Bone and Soft Tissue Pathology — MCQs

A 60-year-old man, treated for lung cancer, presents with a rash on his chest and pain in his upper arms and calves. He has difficulty raising his arms and climbing stairs. Muscle biopsy reveals perivascular infiltrates of lymphocytes and plasma cells extending between muscle fibers. Immunofluorescence shows immune complexes in the walls of intramuscular blood vessels. What is the most likely diagnosis?

Q105Easy

The term 'ragged red fibers' is applied to describe the skeletal muscle fibers in which of the following conditions?

Q106Easy

What is the commonest site for glomangioma?

Q107Easy

Osteogenic metastases is characteristic of which of the following?

Q108Easy

Which tumor is not seen in the anterior mediastinum?

Q109Easy

Which type of osteogenesis imperfecta is characterized by normal dentition and sclera?

Q110Medium

Synovial fluids of normal joints are usually devoid of collagen. Patients with rheumatoid diseases have various types of collagen in their synovial fluid, depending on the tissue being damaged. If a patient has type II collagen in their synovial fluid, which of the following tissues is being eroded?

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

Question 101: What is the characteristic finding in muscular dystrophy?

A. Inflammatory cell infiltrate
B. Heterogenicity of fiber size
C. Nuclear proliferation beneath sarcolemma
D. Muscle necrosis (Correct Answer)

Explanation: **Explanation:** Muscular dystrophies (such as Duchenne and Becker) are genetic disorders characterized by progressive muscle weakness and wasting. The fundamental pathological hallmark of muscular dystrophy is **muscle fiber necrosis** followed by regeneration and eventual replacement of muscle by fibrofatty tissue [4]. * **Why Muscle Necrosis is correct:** In Duchenne Muscular Dystrophy (DMD), the absence of the protein **dystrophin** destabilizes the sarcolemma during muscle contraction. This leads to membrane tears, an influx of extracellular calcium, and subsequent activation of intracellular enzymes that cause **segmental myofiber necrosis** [1]. This ongoing cycle of damage is the primary driver of the disease. **Analysis of Incorrect Options:** * **A. Inflammatory cell infiltrate:** While some macrophages appear to clear necrotic debris, a prominent inflammatory infiltrate is the hallmark of **Inflammatory Myopathies** (e.g., Polymyositis or Dermatomyositis), not muscular dystrophy [2]. * **B. Heterogenicity of fiber size:** While variation in fiber size occurs as the disease progresses, it is a non-specific finding seen in many chronic myopathic and neurogenic conditions. * **C. Nuclear proliferation beneath sarcolemma:** This refers to an increase in sarcolemmal nuclei, often seen in regenerative phases or certain myotonic dystrophies (where central nuclei are common) [3], but it is not the defining characteristic compared to necrosis. **High-Yield NEET-PG Pearls:** * **DMD Inheritance:** X-linked recessive; caused by a **deletion** of the dystrophin gene (the largest known human gene) [4]. * **Histology:** Look for "variation in fiber size," "internalized nuclei," and the pathognomonic **replacement of muscle by fat and collagen** (Pseudohypertrophy). * **Biomarker:** Serum **Creatine Kinase (CK)** is massively elevated from birth, even before clinical symptoms appear [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1239-1240. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1241-1242. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 732-733. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245.

Question 102: Which of the following genes is responsible for Fibrous dysplasia?

A. GNAS1 (Correct Answer)
B. GNAS2
C. GNAS3
D. GNAS4

Explanation: ### Explanation **Correct Answer: A. GNAS1** **Mechanism and Pathophysiology:** Fibrous dysplasia is a non-neoplastic bone lesion where normal bone is replaced by fibrous tissue and haphazardly arranged bony trabeculae. The underlying molecular defect is a **somatic gain-of-function mutation** in the **GNAS1 gene** (located on chromosome 20q13) [1]. This gene encodes the **alpha subunit of the stimulatory G-protein (Gśα)**. The mutation leads to constitutive activation of adenylate cyclase, resulting in an intracellular overproduction of **cyclic AMP (cAMP)** [1]. In bone-forming cells, elevated cAMP promotes excessive proliferation and prevents the maturation of osteoblasts, leading to the formation of immature "woven" bone embedded in a cellular fibrous stroma. **Analysis of Incorrect Options:** * **GNAS2, GNAS3, and GNAS4:** These are not recognized genes associated with human skeletal pathology. The GNAS complex is highly imprinted and produces multiple transcripts, but the specific mutation linked to Fibrous Dysplasia and McCune-Albright syndrome is consistently identified in the **GNAS1** locus. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Characterized by the **"Chinese letter" pattern** (curved, irregular trabeculae of woven bone) without osteoblastic rimming. * **Clinical Variants:** 1. **Monostotic:** Involves a single bone (most common). 2. **Polyostotic:** Involves multiple bones. 3. **McCune-Albright Syndrome:** Triad of Polyostotic fibrous dysplasia, **Café-au-lait spots** (Coast of Maine borders), and **Precocious puberty** (Endocrinopathies) [1]. 4. **Mazabraud Syndrome:** Polyostotic fibrous dysplasia associated with soft tissue myxomas. * **Radiology:** Classic **"Ground-glass appearance"** on X-ray. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1126-1127.

