Bone and Soft Tissue Pathology — MCQs

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

Question 41: Arnold head is a feature of which of the following conditions?

A. Fibrous dysplasia.
B. Paget's disease.
C. Cleidocranial dysplasia. (Correct Answer)
D. Cherubim.

Explanation: **Explanation:** **Cleidocranial Dysplasia (CCD)** is the correct answer. It is an autosomal dominant skeletal disorder caused by a mutation in the **RUNX2 gene**, which is essential for osteoblast differentiation [1]. The "Arnold head" (or "Arnold-Chiari appearance" in some texts, though distinct from the malformation) refers to the characteristic **brachycephaly** (broad head) with frontal and parietal bossing, giving the skull a large, globular appearance relative to a small face. **Why other options are incorrect:** * **Fibrous Dysplasia:** Characterized by the replacement of bone with fibrous tissue [2]. While it can cause facial asymmetry (especially in the monostotic form), it is classically associated with "ground-glass" appearance on X-ray and "Chinese-letter" trabeculae histologically. * **Paget’s Disease:** Known for causing an increase in head size ("the hat no longer fits"), but this is due to cortical thickening and is referred to as **Leontiasis ossea** (lion-like face) rather than Arnold head [3]. * **Cherubism:** A genetic disorder causing bilateral, symmetrical painless swelling of the jaws. This creates a "cherubic" (angelic) look due to the upward tilting of the eyes, not the specific cranial bossing seen in CCD. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of CCD:** 1. Delayed closure of cranial sutures (persistent fontanelles), 2. Hypoplastic or absent clavicles (allowing the patient to touch shoulders in the midline), and 3. Dental anomalies (supernumerary teeth) [1]. * **Radiology:** Look for "Wormian bones" (small sutural bones) in the skull [1]. * **RUNX2 (CBFA1):** Remember this gene for MCQ purposes as it is the "master switch" for bone formation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1186. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1208. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1192-1194.

Question 42: Which of the following genetic abnormalities is associated with Ewing's sarcoma?

A. Defective gene at 11p13
B. Defective gene at 13q14
C. t(X;18)
D. t(11;22) (Correct Answer)

Explanation: ### Explanation **Correct Option: D. t(11;22)** Ewing’s sarcoma is a highly aggressive, small round blue cell tumor. The hallmark genetic abnormality, present in approximately 90–95% of cases, is the **t(11;22)(q24;q12)** translocation. This results in the fusion of the **EWS gene** (on chromosome 22) with the **FLI1 gene** (on chromosome 11). The resulting EWS-FLI1 fusion protein acts as an aberrant transcription factor that drives oncogenesis. **Analysis of Incorrect Options:** * **A. Defective gene at 11p13:** This refers to the **WT1 gene**, associated with **Wilms tumor** (often part of the WAGR syndrome). * **B. Defective gene at 13q14:** This refers to the **RB1 gene**, associated with **Retinoblastoma** and Osteosarcoma [1]. * **C. t(X;18):** This is the characteristic translocation for **Synovial Sarcoma** [2], resulting in the *SYT-SSX* fusion gene. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Derived from neuroectodermal cells (PAS positive due to cytoplasmic glycogen). * **Radiology:** Classic **"onion-skin"** periosteal reaction. It typically affects the diaphysis of long bones (Femur is the most common site). * **Immunohistochemistry (IHC):** Strong membranous expression of **CD99 (MIC2)** is a highly sensitive marker. * **Differential Diagnosis:** Must be differentiated from other "Small Round Blue Cell Tumors" like Lymphoma (CD45+), Rhabdomyosarcoma (Desmin+), and Neuroblastoma (NSE+). * **Other Translocations:** A less common variant is t(21;22), involving the *ERG* gene. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1200-1202. [2] 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 43: Which of the following conditions is NOT X-linked?

