Menu

Biology, Genetics & Bone Healing MCQs

Practice Set 116 of 212

This practice set contains high-yield board review questions covering key concepts in Biology, Genetics & Bone Healing. Each clinical scenario is designed to test your diagnostic and management skills relevant to this subspecialty.

Question 2301

Topic: Biology, Genetics & Bone Healing
A 68-year-old male with osteoporosis is started on a novel therapeutic agent that targets the Wnt signaling pathway. This agent specifically acts as an anti-sclerostin antibody. Which of the following is the primary mechanism by which anti-sclerostin therapy increases bone formation?
. Inhibition of osteoclast differentiation and activity.
. Direct stimulation of osteoblast proliferation and collagen synthesis.
. Prevention of RANKL binding to RANK on osteoclast precursors.
. Disinhibition of the Wnt/β-catenin pathway, leading to increased osteoblastogenesis.
. Activation of parathyroid hormone receptors on osteocytes.

Correct Answer & Explanation

. Disinhibition of the Wnt/β-catenin pathway, leading to increased osteoblastogenesis.

Explanation

Sclerostin, secreted primarily by osteocytes, acts as an inhibitor of the Wnt/β-catenin signaling pathway. The Wnt pathway is crucial for osteoblast differentiation, proliferation, and bone formation. By binding to LRP5/6 co-receptors, sclerostin prevents Wnt ligands from activating the pathway, thereby suppressing bone formation. An anti-sclerostin antibody neutralizes sclerostin, thus disinhibiting the Wnt/β-catenin pathway. This leads to increased osteoblastogenesis, enhanced osteoblast function, and ultimately, increased bone formation. Options A and C relate to osteoclast inhibition, which is not the primary mechanism of sclerostin's action. Option B describes a direct stimulatory effect, but anti-sclerostin works by removing an inhibitory signal. Option E is related to PTH action, a different mechanism.

Question 2302

Topic: Biology, Genetics & Bone Healing

Osteocytes, embedded within the bone matrix, are critical mechanosensors. Which cellular organelle is thought to play a pivotal role in detecting mechanical strain and initiating downstream signaling pathways in osteocytes?

. Mitochondrion
. Endoplasmic Reticulum
. Primary Cilium
. Golgi Apparatus
. Lysosome

Correct Answer & Explanation

. Primary Cilium

Explanation

The primary cilium, a non-motile, solitary organelle found on the surface of most eukaryotic cells, including osteocytes, is increasingly recognized as a key mechanosensory structure. It acts as an antenna, sensing changes in fluid flow and mechanical strain within the lacunar-canalicular network. Upon mechanical stimulation, the primary cilium initiates intracellular signaling cascades, influencing osteocyte function, bone remodeling, and adaptation. The other organelles listed have different primary functions within the cell (energy production, protein synthesis/folding, packaging, waste degradation).

Question 2303

Topic: Biology, Genetics & Bone Healing

The Basic Multicellular Unit (BMU) is the fundamental operational unit of bone remodeling. Which cell type initiates the remodeling cycle by sensing microdamage or changes in mechanical load, and signals other cells to begin resorption?

. Osteoblast
. Osteoclast
. Osteocyte
. Mesenchymal Stem Cell
. Adipocyte

Correct Answer & Explanation

. Osteocyte

Explanation

Osteocytes, embedded within the bone matrix and interconnected by canaliculi, are recognized as the primary mechanosensory cells of bone. They sense microdamage, fatigue, and changes in mechanical loading. Upon sensing these signals, osteocytes undergo apoptosis or send signals (e.g., sclerostin, RANKL) to recruit and activate osteoclasts, thereby initiating the bone remodeling cycle by targeting specific areas for resorption. Osteoblasts are responsible for bone formation. Osteoclasts resorb bone. Mesenchymal stem cells are precursors. Adipocytes are fat cells, though bone marrow contains adipocytes.

Question 2304

Topic: Biology, Genetics & Bone Healing

Chronic tendinopathy, unlike acute tendonitis, is characterized by a degenerative process rather than a purely inflammatory one. Which of the following is a hallmark pathological finding in chronic tendinopathy at the cellular and molecular level?

. Abundant acute inflammatory cells (neutrophils and macrophages).
. Normal collagen fiber organization with increased tenocyte proliferation.
. Disorganized collagen fibers, increased ground substance, and focal neovascularization.
. Calcification within the tendon matrix due to increased osteoblast activity.
. Complete absence of fibroblasts and cellularity.

