Locomotor System I Bones

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MBBS2 Tutorial - Locomotor System 2 - Bones

1. To be aware of the mechanisms underlying some non-neoplastic conditions of bone, as well as their
characteristic macroscopic appearance
2. Understand the classification of benign and malignant bone tumours
3. Knowledge of the important pathological features of the more important bone tumours
Bones
-

Essential role in mineral homeostasis, house hematopoietic elements

Provides mechanical support for movement
Protects viscera
Determines body size and shape

Differences between ADULT AND CHILD

- Articular cartilage thicker in children and can remodel
- Growth plates specific Salter-Harris classification
- Junction between epiphysis and metaphysis vulnerable to disruption especially from shearing forces
- Apophysis relatively weak cartilaginous plates where tendons attach to bone
- Metaphysis in children more resistant to force without fracturing.
- Periosteum Children thick responsible for growth in circumference influences fracture type and
provides some stability to fracture. Periosteum is thinner in adults.
- Arrangement of protein is paediatric bone differs to adult making in more plastic allowing deformity
before fracturing.

Review the histology of bone and the function of the cells.

- Made up of organic matrix (osteoid) and mineral calcium hydroxyapatite gives bones strength and
hardness
- Different types of cells
o Osteoprogenitor cells pluripotent mesenchymal SC found in vicinity of all bony surfaces
o When appropriately stimulated by growth factors, produce offspring that differentiates into
osteoblasts, process governed by RUNX2/CBFA1 transcription factor network and WNT/catenin signaling pathway
o Osteoblast and lining cells located on surfaces of bone

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Cells synthesize, transport and arrange proteins of matrix and initiate process of
mineralisation
Osteoblast have receptors that bind regulatory hormones (PTH, Vit D, Leptin and
estrogen) , cytokines, growth factors, and ECM proteins
In turn express several factors that regulate differentiation and function of
osteoclasts
If osteoblast become surrounded by newly deposited organic matric, transform
into osteocytes
Osteoblast remaining on bone surface may become flattened and quiescent bone
lining cells
o Osteocytes communicate with each other and with cells on bone surface via intricate network of
cytoplasmic processes that traverse tunnels in matric (cannaliculo)
Osteocytes control calcium and phosphate levels in microenvironement and detect
mechanical forces and translate them into biologic activity (mechanotransduction )
o Osteoclasts responsible for bone resorption, derived from same hematopoietic progenitor cells
that also giver rise to monocytes and macrophages
Cytokines and growth factors that regulate human osteoclast differentiation and
maturation include macrophage colony-stimulating factor (M-CSF) , interleukin-1 (IL-1)
and TNF
Mature multinucleated osteoclasts (containing 6-12 nuceli) from fusion of circulating
monoculear precursors and have limited lifespan
Bind to bone surface via integrins
Form underlying resorption pit (self-contained extracellular space analogous to secondary
lysosome )
Cell membranes overlying resoprtion pit thrown into numerous folds (ruffled border)
increasing its digestion products
Osteoclast removes mineral by generating acidic environment utilizing proton pump
system , digest organic component by releasing proteases

Hormones, cytokines, growth

factors, and signal-transducing
molecules are key in their formation
and maturation, and allow
communication between osteoblasts
and osteoclasts. Bone resorption and
formation in remodeling are coupled
processes that are controlled by
systemic factors and local cytokines,
some of which are deposited in the
bone matrix. BMP, bone
morphogenic protein; LRP5/6, LDL
receptor related proteins 5 and 6.
A, Active osteoblasts
synthesizing bone
matrix. The
surrounding spindle
cells represent
osteoprogenitor cells.
B, Two
osteoclasts resorbing
bone.

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Control mechanisms
- Transmembrane receptor RANK receptor activator for NF-KB expressed on osteoclast precursor
- RANKL expressed on osteoblast and marrow stromal cells
- Osteoprotegerin (OPG) secreted decoy receptor made by osteoblast and other types of cells that
can bind RANKL
- When stimulated by RANKL, RANK signaling activates transcription factor NF-KB essential for
generation and survival of osteoclasts
- Second important pathway involves M-CSF produced by osteoblasts and M0CSF receptor, which is
expressed by osteoclast progenitors
o Activation of M-CSF receptor stimulates tyrosine kinase activity that is also crucial for
generation of osteoclasts
o Other notable pathways, WNT/P-catenin pathway
WNT proteins produced by marrow stromal cells bing to LRP5 and LRP6 receptors on
osteoblasts and thereby trigger activation of -catenin and production of OPG
- Bone formation and resoprtion are tightly coupled
o Systemic factors affecting RANKL and OPG expression
Hormones (PTH. Estrogen, testosterone and glucocortoids)
Vit D
IL-1
mechanisms
Growth factors
Paracrine molecular
that regulate
osteoclast formation and function. Osteoclasts are
derived from the same stem
cells that produce macrophages. Osteoblast/stromal
cell membraneassociated RANKL binds to its
receptor RANK located on the cell surface of
osteoclast precursors. This interaction in the
background of macrophage colony-stimulating factor
(M-CSF) causes the precursor cells to produce
functional osteoclasts. Stromal cells also secrete
osteoprotegrin (OPG), which acts as a decay receptor
for RANKL, preventing it from binding
the RANK receptor on osteoclast precursors.
Consequently, OPG prevents bone resorption by
inhibiting osteoclast differentiation.

Proteins of bone
- Type 1 collagen
- Many non-collagenous proteins derived mainly from osteoblasts

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Osteoblast deposit collagen either in random weave woven bone or in orderly layered manner
designated lamellar bone
Normally woven bone is seen in sites of rapid bone formation such as fetal skeleton and base of growth
plates
Produced quickly and resist forces equally from all directions
Presence of woven bone in adults is always abnormal
Lamellar bone gradually replaces woven bone during growth, is deposited much more slowly and is
stronger than woven bone

Bone modeling, remodeling and peak bone mass

- Local collections of osteocytes, osteoblasts and osteoclasts work together to control bone formation and
resorption creating functional unit basic multicellular unit (BMU)
- Early life skeleton grows and enlarges (modeling)
o Bone formation predominates
- Skeletal maturity breakdown and renewal of bone that constitutes skeletal maintenance = remodeling
o Initiated at sites experiencing fatigue, microdamage
- Peak bone mass achieved in early adulthood after cessation of growth
o Determined by polymorphism in receptors for vit D and LRP 5/6, nutrition, physical activity.
Age and hormonal status
o Beginning of 4th decade, amt of bone resorbed by BMU exceeds that formed steady decrement
in skeletal mass
Bone growth and development
- Most bone first formed as cartilage model or anlage
- Subsequently, around 8th week of gestation, process of
enchondral ossification begins, cartilage is removed by
osteoclast0type cells form medullary canal
- Process progresses along length of bone
- Concurrently periosteum in midshaft generates osteoblast that
deposit the beginnings of cortex Primary center of ossification
- Similar events occur in epiphysis resulting in removal of
cartilage and deposition of bone in centrifugal fashion (secondary
center of ossification)
o Plate of cartilage analage become entrapped between
expanding centers of ossification
o Form physis or growth plate
- Chondrocytes within growth plate responsible for longitudinal
growth
o Undergo series of changes, including proliferation ,
growth, maturation and apoptosis
o Controlled by number of signaling pathways, including
those involving FGF receptors and bone morphogenetic
protein, hedgehog protein and PTH related protein
- In region of apoptosis matrix mineralizes and is resorbed by
osteoclast
o But remnant struts persist and act as scaffolding for
deposition of bone on surfaces
o These structures are known as primary spongiosa and are
the first bony trabeculae

Active growth plate with ongoing

enchondral ossification. 1, Reserve
zone. 2, Zone of proliferation.
3, Zone of hypertrophy.
4,Zone of mineralization.
5, Primary spongiosa.