A. Duchenne muscular dystrophy
B. Emery-Dreifuss muscular dystrophy
C. Facioscapulohumeral muscular dystrophy (Correct Answer)
D. Becker muscular dystrophy

Explanation: ### Explanation The correct answer is **Facioscapulohumeral muscular dystrophy (FSHD)**. **1. Why Facioscapulohumeral Muscular Dystrophy is the correct answer:** Unlike the other options, FSHD is an **Autosomal Dominant** disorder [1]. It is most commonly associated with a deletion on **chromosome 4q35** (specifically the D4Z4 repeat unit), which leads to the overexpression of the *DUX4* gene [1]. Clinically, it presents with weakness in the facial muscles (inability to whistle or close eyes tightly), scapular winging, and upper arm weakness, typically appearing in the second decade of life [1]. **2. Why the other options are incorrect:** * **Duchenne Muscular Dystrophy (DMD):** This is the most common and severe form of muscular dystrophy. It is an **X-linked recessive** disorder caused by a "frameshift" mutation in the *DMD* gene, leading to a total absence of the protein **dystrophin** [2]. * **Becker Muscular Dystrophy (BMD):** This is also an **X-linked recessive** disorder. It involves "non-frameshift" mutations in the same *DMD* gene, resulting in a truncated but partially functional dystrophin protein [2]. It is clinically milder than DMD. * **Emery-Dreifuss Muscular Dystrophy (EDMD):** This condition has multiple inheritance patterns, but the **classic form is X-linked recessive** (mutations in the *EMD* gene encoding **Emerin**). It is characterized by the triad of early contractures, slowly progressive muscle weakness, and life-threatening cardiac conduction defects. **3. NEET-PG High-Yield Pearls:** * **Gower’s Sign:** Classically seen in DMD due to pelvic girdle weakness. * **Calf Pseudohypertrophy:** In DMD/BMD, muscle tissue is replaced by fat and connective tissue [2]. * **Death in DMD:** Usually occurs by age 20 due to respiratory failure or heart failure (dilated cardiomyopathy). * **Myotonic Dystrophy:** Another common dystrophy, but it is **Autosomal Dominant** and characterized by **Trinucleotide repeats (CTG)** and "hatchet-like" facies [1], [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 732-733. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1245-1246.

Question 44: Multiple osteomas, multiple polyposis, and supernumerary teeth are found in which syndrome?

A. Reiter's
B. Peutz-Jeghers
C. Gardner's (Correct Answer)
D. Behcet's

Explanation: **Explanation** **Gardner’s Syndrome** is a clinical variant of **Familial Adenomatous Polyposis (FAP)**, inherited in an autosomal dominant fashion due to mutations in the **APC gene** on chromosome 5q21 [3]. The hallmark of this syndrome is the triad of: 1. **Colonic Polyposis:** Hundreds to thousands of adenomatous polyps with a 100% risk of progression to colorectal carcinoma [3]. 2. **Skeletal Abnormalities:** Multiple **osteomas** (most commonly in the mandible, skull, and long bones) and supernumerary teeth. 3. **Soft Tissue Tumors:** Epidermoid cysts, desmoid tumors, and fibromas [2]. **Analysis of Incorrect Options:** * **Reiter’s Syndrome (Reactive Arthritis):** Characterized by the triad of urethritis, conjunctivitis, and arthritis ("Can't see, can't pee, can't climb a tree"). It is associated with HLA-B27 and follows GI or GU infections. * **Peutz-Jeghers Syndrome:** An autosomal dominant condition (STK11 mutation) featuring **hamartomatous polyps** and mucocutaneous hyperpigmentation (melanotic spots on lips/oral mucosa) [1]. * **Behcet’s Syndrome:** A multisystem inflammatory disorder (vasculitis) presenting with recurrent oral ulcers, genital ulcers, and uveitis. **High-Yield Clinical Pearls for NEET-PG:** * **Turcot Syndrome:** FAP/Lynch syndrome associated with **CNS tumors** (Medulloblastoma or Glioma). * **Osteoma Location:** In Gardner’s, the mandible is the most common site for osteomas; their presence often precedes the detection of intestinal polyps. * **Desmoid Tumors:** These are aggressive fibromatoses that frequently occur post-surgery in Gardner’s patients [2]. * **CHRPE:** Congenital Hypertrophy of Retinal Pigment Epithelium is a highly specific screening marker for Gardner’s/FAP. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 813. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 691-692. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817.

