Week 2 Physiology Musculoskeletal System

### Bone Structure

Long bone

Bone with a shaft (diaphysis) and two distinct ends (epiphyses); functions as a lever for movement (e.g., femur, humerus)

Short bone

Cube-shaped bone; functions to provide stability and shock absorption (e.g., carpals, tarsals)

Flat bone

Thin, flattened bone; provides broad surface for muscle attachment and protection of underlying structures (e.g., scapula, skull bones)

Irregular bone

Bone with a variety of complex shapes; allows specialized functions (e.g., vertebrae, facial bones)

Periosteum

Outer fibrous covering of bone; tough structural protection and attachment point for tendons/ligaments; drives appositional (width) growth and bone repair, and is densely innervated (source of most fracture pain)

Epiphyseal plate

Cartilage growth plate near the ends of long bones; allows bones to grow in length (longitudinal growth) until skeletal maturity

Why do fractures hurt so much?

The periosteum is densely innervated with sensory nerve fibers, so disrupting it (as in a fracture) produces intense pain

Compact (cortical) bone

Dense outer bone layer built of osteons; provides strength against bending and fracture

Osteon (Haversian system)

The fundamental structural/functional unit of compact bone; a microscopic weight-bearing cylinder aligned parallel to the bone's long axis that acts like a structural pillar for strength

Spongy (trabecular) bone

Porous inner bone with a network of struts (trabeculae) that maximizes strength while minimizing skeletal weight; contains active marrow with high blood flow

Trabeculae

Structural struts of spongy bone that align along lines of mechanical stress to efficiently handle everyday loads

Osteocyte

Mature bone cell embedded in lacunae that senses fluid shear stress via the lacunocanalicular network and signals osteoblasts/osteoclasts to initiate remodeling

Osteoblast

Bone cell that lays down new organic bone matrix (osteoid, mostly collagen); site of bone formation

Osteoclast

Large multinucleated cell that resorbs bone by releasing acid and enzymes to dissolve mineral and collagen matrix

Wolff's Law

Principle that bone adapts its size, shape, and internal architecture (trabecular alignment) in response to the mechanical forces/loads placed on it

Bone modeling

Process where bone is removed from one surface and formed on another to change a bone's size, shape, and density; occurs primarily during childhood/adolescence until skeletal maturity (~25-30 years) to achieve peak bone mass

Bone remodeling

Continuous lifelong process that replaces old/damaged bone with new bone to maintain strength, repair micro-damage, and regulate mineral balance

What triggers the bone remodeling cycle to begin?

Micro-damage to bone or hormonal signals, which alert bone cells and recruit pre-osteoclasts to the targeted bone surface (Activation phase)

### Bone Remodeling Sequence & Wide Applications

Bone remodeling phase 1: Activation

Micro-damage or hormonal signals alert bone cells; pre-osteoclasts are recruited to the targeted bone surface

Bone remodeling phase 2: Resorption

Osteoclasts attach to bone and release acid and enzymes; minerals and collagen matrix dissolve, creating a small pit

Bone remodeling phase 3: Reversal

Osteoclasts disappear from the site; mononuclear cells prepare the resorption pit surface for new bone formation

Bone remodeling phase 4: Formation

Osteoblasts arrive and lay down new organic matrix (osteoid) that fills the cavity left by resorption

Bone remodeling phase 5: Mineralization

Calcium and phosphate crystals deposit into the new osteoid, hardening the tissue into mature, strong bone

Put in order: Reversal, Mineralization, Activation, Formation, Resorption

Activation to Resorption to Reversal to Formation to Mineralization

In the bone remodeling cycle, what event marks the transition from the Reversal phase to the Formation phase?

Osteoblasts are recruited to the prepared resorption pit and begin laying down osteoid

Why can a fresh resorption pit not yet be called "remodeled bone" even after osteoblasts arrive?