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o Similar process occurs at base of articular cartilage, and by this mechanism bones increases in
length and articular surfaces increase in diameter
o In contrast, bones derived from intramembranous formation, such as cranium and lateral portions
of clavicles are formed by osteoblast directly from fibrous layer of tissue that is derived from
mesenchyme
o Because bone tissue is made only by osteoblasts enlargement of bones is achieved by the
deposition of new bone on pre-existing surface
o Mechanism of appositional growth is key understanding bone growth and modeling
Non-neoplastic conditions of bone
Hereditary:
Disease caused by defects in hormones and signal transduction mechanisms
Achondroplasia
- Autosomal dominant disorder (80% from new mutations, most occur in paternal allele)
- Point mutation in the FGF receptor 3 gene
o Normally FGF mediated activation of FGFR3 inhibits cartilage proliferation
o In achondroplasia, mutations cause constitutive activation of FGFR3 Suppress growth
- Most common disease of the growth plate and is a major cause of dwarfism.
- Premature closure of the growth plate due to reduced chondrocyte proliferation with normal appositional
bone formation.
o Affected individuals have shortened proximal extremities
o Trunk of relative normal length
o Enlarged head with lubing forehead
o Conspicuous depression of root of nose
o Skeletal abnormalities not associated with changes in longevity, intelligence or reproductive
status
X4329B. Lower limb bones from a
Tyrion lannister
man aged 68 with achondroplasia.
- Large head
Death was due to myocardial
- Frontal bossing of head
infarction. See the short and
- Forearm is relatively normal sized, proximal arm
disproportionately thick bones
bones shortened
- Trunk is relatively normal sized
Cortical bone thickness is increased
- Have intelligence and life span
Affected patients have normal intelligence and life-span.
Thanatophoric dwarfism most common lethal form of dwarfism
- Gain of function mutation in FGFR3 (differ from those in achrondroplasia)
- Affected individuals have micromelic shortening of limbs, frontal bossing, relative macrocephaly, small
chest cavity and bell-shaped abdomen
- Underdeveloped thoracic cavity leads to respiratory insufficiency
- Individuals frequently die at birth or soon after
Disease associated with defects in extracellular structural proteins
Importance of structural bone proteins exemplified by diseases associated with deranged metabolism of
collagens important in bone and cartilage formation
Clinical manifestations highly variable

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Osteogenesis Imperfecta Type 1 collagen disease

- Brittle bone disease
- Phenotypically diverse disorder caused by deficiencies in synthesis of type 1 collagen
- Most common inherited disorder of connective tissue
- Principally affects bone
- Also impacts other tissues rick in type 1 collagen (joints, eyes, ears, skin, teeth)
- More common types are inherited as autosomal dominant but sporadic mutations can occur
o Most involve genes that encode 1 and 2 chains of collagen
o Many of these mutations involve substitution of glycine residues in triple-helical domain
o Genotypephenotype relationship underlying osteogenesis imperfect, based on location of
mutation within protein
Mutation resulting in decreased synthesis of qualitatively normal collage associated with
mild skeletal abnormalities
More severe or lethal phenotypes have abnormal polypeptide chain that cannot be
arranged in triple helix
Type 1 collagen major component of all strong bones, triple helix structure strong and stable
- If 1 branch of triple helix is down helical structure not formed properly
- Lack of synthesis
- Lack of helical formation
Severe osteoporosis with marked cortical and trabeculae thinning resulting in extreme skeletal fragility.
Characteristic blue sclera thinning of outer layer of sclera, therefor looking straight into choroid

Skeletal
radiogram of a
fetus with lethal
type II OI. Note
the numerous
fractures of
virtually all
bones,
resulting in
accordion-like
shortening of the
limbs.

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Clinically OI separated into 4 major subtypes

Type II variants uniformly fatal in utero or during perinatal period
- Characterized by extraordinary bone fragility with multiple intrauterine
fractures
Type 1 form normal life span, experience childhood fractures that decrease in
frequency following puberty
- Other findings, blue sclerae caused by decrease collagen content, making
sclera translucent and allowing partial visualization of underlying choroid
- Hearing loss related to both sensorineural deficit and impeded conduction
due to abnormalities in bones of middle and inner ear
- Dental imperfections
- Small misshapen blue yellow teeth secondary to deficiency in dentin
- Basic abnormality in all forms of OI too little bone, thus constituting
type of osteoporosis with marked cortical thinning and attenuation of
trabacula

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Multiple rib fractures in a

neonate with OI
congenita. There were
severe limb deformities.
The patient made only a
few ineffectual respiratory
movements after birth.

Osteopetrosis
Radiogram of the
- Aka marble bone disease and Albers-schoneberg disease
upper extremity in
rare genetic disease that are characterized by reduced
an individual with
bone resoprtion and diffuse symmetric skeletal sclerosis
osteopetrosis. The
due to impaired formation or function of osteoclasts
bones are diffusely
- Osteopetrosis stonelike quality of bones
sclerotic, and the
o Bones are abnormally brittle and fracture easily
distal
o Autosomal recessive and dominant forms
metaphyses of the
Mild
ulna and radius are
poorly formed
Severe
Pathogenesis
- Interfere with process of acidification of osteoclast
resorption pit, required for dissolution of calcium
hydroxyapatite within matrix
o Eg: CA2 encodes enzyme carbonic anhydrase II
o Required by osteoclast and renal tubular cells to generate protons from carbon dioxide and water
o Lack of CAII Prevents osteoclast from acidifying
resoprtion put and solubilizing hydroxyapatite
o Blacks acidification of urine by renal tubular cells
Morphology
- Due to deficient osteoclast activity
- Bones lack medullary canal and ends of long bones are
bulbous (Erlenmeyere fask deformity) and misshapen
- Neural foramina are small and compress exiting nerves

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Primary spongiosa normally removed during growth, persists and fills medullary cavity no room
for hematopoietic marrow and preventing formation of mature trabeculae
Deposited bone not remodeled
o Woven in architecture
Section of proximal tibial diaphysis
o Intrinsic abnormalities cause bone to be brittle and
from a fetus with osteopetrosis. The
predisposed to fracture
cortex (1) is present, but the
o Histologically number of osteoclast may be normal,
medullary cavity (2) is filled with
increased or decreased depending on underlying
primary spongiosa, which replaces
genetic defect
the hematopoietic elements.

Clinical features
- Severe infantile malignant osteopetrosis autosomal recessive
- Becomes evident in utero and facial paralysis , repeated often fatal infections because of inadequacies
of marrow produced in extramedullary sites also causes prominent hepatosplenomegaly
- Mild autosomal dominant begin
Osteoporosis
- Disease characterized by porous bones and reduced bone mass
- Causes
o Primary
Post menopausal
Senile
o Secondary
Endocrine disorders
Hyperparathyroidism
Hyperthyroidism
Hypothyroidism
Pituitary tumors
DM 1
Addisons disease
Neoplasia
MM
Carcinomatosis
GIT
Malnutrition
Malabsorption
Hepatic insufficiency
V C,D, deficiencies
Drugs
Antico-agulants
Chemo
Corticosteroids
Anticonvulsants
Osteoporotic vertebral body (right) shortened by
OH
compression fractures compared with a normal
Pathogenesis
vertebral body. Note that the osteoporotic vertebra
- Peak bone mass archived during young
has a characteristic loss of horizontal trabeculae
adulthood
and thickened vertical trabeculae

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Magnitude determined hereditary factors polymorphisms in genes that influence bone metabolism
Physical activity, muscle strength, diet hormonal state also make important contributions
Imbalance between bone resopriton and bone formation
Accordingly, age-related bone cells and matrix and strong impact on bone metabolism
o Osteoblast from elderly individuals have reduced proliferative and biosynthetic potential
o Proteins bound to extracellular matrix (such as growth factors, which are mitogenic to
osteoprogenitor cells and stimulate osteoblastic synthetic activity)
Losing biologic punch over time
o Net result is diminished capacity to make bone
o This form osteoporosis, known as senile osteoporosis low-turnover variant
Reduced physical activity increases the rate of bone loss in experimental animals and humans
o Because mechanical forces stimulate normal bone remodeling
o Bone loss in an immobilized or paralyzed extremity
o Load magnitude influences bone density more than number of load cycles
o Muscle contraction is dominant source of skeletal loading (resistance exercise impt)
Genetic factors RANKL, OPG, RANK
Bodys calcium nutritional state impot
o Calcium deficiency occurring during period of rapid growth stunt peak bone mass
o Calcium deficiency increase PTH conc reduced levels of vitamin D
Hormonal influences decade after menopause poste menopausal osteoporosis
o Hormone-dependent acceleration of bone loss that occurs during decade after menopause
o Effects of estrogen mediated by cytokines
Decreased estrogen levels increased secretion of inflammatory cytokines by blood
monocytes and bone marrow cells
Cytokines stimulate osteoclast recruitment and activity by increasing RANKL and
diminish OPG

3 main
- Inadequate peak bone mass mechanism
- Excessive bone resorption
- Inadequate formation of bone during remodeling
Morphology entire skeleton affected in postmenopausal and senile osteoporosis
- Post menopausal osteoporosis inc osteoclast activity affects mainly bones or portions of bones
that have increased surface area cancellous compartment of vertebral bodies
- Trabecular plates become perforated, thinned and lose interconnections leading to progressive
microfractures and eventual vertebral collapse
- Senile osteoporosis cortex thinned by subperiosteal and endosteal resorption
- Haversian systems widened
Clinical course
- Clinical manifestations of osteoporosis depend on which bones involve
- Vertebral fractures that frequently occur in thoracic and lumbar regions are painful
o Multiple cause significant loss of height and various deformities
o Including lumbar lordosis and kyphoscoliosis
o Complications of fractures of femoral neck, pelvis or spine PE, pneumonia
- Osteoporosis cannot be reliably detected until 30-40% of bone mass is lost and measurement of blood
levels of calcium, phosphorus and alkaline phosphatase are not diagnostic
Infections:

