Basic Science in Orthopaedics Practice Questions

Q: What is the last step in fracture healing?

Remodeling. **Explanation:** Fracture healing is a continuous biological process typically divided into four distinct histological stages. The correct answer is **Remodeling**, which represents the final and longest phase of bone repair. **1. Why Remodeling is correct:** Remodeling (Phase of Modeling) begins once the fracture has been bridged by firm bone. In this stage, the bulky clinical callus is reshaped. Osteoclasts resorb unnecessary bone (external callus), while osteoblasts lay down lamellar bone along the lines of mechanical stress (**Wolff’s Law**). This process restores the bone to its original shape and restores the medullary canal. It can take months to years to complete. **2. Why other options are incorrect:** * **A. Hematoma:** This is the **first stage** (Inflammation). It occurs within hours of injury, providing a fibrin scaffold for signaling molecules and progenitor cells. * **B. Callus formation:** This occurs in the middle stages. **Soft callus** (cartilage/fibrous tissue) is formed first, followed by **Hard callus** (woven bone), which provides initial structural stability. * **C. Consolidation:** This is the stage where the woven bone of the hard callus is transformed into mature lamellar bone. While it signifies clinical union, it precedes the final structural "fine-tuning" of remodeling. **NEET-PG High-Yield Pearls:** * **Sequence of Healing:** Hematoma → Inflammation → Soft Callus → Hard Callus → Consolidation → Remodeling. * **Primary Bone Healing:** Occurs via absolute stability (e.g., compression plating). There is **no callus formation**; healing happens via "cutting cones." * **Secondary Bone Healing:** Occurs via relative stability (e.g., intramedullary nailing or casts). It involves **callus formation**. * **Wolff’s Law:** Bone grows or remodels in response to the forces or demands placed upon it.

Q: Marie and Sainton's disease is also known as:

Cleidocranial dysostosis.. **Explanation:** **Marie and Sainton’s disease** is the eponym for **Cleidocranial Dysostosis (CCD)**. It is an autosomal dominant skeletal dysplasia caused by a mutation in the **RUNX2 gene** (located on chromosome 6), which is essential for osteoblast differentiation and intramembranous ossification. **Why Cleidocranial Dysostosis is correct:** The disease primarily affects bones formed via intramembranous ossification (skull and clavicles). Key clinical features include: * **Aplasia or hypoplasia of clavicles:** Patients can often approximate their shoulders in the midline. * **Skull abnormalities:** Delayed closure of fontanelles, presence of multiple **Wormian bones**, and frontal bossing. * **Dental anomalies:** Failure of eruption of permanent teeth and the presence of multiple **supernumerary teeth**. **Why other options are incorrect:** * **Dentinogenesis imperfecta:** A genetic disorder of tooth development resulting in discolored (opalescent) and weak teeth; it is often associated with Osteogenesis Imperfecta but is not Marie and Sainton’s disease. * **Turner’s hypoplasia:** An enamel defect in permanent teeth caused by periapical infection or trauma to the preceding deciduous tooth. * **Amelogenesis imperfecta:** A group of hereditary disorders affecting enamel formation in the absence of systemic features. **High-Yield Clinical Pearls for NEET-PG:** * **Gene:** RUNX2 (CBFA1). * **Radiology:** "Hot cross bun" appearance of the skull (due to prominent sutures) and widened symphysis pubis. * **Classic Sign:** Ability to touch shoulders together anteriorly. * **Inheritance:** Autosomal Dominant (though 1/3rd are spontaneous mutations).

Q: The Trendelenburg test is primarily performed to assess the integrity of which muscle group?

