SBMS1431- Anatomy of Muskoskeletal System II

Muscoskeletal system - Key Components

Bones: Rigid framework providing structure and protection

Muscles: Contractile tissues enabling movement

Joints: Connections between bones allowing mobility

Tendons: Connects muscles to bones

Ligaments: Connects bones to other bones

Muscoskeletal system - Primary Functions

Support and movement of the body

Protection of vital organs

Blood cell formation (hematopoieses)

Mineral Stirage and homeostasis

Overview: Joints

Forms connections between bones that allow various types of movement

Overview: Tendons

Transfer force from muscles to bones to create movement

Overview: Ligaments

Connect bones to other bones, stabilizing joints and guiding movement

Overview: Cartilage

Cushions joints and reduces friction between moving parts

Integration of the muscoskeletal system

The system works through linked roles: support (bones), movement (joints), force, (tendons), stability (ligaments), low-friction (cartilage), and generate (muscles)

Movement Pathways

When you decide to move, your brain sends signals yjtough nerves to skeletal muscles, which contract and pull-on tendons → movement occurs at a joint

Stability + Protection

Ligaments stabilise and guide joint motion. Cartilage cushions, distributes load and reduces friction.

Cartillage: Nature’s shock absorber

Hyaline Cartilage

Elastic Cartilage

Fibrocartilage

Hyaline Cartilage

Found in joints, ribs, and respiratory tract

Smooth, glassy appearance with high collagen content

Primary type in articulation surfaces of synovial joints

Elastic Cartilage

Present in ear, epiglottis, and parts of the larynx

Contains elastic fibers allowing flexibility

Supports structures that bend repeatedly

Fibrocartilage

Located in menisci (of the knee), intervertebral discs (spine), and pubic symphysis (pelvis)

Contains abundant collagen fibers for strength

Strongest cartilage type

Designed to resist compression and tension

The Muscular System: Types of muscle

Cardiac Mucle

Smooth Muscle

Skeletal Muscle

Cardiac Muscle

Involuntary, controlled by the autonomic nervous system

Forms the muscular layer of the heart (myocardium)

Striated, involuntary control

Has unique properties allowing it to contract rhythmically

Smooth Muscle

Comprises walls of blood vessels and hollow organs

Non-striated, involuntary control (autonomic nervous system)

Example: Muscles in blood vessels, digestive tract, bladder

Skeletal Muscle

Attaches to bones and provides voluntary movement

Striated, voluntary control (somatic nervous system)

Example: Biceps, quadriceps, hamstrings

Anterior View

Deltoid (flex, abduct, and extend arm)

Biceps (flex forearm)

Abdominal muscles (flex and rotate trunk, hip)

Wrist flexors (flex wrist and fingers)

Pectoralis major (adduct arm)

Triceps (extend forearm)

Rectus abdominis ( flex trunk, hip)

Quadriceps (flex hip, extend leg)

Calf Muscles (plantarflexion & invert foot, flex toes)

Posterior View

Trapezius- (extend head, elevate shoulder)

Deltoid- ( posterior fibers extend arm)

Triceps- (extend forearm)

Latissimus dorsi- (extend, adduct arm)

Gluteus maximus- (extend, abduct hip/thigh)

Hamstring- biceps femoris ( extend hip, flex knee)

Calf muscles- (olantarflexion foot & invert foot, flex toes)

Skeletal Muscle Attachments: Original, Insertion, & Belly

Origin- the relatively fixed attachment of a muscle; often proximal (closer to the center of the body/ trunk), but this depends on the action being performed.

Insertion- The attachment that usually moves toward the origin during contraction. It is often the end farther from the body’s center (distal)

Muscle belly- The thick, contractile middle region of the muscle, made up of fascicles and muscle fibers. When the region shortens, it generates tension that is passed on to the bone through tendons.

Tendon- A connective tissue structure that attaches muscle to bone and carries the force produced by the muscle belly to the bone.

In short: A muscle anchors at its origin (stays put), pulls at its insertion (moves), generates force in its belly (the fleshy contractile part), and delivers that force to bone through its tendon.

Skeletal Muscle: Organization

Muscle → Fascicle → Muscle Fiber → Myofibril → Sarcomere

Muscle

Organ composed of fascicles, blood vessels, nerves and connective tissue coverings.

Fascicle

Bundle of muscle fibers wrapped by perimysium

Muscle Fiber

Long multinucleated muscle cell surrounded by sarcolemma.

Myofibril

Cylindrical bundle of repeating contractile units

Sarcomere

Functional contractile unit containing actin and myosin. Actin and myosin are arranged in repeating sarcomeres. Their orderly pattern produces skeletal-muscle striations.

Skeletal Muscle: Overview

Connective Tissue coverings organize force transmission

Epimysium: wraps whole muscle

Perimysium: wraps each fascicle

Endomysium: wraps each fibe

Sliding Filament Theory

1. Calcium exposes binding sites

A nerve signal triggers the release of calcium ions (Ca2+) inside the muscle Fiber. The calcium binds to troponin (a protein on the Acton filament), which causes tropomyosin to shift out of the way. This uncovers the myosin- binding sites on actin that were previously blocked.

Sliding Filament Theory

2. Cross-Bridge Formation

The myosin head (already energized by ATP) now attaches to the exposed binding sites on actin. This connection is called a cross-bridge

Sliding Filament Theory

3. Power stroke pulls actin

Once attached, the myosin head pivots (tilts), dragging the actin filament toward the centre of the Sarcomere. This is the power stroke- the actual pulling motion that generates force.

Sliding Filament Theory

4. ATP resets myosin

For the cycle to continue, myosin must let go of actin. ATP binds to the myosin head, causing it to detach from actin. Then the ATP is broken down (hydrolysis), which re-cocks the myosin head back into its energized, ready position.