Because the newly formed osteoid matrix (Formation phase) has not yet been mineralized with calcium/phosphate (Mineralization phase); it is still soft, unmineralized collagen

### Scoliosis

Scoliosis

3D spinal deformity involving lateral curvature of the spine >10° plus vertebral rotation

Idiopathic scoliosis

Most common form of scoliosis; cause unknown, though genetic, hormonal, and asymmetric growth theories exist

Congenital scoliosis

Scoliosis caused by vertebral malformations present from birth

Neuromuscular scoliosis

Scoliosis related to underlying neuromuscular conditions such as cerebral palsy or muscular dystrophy

Degenerative scoliosis

Adult-onset scoliosis caused by asymmetric disc/facet joint degeneration, often accompanied by spinal stenosis

Relative anterior spinal overgrowth (AIS theory)

In adolescent idiopathic scoliosis, anterior spinal structures grow relatively longer than posterior structures, contributing to vertebral rotation and sagittal-plane changes

In adolescent idiopathic scoliosis, why does the concave side of the curve become progressively more curved over time?

Greater compression on the concave side inhibits growth plate cartilage but triggers osteoblasts to lay down more dense bone, while the convex side has lower loading, permitting more cartilage growth and triggering more osteoclast activity — this asymmetric loading creates a self-reinforcing progression cycle

On which side of a scoliotic curve are osteoclasts out-pacing osteoblasts, and why does this matter?

The convex (less compressed) side; the resulting relative bone loss versus the concave side's bone deposition perpetuates and worsens the curve over growth

Adam's forward bend test

Clinical exam for scoliosis where the patient bends forward; used to detect a rib hump/torso shift indicating asymmetric rib cage protrusion

Scoliosis Cobb angle 10-25°

Mild scoliosis; typically managed with observation and targeted physical therapy

Scoliosis Cobb angle 25-40°

Moderate scoliosis; often treated with bracing in growing teens alongside specialized physical therapy

Scoliosis Cobb angle 40-50°+

Severe curvature; frequently evaluated for surgical intervention or intensive conservative care

### Bone Function

Six major functions of bone

Support, movement (muscle attachment/leverage), protection of organs, mineral storage (Ca/phosphate), hematopoiesis (in red marrow), and endocrine organ function

How does bone act as an endocrine organ?

Osteoblasts and osteoclasts release hormones that regulate whole-body metabolism, blood sugar, kidney function, and brain development

What physiological processes depend on adequate blood calcium, and what happens if calcium drops too low?

Calcium is required for muscle contraction, nerve signaling, and blood clotting; hypocalcemia can cause muscle cramps/tetany, numbness/tingling, and cardiac arrhythmias

### Bone Pathologies — Osteoporosis & Osteomalacia

Osteoporosis

A "silent" bone disease characterized by decreased bone mineral density and deterioration of trabecular microarchitecture, making bone fragile and prone to low-trauma (fragility) fractures

Type I (postmenopausal) osteoporosis mechanism

Decreased estrogen suppresses osteoclast apoptosis, leading to increased osteoclast activity/lifespan and net bone resorption

Type II (age-related) osteoporosis mechanism

Gradual decline in osteoblast number/activity and decreased calcium absorption with aging, leading to reduced bone formation

A postmenopausal woman and an elderly man both have osteoporosis — how do the underlying mechanisms differ?

The woman's (Type I) is driven by estrogen loss increasing osteoclast lifespan/resorption; the man's (Type II) is driven by age-related decline in osteoblast number/function and reduced calcium absorption — one is excess breakdown, the other is inadequate formation

Secondary osteoporosis causes

Endocrine disorders (hyperthyroidism, hyperparathyroidism, Cushing's), chronic corticosteroid use, GI malabsorption (celiac, Crohn's), chronic kidney disease, sedentary lifestyle/smoking/alcohol, and nutritional deficits (calcium, vitamin D, protein)

Osteoporosis red flags for a PT

Sudden severe back pain in an older adult, height loss >2 cm, and new kyphosis — suggest possible vertebral compression fracture

