to advanced stage at presentation. **2. Why the other options are incorrect:** * **Orbit (A):** This is considered a **favorable site**. Tumors here are usually detected early due to visible proptosis and have a high cure rate (often >90%). * **Paratesticular (C):** This is a **favorable site**. These are typically of the embryonal subtype and are easily accessible for surgical resection and early diagnosis. * **Urinary Bladder (D):** While internal, the genitourinary system (excluding the prostate) is generally categorized as having a better prognosis than extremity or parameningeal sites, particularly when the tumor is the "botryoid" variant. [1] **Clinical Pearls for NEET-PG:** * **Most common subtype:** Embryonal RMS (60%, better prognosis). [1] * **Most aggressive subtype:** Alveolar RMS (associated with t(2;13) or t(1;13) translocation involving the *PAX3/7-FOXO1* genes). * **Favorable Sites:** Orbit, Non-parameningeal Head & Neck, Paratesticular/Genitourinary (excluding bladder/prostate). * **Unfavorable Sites:** Extremities, Parameningeal (skull base), Prostate, and Trunk. * **Sarcoma Botryoides:** A variant of embryonal RMS found in hollow organs (vagina/bladder) characterized by a "grape-like" appearance and the presence of a **Cambium layer** under the epithelium. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225.

Question 246: Which of the following is an example of X-linked muscular dystrophy?

A. Myotonic dystrophy
B. Spinal muscular atrophy
C. Neurogenic muscular atrophy
D. Duchenne muscular dystrophy (Correct Answer)

Explanation: **Explanation:** **Duchenne Muscular Dystrophy (DMD)** is the correct answer because it is an **X-linked recessive** disorder caused by a mutation in the *DMD* gene located on the short arm of the X chromosome (Xp21) [1]. This mutation leads to a complete absence of **dystrophin**, a critical protein that links the intracellular cytoskeleton (actin) to the extracellular matrix [1]. Without dystrophin, muscle membranes become fragile, leading to progressive myofiber necrosis and replacement by fibrofatty tissue. **Analysis of Incorrect Options:** * **A. Myotonic Dystrophy:** This is an **Autosomal Dominant** disorder [2]. It is characterized by CTG trinucleotide repeat expansions in the *DMPK* gene. Clinical hallmarks include "myotonia" (delayed muscle relaxation) and "hatchet facies" [2]. * **B. Spinal Muscular Atrophy (SMA):** This is an **Autosomal Recessive** motor neuron disease caused by mutations in the *SMN1* gene. It involves the destruction of anterior horn cells in the spinal cord, leading to secondary muscle wasting. * **C. Neurogenic Muscular Atrophy:** This is a broad category of muscle wasting resulting from nerve injury (e.g., peripheral neuropathy or polio) rather than a primary genetic muscle pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Gower’s Sign:** A classic clinical finding in DMD where the child uses their hands to "climb up" their own legs to stand. * **Pseudohypertrophy:** The calves appear enlarged due to fat and connective tissue replacement, not actual muscle growth. * **Becker Muscular Dystrophy (BMD):** Also X-linked, but involves *truncated* (functional) dystrophin, resulting in a milder clinical course than DMD [1]. * **Lab Marker:** Serum **Creatine Kinase (CK)** levels are massively elevated from birth in DMD patients. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1245-1246.

Question 247: Which of the following has a propensity to metastasize through lymph nodes?

A. Alveolar rhabdomyosarcoma (Correct Answer)
B. Osteosarcoma
C. Both
D. None

Explanation: Explanation: In general, sarcomas (malignant mesenchymal tumors) characteristically spread via the **hematogenous route** (bloodstream), most commonly to the lungs [2]. However, a specific subset of soft tissue sarcomas is known for its unusual propensity for **lymphatic spread**. **1. Why Alveolar Rhabdomyosarcoma is Correct:** Alveolar rhabdomyosarcoma (ARMS) is a highly aggressive subtype of rhabdomyosarcoma, often associated with the $t(2;13)$ or $t(1;13)$ translocation [1]. Unlike most sarcomas, ARMS frequently involves regional lymph nodes. This characteristic is shared with a few other "exceptions to the rule" in sarcoma pathology. **2. Why Osteosarcoma is Incorrect:** Osteosarcoma is the most common primary malignant bone tumor. It follows the classic rule for sarcomas: it spreads almost exclusively via the hematogenous route. At the time of diagnosis, subclinical pulmonary metastases are often already present, but lymph node involvement is extremely rare (usually <3%). **3. High-Yield Clinical Pearls for NEET-PG:** To excel in pathology questions regarding metastasis, remember the mnemonic **"SCARE"** for sarcomas that frequently spread via **Lymph Nodes**: * **S:** **S**ynovial sarcoma [3] * **C:** **C**lear cell sarcoma * **A:** **A**ngiosarcoma / **A**lveolar rhabdomyosarcoma * **R:** **R**habdomyosarcoma (specifically Alveolar) [1] * **E:** **E**pithelioid sarcoma (The most common sarcoma to spread via lymphatics) **Key Takeaway:** While the "Sarcoma = Hematogenous" rule is generally true, Alveolar Rhabdomyosarcoma is a classic exception frequently tested in postgraduate exams. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 282. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1225-1226.

Question 248: Which of the following is a complication of rheumatoid arthritis of the mandibular condyle?