Correct Answer & Explanation

. Disorganized collagen fibers, increased ground substance, and focal neovascularization.

Explanation

Chronic tendinopathy is histologically characterized by a degenerative process, often referred to as 'tendinosis,' rather than an acute inflammatory response. Key pathological findings include disorganized and poorly aligned collagen fibers, an increase in the amount of ground substance (proteoglycans), increased cellularity with rounded tenocytes (often referred to as angiofibroblastic hyperplasia), and focal neovascularization (ingrowth of small blood vessels and nerves). Acute inflammatory cells are generally absent or sparse. Option B describes normal collagen, which is incorrect. Option D describes calcific tendinopathy, a specific subtype. Option E is incorrect as there is often increased cellularity.

Question 2305

Topic: Biology, Genetics & Bone Healing

Autologous bone graft is considered the gold standard for many reconstructive procedures due to its osteoinductive, osteoconductive, and osteogenic properties. Which component of autologous cancellous bone graft is primarily responsible for its osteoinductive capability?

. Cortical bone fragments acting as a scaffold.
. The mineralized hydroxyapatite matrix.
. Living osteocytes providing mechanical integrity.
. Bone morphogenetic proteins (BMPs) and other growth factors.
. Red bone marrow providing hematopoietic stem cells.

Correct Answer & Explanation

. Bone morphogenetic proteins (BMPs) and other growth factors.

Explanation

Osteoinduction refers to the ability of a material to induce the differentiation of undifferentiated mesenchymal stem cells into osteoblasts, leading to new bone formation. In autologous bone graft, this property is primarily attributed to growth factors, particularly Bone Morphogenetic Proteins (BMPs), which are embedded within the demineralized bone matrix or present in the progenitor cells. BMPs are powerful osteoinductive agents. The mineralized matrix provides osteoconduction (a scaffold), living cells provide osteogenesis (actual bone-forming cells), and red marrow contributes hematopoietic cells, but the inductive signal comes from growth factors like BMPs.

Question 2306

Topic: Biology, Genetics & Bone Healing

Osseointegration, the direct structural and functional connection between ordered, living bone and the surface of a load-bearing implant, involves specific proteins mediating the bone-implant interface. Which two non-collagenous proteins are critical early mediators for osteoblast attachment and subsequent mineralization on titanium implant surfaces?

. Collagen Type I and Type II
. Elastin and Fibrillin
. Osteopontin and Bone Sialoprotein
. Aggrecan and Decorin
. Tenascin-C and Fibronectin

Correct Answer & Explanation

. Osteopontin and Bone Sialoprotein

Explanation

Osteopontin (OPN) and Bone Sialoprotein (BSP) are highly phosphorylated, acidic non-collagenous proteins that are abundantly expressed by osteoblasts and are crucial for mediating cell-matrix interactions and mineralization during bone formation and osseointegration. They act as 'glue' molecules, promoting initial osteoblast adhesion to implant surfaces (often via integrins) and playing a key role in the nucleation and growth of hydroxyapatite crystals, thus facilitating the direct apposition of new bone onto the implant. Collagen is a structural protein. Elastin and Fibrillin are extracellular matrix proteins involved in elasticity. Aggrecan and Decorin are proteoglycans of cartilage and connective tissue. Tenascin-C and Fibronectin are ECM proteins involved in cell adhesion and migration but less specific to direct bone-implant mineralization compared to OPN/BSP.

Question 2307

Topic: Biology, Genetics & Bone Healing

Mutations in the LRP5 gene (low-density lipoprotein receptor-related protein 5) can lead to varied bone phenotypes. Which of the following conditions is associated with a gain-of-function mutation in LRP5, leading to abnormally high bone mass?

. Osteogenesis Imperfecta
. Osteopetrosis
. Van Buchem Disease
. Sclerosteosis
. High Bone Mass (HBM) syndrome

Correct Answer & Explanation

. High Bone Mass (HBM) syndrome

Explanation

Gain-of-function mutations in LRP5 lead to the High Bone Mass (HBM) syndrome. LRP5 is a co-receptor for Wnt signaling, which is a crucial pathway for osteoblastogenesis and bone formation. Gain-of-function mutations in LRP5 enhance Wnt signaling, resulting in increased bone formation and consequently, abnormally high bone mineral density and bone mass, typically without other systemic abnormalities. Van Buchem disease and Sclerosteosis are also high bone mass disorders, but they are typically caused by mutations in the SOST gene (sclerostin) or LRP4 (for sclerosteosis). Osteogenesis Imperfecta is brittle bone disease (collagen mutation), and Osteopetrosis is dense, brittle bone due to osteoclast dysfunction. Thus, HBM syndrome is directly linked to gain-of-function LRP5 mutations.