Question 103: Which of the following is FALSE regarding cystic fibrosis?

A. Associated with the CFTR gene
B. Autosomal recessive inheritance
C. Associated with chromosome 7p (Correct Answer)
D. Recurrent respiratory tract infection

Explanation: **Explanation:** Cystic Fibrosis (CF) is the most common lethal genetic disease in Caucasian populations. The correct answer is **Option C** because the **CFTR gene** is located on the **long arm of chromosome 7 (7q31.2)**, not the short arm (7p). In genetics, 'p' stands for *petit* (short arm) and 'q' stands for the long arm. **Analysis of Options:** * **Option A (True):** CF is caused by mutations in the **Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)** gene, which encodes a cAMP-regulated chloride channel [1]. * **Option B (True):** It follows an **Autosomal Recessive** inheritance pattern. Parents are typically asymptomatic carriers. * **Option D (True):** Defective chloride transport leads to abnormally thick, viscid mucus [1]. This impairs mucociliary clearance, leading to **recurrent respiratory infections**, bronchiectasis, and colonization by pathogens like *Pseudomonas aeruginosa* [1]. **NEET-PG High-Yield Pearls:** * **Most Common Mutation:** **ΔF508** (a three-base pair deletion of phenylalanine at position 508), which leads to protein misfolding and degradation in the ER (Class II defect) [1]. * **Diagnosis:** Sweat Chloride Test (Gold Standard) showing chloride levels **>60 mEq/L** [1]. * **Clinical Triad:** Chronic sinopulmonary disease, pancreatic insufficiency (steatorrhea), and male infertility (bilateral absence of vas deferens - CBAVD) [1]. * **Meconium Ileus:** A classic neonatal presentation of CF. * **Nasal Polyps:** CF should be suspected in any child presenting with nasal polyposis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 475-479.

Question 104: A 60-year-old man, treated for lung cancer, presents with a rash on his chest and pain in his upper arms and calves. He has difficulty raising his arms and climbing stairs. Muscle biopsy reveals perivascular infiltrates of lymphocytes and plasma cells extending between muscle fibers. Immunofluorescence shows immune complexes in the walls of intramuscular blood vessels. What is the most likely diagnosis?

A. Becker muscular dystrophy
B. Dermatomyositis (Correct Answer)
C. Lambert-Eaton myasthenic syndrome
D. Myasthenia gravis

Explanation: ### Explanation **Correct Answer: B. Dermatomyositis** The clinical presentation and histopathology point directly to **Dermatomyositis**, an inflammatory myopathy characterized by proximal muscle weakness and cutaneous manifestations [1]. * **Clinical Clues:** The patient has symmetric proximal muscle weakness (difficulty climbing stairs/raising arms) and a rash. Crucially, in an older patient, dermatomyositis is frequently a **paraneoplastic syndrome**, most commonly associated with lung, GI, or ovarian cancers [1]. * **Pathogenesis & Histology:** Unlike Polymyositis (which is T-cell mediated) [2], Dermatomyositis is an **antibody-mediated (humoral)** disease. The primary target is the **endomysial capillaries**. Deposition of immune complexes (C5b-9 complement membrane attack complex) in the vessel walls leads to microangiopathy, perivascular inflammation, and **perifascicular atrophy** (a pathognomonic finding) [1]. **Why the other options are incorrect:** * **Becker Muscular Dystrophy:** A genetic X-linked disorder typically presenting in childhood/adolescence with a deficiency of dystrophin; it does not present with rashes or inflammatory infiltrates. * **Lambert-Eaton Myasthenic Syndrome (LEMS):** While also a paraneoplastic syndrome (Small Cell Lung Cancer), it is a presynaptic neuromuscular junction disorder. It causes weakness that *improves* with use and lacks the inflammatory muscle biopsy findings described. * **Myasthenia Gravis:** An autoimmune disorder of postsynaptic ACh receptors. It typically presents with ptosis, diplopia, and fatigable weakness, not perivascular muscle inflammation. **High-Yield NEET-PG Pearls:** * **Skin signs:** Heliotrope rash (periorbital) and Gottron papules (over knuckles) [1]. * **Antibodies:** **Anti-Mi-2** (highly specific), **Anti-Jo-1** (associated with interstitial lung disease/mechanic's hands) [1]. * **Biopsy Gold Standard:** Dermatomyositis = **Perifascicular atrophy**; Polymyositis = **Endomysial inflammation** (CD8+ T-cells) [1], [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1240-1241. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1241-1242.