A. Fibrous ankylosis (Correct Answer)
B. Subluxation
C. Dislocation
D. None of the above

Explanation: **Explanation:** Rheumatoid Arthritis (RA) is a chronic systemic inflammatory disorder that primarily affects synovial joints [1]. When the **Temporomandibular Joint (TMJ)** is involved, the chronic inflammatory process leads to the formation of **pannus** (inflamed synovial granulation tissue) [1]. 1. **Why Fibrous Ankylosis is correct:** In the TMJ, the persistent presence of pannus causes destruction of the articular cartilage and the underlying subchondral bone of the mandibular condyle [1]. As the inflammatory process progresses and attempts to heal, the granulation tissue undergoes fibrosis. This leads to the formation of dense fibrous adhesions between the condyle and the glenoid fossa, resulting in **fibrous ankylosis** [2]. While bony ankylosis can occur, fibrous ankylosis is the more characteristic end-stage complication in RA patients [2]. 2. **Why other options are incorrect:** * **Subluxation and Dislocation:** These typically involve hypermobility or trauma where the condyle moves out of the articular eminence. In RA, the primary pathology is **hypomobility** due to structural destruction and scarring, rather than excessive joint laxity [2]. **NEET-PG High-Yield Pearls:** * **TMJ Involvement in RA:** Occurs in approximately 50-75% of chronic RA patients, often manifesting as bilateral preauricular pain and limited mouth opening. * **Radiographic Hallmark:** "Sharpened pencil" or "Pencil-in-cup" appearance of the mandibular condyle due to extensive erosions [1]. * **Ankylosis Comparison:** While RA typically leads to **fibrous** ankylosis, **Septic Arthritis** (especially in children) is a more common cause of **bony** ankylosis of the TMJ. * **Key Histology:** Presence of synovial hyperplasia, lymphoplasmacytic infiltrates, and fibrinoid necrosis [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1214.

Question 249: In Osteomalacia, which of the following is defective?

A. Osteoid formation
B. Mineralization of bone (Correct Answer)
C. Both osteoid formation and mineralization of bone
D. None of the above

Explanation: **Explanation:** **1. Why Option B is correct:** Osteomalacia is a metabolic bone disease characterized by a **defect in the mineralization of the organic bone matrix (osteoid)**. In adults, this is most commonly due to Vitamin D deficiency, which leads to inadequate levels of calcium and phosphate [1]. While the osteoblasts continue to synthesize the organic matrix (osteoid) at a normal rate, there is insufficient mineral deposition to harden it. This results in an accumulation of excess, unmineralized osteoid, making the bones "soft" and prone to fractures and deformities [2]. **2. Why other options are incorrect:** * **Option A:** Osteoid formation is the synthesis of the organic matrix (primarily Type I collagen) by osteoblasts. In osteomalacia, the **formation** of osteoid is generally normal or even increased as a compensatory mechanism; the pathology lies in the inability to mineralize that matrix. * **Option C:** This is incorrect because the primary defect is isolated to mineralization. A defect in both osteoid formation and mineralization would be seen in more complex systemic states or severe protein-calorie malnutrition, but it does not define the pathophysiology of osteomalacia. **3. NEET-PG High-Yield Pearls:** * **Rickets vs. Osteomalacia:** Both involve defective mineralization. Rickets occurs in children (affecting the growth plates/epiphyses), while Osteomalacia occurs in adults (after epiphyseal closure) [1]. * **Histology:** The hallmark is an **increased thickness of osteoid seams** (unmineralized matrix) and an increase in the **osteoid volume**. * **Radiology:** Look for **Looser’s zones** (pseudofractures or Milkman’s fractures), which are pathognomonic for osteomalacia. * **Biochemical Markers:** Typically shows Low/Normal Calcium, Low Phosphate, and **Elevated Alkaline Phosphatase (ALP)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 448-449. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1194-1195.

Question 250: Articular cartilage is made up of-

A. Type I collagen
B. Type II collagen (Correct Answer)
C. Type III collagen
D. Type IV collagen

Explanation: **Explanation:** Articular cartilage is a specialized form of **hyaline cartilage** that covers the ends of bones in synovial joints [1]. Its primary function is to provide a smooth, lubricated surface for low-friction articulation and to facilitate the transmission of loads to the underlying bone. **Why Type II Collagen is Correct:** The extracellular matrix of hyaline cartilage is unique. Approximately 90-95% of the collagen found in articular cartilage is **Type II collagen** [1]. These fibers form a dense, cross-linked network that provides tensile strength and anchors the proteoglycan aggregates (like aggrecan), which are essential for the cartilage's shock-absorbing properties. **Analysis of Incorrect Options:** * **Type I Collagen:** Found in "tough" tissues like **bone**, skin, tendons, and ligaments. It is also the primary collagen in **fibrocartilage** (e.g., intervertebral discs, pubic symphysis). * **Type III Collagen:** Known as **reticulin** fibers. It is prevalent in distensible organs like blood vessels, the uterus, and during the early stages of wound healing (granulation tissue). * **Type IV Collagen:** A non-fibrillar collagen that forms the structural framework of the **basement membrane**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** "Type **Two** is for Car-ti-lage" (Two syllables for Type II). * **Osteoarthritis:** Characterized by the degradation of Type II collagen and proteoglycans, leading to joint space narrowing [1]. * **Relapsing Polychondritis:** An autoimmune condition where antibodies are directed specifically against Type II collagen. * **Water Content:** Articular cartilage is composed of nearly 70-80% water, which is vital for its load-bearing capacity [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1209-1210.

Practice by Chapter

Bone Development and Growth

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Fracture Healing

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Osteomyelitis and Infectious Diseases

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Metabolic Bone Diseases

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Bone Tumors and Tumor-like Lesions

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Joints and Rheumatologic Diseases

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Soft Tissue Tumors

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Muscular Dystrophies and Myopathies

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Diseases of Tendons and Fascia

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Pathology of Orthopedic Implants

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