Question 2308

Topic: Biology, Genetics & Bone Healing
A 55-year-old male presents with severe osteoporosis. His treatment includes an agent that targets sclerostin. Sclerostin, primarily produced by osteocytes, exerts its catabolic effects by directly:
. Activating RANKL on osteoblasts, promoting osteoclastogenesis.
. Inhibiting the Wnt/β-catenin signaling pathway, reducing osteoblast activity.
. Increasing the production of PTHrP, which enhances bone resorption.
. Stimulating the differentiation of mesenchymal stem cells into adipocytes instead of osteoblasts.
. Downregulating the expression of OPG, leading to increased osteoclast survival.

Correct Answer & Explanation

. Inhibiting the Wnt/β-catenin signaling pathway, reducing osteoblast activity.

Explanation

Sclerostin, a glycoprotein produced by osteocytes, acts as a negative regulator of bone formation. Its primary mechanism of action is to inhibit the Wnt/β-catenin signaling pathway. This pathway is crucial for osteoblast differentiation, proliferation, and survival, as well as for the production of bone matrix proteins. By binding to LRP5/6 co-receptors, sclerostin prevents Wnt ligands from activating the pathway, thereby reducing osteoblast activity and bone formation. This makes Option B correct. Option A is incorrect; RANKL activation is primarily regulated by osteoblasts/stromal cells, and sclerostin's effect is more direct on Wnt. Option C is incorrect; PTHrP is involved in endochondral ossification and calcium homeostasis, not directly targeted by sclerostin's catabolic effects on bone formation. Option D is incorrect; while MSC differentiation is relevant, sclerostin's direct action is on osteoblast activity via Wnt. Option E is incorrect; OPG (osteoprotegerin) regulation is complex, but sclerostin's main direct action is not OPG downregulation.

Question 2309

Topic: Biology, Genetics & Bone Healing
In the context of bone fracture healing, secondary fracture healing (endochondral ossification) is initiated by the formation of a soft callus. Which of the following conditions is most crucial for the successful progression from soft callus to hard callus via endochondral ossification?
. Absolute rigidity and complete absence of micromotion at the fracture site.
. Adequate vascularization of the hypertrophic chondrocytes within the callus.
. High oxygen tension and a pH below 7.0 within the soft callus.
. The absence of inflammatory cytokines such as TNF-α and IL-6.
. Dominance of intramembranous ossification in the periosteal regions.

Correct Answer & Explanation

. Adequate vascularization of the hypertrophic chondrocytes within the callus.

Explanation

For secondary fracture healing (endochondral ossification) to progress from a soft callus (cartilaginous) to a hard callus (bony), the hypertrophic chondrocytes within the cartilage template must undergo apoptosis and be replaced by invading blood vessels and osteoblasts, a process known as chondroclastic resorption and vascular invasion. This vascularization is absolutely crucial for bringing in osteoprogenitor cells and nutrients, and for establishing the oxygen gradient necessary for bone formation. Option B is correct. Option A is incorrect; some controlled micromotion (interfragmentary strain) is beneficial for secondary healing, unlike primary healing which requires absolute rigidity. Option C is incorrect; cartilage is typically maintained in relatively low oxygen tension, and the progression to bone requires an increase in oxygenation associated with vascularization. Option D is incorrect; inflammatory cytokines play an essential role in the initial phases of fracture healing. Option E is incorrect; while intramembranous ossification occurs in the periosteal regions, the question specifically asks about the progression of the soft callus via endochondral ossification.

Question 2310

Topic: Biology, Genetics & Bone Healing

Osteocytes, embedded within the bone matrix, are considered master regulators of bone remodeling. They communicate with surface osteoblasts and osteoclasts through various mechanisms. Which of the following is the most established primary mode of long-range communication for osteocytes to coordinate remodeling events across significant distances within bone?

. Direct cell-to-cell contact via gap junctions within the lacunar-canalicular network.
. Secretion of systemic hormones like PTH and calcitonin.
. Release of soluble factors such as sclerostin and FGF23.
. Neural innervation signaling directly to osteocytes.
. Direct sensing of systemic cytokine levels in the interstitial fluid.