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Osteomyelitis 2288
Most commonly affects children with pain in a long bone.(but may present in any form, mild fever)
Spread
1) Haematogenous spread most cases in children
2) Extension from contiguous site
3) Direct implantation often in adults open fracture, surgical complication, diabetic infections
Usually bacterial Staphylococcus Aureas 80-90% as a result of direct entry (compound fracture, complication
of internal fixation of fracture) or haematogenous (septicaemia).
Organisms express receptors for bone matrix components such as collagen
- Facilitates adherence to bone tissue
E.coli, pseudomonas, klebsiella more frequently isolated from individuals with gentiurinary tract infections
or IV drug users
Mixed bacterial infection seen in direct spread or inoculation of organisms during surgery or open fractures
Haemophillus influenza ad Group B strep neonatal period
Salmonella sickle cell disease
Location of infection within bone influenced by osseos vascular circulation varies with age
Age
Location
Neonates
Metaphyseal vessels penetrate growth plate
- Infection of metaphysis, epiphysis or both
Children
Localization of micro-organisms in metaphysis is typical
Adults after growth plate closure Metaphyseal vessels reunite with epiphyseal counterparts provide route
for bacteria to seed epiphyses and subchondral regions
Morphology Depends on
Stage
- Acute
- Subacute
- Chronic
Location of infection
Once in bone, bacteria proliferate and induce acute inflammatory reaction
Entrapped bone undergo necrosis within first 48 hours bacteria and
inflammation spread within shaft of bone
- May percolate within haversian system to reach periosteum
- In children periosteum loosely attached to cortex
o Sizable subperiosteal abscess may form (may track for long distances
along bone surface)
- Lifting of periosteum further impairs blood supply to affected region
o Suppurative and ischemic injury cause segmental necrosis
- Necrotic bone forms the inner sequestrum
- Rupture of periosteum soft tissue abscess and eventual formation of
draining sinus
- After 1st week chronic inflammatory cells become more numernous
release cytokines
o Stimulate osteoclastic bone resprtion
o Ingrowth of firous tissue

In infants, epiphyseal
infection spreads
through Articular
surface or along
capsular and
tendoliagmentous
insertions
producing septic
arthritis

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o Deposition of reactive bone in periphery

Newly deposited bone forms sleeve of living tissue around segment of infected bone (outer
involucrum)
Other variants
The drainage tract in
o Broadie abbess small intraosseous abscess that involves cortex,
the subperiosteal shell
walled off by reactive bone
of viable new
o Sclerosis osteomyelitis of Garre in jaw associated with extensive
bone (involucrum)
new bone formation that obscures much of underlying osseous
reveals the inner
structure
native necrotic cortex

Pathogenesis brief: bacteria focus of acute inflammation compression of blood vessels necrosis of bone
fragments reactive new bone formation. Hervation system bacterial can travel
Pus underneath periosteum and can be lifted of causing multiple segments of bone necrosis
Osteoclast engulf necrotic bone and release growth factor within necrotic bone formation of new bone
around necrotic bone (involucrum)
Clinical course
- Haematogenous osteomyelitis manifests as acute systemic illness
o Malaise
o Fever
o Chills
o Leukocytosis
o Marked to intense throbbin pain over affected region
Radioogical Finding
- Lytic focus of bone destruction surrounded by zone of sclerosis
Treatment antibiotics + surgical drainage
Chronicity may develop
- Delay in diagnosis
- Extensive bone necrosis
- Inadequate antibiotic therapy or surgical debridement
- Weakened host defenses
- Other complications
o Pathological fracture
o Secondary amyloidosis
o Endocarditis
o Sepsis
o Development of squamous cell carcinoma in sinus tract
o Sarcoma in infected bone
Pagets Disease (Osteitis Deformans)
Chronic disease of unknown aetiology. Some people say may be related to
measles virus (paramaxyal virus)
Characterised by the presence of regions of major osteoclastic bone
resorption followed by periods of uncoordinated bone formation.
May affect part of one bone, an entire bone or many bones.
Patients have few symptoms.
3 stages :
1. initial osteolytic stage

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2. a mixed osteoclastic osteoblastic stage which is ultimately predominantly osteoblastic

3. Burn-out quiescent osteosclerotic phase
Net effect newly formed bone is disordered and architecturally unsound
The affected bones become larger than normal and are composed of coarsely thickened trabecular and
cortices.
- Frantic bone resorption and unorganized laying down in bone structure is less stable
- Bones are much thicker but are softer and porous than normal bones therefore weaker
Epidemiology
- Begins in late adulthood (avg age at diagnosis 70years)
- Becomes progressively more common thereafter
- Pagets disease relatively common in whites
Pathogenesis
- Cause of Pagets disease remains uncertain
- Risk of developing disorder is approximately 7 times greater in first-degree relatives of affected
individuals
- Mutations in SQSTM1 present in 40 50% of cases of familial Pagets disease and in 5% to 10 of pt
without family history
- SQSTM mutations enhance NF-KB activation by RANK signaling leading to increased osteoclast
activity and an increased susceptibility to disease
- Mutations in RANKL and RANK/OPG
Morphology
- Hallmark mosaic pattern of lamellar bone produced by prominent cement lines that anneal units of
lamellar bone
- Initial lytic phase waves of osteoclastic activity and numerous resorption pits
- Osteoclasts abnormally large, have many more than normal 10-12 nuclei
- Osteoclast persist in mixed phase forming surface replaced by loose connective tissue that contains
osteoprogenitor cells and numerous blood vessels transports nutrients and catabolites to and from
metabolically active sites
- Newly formed bone may be woven or lamellar eventually all remodled into lamellar bone
- As mosaic pattern unfolds cell activity decreases periosseous fibrovascular tissue recedes, replaced
by normal marrow bone becomes larger than normal, composed of coarsely thickened trabeculae
- Cortices are soft, porous, lack structural stability
- Bone vulnerable to deformation under stress, fractures easily
Clinical course
- Variable depend on extent and site of disease
- Most cases are mild, discovered as incidental radiographic finding
- Pagets disease monosotic in 15%, polystotic mostly
- Axial skeleton or proximal femur involved in 80%
- Pain localized to affected bone common
o Caused by microfractures or by bony overgrowth that compresses
spinal and cranial nerve roots
o Enlargement of craniofacial skeleton produce leontiasis ossea
heavy cranium
o Weakened pagetic bone invagination of skull base (platybasia),
compression of posterior fossa structures
o Weight bearing anterior bowing of femurs & tibae & distorts femoral
heads development of severe secondary osteoarthritis
o Chalkstick-type fractures freq in long bones of lower extremities
o Compression fractures spinal cord injury + development of kyphosis

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o Increased blood flow creates AV shunt high-output heart failure or exacerbation of

underlying cardiac disease
Tumours
Severe Paget Tibia
o Benign
bowed, affected
Giant-cell tumors
portion enlarged,
Giant-cell reparative granuloma
sclerotic, exhibits
Extra-osseous masses of hematopoiesis
irregular thickening of
o Malignant (most serious)
cortical & cancellous
Sarcoma (0.7-0.9% but 5 10% in severe polyostotic disease
Commonly osteosarcoma or fibrosarcoma
Arise in paget lesions in long bones, pelvis, skull and spine
Diagnosis, frequently be made from radiographic findings
o Typically enlarged with thick coarsened corticies and cancellous bone
o Active disease wedge-shaped lytic leading edge that may progress along length of bone
o Affected individuals elevated serum alkaline phosphatase levels and increased urinary
excretion of hydroxyproline
o In absence of malignant transformation: Paget disease usually not serious or life-threatening
disease most have mild symptoms that are readily suppressed by calcitonin and
bisphosphonates
This shows severe
Pagets disease of
bone from a 77
year old female.

Mosaic pattern of
lamellar bone
pathognomonic of
Paget disease.

Histology in a late stage of the disease. The trabeculae of the

cancellous bone are markedly thickened. This picture is
described as a mosiac pattern, with haphazardly arranged cement
lines which link haphazardly arranged units of lamellar (cancellous)
bone. Here, the osteoblastic and osteoclastic activity has
subsided. Arrows indicate the reversal lines.
Though thicker the bones are much softer and porous than normal bones therefore they are weaker.
Signs and symptoms
- Deformities
- Bone pain
- Fractures
- Nerve or spinal cord compression
- Deafness
- Osteosarcoma
- Heart failure new bone formation required a lot of blood supply to new area- vascular genesis act
like AV shunts leading to high-output heart failure impt in pt with existing HF

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Disease associated with abnormal mineral homeostasis

Rickets and Osteomalacia
- Disorders characterized by defect in matrix mineralization most often related to vitamin D or
disturbance in metabolism
- Rickets disorder in children
o Deranged bone growth produces distinctive skeletal deformities
- Osteomalacia bones that forms during remodeling process is inadequately mineralized
o Results in osteopenia and predisposes to insufficiency fractures
Hyperparathyroidism
Primary
- Autonomous hyperplasia or tumor
- Usually adenoma of parathyroid gland
Secondary
- Commonly caused by prolonged states of Hypocalcemia resulting in compensatory hypersecretion of
PTH
- Increased PTH concentration are detected by receptors on osteoblast
- Release factors that stimulate osteoclast activity
o Skeletal manifestations of hyperparathyroidism unabated osteoclastic bone resoprtion
Entire skeleton affected in hyperparathyroidism (some areas more than others)
Anatomic changes of severe hyperparathyroidism osteitis fibrosa cystica (now rarely
encounted due to brisk treatment)
Secondary hyperparathyroidism nor as severe as primary skeletal abnormalities milder
Morphology
- Increased osteoclast activity in hyperparathyroidism affects cortical bone more severely than
cancellous bone
o Subperiosteal thinned cortices and loss of lamina dura around teeth
X-ray pattern revel radiolucency
o osteonal, endosteal surfaces
o In cancellous bone, osteoclast tunnel and dissect centrally along length of trabeculae creating
pattern of railroad tracks and producing dissecting osteritos
o Radiographic finding
Decreased bone density or osteopenia
o Osteoblast activity also increased marrow spaces around affected surfaces replaced by
fibrovascular tissue
o Brown tumor
Bone loss predisposes to microfractures and secondary hemorrhages
Elicit influx of macrophages and ingrowth of reparative fibrous tissue
Brown color result of vascularity, hemorrhage and hemosiderin deposition
Not uncommon for lesion to undergo cystic
degeneration
- Generalised osteitis fibrosa cystica (von Recklinghausen
disease of bone) severe hyperparathyroidism
o Combined increased bone cell activity, peritrabecular
fibrosis and cystic brown tumor

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Hyperparathyroidism with
osteoclasts boring into center of
the trabeculum (dissecting
osteitis).

