MEDICAL AND SURGICAL FOUNDATION 1 REVIEWER At the end of long bones:

1. Metaphysis
GENERALITIES 2. Epiphysis
GENERAL CONDITIONS AFFECTING THE BONES -both mainly made up of cancellous bone
covered with thin cortex of compact bone
BONE - highly vascular form of CT -Physis (growth plate) separates metaphysis
-collagen, calcium phosphate, water, amorphous proteins and cells and epiphysis in children
-most rigid of the CTs
-dynamic tissue that undergoes constant metabolism and Bone Gross Anatomy:
remodeling -Epiphysis
-Metaphysis
Functions: -Diaphysis
➡
Support
➡
Enhance leverage Cortical vs Cancellous Bone
➡
Protect vital structures
➡
Provide attachments for both tendons and ligaments CORTICAL (COMPACT) BONE
➡
Store minerals (calcium) -constitutes 80% of the skeleton
➡
Used as landmarks during palpation phase of examination -Consists of tightly packed osteons or
Haversian systems
Embriology, anatomy and physiology: ✤ connected by Haversian or Volkmann’s

❖ Bone is derived from mesenchyme or primitive connective tissue canal

✤ contains arterioles, venules, capillaries,
OSTEOGENESIS (OSSIFICATION)
- process of bone formation from osteoblast. nerves, lymphatic channels
- Starts at 6 weeks after fertilization
- Growth ends at 25 years
- After 25 more of remodeling and repairen destroyed and replaced by HAVERSIAN SYSTEM OR OSTEON
-long patent columns irregularly parallel to the
bone.
✤ Bone development may either come from fibrous membrane
long axis of the shaft of bone
(membranous development) or hyaline (cartilaginous development) Description
✤ Undergoes membranous or cartilaginous phase during development

from osteoblasts Central Canal Central space of the column

✤ Membranous bone formation

➡ Common in cranial vault and face

Lamellae Concentric layers of calcified intracellular
➡ Gradual replacement of primitive connective tissue by osteoid matrix
substance
which calcifies promptly to become bone
✤ Cartilaginous Lacunae Spaces within lamellae; contains osteocytes
➡ Also known as enchondral type

➡ Long bones, spine, scapula, ribs, sternum and pelvis Canaliculi Tiny irregular channels that connect lacunae
➡ Cartilage is invaded by blood vessels then destroyed and replaced from one another
by bone.
✤ All bones that replace cartilage in turn replace by more mature bone
Volkmann’s canal Transverse or oblique channels that connect
✤ In adults, none of the existing bone is enchondral origin
Haversian canal and transmit part of the
vascular supply to osteons
3 shapes of bones:
flat (scapula)
cuboidal (vertebra)
long (femur, tibia)
-all bones are histologically similar except for the Haversian system found in
the compact parts of long bones
-flat and cuboidal bone consists of inner and outer plate of compact bone,
cancellous bone in between

LONG BONE
1. Elongated medullary canal
2. Endosteum - fine layer of connective tissue
3. Cortex of diaphysis or shaft: composed of
compact bone with Haversian system
4. Periosteum : outer fibrous covering

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CORTICAL (COMPACT) BONE
Microscopic Subtypes Characteristics Examples
‣ Interstitial lamellae: between osteons
Appearance
-fibrils connect lamellae but do not cross cement lines
-cement line define the outer border of an osteon Woven Immature Not stress- Fractured callus
‣ Nutrition provided by intraosseous circulation oriented
-canals and canaliculi (cell processes of osteocytes)
‣ Characterized by slow turnover rate, higher modulus of elasticity, more Pathologic Random Osteosarcoma
stiffness. organization Fibrous
Increased dysplasia
turnover
Weak, flexible

Cellular Biology
OSTEOBLASTS

-Associated with formation of new bone tissue

-Found in surface of actively growing bone

-Functions in manufacturing organic bone matrix and plays a role in
CANCELLOUS (SPONGY OR TRABECULAR) BONE
mineralization

‣ mostly found in the metaphyseal and epiphyseal area
-Derived from undifferentiated mesenchymal stem cells 0 Differentiation
‣ Consists of fine trabeculae oriented in the bone in a manner best to
affected by interleukins, PDGF, IDGF
withstand stress
‣ Less dense
OSTEOCYTES

‣ Arranged parallel to the surface lamellae
-Maintain bone; living element of bone tissue

‣ More remodeling according to lines of stress
-Constitute 90% of the cells in the mature skeleton