Correct Answer & Explanation

. Release of soluble factors such as sclerostin and FGF23.

Explanation

While osteocytes communicate extensively via gap junctions within the lacunar-canalicular network (Option A), this is primarily for local, short-range signaling. For coordinating remodeling events across significant distances, osteocytes act as endocrine-like cells, releasing soluble factors that can act on distant osteoblasts, osteoclasts, or other cells. Key examples include sclerostin (a Wnt pathway inhibitor, discussed in Q1) which regulates bone formation, and FGF23 (fibroblast growth factor 23) which regulates phosphate homeostasis. These soluble factors allow for long-range communication and coordination. Option C is correct. Option B is incorrect; osteocytes respond to systemic hormones but do not primarily secrete them to regulate remodeling. Option D is incorrect; while bone has neural innervation, it's not the primary long-range communication method for osteocytes. Option E is part of their mechanosensing environment but not their primary long-range communication output.

Question 2311

Topic: Biology, Genetics & Bone Healing
The growth plate (physis) is a critical structure for longitudinal bone growth. The transition of chondrocytes from proliferation to hypertrophy and subsequent apoptosis is tightly regulated. Which of the following signaling pathways primarily maintains the balance between chondrocyte proliferation and hypertrophy by negatively regulating hypertrophy and promoting proliferation?
. Wnt/β-catenin signaling pathway.
. Indian Hedgehog (IHH) and Parathyroid Hormone-related Protein (PTHrP) feedback loop.
. Bone Morphogenetic Protein (BMP) signaling pathway.
. Fibroblast Growth Factor (FGF) receptor signaling.
. Transforming Growth Factor-beta (TGF-β) signaling pathway.

Correct Answer & Explanation

. Indian Hedgehog (IHH) and Parathyroid Hormone-related Protein (PTHrP) feedback loop.

Explanation

The Indian Hedgehog (IHH) and Parathyroid Hormone-related Protein (PTHrP) feedback loop is a central regulator of chondrocyte differentiation and the rate of endochondral ossification in the growth plate. Chondrocytes in the prehypertrophic zone produce IHH, which diffuses to the perichondrium, inducing PTHrP expression. PTHrP then acts on receptors on proliferating chondrocytes, preventing their premature differentiation into hypertrophic chondrocytes and promoting their proliferation. As chondrocytes move away from the PTHrP source, PTHrP levels drop, allowing them to differentiate into hypertrophic chondrocytes. This finely tuned feedback loop maintains the correct proportions of the proliferating and hypertrophic zones. Option B is correct. Wnt, BMP, FGF, and TGF-β all play roles in skeletal development but the IHH/PTHrP loop is the most specific and primary pathway for this particular balance in the growth plate.

Question 2312

Topic: Biology, Genetics & Bone Healing

When considering the long-term success of an orthopedic implant designed for osseointegration, the most critical factor at the cellular level is the direct interaction between osteoblasts and the implant surface. This interaction is primarily mediated by:

. The overall bulk modulus and stiffness of the implant material.
. The electrical conductivity of the implant surface.
. Specific adsorbed proteins from host fluids, like fibronectin and vitronectin.
. The macroscopic surface roughness and geometry of the implant.
. The rate of release of growth factors from the implant's core.

Correct Answer & Explanation

. Specific adsorbed proteins from host fluids, like fibronectin and vitronectin.

Explanation

Osseointegration is a complex biological process, and while many factors contribute, the initial and most critical cellular event is the adsorption of host proteins onto the implant surface. Within minutes to hours of implantation, proteins from blood and interstitial fluid, such as fibronectin, vitronectin, collagen, and albumin, rapidly adsorb to the implant surface. These adsorbed proteins form a 'conditioning film' that then dictates how host cells, particularly osteoblasts and osteoprogenitor cells, will interact with the surface. Integrins on the cell membrane bind to specific recognition sequences within these adsorbed proteins, mediating cell adhesion, spreading, and subsequent differentiation and matrix production. Option C is correct. While bulk modulus (Option A), surface roughness (Option D), and even electrical properties (Option B) influence osseointegration, they do so indirectly by affecting protein adsorption and subsequent cellular responses, not by direct interaction between the cell and the 'naked' implant. Option E is less about the surface interaction itself, but more about drug delivery.