Gluteus medius. ### Explanation The **Trendelenburg test** is a clinical examination used to assess the integrity of the **hip abductor mechanism**. **Why Gluteus Medius is the Correct Answer:** The primary muscle responsible for stabilizing the pelvis during the stance phase of the gait cycle is the **Gluteus medius** (assisted by the gluteus minimus and tensor fasciae latae). When a person stands on one leg, the gluteus medius on the weight-bearing side contracts to prevent the opposite (unsupported) side of the pelvis from sagging. A positive Trendelenburg sign occurs when the pelvis drops on the unsupported side, indicating weakness or paralysis of the gluteus medius on the **standing (weight-bearing) side**. **Analysis of Incorrect Options:** * **Gluteus maximus (A):** This is the primary extensor of the hip. While crucial for climbing stairs and rising from a seated position, it does not play a primary role in lateral pelvic stabilization. * **Gluteus minimus (C):** Although it is an abductor, it is significantly weaker than the gluteus medius. While it contributes to the mechanism, the test is clinically defined by the failure of the gluteus medius. * **All of the above (D):** Incorrect because the test specifically targets the abductor group, excluding the maximus. **NEET-PG High-Yield Pearls:** 1. **Nerve Supply:** The gluteus medius and minimus are supplied by the **Superior Gluteal Nerve (L4, L5, S1)**. Injury to this nerve results in a positive Trendelenburg sign. 2. **Trendelenburg Gait:** Also known as a "lurching gait." To compensate for the pelvic drop, the patient tilts their trunk *toward* the affected side to shift the center of gravity. 3. **Causes of Positive Sign:** Polio, Superior Gluteal Nerve injury, L5 radiculopathy, Congenital Dislocation of the Hip (CDH/DDH), and ununited fractures of the femoral neck.

Q: After bone fracture, primary healing will show which of these features?

The fracture line disappears very soon radiographically.. ### Explanation **Primary Bone Healing (Direct Healing)** occurs when there is absolute stability (no movement at the fracture site) and anatomical reduction. This is typically achieved through internal fixation using compression plates and screws. **Why the correct answer is right:** In primary healing, there is no formation of an external callus. Instead, "contact healing" or "gap healing" occurs via **Haversian remodeling**. Osteoclasts form "cutting cones" that cross the fracture line, followed by osteoblasts laying down new bone. Because the bone ends are compressed and the gap is bridged directly by new bone without a precursor callus, the **fracture line disappears very soon radiographically** as it is replaced by new lamellar bone. **Analysis of Incorrect Options:** * **Option A & B:** Callus molding is a feature of **Secondary Bone Healing** (indirect healing), which occurs in the presence of micromotion (e.g., casts, intramedullary nails). In primary healing, there is **no callus formation**, so there is nothing to mold or evaluate on a radiograph. * **Option D:** The fracture line *must* disappear for union to be considered complete. If the fracture line persists indefinitely, it suggests a non-union or failure of fixation. **Clinical Pearls for NEET-PG:** * **Primary Healing:** Requires **Absolute Stability**. No callus formation. Mechanism: Cutting cones/Haversian remodeling. * **Secondary Healing:** Requires **Relative Stability**. Characterized by four stages: Inflammation, Soft Callus, Hard Callus, and Remodeling. * **Gold Standard for Primary Healing:** Compression plating. * **Radiographic Sign of Primary Union:** Gradual disappearance of the fracture line without external callus.

Q: Following nerve injury, at what rate does the injured nerve regenerate?

0.1 cm/day. **Explanation:** The correct answer is **0.1 cm/day (Option B)**. Following a peripheral nerve injury (specifically Seddon’s Axonotmesis or Sunderland’s Grade II-IV), the distal segment undergoes **Wallerian degeneration**. Once the debris is cleared, the proximal axon begins to sprout and regenerate along the preserved endoneurial tubes. In clinical practice, the standard accepted rate of axonal regeneration is approximately **1 mm per day**. Converting this to centimeters: * 1 mm = 0.1 cm * Therefore, the rate is **0.1 cm/day**. **Analysis of Incorrect Options:** * **Option A (0.001 cm/day):** This equals 0.01 mm/day, which is far too slow to be clinically significant. * **Option C (1 cm/day):** This equals 10 mm/day. This is an overestimation; while regeneration can occasionally reach 2-3 mm/day in proximal segments, 10 mm/day is physiologically impossible for human nerves. * **Option D (0.0001 cm/day):** This is an infinitesimal rate (0.001 mm/day) and does not represent biological growth. **High-Yield Clinical Pearls for NEET-PG:** 1. **Tinel’s Sign:** This is used to track regeneration. A positive Tinel’s sign (tingling on percussion) at a site distal to the injury indicates the presence of regenerating axonal sprouts. 2. **Order of Recovery:** Nerve recovery typically follows a specific sequence: **Sympathetic function → Pain → Temperature → Touch → Proprioception → Motor function.** 3. **Hoffmann-Tinel Sign:** If the distal point of tingling advances by roughly 1 mm/day, it indicates successful progression of regeneration. 4. **Factors:** Regeneration is faster in children and in proximal injuries compared to distal ones.