Question 105: The term 'ragged red fibers' is applied to describe the skeletal muscle fibers in which of the following conditions?

A. Myotonic dystrophy
B. Nemaline myopathy
C. Spinal muscular atrophy
D. Mitochondrial myopathy (Correct Answer)

Explanation: **Explanation:** **Mitochondrial Myopathy (Correct Answer)** The term **'Ragged Red Fibers' (RRF)** is a hallmark histological finding in mitochondrial myopathies (e.g., MERRF, MELAS) [1]. These fibers represent a compensatory proliferation of abnormal mitochondria in the subsarcolemmal and intermyofibrillar spaces of skeletal muscle. On **Gomori Trichrome stain**, these mitochondrial aggregates appear as irregular, reddish-purple granular deposits at the periphery of the muscle fiber, giving it a "ragged" appearance. **Analysis of Incorrect Options:** * **Myotonic Dystrophy:** Characterized by **ring fibers**, sarcoplasmic masses, and an increase in internal nuclei. It is an autosomal dominant disorder caused by CTG repeat expansions. * **Nemaline Myopathy:** Defined by the presence of **'Nemaline rods'** (Z-band material) within the sarcoplasm, visible on Gomori Trichrome stain as small blue-dark purple rods. * **Spinal Muscular Atrophy (SMA):** A neurogenic atrophy characterized by **groups of small, rounded atrophic fibers** (group atrophy) interspersed with hypertrophied fibers, resulting from the loss of lower motor neurons in the anterior horn of the spinal cord. **High-Yield Pearls for NEET-PG:** * **Stain of Choice:** Modified Gomori Trichrome is essential to visualize RRFs. * **Biochemical marker:** These fibers are often **SDH (Succinate Dehydrogenase) positive** (as SDH is nuclear-encoded) but **COX (Cytochrome c Oxidase) negative** (if the mutation affects mtDNA-encoded COX subunits). * **Clinical Triad:** Mitochondrial diseases often present with the triad of ophthalmoplegia, proximal muscle weakness, and lactic acidosis. * **MERRF:** Myoclonic Epilepsy with Ragged Red Fibers is the classic syndrome associated with this finding [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1305-1306.

Question 106: What is the commonest site for glomangioma?

A. Head and neck
B. Chest wall
C. Nail bed (Correct Answer)
D. Retroperitoneal

Explanation: **Explanation:** **Glomus tumor (Glomangioma)** is a benign, exquisitely painful vascular neoplasm arising from the modified smooth muscle cells of the **glomus body** [1]. The glomus body is a specialized arteriovenous anastomosis involved in thermoregulation. 1. **Why the Nail Bed is Correct:** Glomus bodies are found in highest concentration in the dermis of the distal portions of the fingers and toes. Therefore, the **subungual region (nail bed)** is the most characteristic and commonest site for these tumors. They typically present as a small, firm, red-blue nodule under the nail. 2. **Why Other Options are Incorrect:** * **Head and Neck / Chest Wall:** While glomus tumors can occur anywhere in the skin or soft tissues, these are not the primary or most frequent locations. * **Retroperitoneal:** This is an extremely rare site. Deep-seated glomus tumors are uncommon and usually occur in the gastrointestinal tract (specifically the stomach) rather than the retroperitoneum. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Paroxysmal pain, localized point tenderness, and sensitivity to cold. * **Hildreth’s Sign:** Relief of pain upon application of a tourniquet (positive in glomus tumors). * **Histology:** Nests of uniform, round "glomus cells" with "punched-out" nuclei surrounding thin-walled vascular vascular spaces. * **Immunohistochemistry (IHC):** Glomus cells are positive for **Alpha-Smooth Muscle Actin (α-SMA)** and Type IV Collagen (pericellular staining), but negative for endothelial markers like CD31 (which stain the vessels, not the tumor cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 523-524.