Most common fracture patterns in osteoporosis

Vertebral compression fractures (most common), hip fractures (femoral neck/intertrochanteric), and distal radius (Colles) fractures

Osteoporosis PT/lifestyle management

Weight-bearing exercise and resistance training (bone-loading stimulus), balance training (fall risk reduction), postural training (reduce kyphotic stress), and fall-prevention education

Osteomalacia/rickets

Condition where vitamin D deficiency (or related cause) leads to low calcium/phosphorus, preventing osteoblasts from mineralizing the osteoid — bone quantity is normal but bone quality/mineralization is defective

Osteoporosis vs. osteomalacia — what is the fundamental distinction?

Osteoporosis is a problem of bone quantity (reduced mineral density/mass with normally mineralized bone), whereas osteomalacia is a problem of bone quality (normal or near-normal amount of bone matrix that is inadequately mineralized due to vitamin D/calcium deficiency)

Osteomalacia clinical presentation

Bone pain, muscle weakness, skeletal deformities, fractures, and hypocalcemia

Osteomalacia treatment

High-dose vitamin D and calcium, sunlight exposure, dietary changes, and orthopedic care

### Bone Pathologies — Paget, OI, HO, Osteomyelitis

Paget disease of bone

Disorder of enlarged, hyperactive osteoclasts causing intense bone breakdown followed by rapid, disorganized new bone formation by osteoblasts, most affecting the axial skeleton, femur, tibia, and humerus

Paget disease clinical presentation

75% asymptomatic; can present with bone pain, deformities, hearing loss, fractures, warmth/redness over bone, and secondary osteoarthritis

Osteogenesis imperfecta (OI)

Autosomal dominant disorder from COL1A1 or COL1A2 gene mutations causing structurally altered or reduced Type I collagen, resulting in weak, poorly mineralized, brittle bone

OI clinical presentation

Bone fragility with frequent fractures from minor trauma, deformities (scoliosis, bowing), short stature, and dental issues

Heterotopic ossification (HO)

Inappropriate differentiation of mesenchymal stem cells into osteoblasts within non-osseous (soft) tissue, typically triggered by trauma/neurological injury creating a cytokine- and macrophage-rich inflammatory environment

HO clinical presentation and PT-relevant treatment

Loss of motion, inflammation, pain, palpable mass, and functional limitations; managed with NSAID prevention, PROM/AROM, and surgical excision only once the lesion is mature and symptomatic

Osteomyelitis

Bacterial (most commonly Staphylococcus aureus), fungal, or viral infection of bone, reaching bone via hematogenous spread, contiguous spread, or direct inoculation

Osteomyelitis risk factors

Diabetes, peripheral vascular disease, immunosuppression, IV drug use, recent surgery, and chronic wounds

Sequestrum

A segment of dead (necrotic) bone formed in osteomyelitis when increased intramedullary pressure from inflammation reduces blood flow, causing bone necrosis

Involucrum

New bone that forms around a sequestrum as the body attempts to wall off the infection in osteomyelitis

In osteomyelitis, what is the sequence from infection to sequestrum/involucrum formation?

Microorganisms enter bone to trigger inflammation, which raises intramedullary pressure and reduces blood flow, causing bone necrosis (sequestrum); the body then walls off the infection by forming new bone around it (involucrum); in chronic cases, persistent infection/poor perfusion impairs healing and may cause abscesses or draining sinus tracts

Acute vs. chronic osteomyelitis presentation

Acute: sudden localized bone pain, tenderness/warmth/swelling/erythema, fever/chills (esp. children), reduced weight-bearing. Chronic: persistent/recurrent bone pain, less dramatic swelling/warmth, history of prior infection/wound/hardware, possible low-grade or absent fever

### Cartilage

Chondrocyte

Specialized cartilage cell embedded within the cartilage extracellular matrix; produces and maintains the ECM

Cartilage extracellular matrix components

Water, collagen fibers, proteoglycans, and glycosaminoglycans (GAGs), produced by chondrocytes

Perichondrium

Connective tissue layer surrounding cartilage (except articular cartilage), containing blood vessels that supply nutrients via diffusion since cartilage itself is avascular

Why does cartilage heal so slowly compared to bone?