Q: All are true regarding bone remodeling, EXCEPT:

It involves the replacement of lamellar bone by woven bone.. **Explanation:** Bone remodeling is a lifelong physiological process where mature bone tissue is removed (resorption) and new bone tissue is formed (ossification). **1. Why Option A is the Correct Answer (The Exception):** In bone remodeling, the goal is to maintain structural integrity. Therefore, **woven bone (immature, disorganized bone) is replaced by lamellar bone (mature, organized bone)**, not the other way around. Woven bone is typically seen during rapid growth, initial fracture healing (callus), or pathological states (e.g., Paget’s disease). Remodeling converts this weak woven bone into strong, load-bearing lamellar bone. **2. Analysis of Other Options:** * **Option B:** Resorption is the first stage of the remodeling cycle (ARF: Activation-Resorption-Formation). This is carried out by **osteoclasts**, which create Howship’s lacunae. * **Option C:** Both cortical and cancellous bones undergo remodeling via **Basic Multicellular Units (BMUs)**, which consist of a coordinated team of osteoclasts (cutting cone in cortical bone) and osteoblasts (closing cone). * **Option D:** Once osteoblasts finish secreting the bone matrix (osteoid), some become trapped within the matrix and differentiate into **osteocytes**, which act as mechanosensors. **High-Yield NEET-PG Pearls:** * **Woven Bone:** Characterized by random collagen arrangement; it is always pathological in adults except during fracture healing. * **Lamellar Bone:** Characterized by parallel collagen layers; it is the hallmark of healthy mature bone. * **Wolff’s Law:** Bone remodels in response to the mechanical stresses placed upon it. * **RANKL/OPG Pathway:** The primary regulator of osteoclast differentiation and activity during remodeling.

Q: Which of the following is NOT a cause of pathological fractures?

Anemia. **Explanation:** A **pathological fracture** is defined as a fracture occurring through a bone weakened by a pre-existing disease, often resulting from trivial trauma or normal physiological stress. **Why Anemia is the Correct Answer:** Anemia is a hematological condition characterized by a decrease in red blood cells or hemoglobin. While certain chronic anemias (like Thalassemia or Sickle Cell Disease) can lead to compensatory bone marrow hyperplasia and secondary osteoporosis, **anemia itself is not a direct cause of bone weakening** that leads to pathological fractures. It affects the blood's oxygen-carrying capacity, not the structural integrity of the bone matrix. **Analysis of Incorrect Options:** * **Radiation Therapy:** High-dose radiation causes endarteritis obliterans, reducing the blood supply to the bone (osteoradionecrosis). This leads to cell death and a brittle matrix, making it a classic cause of pathological fractures. * **Osteoporosis:** This is the most common cause of pathological fractures worldwide. It involves a decrease in both bone mass and density, leading to micro-architectural deterioration (common in vertebral bodies and the femoral neck). * **Osteomalacia:** This is a qualitative defect in bone mineralization (soft bones) due to Vitamin D deficiency. The unmineralized osteoid is weak, leading to Looser’s zones (pseudofractures) and true pathological fractures. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of pathological fracture:** Osteoporosis. * **Most common site for pathological fracture:** Vertebral bodies (compression fractures). * **Most common benign bone tumor causing fracture:** Unicameral Bone Cyst (UBC), often showing the "Fallen Leaf Sign" on X-ray. * **Most common malignancy causing pathological fracture:** Metastatic bone disease (Breast cancer in females, Prostate cancer in males).

Q: A 20-year-old man was diagnosed with myositis ossificans progressiva. He died five years later. What was the most probable cause of his death?