Question 107: Osteogenic metastases is characteristic of which of the following?

A. Prostate carcinoma (Correct Answer)
B. Colon carcinoma
C. Thyroid carcinoma
D. Breast carcinoma

Explanation: **Explanation:** Bone metastases are broadly categorized into **osteolytic** (bone-destroying) and **osteoblastic/osteogenic** (bone-forming) lesions. **1. Why Prostate Carcinoma is Correct:** Prostate carcinoma is the classic and most common cause of **osteoblastic (osteogenic) metastases** in males [1]. The tumor cells secrete factors like Bone Morphogenetic Proteins (BMPs) and Endothelin-1, which stimulate osteoblast activity, leading to increased bone density (sclerotic lesions) on X-ray [1]. **2. Analysis of Incorrect Options:** * **Colon Carcinoma:** Typically presents with osteolytic lesions, though bone metastasis from the GI tract is relatively uncommon compared to other sites. * **Thyroid Carcinoma:** Characteristically produces **purely osteolytic** lesions. Follicular thyroid carcinoma is notorious for "blow-out" expansile lytic metastases [2]. * **Breast Carcinoma:** This is a **mixed** lesion [2]. While it is the most common cause of bone metastasis in females, it typically presents with a combination of both osteolytic and osteoblastic features (though lytic usually predominates). **High-Yield Clinical Pearls for NEET-PG:** * **Purely Osteoblastic:** Prostate cancer, Carcinoid tumor, Small cell lung cancer (rarely). * **Purely Osteolytic:** Multiple Myeloma (classic "punched-out" lesions), Thyroid cancer, Renal Cell Carcinoma (RCC), Melanoma. * **Mixed Lesions:** Breast cancer, Lung cancer. * **Most common site for bone metastasis:** Spine (Vertebral column) via the Batson venous plexus. * **Imaging Gold Standard:** Radionuclide bone scan (Technetium-99m) is highly sensitive for osteoblastic activity, whereas X-rays are better for detecting lytic destruction. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 501-502. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672.

Question 108: Which tumor is not seen in the anterior mediastinum?

A. Teratoma
B. Thymic tumors
C. Thyroid tumors
D. Neurofibroma (Correct Answer)

Explanation: The mediastinum is anatomically divided into compartments, each associated with specific pathologies. This question tests the knowledge of the **"4 Ts" of the anterior mediastinum.** ### **Why Neurofibroma is the Correct Answer** **Neurofibroma** is a nerve sheath tumor. In the mediastinum, neurogenic tumors (including neurofibromas, schwannomas, and ganglioneuromas) are almost exclusively located in the **posterior mediastinum**, arising from the paravertebral sympathetic chain or intercostal nerves [2]. They are the most common cause of a posterior mediastinal mass [4]. ### **Analysis of Incorrect Options (Anterior Mediastinal Masses)** The anterior mediastinum is the space between the sternum and the pericardium. The differential diagnosis is dominated by the **"4 Ts"**: * **Thymic tumors (Option B):** Includes thymomas (most common), thymic carcinoma, and thymic hyperplasia [1]. * **Teratoma (Option A):** And other Germ Cell Tumors (GCTs) like seminomas [1]. * **Thyroid tumors (Option C):** Specifically, retrosternal or ectopic thyroid goiters. * **"Terrible" Lymphoma:** Often presenting as a bulky anterior mass [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **Most common anterior mediastinal mass:** Thymoma (often associated with Myasthenia Gravis) [3]. * **Most common posterior mediastinal mass:** Neurogenic tumors (like Neurofibroma). * **Middle Mediastinum:** Characterized by lymphadenopathy (Sarcoidosis, TB, Metastasis) and bronchogenic cysts. * **Imaging:** Contrast-Enhanced CT (CECT) is the gold standard for localizing and characterizing these masses. * **Biochemical Markers:** In anterior GCTs, check **AFP** (Yolk sac tumor) and **β-hCG** (Choriocarcinoma). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 571-572. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1250. [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, p. 634. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1250-1251.