Question 45: Which of the following is the most accepted theory?

A. Chemioparasitic theory. (Correct Answer)
B. Proteolytic theory.
C. Proteolytic chelation theory.
D. Dissolution theory.

Explanation: ### Explanation The question pertains to the theories of **dental caries** formation, a fundamental topic in oral pathology. **1. Why Chemioparasitic Theory is Correct:** Proposed by **W.D. Miller in 1890**, the **Chemioparasitic Theory** (also known as Miller’s Theory) is the most widely accepted explanation for the initiation of dental caries. It posits a two-step process: * **Chemical Phase:** Acid is produced by the fermentation of dietary carbohydrates by oral bacteria. Caries is the result of acid destruction of the calcified components of the teeth [1]. * **Parasitic Phase:** This acid causes the demineralization of the enamel and dentin, followed by the bacterial degradation of the remaining organic matrix. It identifies three essential factors: a susceptible host (tooth), micro-organisms (bacteria), and a substrate (carbohydrates). **2. Why Other Options are Incorrect:** * **Proteolytic Theory (Gottlieb):** This theory suggests that the organic matrix of the tooth is destroyed first by proteolytic enzymes, followed by the dissolution of inorganic crystals. It is less accepted because caries can occur in areas with very low organic content. * **Proteolytic Chelation Theory (Schatz):** This proposes that the products of bacterial proteolysis act as chelating agents that remove calcium ions from the tooth even at neutral or alkaline pH. While scientifically interesting, it is not the primary mechanism. * **Dissolution Theory:** This is a general term and not a recognized standalone theory for the complex biological process of caries formation. **3. NEET-PG High-Yield Pearls:** * **Primary Organism:** *Streptococcus mutans* is the chief etiologic agent in the initiation of enamel caries. * **Critical pH:** Enamel demineralization typically begins when the oral pH drops below **5.5**. * **Stephan Curve:** A graph representing the drop and subsequent recovery of plaque pH after carbohydrate consumption. * **Vipeholm Study:** A landmark study establishing the link between the frequency of sugar intake and caries activity. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 343-344.

Question 46: Regarding Burkitt's lymphoma, which of the following statements is true?

A. CD34 positive and Surface Ig positive
B. CD34 positive and Surface Ig negative
C. CD34 negative and Surface Ig negative
D. CD34 negative and Surface Ig positive (Correct Answer)

Explanation: **Explanation:** Burkitt’s Lymphoma (BL) is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the proliferation of **mature, germinal center-derived B-cells** [1]. Understanding the maturation state of the lymphocyte is key to identifying its immunophenotype [3]. **1. Why Option D is Correct:** * **Surface Ig Positive:** Since BL arises from mature B-cells (post-antigenic stimulation in the germinal center), these cells express surface Immunoglobulins (typically IgM with kappa or lambda light chain restriction). * **CD34 Negative:** CD34 is a marker of hematopoietic stem cells and early lymphoid progenitors (blasts). Because BL cells are mature B-cells and not immature "blasts" (despite their aggressive growth), they lose the expression of CD34 [2]. **2. Why Other Options are Incorrect:** * **Options A & B (CD34 positive):** These are incorrect because CD34 is a marker for **Acute Lymphoblastic Leukemia (ALL)** or precursor B-cell neoplasms [2]. BL cells are mature, not precursor cells [3]. * **Options B & C (Surface Ig negative):** These are incorrect because mature B-cell neoplasms characteristically express surface immunoglobulins, unlike very early precursor B-cells which may only show cytoplasmic mu chains or no Ig expression at all. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Characterized by **t(8;14)** involving the *MYC* gene and IGH gene. Less commonly t(2;8) or t(8;22). * **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages against a sea of cohesive tumor cells) [2]. * **Immunophenotype:** Positive for B-cell markers (**CD19, CD20, CD22, CD10**) and **BCL-6**. Crucially, it is **BCL-2 negative** (unlike Follicular Lymphoma). * **Proliferation Index:** Ki-67 is typically **>99%**, indicating nearly all cells are in the cell cycle. * **Associations:** Strongly linked to **Epstein-Barr Virus (EBV)**, especially the endemic (African) variant involving the jaw [1]. **References:** [1] 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, pp. 605-606. [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. 606. [3] 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, pp. 596-598.