Starvation and chest infection. **Explanation:** **Myositis Ossificans Progressiva (MOP)**, also known as **Fibrodysplasia Ossificans Progressiva (FOP)**, is a rare genetic connective tissue disorder characterized by the progressive replacement of muscles, tendons, and ligaments by mature bone (heterotopic ossification). **Why Option A is correct:** The cause of death in MOP is typically related to the anatomical sites of ossification: 1. **Starvation:** Ossification of the **masseter and temporomandibular joints** leads to "jaw locking" (ankylosis). This makes mastication impossible, leading to severe malnutrition and starvation. 2. **Chest Infection:** Ossification of the **intercostal muscles and paraspinal ligaments** creates a "stone man" effect, severely restricting chest wall expansion. This results in **Thoracic Insufficiency Syndrome**, leading to restrictive lung disease, poor cough reflex, and recurrent, ultimately fatal, bronchopneumonia. **Why the other options are incorrect:** * **B. Myocarditis:** MOP specifically spares smooth muscles and cardiac muscle. The heart is not involved in the ossification process. * **C & D. Hypercalcemia/Hyperphosphatemia:** While MOP involves abnormal bone formation, it is a disorder of tissue induction (ACVR1 gene mutation), not a primary metabolic bone disease. Serum calcium and phosphate levels are typically **normal**. **Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant (Mutation in **ACVR1/ALK2 gene**). * **Pathognomonic Sign:** Congenital **short/deviated great toe** (hallux valgus) or thumb. * **Progression:** Follows a cranio-caudal and dorso-ventral pattern (starts at the neck/shoulders and moves down). * **Management Caution:** Avoid biopsies or intramuscular injections, as trauma triggers "flare-ups" and rapid new bone formation.

Question 1

What is the last step in fracture healing?

Accepted Answer

Remodeling

Answer

Hematoma

Answer

Callus formation

Answer

Consolidation

Question 2

Marie and Sainton's disease is also known as:

Accepted Answer

Cleidocranial dysostosis.

Answer

Dentinogenesis imperfecta.

Answer

Turners hypoplasia.

Answer

Amelogenesia imperfecta.

Question 3

The Trendelenburg test is primarily performed to assess the integrity of which muscle group?

Accepted Answer

Gluteus medius

Answer

Gluteus maximus

Answer

Gluteus minimus

Answer

All of the above

Question 4

Wolff's law states that:

Accepted Answer

If a bone is continuously subjected to a particular stress, it will adapt to become stronger to resist that loading.

Answer

Only the diaphysis allows longitudinal growth in childhood.

Answer

Any infection not showing periosteal reaction within 1 week of symptoms can be ruled out to be osteomyelitis.

Answer

Angular deformities will progress until the closure of the physis.

Question 5

After bone fracture, primary healing will show which of these features?

Accepted Answer

The fracture line disappears very soon radiographically.

Answer

Callus molding can be evaluated on the radiograph.

Answer

Cannot be seen.

Answer

The fracture line does not disappear.

Question 6

What is the difference between neuropraxia and axonotmesis?

Accepted Answer

Electromyography (EMG) finding

Answer

Sensory loss

Answer

Motor loss

Answer

All of the above

Question 7

Following nerve injury, at what rate does the injured nerve regenerate?

Accepted Answer

0.1 cm/day

Answer

0.001 cm/day

Answer

1 cm/day

Answer

0.0001 cm/day

Question 8

All are true regarding bone remodeling, EXCEPT:

Accepted Answer

It involves the replacement of lamellar bone by woven bone.

Answer

Osteoclastic activity at the resorption site.

Answer

Osteoclastic activity and osteoblastic activity are both needed for bone remodeling in cortical and cancellous bones.

Answer

Osteoblasts transform into osteocytes.

Question 9

Which of the following is NOT a cause of pathological fractures?

Accepted Answer

Anemia

Answer

Radiation therapy

Answer

Osteoporosis

Answer

Osteomalacia

Question 10

A 20-year-old man was diagnosed with myositis ossificans progressiva. He died five years later. What was the most probable cause of his death?

Accepted Answer

Starvation and chest infection

Answer

Myocarditis

Answer

Hypercalcemia

Answer

Hyperphosphatemia

Basic Science in Orthopaedics — MCQs

Basic Science in Orthopaedics — MCQs

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