Cartilage is avascular (no blood vessels) and aneural (no nerve supply); nutrients must reach chondrocytes by passive diffusion through the matrix, making repair slow and limiting pain sensation until damage is advanced

Why is articular cartilage damage often painless until late-stage disease?

Cartilage is aneural (has no nerve supply), so cartilage breakdown itself does not directly cause pain — pain arises later from subchondral bone changes and synovial inflammation

Elastic cartilage

Cartilage type containing more elastic fibers for flexibility; found in structures like the ear and epiglottis

Hyaline cartilage

Cartilage type that is less elastic and provides stability/smooth surfaces; found as articular cartilage on joint surfaces and in the trachea/rib cage

Fibrocartilage

Cartilage type that provides padding/shock absorption in joints; found in structures like the intervertebral discs and menisci

Functions of cartilage

Joint movement (smooth lubricated gliding surface via articular cartilage), shock absorption (cushions compressive forces), structural support (rib cage, ear, nose, trachea), and flexibility/resilience (water-rich gel matrix reinforced with collagen)

### Joints — Classification

Structural joint classification

Classifies joints by the type of connective tissue present and whether a joint cavity exists: fibrous, cartilaginous, or synovial

Functional joint classification

Classifies joints by the degree of movement allowed: synarthrosis, amphiarthrosis, or diarthrosis

Synarthrosis ("syn-")

Functional joint classification meaning immovable joint (e.g., skull sutures)

Amphiarthrosis ("amphi-")

Functional joint classification meaning slightly movable joint (e.g., pubic symphysis, intervertebral discs)

Diarthrosis ("dia-")

Functional joint classification meaning freely movable joint — this is the functional category that all synovial joints belong to

Trap: a synovial joint is structurally "synovial" — what is it functionally classified as, and why is this a common point of confusion?

Functionally, a synovial joint is a diarthrosis (freely movable) — NOT a "synarthrosis," despite "synovial" sounding like it shares the "syn-" (immovable) prefix; the "syn-" in "synovial" is unrelated to the "syn-" functional prefix meaning immobile, so students must not let the word similarity mislead them

Synovial joint capsule — outer fibrous layer

Dense irregular connective tissue layer that is highly innervated, providing proprioception and pain sensation

Synovial joint capsule — inner synovial membrane

Contains Type A synoviocytes (macrophage-like, remove debris) and Type B synoviocytes (produce hyaluronic acid and lubricin for joint lubrication)

### Joints — Synovial Types by Plane of Motion

Hinge joint

Uniaxial joint allowing only flexion and extension, like a door hinge (e.g., elbow, knee)

Pivot joint

Uniaxial joint allowing rotation around a central axis (e.g., atlantoaxial joint, proximal radioulnar joint)

Condyloid (ellipsoid) joint

Biaxial joint where an oval-shaped bone fits into a depression, allowing flexion/extension and abduction/adduction (e.g., wrist/radiocarpal joint)

Saddle joint

Biaxial joint similar to condyloid but with greater range, allowing flexion/extension, abduction/adduction, and some rotation (e.g., thumb CMC joint)

Plane (gliding) joint

Nonaxial/multiaxial joint where flat surfaces glide past one another (e.g., intercarpal joints, facet joints)

Ball-and-socket joint

Multiaxial joint where a spherical head fits into a cup-like depression, allowing flexion/extension, abduction/adduction, and rotation (e.g., hip, shoulder)

A joint allows flexion/extension only, like a door — what type of joint and what axial category?

Hinge joint; uniaxial

A joint allows flexion/extension, abduction/adduction, AND rotation, with a spherical head in a cup depression — what type of joint?

Ball-and-socket joint (multiaxial)

### Joint Pathologies — Osteoarthritis