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Resected rib, harboring an expansile brown tumor

adjacent to the costal cartilage.

Renal osteodystrophy Skeletal changes of chronic renal disease

- Increased osteoclastic bone resoprtion mimicking osteitis fibrosa cystica (severe hyperparathyroidism)
- Delayed matric mineralization (osteomalacia)
- Osteoscelrosis
- Growth retardation
- Osteoporosis
Caused by 3 major types of disorders
- High turnover osteodystrophy increased bone resorption and bone formation
- Low turnover/aplastic disease adynamic bone (little osteoclastic and osteoblastic acitivity
- Mixed pattern of disease
Pathogenesis
- Phosphate retention + Hyperphosphatemia induces secondary hyperparathyroidism (phosphate
regulate PTH secretion directly)
- Hypocalcemia develops as vit D (125 dihydroxyvitamine) fall
o Due to decrease conversion from vit D metabolite by damaged kidney
o Inhibition of renal hydroxylase
- PTH secretion increases all levels of serum calcium, suppresses PTH gene expression and secretion
o In renal failure: decrease binding of Vit D to parathyroid cells decrease degradation of PTH
- Secondary hyperparathyroidism increase osteoclast activity
Fractures
An example of an acute fracture
of the femur in a child, with
displacement, shortening and a
large haematoma. Fracture of a
femur results in a great loss of
blood and may cause death if not
treated quickly.

This shows healing fractures

of tibia and fibula. See the
early resorption of
haematomas and callus
formation.

Stages in fracture healing:

1. Vessels will be torn hematoma and fibrin clot formation. Inflammatory cell influx

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2. Debris removed and releases local growth factors attracting fibroblast fibroblast in growth and
angiogenesis new blood vessels
3. Provisional fibro-cartilaginous callus
4. Osseous callus- women bone Spongy structure (can try to weight bear now, so that osteoclast can
reabsorb disorganized bone
5. Remodeling lamellar bone
Fractures
- Classification
o Complete or incomplete
o Closed when overlying tissue is intact
o Compound fracture site communicates with skin surface
o Comminuted bone is splintered
o Displaced ends of bone at fracture site not aligned
o Pathological fracture break occurring in bone already altered by disease process
o Stress fracture slowly developing fracture follows period of increased physical activity where
bone is subjected to new repetitive loads
Repair process
- Immediately after fracture
o Rupture of blood vessels hematoma
Fills fracture gap and surrounds area of bone injury
Clotted blood provides fibrin mesh
Helps seal off fracture site + framework for influx of inflammatory cells and
ingrowth of fibroblast and new capillary vessels
Degranualted platelets and migrating inflammatory cells release PDGF, TGF-B,
FGF and interleukins , which activate osteoprogenitor cells in periosteum,
medullary cavity and surrounding soft
A, Recent fracture of the fibula. B, Marked
tissues
callus formation 6 weeks later.
Simulate osteoclastic and
osteoblastic activity
By end of first week, hematoma is organizing adjacent tissue is being modulated for
future matrix production
Fractured ends of bones are being remodeled
Fusiform and uncalcified tissue soft-tissue
or procallus provides anchorage between
ends of fractured bones but offers no
structural rigidity for weight bearing
- Activated osteoprogenitor cells deposit subperiosteal
trabeculae of woven bone that orients perpendicular to
cortical axis and within medullary cavity
- In uncomplicated fracture, repair tissue reaches maximal
girth at end of second or third week
o Helps stabiles fracture site
o Newly formed cartilage along fracture line undergoes
enchondral ossification (which normally occurs at
growth plate)
Forms network of bone that connects to reactive trabeculae deposited elsewhere in
medullary cavity and beneath periosteum

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Fractured ends are bridged by bony callus, as it mineralizes, stiffness and strength of
callus increases
o In early stages of callus formation excess fibrous tissue, cartilage and bone produced
If bone nor perfectly aligned, volume of callus greatest in concave portion of fracture site
As callus matures , subjected to weight bearing forces , portions that are not physically
stressed are resorbed
Callus is reduced in size until shape has been re-established
Medullary cavity also restored

Osteonecrosis (Avascular Necrosis)

- Infarction of bone and marrow relatively common
o Can occur in medullary cavity of metaphysis or diaphysis and subchondral region of epiphysis
o Ischemia underlies all forms of bone necrosis
o Predisposing conditions
Trauma (fractures)
Corticosteroid administration
Infection
Dysbarism (bends)
Radiation theryapy)
Pregnancy
Femoral head with a subchondral, wedge Sickle cell and other anemias
shaped pale yellow area of osteonecrosis. The
- Commonest injuries
space between the overlying articular
o Neck of femur (fractures of femoral neck may
cartilage and bone is caused by trabecular
compression fractures without repair.
cut blood supply to head artery of ligament
teres inadequate in 80%)
o Prox scaphoid
o Neck of talus
- Medullary infarcts geographic and involve cancellous bone and
marrow
o Cortex usually not affected due to collateral flow
- In subchondral infarcts, triangular or wedge shaped segment
of tissue that has subchondral plate as its base undergoes
necrosis
- Overlying articular cartilage remains viable due to nutrition
received from synovial fluid

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Deadbone empty lacunae, surrounded by necrotic adipocytes that frequently rupture, releasing fatty
acids
o Ding calcium and form insoluble calcium soaps that may persist for life
- Healing response osteoclast reabsorb necrotic trabeculae
o Those that remain act as scaffolding for deposition of new bone creeping substitution
- In subchondral infarcts, pace of this substitution is too slow to be effective so there is eventual collapse
of necrotic cancellous bone and distortion, fracture and even sloughing of articular cartilage
Clinical course
- Symptoms depend on location and extent of infarction
- Typically subchondral infarcts cause chronic pain initially associated with activity
o Then becomes progressively more constant as secondary changes supervene
o Often collapse and may predispose to severe, secondary osteoarthritis
- Medullary infarcts clinically silent except for large ones occurring in gaucher disease, dysbarism and
sickle cell anemia
- Cause
o Pain
o Bone collapse
o Arthritis
Pre-reading Ankle sprain
Anterior talo-fibular ligament
- Spans anterior lateral ankle joint
- Originates from anterior edge of fibula
lateral to articular cartilage of lateral
malleolus and insert into talus
Posterior tibiofibular ligament
- Arises form medial surface of lateral
malleolus and courses medially in
horizontal fashion to posterior aspect
of talus
Calcenofibular ligament
- Attahced on anterior edge of distal
fibula
- Calcenal insertion
Injuries
- Inversion injury lateral ligament damage
- Eversion injury medial ligament strains or ruptures
- Injuries that involve jumping or compression osteochondral damage
- Important to ask if pt can weight bear afterwards indicates more severe injury
Examination
- Degree of swelling generally correlates with soft tissue damage , distribution indicates site of maximal
trauma
- Anatomical factors what can predispose to injury
o Hind foot varus or cavovarus foot should be noted
- Direct tenderness important clinical sign in ankle injury
- Initially tenderness may be less localized after a few days finely localizing specific area of tenderness
correlates closely with damage to specific underlying structure

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Grade 1 tenderness on lateral side

Grade 2 medial and lateral tenderness
sue to impact contusion
Grade 3 sprains associated with brusing
and swelling
Grade 2 &3 often have co-exsiting injury to
other structures, most common deltoid
ligament contusions and sinus rasi injuries
Treatment
- Reduce all swelling (and therefore pain)
- Restore range of movement
- Arrange graduated return to sport with muscle strengthening and proprioceptione exercises
Sprains that do not get better
1) Sinus tarsi sybdrome inflammation of structures in sinus tarso secondary to injury
- Frequent complication of severe ankle sprain
- Also seen in pt with pers cavus, hypermobile pes planus and chronic subtalar joint instability
- Usually pt has tenderness over sinus tarsi ( conical shaped anatomical space just anterior to lateral
malleolus)
o Must be differentiated from tenderness over anterolateral ligament
Peroneal tendon pathology
- Peroneal tendon runs in common sheath contained within sulcus on posterolateral aspect of fibula
- Sulcus supplemented by superior peroneal retinulum prevents subluxation
- When sublaxation occurs pt decribes snapping sensation
- Delayed diagnosis common as sublazation may not be apparent unitl normal activity resumes
Syndemosis injury
Syndesomosis slightly movable articulation where contiguous bony surfaces are united by interosseos
ligament
- Commonly mistake for lateral liament sprains and may cause persistent disability
- Injures graded from I-III