Question 2313

Topic: Biology, Genetics & Bone Healing

A biopsy from a patient with a rare bone disorder shows abnormally increased activity of cathepsin K. Cathepsin K is a cysteine protease primarily associated with:

. Osteoblast differentiation and collagen synthesis.
. Osteoclast-mediated bone matrix degradation.
. Chondrocyte proliferation in the growth plate.
. Myoblast fusion and muscle repair.
. Tendon fibroblast collagen cross-linking.

Correct Answer & Explanation

. Osteoclast-mediated bone matrix degradation.

Explanation

Cathepsin K is a potent lysosomal cysteine protease that is highly expressed by osteoclasts. It plays a critical role in the degradation of organic components of the bone matrix, particularly type I collagen, within the acidified resorption lacuna. Inhibitors of cathepsin K have been investigated as potential treatments for osteoporosis due to their specific targeting of osteoclast activity without affecting osteoblast function. Option B is correct. Options A, C, D, and E describe processes associated with other cell types or different enzymatic activities.

Question 2314

Topic: Biology, Genetics & Bone Healing

In the process of bone remodeling, activation of bone multicellular units (BMUs) involves a highly coordinated sequence of cellular events. The initial signal for BMU activation and the recruitment of osteoclast precursors often originates from:

. Direct sensing of microcracks and fatigue damage by osteoclasts.
. Osteocytes releasing RANKL and other signaling molecules in response to mechanical changes.
. Parathyroid hormone (PTH) directly stimulating osteoclast differentiation.
. Mesenchymal stem cells differentiating directly into osteoclasts.
. Systemic calcitonin acting to suppress initial osteoclast activation.

Correct Answer & Explanation

. Osteocytes releasing RANKL and other signaling molecules in response to mechanical changes.

Explanation

Osteocytes, embedded within the bone matrix, are considered the primary mechanosensors and orchestrators of bone remodeling. In response to microdamage (microcracks) or changes in mechanical loading, osteocytes undergo apoptosis or release signaling molecules (e.g., RANKL, sclerostin, FGF23). Specifically, osteocytes can increase RANKL expression (or reduce OPG expression) and other pro-resorptive factors, which signals to osteoblasts and stromal cells to recruit and activate osteoclast precursors, thereby initiating the remodeling cycle. Option B is correct. Option A is incorrect; osteoclasts resorb bone but are not the primary sensors of microcracks. Option C is incorrect; PTH primarily acts on osteoblasts to induce RANKL expression, which then stimulates osteoclast activity, not directly on osteoclasts themselves. Option D is incorrect; osteoclasts derive from hematopoietic stem cells, not mesenchymal stem cells. Option E describes calcitonin's role in inhibiting osteoclasts, which is a counter-regulatory mechanism, not an activating signal.

Question 2315

Topic: Biology, Genetics & Bone Healing
Which of the following non-collagenous proteins in bone matrix is primarily known for inhibiting osteoblast differentiation and promoting osteoclastogenesis via the canonical Wnt/β-catenin pathway?
. Osteocalcin
. Osteopontin
. Sclerostin
. Bone Sialoprotein
. Matrix Gla Protein

Correct Answer & Explanation

. Sclerostin

Explanation

Sclerostin (SOST) is a glycoprotein produced by osteocytes that acts as a negative regulator of bone formation by binding to LRP5/6 co-receptors, thereby inhibiting the canonical Wnt/β-catenin signaling pathway. This inhibition reduces osteoblast differentiation and activity, and indirectly promotes osteoclastogenesis. Osteocalcin and Bone Sialoprotein are involved in mineralization. Osteopontin is involved in cell attachment and crystal formation. Matrix Gla Protein inhibits ectopic calcification.

Question 2316

Topic: Biology, Genetics & Bone Healing

In the process of bone graft incorporation, which of the following mechanisms describes the process by which a graft material serves as a scaffold for the ingrowth of host osteogenic cells and blood vessels, ultimately leading to new bone formation on its surface?

. Osteoinduction
. Osteogenesis
. Osteoconduction
. Osseointegration
. Osteoclasis

Correct Answer & Explanation

. Osteoconduction

Explanation

Osteoconduction describes the ability of a bone graft material to serve as a passive scaffold for the ingrowth of new bone from the surrounding host tissue. It provides a framework for osteoblasts, capillaries, and mesenchymal stem cells to migrate, proliferate, and differentiate. Osteoinduction is the active stimulation of undifferentiated mesenchymal stem cells to differentiate into osteoblasts and form bone. Osteogenesis refers to the formation of new bone by viable cells within the graft itself. Osseointegration is the direct structural and functional connection between ordered, living bone and the surface of a load-bearing implant. Osteoclasis is bone resorption.