‣ Characterized by high turnover rate, smaller modulus of elasticity, more
-Former osteoblasts surrounded by newly formed matrix

elasticity
-Less active in matrix production

-Important for control of flow of extracellular minerals (calcium and
phosphorus concentration) in and out of the bone

OSTEOCLASTS
-Resorb bone
- Multinucleated, irregular giant cells

- Derived from hematopoietic cells in macrophage lineage

- Has a ruffled brush border consisting of plasma membrane
enfoldings that increase surface area for resorption

- Bone resorption occurs in depressions (Howship’s lacunae)

OSTEOPROGENITOR CELLS
-Originate from mesenchymal cells
-Become osteoblasts under conditions of low strain and increased oxygen
tension
Bone Histology
-Become cartilage under conditions of intermediate strain and low oxygen
Lamellar - fine, altering layers
tension
Woven - a complex pattern of interconnected elements
-Become fibrous tissue under conditions of high strain
Microscopic Subtypes Characteristics Examples -Line Haversian canals, endosteum and periosteum
Appearance
BONE RECEPTOR EFFECTS
Lamellar Cortical Structure is Femoral shaft
oriented along
lines of stress
Strong

Cancellous More elastic Distal femoral

than cortical metaphysis
bone

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 BONE MATRIX TISSUES SURROUNDING BONE
Organic components : 40% of dry weight of bone Periosteum

1. Collagen (90%) -Connective tissue membrane which covers the bone
-primarily collagen type 1 -Highly developed in children
-provides tensile strength Parts :
2. Proteglycans 1. Cambium layer
-partly responsible for compressive strength -inner periosteum
3. Matrix proteins -Loose and vascular

-promotes mineralization and bone formation -contains cells capable of becoming
-osteocalcin, osteonectin osteoblasts which enlarge the diameter
4. Growth factors and cytokines of bone during growth and form
periosteal callus during fracture healing
Inorganic components: 60% of dry weight of bone
1. Calcium Hydroxyapatite 2. Fibrous layer
-Ca10(PO4)6(OH)2 -Outer periosteum

-provides compressive strength -Less cellular and contiguous with joint capsules
2. Calcium phosphate
Bone Marrow
Bone Remodeling -Source of progenitor cells
-cortical and cancellous bone are continuously remodeled throughout life Types :
by osteoblastic and osteoclastic activity 1. Red marrow

-Hematopoietic
WOLFF’s LAW : remodeling occurs in response to mechanical stress -40% water, 40% fat, 20% protein
-Slowly changes to yellow marrow with age
HEUTER-VOLKMANN LAW: compressive forces inhibits growth; tension 2. Yellow marrow
stimulates it -Inactive
-15% water, 80% fat, 5% protein
CORTICAL BONE
-osteoclastic tunneling (cutting cones) BONE FORMATION
-followed by layering of osteoblasts and successive deposition of layers of
lamellae
-the head of the cutting cone is made up of osteoclasts

CANCELLOUS BONE
-osteoclastic resorption occurs and then osteoblasts lay down new bone

BONE CIRCULATION
-bone receives 5-10% of the cardiac output
-long bones receive blood from 3 systems:

*Nutrient artery system

-Branch from systemic arteries, enter the diaphyseal cortex
through the nutrient foramen, enter the medullary canal and branch into
ascending and descending arteries
-Blood pressure is high
ENCHONDRAL OSSIFICATION
*Metaphyseal-epiphyseal system
-this system arises from the periarticular vascuilar plexus (e.g.
geniculate arteries)

*Periosteal system
-consists mostly of capillaries that supply the outer third of the
mature diaphyseal cortex
-blood pressure in this system is low

Direction of Blood Flow:

-Arterial flow in mature bone centrifugal (inside to outside) due to
the net effect of the high-pressure nutrient artery system and the
low-pressure periosteal system

-In fractures and in immature, developing bone, blood flow is
centripetal (outside to inside) because the nutrient artery system
is disrupted
-Venous flow in mature bone is centripetal (cortical capillaries
drain to venous sinusoids which drain to the emissary venous system)

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PHYSIS Diastrophic dwarfism
-growth plates in immature long bones -Characterized by short limbs, multiple joint contractures, external ear
Physeal cartilage zones: deformities and proximally set hitchhiker’s thumb
1. Reserve zone -Kyphoscoliosis and very resistant clubfoot deformity
2. Proliferative zone -Autosomal recessive disorder
3. Hypertrophic zone
3.1 Maturation zone PROLIFERATIVE ZONE
3.2 Degenerative zone •Growth is longitudinal
3.3 Zone of provisional calcification • Stacking of chondrocytes
• Cellular proliferation and matrix production
• Increased oxygen tension and increased proteoglycans inhibit
calcification
• Growth hormone exerts its effect in this zone
• Example disease : Gigantism, Achondroplasia