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Osteochondral lsisons
- Damage o cartilage of talus generally caused by trauma
- Lateral lesions caused by ijuies during inversion and dorsiflexion
- Medial lesions eversion and plantar flexion (more common)
- Not diagnoised at time of trauma but present later with continuing ache , generally felt deep in ankle
- Swelling common adter weight bearing
Impingement lesions
- Soft-tssue or bony impingement lesions persisting pain at extremes of movement
- Fibrotic scar tissue may develop in lateral gutter after inversion injury
- Scar tissue may become chronically inflamed causing reactive hyperplastic synovitis
- Synovitis forms meniscoid lesion that can become trapped between lateral malleolus and talus during
dorsiflexion
Exercise and lower-limb related pain
Clinical assessment everyone asks for detailed history
Pain history
- Focal tibial pain raise suspicion of stress injury
- Diffuse pain compartment syndrome or medial tibial stress syndrome or referred pain
Nature of pain
- Deep aching pain somatic in nature
- Sharp shooting pain in narrow band radicular pain radicular pain
- Both somatic referred pain and radicular pain can arise from lumbosacral and pelvic structures
Address red and yellow flag conditions
- Neoplastic disease (primary and secondary)
- Vascular compromise (DVT, arterial obstruction)
- Osteomyelitis/septic arthritis
- Inflammatory arthritis

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- Neurological disease (neuropathes, MS, cauda equine)

Medial Tibial Stress Syndrome (MTSS)
- Stress reaction in tibia
- If not recognized early enough, can progress to stress
fracture and more protracted recovery
- Most commonly found in runners but also in ballistic
sports eg basketball, dancing
- Often presentswhen players concentrate on regaining
aerobic fitness
- First symptom
o Diffuse pain along posteromedial border of
middle and distal thirds ob tibia
o Early on: pain only at start and end of physical
activity
o Pains subsides quickly after stopping activity
- As condition progresses, pain lasts longer and occurs
even with gentle activities
- Main physical finding diffuse tenderness along
posteromedial tibia
- No tenderness to percussion or vibration vs stress
fractures (often tenderness
- No swelling or erythema
- X-Ray often normal occasional posterior cortical
thickening due to persistent bone remodeling
- Bone scan: characteristic longitudinally oriented diffuse
tracer uptake
Tibial Stress Fractures
- Bones ability to repair itself has been compromise
- Bone resorption outstrips bone formation
- Occurs when there has been increase in training or
change in training surface (shoes)
- Women particularly at risk of stress fractures pay
attention to menstrual x, weight changes, level of
nutrition, OCP
- Classically tibial stress fractures start insidiously with
ache in lower leg after exercise that settles quickly with
rest
- Progression: ache becomes pain, comes on more
quickly and lasts longer. Pain more focal and proximal
compared with MTSS
- Xray small fracture line, periosteal reaction of callus
formation.
o Anterior cortex defect dreaded black line
hallmark of anterior tibial stress fractures
- Management : reducing bony stress and identifying
modifiable risk factors
o Pt should not weight bear for 2-4 weeks
- Pt can expect to return to trainng in 8-16 weeks
o Anterior cortex fractures 6 months

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o Longitudinal stress fractures and chornic non-union proximal medial stress fractures surgery
Other stress fractures
- Tibial stress fracture most common
- Low risk fractures
o Metatarsal shaft
o Femoral shaft
o Tibial shaft
o Fibula
o Calcenus
o Sacrum
o Pubic rami
- High risk prone to non-union and progression to complete fracture
o Femoral neck
o Patella
o Anterior cortex of tibia
o Navicular
o Talus
o Medial malleolus
o Base of 5th metatarsal
o Sesamoid
Tendinosis
- Non-inflammatory condition that results in intra-tendinous degerneation related to ageing, decreased
vascular supply and microtrauma
- Needs to be distiguised from tendinitis and paraptenonitits
o Tendinitis associated inflammatory disorder (RA)
o Paratenonitis inflammation of ouerlayer of tendon (paratenon)
Responsible for crepitus felt with movement
- Tendinosis responsible for 30% of all overuse sports injuries: most common persistent forms
o Achilles running activities
May be insertional or mid-tendon
Insertional associated with haglunds deformity, prominence of posteror superior
calcaneal tuberosity that contributes to irritation of overlying tissues and Achilles tendon
o Mid-tendon Achilles tendinosis most commonly seen in recreational atheletes (30-50)
Men more risk than women (3xs)
Pain starts insidiously with some discomfrit after exercise
As it progressed pt notice pain during exercise and stiffness after inactivity
CLinicallu tneder nodular thickening in mid-tendon
o Paratenonitis
Swelling is more sausage-like
Stays fixed when foot is plantar or dorsiflexed
Thompson test performed if concern of complete tear of tendon
o Patellar tendinosis jumping activities
Insidious condition that often presents late
Tenderness to palpation usually in inferior pole of patella
Tendon may be thickened, often associated patella-femoral dysfunction
Fapina ggravated by decline squats
Chronic exertional compartment syndrome

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Bilateral, occur in men and women equally

4 distinct compartments
o Anterior most commonly affected
o Lateral
o Superficial
o Deep posterior
- Pressures become raised during exercise and stay raised for 30 mins results in myoneural ischaemia
- Pt present with pain, cramping or burning over affected compartment
- Comes with exercise, at predictable times and level of intensity, subsides when exercise stops
- Clinically tight tender musculature over affected compartment, more noticeable straight after exercise
- After exercise: neurological changes may be detectable
o Anterior compartment weakness
Weakness of dorsiflexion and loss of sensation in web of first to
o Lateral compartment
Weakness upon inversion with loss of sensation on anterolateral part of shin and dorsum
of foot
o Posterior compartment
Pt may exhibit weakness in foot muscles and loss of sensation in foot arch
Nerve entrapments
- Entrapment of common, superficial and deep peroneal nerves and saphenous nerve
- Nerve entrapments cause pain with exercise may mimic claudication
Common Peroneal
- May be irritated in peroneal tunnel by repetitive inversion and pronation of foot
- Crossed-leg position
- Pain with exercise causes anterolateral pain
- May be weakness of ankle dorsiflexion
- Food drop only present in this syndrome
Superficial peroneal nerve
- Supplies both peroneal muscle and is vulnerable where it crosses ankle anteriorly and where it
penetrates crural fascia at junction of middle and distal thirds of tibia
- Usually loss of sensation over laerla calf or dorsum of foor during exercise
Saphenous nerve
- Longest sensory branch of femoral nerve and may be irritated in adducator canal or where it crosses
medial femoral condyle
Illiotibial band syndrome
- Illiotibial band assist leg in abduction and anterolateral stability of knee
- COntiuation of tensor fascia lata with indirect attachements form gluteus medius, maximus and vastus
lateralis muscels
- With running posterior edge of and may impinge against lateral femoral epidondyle just after foot strike
- Setting up irritation in underlying tissue
- Related to increased runnin distance, knee flexion or extension, weakness and hip abductor weakness
- Pt presents with lateal knee pain that my be sharp, burning or aching
- Comes on at predictable time or distance with runnin
- Settles down quickly after run

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Laxity: is the measured amplitude of joint movement within the

constraints of its ligaments.
Physiological Laxity: implies no ligament is stretched pathologically.
Pathological Laxity: means a ligament has been stretched by injury.
Instability: is a complaint by a patient that they lose single leg stance
because the joint subluxes due to pathological laxity.
Disability: is instability that interferes with the required function of the
knee.
Knee anatomy
- Separated into 3 physiological anatomical components
o Patellofemoral compartment
o Medial compartment
Medially deep third of mid-capsular ligament + Medial collateral ligament
Posterior posterior oblique ligament and laterally by posterior cruciate ligament
o Lateral compartment
Ligaments bound medially by anterior cruciate ligament
Laterally by lateral capsular ligament + ilio-tibial tract + fibular lateral ligament
Posteriorly arcuate complex + posterior capsule
- Each of ligaments and all muscles have proprioceptive fibers
- Ligaments and tendons blend in local proprioceptive reflex arcs give rise to dynamic protection as
well as static protection
Pediatric limb fractures and dislocations
- 42% boys 27% girls
- Pediatric musculoskeletal system differs from adult in anatomy, biomechanics and physiology
- Injury patterns are unique to child
- Most pediatric fractures due to relatively low-velocity impacts during play and recreation
- Fractures and dislocations
o Direct blow
o Indirect forces
- Upper limbs especially vulnerable
- Age of child
o Fracture of scaphoid
o Distal radius
o Supracondylar region of elbow
o Clavicle
- Stress fractures uncommon until adolescences
- Pathological fractures may occur through areas of weakness benign bone cyst
- Shoulder dislocation UNCOMMON PAEDIATRIC INJURY
Unique aspects of growing bone
- Immature bone comprises
o Diaphysis s haft of long bone
Product of periosteal membrous osseous tissue laid on original endochondral model
Membranous ossification leads to increase in overall diameter of shaft
o Metaphysis expanded ends of shaft
Decreased cortical bone thickness
Considerable bone turnover