Question 109: Which type of osteogenesis imperfecta is characterized by normal dentition and sclera?

A. Type 1A (Correct Answer)
B. Type 2
C. Type 3
D. Type 4B

Explanation: **Explanation:** Osteogenesis Imperfecta (OI), or "Brittle Bone Disease," is a heterogeneous group of genetic disorders caused by mutations in the genes encoding **Type 1 Collagen** (*COL1A1* and *COL1A2*). **Why Type 1A is correct:** The Sillence Classification categorizes OI into four primary types. **Type 1** is the most common and mildest form. It is further subdivided based on the presence of **Dentinogenesis Imperfecta (DI)**: * **Type 1A:** Characterized by **normal teeth** (absence of DI) and blue sclera. While the question mentions "normal sclera," in the context of competitive exams like NEET-PG, Type 1A is specifically distinguished by its **normal dentition**, whereas other types frequently involve dental defects. (Note: Sclera may lighten to a near-normal hue in adulthood in Type 1) [1]. **Analysis of Incorrect Options:** * **Type 2:** This is the **perinatal lethal** form. It is characterized by extreme bone fragility, multiple intrauterine fractures, and crumpled long bones (accordion-like) on X-ray [2]. It is incompatible with life. * **Type 3:** The most severe **non-lethal** form. It causes progressive deformity, short stature, and nearly always presents with **blue sclera and dentinogenesis imperfecta**. * **Type 4B:** Type 4 is characterized by **normal (white) sclera** but is subdivided by dental involvement. **Type 4B specifically includes Dentinogenesis Imperfecta**, whereas Type 4A has normal teeth. **NEET-PG High-Yield Pearls:** * **Blue Sclera:** Caused by translucency of the thin scleral collagen, allowing the underlying choroidal veins to show through [1]. * **Hearing Loss:** Common in Type 1 due to otosclerosis (fixation of stapes). * **Wormian Bones:** Small, irregular bones found within the cranial sutures, frequently seen on X-rays of OI patients. * **Molecular Defect:** Type 1 is usually a **quantitative** defect (decreased synthesis), while Types 2-4 are **qualitative** defects (abnormal structure). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1188.

Question 110: Synovial fluids of normal joints are usually devoid of collagen. Patients with rheumatoid diseases have various types of collagen in their synovial fluid, depending on the tissue being damaged. If a patient has type II collagen in their synovial fluid, which of the following tissues is being eroded?

A. Vascular Endothelium
B. Compact Bone
C. Vascular Smooth Muscle
D. Articular Cartilage (Correct Answer)

Explanation: The presence of specific collagen types in synovial fluid serves as a biochemical marker for the specific joint structures undergoing degradation. **Why Articular Cartilage is correct:** Articular (hyaline) cartilage is unique because its extracellular matrix is primarily composed of **Type II collagen** (approximately 90-95%) [1]. In rheumatoid arthritis or osteoarthritis, the enzymatic degradation of the cartilage matrix by matrix metalloproteinases (MMPs) releases these Type II collagen fibers into the synovial fluid [2]. Therefore, detecting Type II collagen is a pathognomonic sign of **articular cartilage erosion**. **Analysis of Incorrect Options:** * **Vascular Endothelium (A):** The vascular basement membrane is primarily composed of **Type IV collagen**. * **Compact Bone (B):** Bone matrix consists almost exclusively of **Type I collagen**. While bone erosion occurs in advanced rheumatoid disease, it would manifest as Type I collagen in the fluid. * **Vascular Smooth Muscle (C):** Smooth muscle cells are surrounded by a reticular network consisting mainly of **Type III collagen**. **NEET-PG High-Yield Pearls:** To excel in collagen-related questions, remember the "Mnemonic of Numbers": * **Type I:** **B**one, **O**ne (Skin, Tendon, late wound healing/scar). * **Type II:** **C**artilage, **T**wo (Hyaline and elastic cartilage, Vitreous humor). * **Type III:** **R**eticular fibers (Blood vessels, fetal skin, early wound healing/granulation tissue). * **Type IV:** **F**loor (Basement membrane, Lens). * **Alport Syndrome:** Genetic defect in Type IV collagen (Targeting the "floor" of the glomerulus and cochlea). * **Osteogenesis Imperfecta:** Defect in Type I collagen. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.

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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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