Question 47: What is the most common epicenter of a radicular cyst?

A. Distal surface of tooth
B. Apex of tooth involved (Correct Answer)
C. Mesial surface of tooth
D. Deep periodontal pocket

Explanation: ### Explanation **1. Why "Apex of tooth involved" is correct:** A radicular cyst (also known as a periapical cyst) is the most common inflammatory odontogenic cyst [1]. Its pathogenesis begins with **pulpal necrosis** (usually due to dental caries or trauma). The necrotic pulp releases inflammatory mediators and toxins into the periapical tissues through the **apical foramen**. This chronic inflammation stimulates the **Rests of Malassez** (epithelial remnants of Hertwig’s epithelial root sheath in the periodontal ligament) to proliferate. As the epithelial mass grows, the central cells undergo ischemic necrosis, forming a fluid-filled cavity centered at the **root apex**. **2. Why other options are incorrect:** * **Distal and Mesial surfaces:** While a "lateral radicular cyst" can occur if an accessory canal exits the side of the root, this is statistically rare. The primary exit for necrotic debris is the apical foramen. * **Deep periodontal pocket:** This is the typical site for a **lateral periodontal cyst** (developmental) or a **periodontal abscess** (inflammatory), but not the classic radicular cyst. **3. High-Yield Facts for NEET-PG:** * **Most common odontogenic cyst:** Radicular cyst (~65-70% of all odontogenic cysts) [1]. * **Histopathology:** Characterized by a lining of non-keratinized stratified squamous epithelium. Look for **Rushton bodies** (eosinophilic, linear/curved calcifications) and **cholesterol clefts** with giant cells in the cyst wall. * **Radiology:** Appears as a well-defined, unilocular radiolucency at the apex of a **non-vital tooth**. * **Residual Cyst:** If the tooth is extracted but the cyst is left behind, it is termed a residual cyst. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Question 48: Which of the following statements is NOT true regarding embryonal rhabdomyosarcoma?

A. It is commonly seen in infants and children.
B. It can present as grape-like clusters, a form known as sarcoma botryoides.
C. Tumor cells may exhibit a tennis racket-like appearance.
D. It is associated with prenatal exposure to Diethylstilbestrol (DES). (Correct Answer)

Explanation: **Explanation:** **Embryonal Rhabdomyosarcoma (ERMS)** is the most common subtype of rhabdomyosarcoma, typically occurring in children under the age of 10 [1]. **Why Option D is the Correct Answer (The False Statement):** Prenatal exposure to **Diethylstilbestrol (DES)** is classically associated with **Clear Cell Adenocarcinoma of the vagina**, not embryonal rhabdomyosarcoma. While ERMS can occur in the vaginal wall of young girls, its etiology is linked to genetic mutations (e.g., loss of heterozygosity at 11p15.5) rather than DES exposure. **Analysis of Other Options:** * **Option A:** ERMS is indeed the most common soft tissue sarcoma in **infants and children** (peak incidence 0–4 years) [1]. * **Option B:** When ERMS arises in hollow, mucosal-lined structures (vagina, bladder, nasopharynx), it grows as gelatinous, polypoid masses resembling **"grape-like clusters."** This variant is specifically called **Sarcoma Botryoides** [1][2]. * **Option C:** Microscopically, the tumor cells (rhabdomyoblasts) are elongated with eccentric nuclei and eosinophilic cytoplasm. These are termed **"tadpole cells"** or **"tennis racket cells."** Cross-striations may be visible under high power [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Immunohistochemistry (IHC):** Positive for **Desmin, Myogenin, and MyoD1** (most specific markers for skeletal muscle differentiation) [2]. * **Genetics:** Unlike Alveolar Rhabdomyosarcoma (t(2;13) or t(1;13)), Embryonal RMS lacks specific translocations but often shows gains in chromosome 8 or 2. * **Site:** Most common site is the **Head and Neck** (orbit), followed by the Genitourinary tract. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1004-1005. [2] 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 49: Which type of bone disease is most likely to be associated with a defect in the mineralization of adult bone secondary to abnormalities in vitamin D metabolism?