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Cortex more porous genetrations

Structure explains prominence of buckle fractures in this area
o Pysis epiphyseal or growth plate
Starts as cartilaginous structure at end of long bone
Secondary center of ossification forms and enlarges until cartilage is replaces
Chondro-osseous change is vascularly dependent
Only articular cartilage remains at maturity
Rapid longitudinal and latitudinal growth
Injuries unique to immature pt
- Resilient due to high cartilage content
o Substantial energy and soft tissue damage occur before break
o High collagen content causes immature bone to be more porous with lower tensile strength than
adult bone
o Prone to incomplete fractures , buckling (torus fractures) when compressed and bowing
when bent (plastic deformation)
o Greenstick fracture
When limit of bending leads to fracture on tension side
Plastic deformity or buckle with intact periosteum on compression side
All fractures may be described as
- Open or closed
- Simple 2 bone fragments
- Comminuted multiple fragments (unusual in children)
- Direction of fracture line
o Spiral: encircling portion of shaft
o Transverse at 90 angle to long axis of shaft
o Oblique: 30 40 to long axis
- Relationship of bone fragments to each other compared with anatomical position
o Angulation: angle of distal fragment relative to proximal fragment
o Displacement volar/dorsal, lateral/medial or radial/ulnar offset, measured as a distance or
percentage of width of proximal fragment e.g. 50%
o Length: separation or shortening (due to impaction or over-riding)
o Rotation
- 15-25% of extremity fractures in children involve physis radiotransulent cartilaginous structure
providing longitudinal and circumferential growth
o Weaker than adjacent ligaments
o Fractures more likely than sprains or dislocations

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Type 1 and 2 excellent prognosis as germinal layer is left intact

Type 2 most common often occurring at wrist of ankle
Type 3 and 4 require precise reduction usually under general anesthetic
Type 5 Crushing injury esp. knee or angle (diagnosed in retrospect) poor prognosis
Periosteum surrounding immature bones thicker and stronger than in adults limit displacement, contributing
to stability and reduce possibility of open fractures
- Children periosteum responds with vigorous callus formation
- Healing is rapid non-union is rare
- Potential for remodeling declines with age (30 in young children but 10 in older child)
Response to injury
- Injury stimulates physeal blood flow and longitudinal bone
growth
- Overriding fracture fragments with shortening may be desirable
in circumstances such as fracture of femur
- Fractures no involving growth plate will generally heal in
acceptable position if alignment of limb is maintained
- Rotational deformity remodels poorly and must be correctly
reduced
Limb-threatening injuries
- Dislocations
- Vascular injury
- Skin ischemia
- Compartment syndrome
- Open fractures
Immediate referral to hospital indicated for
- Amputations
- Significant skin loss

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Compound fractures
Clinically deformed fractures
Fractures with axial rotation, significant angulation or displacement
Actual or high risk vascular complication
Neurological compromise
Compartment syndrome indicated by
o Increasing pain in first few hours
o Tightness of muscle compartment (forearm and calf particularly vulnerable
o Pain on passive extension
o Impaired capillary refill
o Abscess of pulses (occurs late)
Suspicion of non-accidental injury
All dislocations requiring reduction under anesthesia

Upper Limb fractures

- Fracture of clavicle common usually 1/3 mid-shaft after fall on outstretched hand or onto shoulder
tip most common in children of all ages
o Rarely severe
- Humerus supracondylar fracture of distal humerus most common paediatric elbow fracture
(peak at 4-8 years)
o Usually due to fall onto outstretched hand or less commonly direct blow to flexed elbow
o Pain is often severe and swelling may be mild or severe
o Injury is transverse metaphyseal fracture
In lateral view of normal elbow, distal Humerus is tilted 30-40 anterior to longitudinal
axis of distal humeral metaphysis
Posteriorly displaced fracture associated with loss of angle and anterior humeral line will
intersect capitellum more anteriorly
o Humeral diaphysis fracture uncommon ( 0-3abuse, >12 sport,MVA)
o Supracondylar fracture median nerve
Common age 4-10 (rare in adults)
Extension pattern >> Flexion
Gartland classification
1) undisplaced and stable
2) Partially displaced but some remaining contact
3) Complete displacement
o Lateral condylar fracture second most common elbow fracture and most common physeal
elbow fracture
Occurs after fall on outstretched hand
Localized swelling on lateral distal Humerus
Injury involves large fragment of cartilaginous tissue and extends into joint (SH
4fracture)
o Medial epicondylar fractures esp. common in adolescent boys
When valgus force combined with contraction of forearm muscles throwing
50% associated with elbow dislocation
15-20% incarceration of fragment in joint
Ulnar nerve palsy not uncommon
Ensure avulsed epicondyle not trapped in joint
o Olecranon fractures rare occur in teenagers with direct trauma to elbow

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Complications
Early
Arterial injury
Absent or reduced pulse
Temp or color difference
Compartment syndrome
Severe pain
Worse with passive extension of digits
Nerve palsy
Sensory
Motor

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LATE
Volkmann Ischemic Contracture
<1%
ischemic muscle becomes
scarred & fibrotic Malunion
usually cubitus varus or
gunstock deformity

Radius and Ulnar

- Radial head fractures Do not occur until adolescences
o Monteggia fractures
Line through radial shaft should bisect capitellum in any view
Never accept isolated # of radius or ulnar without checking elbow and wrist
- In child, fall on outstretched hand causes force to be transmitted to physis and metaphysis check for
associated dislocation of elbow
- Fractures of radius and ulna common
o Range from torus (buckle) fracture of distal radias,
o Salter Harris epiphyseal injury
o Greenstick fracture of distal radius inherently stable and frequently managed by GPs
o Severely angulated fractures of distal radius and ulna
o Galeazzi Fracture Dislocation
Dislocation or subluxation of distal radioulnar joint
Fractures of wrist and hand
- Scaphoid fracture can only occur after scaphoid has ossified at age 9
- Phalangeal fractures occur during ball games reduction required for >50% displacement or
angulation >20%
- Volar plate injury suggested by history of hyperextension of finger (bent back) and small avulsed
fragment at proximal interphalangeal joint
o Fixed flexion deformity may occur if not managed properly
- Inability to extend distal interphalangeal joint mallet finger injury must be treated continuously in
splint maintaining extension
Lower Limb fractures
Femur
- Fracture of mid-shaft femur usually results from motor vehicle trauma
Tibia and fibula
- Midshaft or distal tibia fractures most common leg fracture
o May be isolated injury or combined with fracture or bowing of fibula
- Toddlers fracture
o Hairline spiral fracture of tibia common in children 1-2
o Present with failure to bear weight after minimal or no trauma
o Swelling and tenderness may be absent

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Fibular fractures treated in above-knee backslab

Greater forces may cause displaced or angulated fractures risk of compartment syndrome
o Refer pt for inpatient analgesia, elevation and reduction if required
o Fibular fracture typically results from twisting injury in young children or from motor vehicle
injury in older children
o Peroneal nerve vulnerable to damage from fibular head fractures associated with ankle injury
Ankle and Foot
- Mid-foot fractures rare
- Lisfranc fracture base of second metatarsal after jumping from tiptoe position associated with
impaired stability of midfoot and potential vascular impairment
Complications of fractures
General
- Shock
- Crush syndrome
- DVT
- PE
- Fat embolism
- Compartment Syndrome
- Tetanus
- Gas gangrene
Shock inadequate tissue perfusion
- Inadequate blood volume normal circulation: oligaemic
- Normal blood volume dilated circulation: neurogenic, septic, anaphylaxis
- Potential blood loss with closed fractures can be guesstimated
- Blood loss in open fractures potentially great: no fascia to contain loss
Oligaemic shock
- Due to blood loss
- Impending when >1.5L
Crush syndrome
- Caused by death of large muscle bulk
o Crushed limb
o Prolonged tourniquet
- Due to release of myoglobin
o Kidneys and blocks renal tubules
o Acute renal failure
o Elevated CPK, Lactic acid, creatinine
- Treatment
o >6hrs amputation of limb above crush
o Cool limb
o Treat shock
o Renal dialysis
Deep vein thrombosis
- Common complication of injury
o Fractures: esp. leg and pelvis
o Elderly
o Prolonged immobilization

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o Malignancy
o Hypercoagulability
Clot(thrombus forms in veins due to stasis and injury to vein
Clinical
o Local pain tenderness
o Swelling
o If calf thrombosis increased pain on dorsiflexion Homans sign
Inc. Temp and pulse
Treatment
o Prophylaxis
Early movement
Compression stockings
Sequential mechanical compression
Partial anti-coagulation
Aspirin
Clexane
Low-dose heparin
Established
Full anticoagulation
o Heparin
o Warfarin