Question 2317

Topic: Biology, Genetics & Bone Healing
Regarding cellular events in secondary fracture healing, what is the primary role of the mesenchymal stem cells (MSCs) that migrate into the fracture hematoma during the inflammatory and reparative phases?
. To directly form woven bone without cartilage intermediate.
. To phagocytose cellular debris and inflammatory mediators.
. To differentiate into chondrocytes and osteoblasts, forming the soft and hard callus.
. To secrete growth factors that attract osteoclasts for remodeling.
. To form the initial granulation tissue rich in Type III collagen.

Correct Answer & Explanation

. To differentiate into chondrocytes and osteoblasts, forming the soft and hard callus.

Explanation

During secondary fracture healing, mesenchymal stem cells (MSCs) are recruited to the fracture site and differentiate into chondrocytes to form the soft callus (cartilage) and into osteoblasts to form the hard callus (woven bone). This process involves both endochondral and intramembranous ossification. The initial granulation tissue does form and contain Type III collagen, but the specific role of MSCs is their differentiation potential. Phagocytosis is by macrophages, and osteoclasts are for resorption.

Question 2318

Topic: Biology, Genetics & Bone Healing

In the context of bone remodeling, which cell type is primarily responsible for sensing mechanical loads and initiating appropriate adaptive responses by signaling to osteoblasts and osteoclasts?

. Osteoclasts
. Osteoblasts
. Bone lining cells
. Osteocytes
. Chondrocytes

Correct Answer & Explanation

. Osteocytes

Explanation

Osteocytes, embedded within the bone matrix and interconnected by canaliculi, are recognized as the primary mechanosensors of bone. They detect changes in mechanical strain and fluid flow, then translate these signals into biochemical cues (e.g., sclerostin, RANKL, OPG, prostaglandins, nitric oxide) that regulate the activity of osteoblasts (bone formation) and osteoclasts (bone resorption), thereby coordinating bone remodeling to adapt to mechanical demands. Osteoblasts form bone, osteoclasts resorb bone, and bone lining cells are quiescent osteoblasts.

Question 2319

Topic: Biology, Genetics & Bone Healing
What is the primary mechanism by which platelet-rich plasma (PRP) is theorized to promote tissue healing in orthopedic applications?
. Directly stimulating differentiation of mesenchymal stem cells into chondrocytes or osteoblasts.
. Delivering high concentrations of antibiotics to the injury site.
. Providing a structural scaffold for tissue regeneration.
. Releasing various growth factors, cytokines, and chemokines from alpha granules.
. Inducing a potent inflammatory response to clear damaged tissue.

Correct Answer & Explanation

. Releasing various growth factors, cytokines, and chemokines from alpha granules.

Explanation

Platelet-Rich Plasma (PRP) is an autologous blood product with a supra-physiological concentration of platelets. When activated, platelets release a multitude of growth factors (e.g., PDGF, TGF-β, VEGF, EGF, IGF-1) and other bioactive proteins from their alpha granules. These factors are crucial for promoting cell proliferation, differentiation, angiogenesis, and extracellular matrix synthesis, thereby enhancing tissue healing and regeneration. While it may indirectly influence MSCs or induce some inflammation, its primary mechanism is the delivery of these signaling molecules. It does not provide antibiotics or a structural scaffold directly.

Question 2320

Topic: Biology, Genetics & Bone Healing
Which type of collagen is predominantly found in healthy mature cortical bone, providing its high tensile strength?
. Type I collagen
. Type II collagen
. Type III collagen
. Type IV collagen
. Type X collagen

Correct Answer & Explanation

. Type I collagen

Explanation

Type I collagen is the most abundant protein in the human body and is the primary organic component (approximately 90%) of bone, skin, tendons, and ligaments. Its highly organized triple-helical structure provides immense tensile strength to cortical bone. Type II collagen is found in cartilage. Type III collagen is found in extensible connective tissues like blood vessels and early wound healing. Type IV collagen forms the basement membranes. Type X collagen is associated with hypertrophic cartilage.

Test Yourself

Switch to an interactive, timed exam simulation to truly master this topic.

On this Page