A. Osteogenesis imperfecta
B. Osteopetrosis
C. Osteitis fibrosa cystica
D. Osteomalacia (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Osteomalacia** **Mechanism:** Osteomalacia is characterized by a **defect in the mineralization** of the organic bone matrix (osteoid) in **adults** [1]. It is most commonly caused by Vitamin D deficiency or abnormal Vitamin D metabolism [2]. Vitamin D is essential for maintaining adequate serum levels of calcium and phosphate; without it, the newly formed osteoid cannot be calcified, leading to "soft bones" that are prone to fractures and deformities. In children, this same process is known as Rickets [1]. **Analysis of Incorrect Options:** * **A. Osteogenesis Imperfecta:** This is a genetic disorder (usually autosomal dominant) caused by mutations in genes encoding **Type I collagen**. It is a defect in the *quantity or quality* of the bone matrix itself, not a mineralization defect. * **B. Osteopetrosis:** Also known as "Marble Bone Disease," this is caused by **defective osteoclast-mediated bone resorption**. This leads to overly dense, stone-like bones that are paradoxically brittle. * **C. Osteitis Fibrosa Cystica:** This is a manifestation of **Hyperparathyroidism** (von Recklinghausen disease of bone). Increased PTH leads to excessive osteoclast activity, resulting in bone resorption, marrow fibrosis, and the formation of "Brown tumors." **High-Yield NEET-PG Pearls:** * **Biochemical Profile of Osteomalacia:** Low/Normal Calcium, Low Phosphate, and **Elevated Alkaline Phosphatase (ALP)**. * **Radiological Hallmark:** **Looser’s zones** (pseudofractures) are pathognomonic for osteomalacia. * **Histology:** Characterized by an increased thickness of **unmineralized osteoid seams** [3]. * **Key Distinction:** Osteoporosis involves a decrease in *total bone mass* (matrix + mineral), whereas Osteomalacia is specifically a *mineralization* defect. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 666-667. [3] 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 50: Which of the following is the most common retroperitoneal sarcoma?

A. Liposarcoma (Correct Answer)
B. Leiomyosarcoma
C. Fibrosarcoma
D. Neural sheath sarcoma

Explanation: **Explanation:** **Liposarcoma** is the most common primary retroperitoneal sarcoma, accounting for approximately 30–50% of all retroperitoneal sarcomas [1]. These tumors often remain asymptomatic for long periods, growing to massive sizes before clinical detection. The most frequent histological subtypes found in the retroperitoneum are **well-differentiated** and **dedifferentiated** liposarcomas [1]. **Analysis of Options:** * **Option A (Liposarcoma):** Correct. It is the most common soft tissue sarcoma of the retroperitoneum [1]. It typically presents in the 5th to 7th decades of life. * **Option B (Leiomyosarcoma):** This is the second most common retroperitoneal sarcoma. It often arises from the walls of large veins (like the Inferior Vena Cava) or small vessels. * **Option C (Fibrosarcoma):** Once commonly diagnosed, it is now a rare diagnosis due to better immunohistochemical classification. It is more common in the deep tissues of the extremities. * **Option D (Neural sheath sarcoma):** Malignant Peripheral Nerve Sheath Tumors (MPNST) are rare in the retroperitoneum and are often associated with Neurofibromatosis Type 1 (NF1). **High-Yield NEET-PG Pearls:** * **Most common soft tissue sarcoma in adults (overall):** Liposarcoma (specifically the well-differentiated/atypical lipomatous tumor type). * **Most common soft tissue sarcoma in children:** Rhabdomyosarcoma. * **Cytogenetics:** Well-differentiated liposarcomas are characterized by the amplification of the **MDM2** gene on chromosome 12q15 [1]. * **Myxoid Liposarcoma:** Characterized by the **t(12;16)** translocation involving the *FUS-CHOP* genes [1]. * **Clinical Sign:** Retroperitoneal tumors often present with an increase in abdominal girth or a palpable mass rather than early pain. **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.

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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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