PE
- 2-5% pt get PE
- Dislodgement circulation lung
- Most commonly from proximal leg or pelvic vein thrombosis
- Large thrombus may occlude pulmonary bifurcation sudden death
Clinical signs
- Chest pain-pleuritic
- Dyspnea
- Hemoptysis
- Cyanosis
- Tachycardia
- Shock
- Rales and friction rubs
Fat Embolism
1) Multiple fractures release marrow fat (and marrow)
into circulation. Globules are >7u in size
2) Fat globules filtered out in lung causing acute
respiratory syndrome
a. Some globules pass through lung and
disseminate in systemic circulation and are
filtered out in
i. Skin (petechial rash)
ii. Brain (Confusion, coma)
iii. Kidney (Haematuria, lipiduria)

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- First 72 hrs. after injury

- Half will have multiple fractures
- Fractures of femur and pelvis common
- Tachycardia dyspnea
- Cyanosis
- Hypotension
- RHF
- Pyrexia
Acute Respiratory Distress Syndrome
- Tachypnea
- Dec p02
- Inc. Temp, Inc. PR
- 75% fat embolism confined to lung
Compartment Syndrome
- Injury to muscle within fascial
compartments causes swelling
- Swelling contained within nonexpansile compartments raises
tissue pressure
- If pressure >40mmHg veins then artery will be occluded muscle ischemia
- Treatment surgery
o 4 Compartment fasciotomy
o Leave incision open
o Secondary debridement
o Delayed closure
- Volkmanns contracture
o Ischemic contracture of forearm
Due to compartment syndrome
Arterial injury in forearm or proximally
o Secondary to
Fibrosis of forearm muscles
Ischemic neuritis
Tetanus
- Obligatory anaerobe grows in dead tissue, not in presence of oxygen
- Gram positive rod spores (hibernation form)
- Occurs naturally in soil and faeces
- Sensitive to penicillin
- Produced extonin (neurotoxin)
o Transported by blood and lymphatics
o Fixes to anterior horn cells
o Once fixed cannot be neutralized
o Causes tonic and clonic muscle contraction
- Initially affects face risus sardonicus lock jaw
- Later affects trunk
- Ultimately affects respiratory muscles
- Death by asphyxiation
- Prophylaxis
- Reimmunise after skin wound
- Wound debridement and penicillin

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- Antitoxin for non-immunized with delay in treatment

Gas gangrene
- Obligatory anaerobe grows on dead tissue, not in presence of oxygen
- 7 Species: clostridium welchii most common and most lethal
- Gram positive bacilli (rods) with terminal spores (hibernation form)
- Occurs naturally in soil and bowel
- Sensitive to penicillin
Action
- Produces exotoxin
- Exotoxin spreads locally and destroys cell walls Causes cell death
- Promotes spread of organisms
Clinical
- Contaminated wound
- Clinically appears within 24 hrs. of injury
- Intense pain and swelling
Treatment
- Thorough wound debridement excise dead and devitalized tissue
- Decompression of healthy tissue
- IV Penicillin
- Hyperbaric chamber
Reflex sympathetic Dystrophy sudecls atrophy, complex regional pain syndrome
- Nerve injury may cause short cut in nervous system resulting in sympathetic
overactivity in hand or foot with burning pain, swelling and increased sweating
- Syndrome generally initiated by injury (MI or stoke)
- Burning pain generally hand or foot
- Swelling
- Immobile
- Skin- sweaty, blotchy, warm
- Later joint stiffness and deformity
Myositis ossificans (MO)
- Heterotopic ossification of muscle
- Occurs with injury, head injury and paraplegia
- Commonly brachialis and quadriceps muscles
- Pain and swelling over muscle subsides over 2-3 weeks
- By 8 weeks calcification evident , bone scan hot
Post traumatic arthritis: CAUSED BY
- Intra-articular fracture
- Malunion
- Malalignement of articular surface
- Axial alignment of weight bearing long bone >15 malalignment
- Chondrolysis
- Infection
- Avascular necrosis
Bone Tumours
Primary bone tumours
TABLE 26-6 Classification of Primary Tumors Involving Bones
Histologic Type
Benign
Malignant
Hematopoietic (40%)
Myeloma
Malignant lymphoma

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Chondrogenic (22%)

Osteogenic (19%)
Unknown origin (10%)
Histiocytic origin
Fibrogenic

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Osteochondroma
Chondroma
Chondroblastoma
Chondromyxoid fibroma
Osteoid osteoma
Osteoblastoma
Giant cell tumor
Fibrous histiocytoma
Metaphyseal fibrous defect
(fibroma)

Notochordal
Vascular

Hemangioma

Lipogenic
Neurogenic

Lipoma
Neurilemmoma

Chondrosarcoma
Dedifferentiated chondrosarcoma
Mesenchymal chondrosarcoma
Osteosarcoma
Ewing tumor
Giant cell tumor
Adamantinoma
Malignant fibrous histiocytoma
Desmoplastic fibroma
Fibrosarcoma
Chordoma
Hemangioendothelioma
Hemangiopericytoma
Liposarcoma

Benign
1. Osteochondromas (exostosis) benign cartilage capped tumor attached to underlying skeleton by
bony stalk 2302
- Most common benign tumor 85% solitary
- Remainder part of multiple hereditary exostosis syndrome (autosomal dominant hereditary disease)
- Hereditary exostoses due to germline loss of function mutations in EXT1 or EXT2 genes
- EXT1 and 2 results in defective endochondral ossification sets stage for abnormal growth
- Age usually under 20 years
- But multiple Osteochondromas apparent during childhood
- Men (3) > women
- Only develop in bones of endochondral origin and arise from metaphysis near growth
plate of long tubular bones esp the jaw
- Site near epiphyses of limb bones
- Benign outgrowth of normal bone with cartilage cap
Morphology
- Sessile or mushroom shaped
- Range in size (1-20cm)
- Cap composed of benign hyaline cartilage varying in thickness
- Covered peripherally by perichondrium
- Cartilage has appearance of disorganized growth plate and undergoes enchondral ossification
- Newly made bone forming inner potion of head and stalk
- Cortex of stalk merges with cortex of host bone
o Medually cavity of Osteochondroma and bone are in continuity

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Osteochondroma. A, X-ray of an osteochondroma arising off the posterior surface of the tibia. B,
Axial CT scan shows continuity of the cortex of the bone and the center of the osteochondroma. The
fibula is adjacent to the mass. C, Gross specimen of sessile osteochondroma composed of a cap of
hyaline cartilage undergoing enchondral ossification. D, The cartilage cap has the histologic
appearance of disorganized growth plate-like cartilage
Clinical course
- Osteochondroms slow-growing masses
- Can be painful If imping of nerve or if stalk is fractures
- Detectable as incidental finding
Chondromas benign tumors of hyaline cartilage usually in bones of enchondral origin
- Can arise within meduallary cavity (encondromas)
- Surface of bone (Subperiosteal or juxtacortical condromas)
Enchondromas most common of intraosseous cartilage tumors
- Age range 20-40 years
- Arise in medullary cavity
- Commonly solitary metaphyseal lesion of tubular bones
o Favoured sites short tubular bones of hands & feet
- may be part of syndrome eg Olliers disease or Mafucci.
Olliers disease or Mafucci.
- Olliers All have multiple Enchondromas
- Mafucci lots of Enchondromas + multiple hemangiomas
within enchondromas
Morphology Multiple lesion within medullary cavity Nodular
and translucent
Enchondroma with a nodule of hyaline
- Usually smaller than 3 cm grossly gray-blue and translucent
cartilage encased by a thin layer of
- Composed of well-circumscribed nodules of cyto logically
reactive bone.
benign hyaline cartilage
- Peripheral portion of nodules may undergo encondral
This is an example of
ossification
enchondromatosis or Olliers
o Centre can calcify and die
disease in a boy, 15 years old,
- Chrondomas in olliers disease and Maffuci syndrome
with multiple enchondromas
sometimes more cellular
(arrows) present.
o Can exhibit cytologic atypia (makes it dififcult to
distinguish from chondrosarcoma)
Clinical Features
- Mostly asymptomatic, detected incidentally

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Occasionally they are painful and cause pathologic fracture

Tumors in enchondromatosis numoerus and large, producing severe deformities
Radiological features
o Unmineralised nodules of cartilage
o Well circumscribed oval lucencies
o Surrounded by thin rim of radiodense bone (C or
o If matrix calcifies detected as irregular opacities
o Nodules scallop endosteum but leave cortex intact
o Growth potential of Chondromas limited, most
o Solitary enchodromas rarely undergo sarcomatous
but those associated with enchondromatoses do so
frequently
o Individuals with Maffucci syndrome also at risk
other types of malignancies ovarian carcinoma
gliomas

Enchondroma of
the phalanx with a
pathologic
O ring sign)
fracture. The
radiolucent
nodules
of hyaline
remain stable
cartilage scallop
transformation
the endosteal
more
surface.
of developing
and brain