ACHONDROPLASIA

-is a bone growth disorder that causes disproportionate
dwarfism
-Dwarfism is a pathologic diminution in stature below 10th percentile
Types:
1.Disproportionate dwarfism

Rhizomelia(humerusandfemur)

Mesomelia (radius, ulna, tibia and fibula)
Acromelia (Hands and feet)
2.Proportionate dwarfism (midget)

HYPERTROPHIC ZONE
Divided into 3 zones : maturation, degeneration and provisional
calcification
• Normal matrix mineralization
• Chondrocytes increase 5x in size, accumulate calcium in
mitochondria, die, and release calcium for matrix vesicles
• Osteoblasts migrate from sinusoidal vessels and use cartilage as a
scaffolding for bone formation
• Low oxygen tension and decreased proteoglycan aggregates
• Example disease : rickets (zone of provisional calcification,)
mucopolysaccharide diseases (zone of maturation and degeneration)

RESERVE ZONE
• Cells store lipids, glycogen and proteoglycans
• Decreased oxygen tension
• Example disease : Lysosomal storage diseases (e.g. Gaucher’s disease)

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HURLER’S SYNDROME (MPS I) 6. Tumors

-also called gargoylism -abnormal growths in the bone -benign (more amenable to treatment)
-most common, autosomal recessive or malignant (more serious prognosis)
-defect in α L idurodinase enzyme
-deposition of large cells called 7.Circulatory disorders
Hurler or gargoyle cell • disturbances in blood supply (esp in the physis) causes changes in growth
-worse prognosis; fatal due to heart • lesions are called aseptic, ischemic or osteonecrosis
failure • disturbances that increase blood flow to an epiphysis (e.g healing
-shortened neck, large skull, fracture) may increase bone length
prominent forehead
8. Neurologic disorders
MUCOPOLYSACCHARIDES • lesions in the brain: cerebral palsy
Hurler’s Syndrome: Clinical Manifestations • lesions in the spinal cord: paraplegia, poliomyelitis
-Heavy and grotesque fascies • lesions in the peripheral nerve: localized paralysis
-Large, boat shaped head
-Noisy mouth breathing 9. Psychological disorders
-Gibbus at the dorsolumbar junction • psychiatric disorders may lead to joint lesions (contractures)
-Corneal clouding and retinal degeneration
-Mental retardation

-Enlarged abdomen
 Epiphyseal plate or growth plate - seen in children found between
-Stature may be normal
 metaphysis and diaphysis
-Joint stiffness, usually in flexion Epiphyseal line - seen in adults
Cancellous bones - weaker, more holes
MORQUIO SYNDROME
 osteoBlasts, Builds
-Affects male and female osteoCytes, Consumes
-Autosomal recessive As we age, mas maraming nasisira, kaunti ang napapalit.
-Symptoms noted when child begins to walk, change in spine, femoral head Pag nadisrupt ang lamella, magiging woven, not parallel.
are enlarged with limited external rotation, spine is stiff It takes years to remodel long bones.
-Poor prognosis; death from complications of spinal cord compression or Heuter-Volkman Law - example is scoliosis
cariorespiratory failure in third decade Our growth hormone functions while we are sleeping
Red marrow produces blood cells
Morquio’s syndrome clinical features: Factors of growth: Genetics and hormones
-Severe dwarfing due to short trunk
 Proliferative - most important zone
-Normal intelligence
 -production of new cells
-Marked dorsolumbar kyphosis Diabetes - lesser blood supply in bones
-Pectus carinatus
 Boys - common ang malignant
-Joint laxity

-Mildly cloudy cornea 0 Genu valgus

-Enlarged bone end

ETIOLOGY OF MUSCULOSKELETAL DISORDERS

1. Congenital anomalies: abnormalities in the development of the limbs
and spine
• genetic abnormalities
• environmental changesaffecting the developing fetus
• combination

2. Trauma
• mechanical injury (acute or chronic) causing sprain, fracture,
degenerativedisc disease

3. Infection
-pathogenic organisms enter bone
(osteomyelitis ) or joint septic arthritis)
1. bloodstream
2. directly from open wounds or
3. extension from a neighboring focus

4. Metabolic disorders

-metabolic disturbances causing changes in and about the bones and joints

-e.g. Gouty arthritis - disturbance of purine metabolism

5. Endocrine disorders
• extensive changes in the bone due to abnormalities of the endocrine
gland (e.g. bone resorption with hyperparathyroidism)
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