Sliding Filament Theory

5. Cycle Repeats

As long as calcium and ATP are present, the cycle repeats: bind → pull → detach → reset → bind again. Each cycle pulls the actin a little farther inward.

Sliding Filament Theory: Overview

Actin and myosin filaments themselves don’t get shorter- thin actin filaments just slide past the thick myosin filaments, pulling Z discs closer together and causing the sarcomere to shorten.

Muscle Actions

Agonist: Prime mover that generates the desired movement (e.g, biceps, in elbow flexion)

Antagonist: Opposes the action of the agonist and relaxes during movement (e.g., triceps during elbow flexion)

Synergist: Assists the agonist in producing movement.

Fixator: Stabilizes the origin of the agonist (e.g., deltoid stabilizing shoulder during bicep curl)

Muscle Actions: Example

A person lifting a class uses biceps brachial as the prime mover, brachioradialis acts as the synergist, subcapularis as the fixator and triceps brachial as the antagonist

Four key properties of muscle

1. Excitability

2. Contractibility

3. Extensibility

4. Elasticity

These four physiological properties enable muscles to respond to stimuli, generate force, adapt to movement demands, and maintain their integrity during physical activity.

Excitability

• The ability to detect neural stimuli

Muscle Fibers can respond to an appropriate stimulus (such as a nerve signal) by generating an electrical and mechanical response

Contractibility

• The ability to contract in response to a neural stimulus

When stimulated, muscle fibers develop tension and shorten, producing force and movement

Extensibility

The ability of a muscle to be stretched without tearing

Muscle fibers can be stretched to a longer length and return to their original length, within physiological limits, without being damaged.

Elasticity

The ability to return to normal shape after being extended.

After being stretched or contracted, muscle fibers recoil and return to their original resting length,

Types of Contraction

Isometric: Muscle length does not change during contraction

Isotonic: Tension remains unchanged while length changes

• Concentric: Muscle shortens (lifting a weight)

• Eccentric: Muscle lengthens while maintaining tension (lowering a weight)

Contraction Mechanism

1. Nervous system generates action potential

2. Signal travels through motor neurons to neuromuscular junction

3. Acetylcholine released into the synaptic cleft

4. Calcium ions released into synaptic cleft

5. Actin and myosin slide over each other using ATP

6. Muscle contracts as signal diminishes

The neuromuscular Junction (NMJ)

Presynaptic Nerve Terminal: Contains vesicles filled with acetylcholine (ACh) neurotransmitter

Synaptic Cleft: Space where ACh diffuses from nerve to muscle

Postsynaptic Endplate: Contains nicotinic ACh receptors that trigger muscle contraction.

Acetylcholineesterase (AChE) enzyme rapidly degrades ACh in the synaptic cleft, terminating the signal. This junction is essential for precise muscle contraction control.

Muscoskeletal Pathologies- Osteoporosis

Decreased bone density increasing fracture risk

Osteoclasts: Break down (resort) old bone

Osteoblasts: Build new bone

• In a healthy bone, build up and break down stay balanced. In osteoporosis, osteoclasts break down bone faster than osteoblasts can rebuild it, so bone mass steadily declines.

Result: Bones become porous and fragile → higher fracture risk (especially hip, spine, and wrist)

The pharmacology: Goal is to tip the balance back toward bone preservation- mainly by slowing down osteoclast activity.

• Bisphosphonates, SERMs, calcitonin

• Target: Osteoclast activity and bone remodelling

Muscoskeletal Pathologies- Neuromuscular Junction (NMJ) Disorders

Myasthenia gravis: autoimmune disease that blocks or destroys nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction

Result: acetylcholine can’t bind properly → muscles receive weak signals → muscle weakness and fatigue (especially with repeated use)

Pharmacology: Neostigmine, pyridostigmine (acetylcholinesterase inhibition)

Target: Inhibit the breakdown of acetylcholine in the NMJ by blocking AchEs- allowing ACh to stat longer in the synaptic cleft.

Osteoarthritis

A degenerative joint disease caused by the breakdown of articular cartilage. As cartilage wears away, bones rub together, causing pain, stiffness, and inflammation.

Pharmacology: NSAIDs, corticosteroids, hyaluronic acid (these treat the symptoms by reducing pain/ inflammation to improve joint movement, but not the underlying cartilage loss)

Target: Inflammation and joint lubrication

Gout

Crystal-induced arthritis caused by deposition of urate (uric acid) crystals in joints. The crystals trigger intense inflammation and sudden, severe joint pain.

Pharmacology: allopurinol, febuxostat

Xanthine oxidase is the enzyme that produces uric acid. Allupurinol and febuxostat inhibit xanthine oxidase, lowering uric acid production. Less uric acid in the blood- fewer crystals forming in joints → fewer gout attacks.

Long term prevention drugs as they lower uric acid levels rather than addressing an acute attack

Bone Tissue Engineering Applications

Mesenchymal Stem Cells: Multipotent stem Cells that can differentiate into osteoblasts, chondrocytes, and other connective tissue cells.

Bioactive scaffolds: Three dimensional frameworks, made from hydroxyapatite or other biocompatible materials.

Tissue Regeneration: Cells proliferate, differentiate, and organise into functional bone tissue.

Key Engineering Processes

1. Cell Adhesion: Cells attach to scaffold surfaces through specific protein interactions

2. Proliferation: Rapid cell division increases cell population within the scaffold

3. Differentiation: Stem cells transform into specialized bone-forming osteoblasts

4. Matrix Formation: New bone tissue develops with proper mineral composition and structure

Modern tissue engineering harnesses the natural power of bone cells, combining them with advanced biomaterials to regenerate lost bone tissue and restore function where traditional treatments fall short.