3. Giant cell tumour

- Contains mixture of mononuclear cells and profusion of multinucleated osteoclast-type giant cells
- Osteocalstoma
- Relatively uncommon but locally aggressive neoplasm
- Age range 20-40 benign but locally aggressive.
- Mononuclear cells in giant-cell tumors express RANKL
o Giant osteoclast-like cells believed to form via
RANK/RANKL signaling pathway
Morphology
- Large, red-brown tumors frequently undergo cystic
degradation
- Mostly composed of uniform oval mononuclear cells that
constitue proliferating component of tumor
- Scattered within background numerous osteocaslt-type
giant cells
- Necrosis, hemorrhage, hemosiderin deposition and relative
Benign giant-cell tumor abundance of
bone formation common secondary features
multinucleated giant cells with
Location in bone:
background mononuclear stromal cells.
- Adults involves epiphyses and metaphyses
- Adolescents limited to metaphyses
Magnetic
- Most occur around : knee (distal femur and proximal tibia)
resonance image
of a giant-cell
- Typical location of tumors cause arthritis-like symptoms
tumor that
- Occasionally present with pathologic fractures
replaces most of
- Often erode into subchondral bone plate and destroy
the femoral
overlying cortex producing bulging soft-tissue mass
condyle and
delinated by thin shell of reactive bone
extends to the
- Margins with adjacent bone fairly circumscribed
subchondral
- Conservative surgery curettage 40-60% recurrence 4%
bone plate
mets to lung
The giant cell tumour (arrows) occurred in
the tibia in a man aged 29 years. He had
noticed a slowly growing lump for 11 months
and there had been a dull ache in the region
made worse by walking.
The x-ray appearance would be?

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Malignant
1. Osteosarcoma malignant mesenchymal tumor in which cancerous
cells produce bone matrix
- Most common primary malignant tumor of bone
- 20% of primary bone cancers can occur in all age range BUT
Age range 75% under 20 years common In young men
- SECOND PEAK OCCURS IN ELDERLY
o Usually associated with Pagets disease, infarcts or past
irradiation
Bone location in young people
- Metaphyseal region of long bones of extremities
- Knee most common (50%)
But In persons beyond 25 incidence in flat bones and long bones equal
Pathogenesis
- 70% acquired genetic abnormality (ploidy changes,
chromosomal aberrations)
o RB gene (retinoblastoma)
o P53
- Tend to grow at sites of bone growth as proliferation makes
osteoblastic cells prone to acquire mutations that could lead to
transformation
Pathology: several subtypes of osteosarcoma recgonised
- Site or origin(intramedullary, intracortical or surface
- Degree of differentiation
- Multicentricity (syndrobous, metachoronous)
- Primary (underlying bone unremarkable) secondary (pre-existing dosorders)
- Histologic features
Most common subtype arise in metaphysis of long bone primary, solitary, intramedullary
and poorly differentiated
- Osteosarcomas are generally big, bulky tumours
- gritty and tan-white, with areas of hemorrhage and cystic degeneration.
- Often grow through cortex, producing a soft tissue mass.
- Spread extensively in medullary canal, infiltrating and replacing marrow surrounding
osteosarcoma
pre-existing bone trabecular
(arrows) of the
- When joint invasion occurs tumor grows into it along tendoligamentous structures
femur
or through attacjemtn site of joint capsule
- Tumour cells vary in shape and size frequently have hyperchromatic nuclei
- Formation of bone by tumor cells characteristic
o Neoplastic bone coarse, lace-like architecture
o May also be deposited in broad sheets

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o Primitive trabeculae
Other matrices, including cartilage or fibrous tissue may be present in varying amounts
o When malignant cartilage abundant called chondroblastic osteosarcoma
Vascular invasion conspicuous 50-60% of individual tumor may be necrotic
Osteosarcoma of
upper end of tibia.
The tan-white
tumor fills most of
medullary cavity of
metaphysis and
proximal diaphysis.
infiltrated through
cortex, lifted
periosteum, and
formed soft-tissue
masses on both
sides of bone

Coarse, lacelike pattern of neoplastic bone

produced by anaplastic malignant tumor cells.

Characterized by osteoid formation.

Histology shows an osteosarcoma. You
can see the haphazardly deposited pink osteoid (arrows)
present surrounding and between the malignant tumour
cells. The tumour cells vary considerably in size and
shape and many have large hyperchromatic nucle i.large
hyperchromatic nucle i.

Clinical course
- Typically presents as painful, progressively enlarging masses
- Sometimes sudden fracture of bone is first symptoms
- Radiogram: desctructive, mixed lytic and blastic mass with infiltrative
margins
- Tumor frequently breaks through cortex and lifts periosteum resulting in
periosteal bone formation
- Triagular shadow between cortex and raised ends of periosteum codman
triangle
o Characteristic but not diagnostic of tumor
- Aggressive neoplasms demonstrable pulmonary metastasis (90%)

osteosarcoma with
prominent bone formation
extending into soft tissues.
periosteum, has been
lifted, has laid down a
proximal triangular shell
of reactive bone aka
Codman triangle

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2. Chondrosarcoma 2308
Produces neoplastic cartilage
Second most common malignant matrix-producing bone tumor Chondrosarcoma skeleton is 50% as common
as osteosarcoma.
Age range pt generally >40
Male to female ratio 2:1
Most cases denovo, remainder associated with pre-existing Enchondromas or Osteochondroma
Most common sites central parts of skeleton particularly in pelvis, shoulder and wrist (distal extremities
rarely involved)
Presentation
- Painful progressively enlarging masses
- Radiologically
o Endosteal scalloping
o Flocculent-appearing matrix calcifications
- Slow growing tumors can cause reactive cortical thickening
- High-grade neoplasm destroy cortex and form soft-tissue mass
Treatment wide surgical excision and chemotherapy
Lung and skeleton favored metastatic sites
Morphology
- Malignant hyaline and myxoid cartilage
- Large bulky tumors
o Lobulated, nodules of gray-white translucent glistening tissue
o Necrosis may create cystic spaces
o Spotty calcification common
Microscopically
o Classified by histologic type and as intramedullary or juxtacortical
o 90% intramedullary conventional (hyaline or myxoid) chondromas
o Most tumors low-grade
Grade 1 or 2 5 year survival of 90 -81%
Mild hypercellularity,
Chondrocytes have plump vesicular nuclei with small nucleoli
Grade 3 43% 5 year survival
Marked hypercellularity, extreme pleomorphism , bizzare tumor giant cells and
mitoses
X4291. This is a chondrosarcoma of the scapula in a woman aged 35.
She suffered from multiple hereditary exostoses and a mass arising
from the shoulder blade had recently increased in size and become
painful. This is an operative surgical specimen. Note the white
translucent appearance of the tumour.

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Histology shows a chondrosarcoma. There is

increased and uneven cellularity with
moderately pleomorphic cells present in a
chondroid matrix (blue arrows). A mitotic figure
is seen (red arrow).

Chondrosarcoma with lobules of hyaline

and myxoid cartilage permeating
throughout the medullary cavity, growing
through the cortex, and forming a
relatively well-circumscribed soft-tissue
mass.

Anaplastic chondrocytes within a

chondrosarcoma.

Metastatic bone tumours

The commonest bone tumours are metastatic carcinomas (breast, kidney, thyroid, prostate and lung).

This is the spine and humerus showing metastatic (black arrows)

breast carcinoma from a female aged 51 years. There is a pathological
fracture (red arrows) of the humeral neck and crush fractures of
vertebrae.

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X2928B. This shows multiple metastases to the skull from a

neuroblastoma of the adrenal gland from a one year old child.
What other metastases to bone can occur in children?

Clinical Case
A 80 year old man who is in hospital for radiotherapy complains of pain in his left upper arm. During the night
he turned over and felt his arm crack. On examination the Humerus is tender and swollen at about midshaft.
Q. How would you proceed? Take a Hx, imaging,
Olf X0RAY and x ray from humerus
Hx of lung Ca and metastasis to bone
X-ray shows hairline fracture of left humerus
Pathological fracture especially as no significant history of trauma and known cancer with metastases
Pt complains also complain of nausea, abdominal pain and constipation
What is possible explanation for these symptoms
- Multiple metastases causing raised serum calcium
In the same ward is a 16 year old boy with a tender swelling above his knee. He has been admitted for
haemoptysis.
Q. What is the most likely diagnosis? osteosarcoma (bimodal presentation)
- Possible metastasis to lung
This is his Xray.

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Reproduced from Robbins & Cotran

Pathologic Basis of Disease 7th Ed.
2005

Codmans triangle looks like a triangle

Tumor extending into soft tissue broken through cortex

LOCOMOTOR SYSTEM II BONES

Demonstration pots
Royal Brisbane Clinical School

X4329. Lower limb bones from a man

aged 68. Death was due to myocardial
infaction.

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X1965A. Woman aged 67.

X995. Female aged 77.

X2236A. Man aged 83..

X2874.

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X2908B. Male aged 28 with Ollier's

disease.

X3514. Man aged 78. Recurrent tumour. He

had an amputation through femoral shaft 14
years before the operation that produced the
mounted specimen..