LO MSK 2-2

1. Syarat X-ray

2. Types of fractures at child

The bones of a child are more likely to bend than to break completely because they are softer and
the periosteum is stronger and thicker.[3] The fractures that are most common in children are the
incomplete fractures; these fractures are the greenstick and torus or buckle fractures.
Greenstick fracture

This fracture involves a bend on one side of the bone and a partial fracture on the other side. The
name is by analogy with green (i.e., fresh) wood which similarly breaks on the outside when
bent. The Sub-nanostructure of cortical bone may provide one possible explanation for the
greenstick fractures in children. On the contrary to adults bone tissue, the low ratio between the
mature and the immature enzymatic cross-links in children bone tissue is a potential explanation
of the presence of greenstick fractures in children.[5]

Torus or buckle fracture

This fracture occurs at the metaphyseal locations and resemble the torus or base of a pillar in
architectural terms. Acute angulation of the cortex is noted, as opposed to the usual curved
surface. It is caused by impaction. They are usually the result of a force acting on the
longitudinal axis of the bone: they are typically a consequence of a fall on an outstretched arm,
so they mainly involve the distal radial metaphysis. The word torus is derived from the Latin
word 'torus,' meaning swelling or protuberance.

3. Callus
Shortly after fracture and resolution of hemorrhage, fibroblasts adjacent to the fracture site begin to
replicate and form loose granulation tissue Following granulation tissue formation, fibroblasts within the
fracture site, as well as along the periosteum, differentiate into chondroblasts to form hyaline cartilage,
while those distal to the fracture site develop into osteoblasts to form woven bone. As these populations
of tissue form a new mass of connective tissue bridging the fracture site, a callus is formed. Following
callus formation, hyaline cartilage and fibrous tissue are replaced by trabecular bone through
mineralization of existing collagenous matrix. During a remodeling phase, the callus and lamellar bone
deposition is contoured to the original bone structure. Generally, fracture callus is incomplete or
disordered in cases of secondary fracture due to neoplasia, ongoing inflammatory or infectious disease,
or metabolic bone disease.

1. Fracture healing 1. Reactive phase : - Stage of hematoma formation —> torn vessels will
bleed and form hematoma, a mass of clotted blood (hematoma) formed around the fracture
site - Stage of inflammation and celullar proliferation (0-7 days)—> hematoma is invanded
inflammatory cells and they degrade necrotic tissue, release of TGF-beta, PDGF by
macrophages, procuring osteoprogenitor cells
2. Reparative phase - Stage of callus formation —> new capillaries organize fracture
hematoma into granulation tissue - procallus , fibroblasts and osteogenic cells invade
procallus, make collagen fibers which connect ends together, chondroblasts begin to
produce fibrocartilage, this is called soft callus (7days-6weeks) - Stage of consolidation —>
osteoblasts lay more boney trabecule, fibrocartilagenous frame work is calcified to form
boney callus (6-12wks), now fracture is painless and allows weight bearing.
3. Remodeling phase - Stage of remodeling —> globular callus is slowly remodeled
over years, more trabecule are layed in the line of stress and non stressed area is resorbed,
hence bone will take original shape Types for bone healing 1. Direct (primary) bone
healing : mechanism of bone healing seen when there is no motion at the fracture site,
doesnt involve formation of fracture callus, osteoblasts originate from endothelial and
perivascular cells.
• Components of direct bone healing - Contact healing : direct contact between the fracture
ends allows healing to be with lamellar bone immediately
• Gap healing - Gaps less than 200-5 microns are primarily filled with woven bone thata
us subsequently remodeled into lamellar bone - Larger gaps are healed by indirect bone
healing (partially filled with fibrous tissue that undergoes secondary ossification) 2.
Indirect (secondary) bone healing : mechanism for healing in fracture that have some
motion but not enough disrupt the healing process • Bridging peiosteal (soft) callus and
medullary (hard) callus re-establish structural continuity
• Callus subsequently undergoes endochondral ossification • Process fairly rapid - weeks
Local regulation of bone healing 1. Growth factors : transforming growth factor, bone
morphogenetic proteins, fibroblast growth factprs, platelet derived growth factors, insulin-
like growth factors 2. Cytokines : IL 1, 4, 6,11, macrophage and granulocyte/macrophage
(GM) colonystimulating factors (CSFs) and tumor necrosis factor 3.
Prostaglandins/leukotrienes 4. Hormones 5. Growth factor antagonists
3. Bone remodeling.
a. Reactions of bone to disorders and injuries.
o 4 basic ways:
 local death
 avascular necrosis of bone
 an alteration of bone deposition
 increased/decreased deposition
 an alteration of bone resoprtion
 increased/decreased resorption
 mechanical failure (fracture)
o other:
 localized reaction of bone as a structure
 deposition > resorption
 work hyperthrophy
 degenerative OA
 fractures
 infection
 osteosclerotic neoplasms
 deposition < resorption
 disused atrophy (in OP)
 RA
 Infection
 Osteolytic neoplasms
 generalized reaction of all bone as an organ
 deposition > resorption
 osteopetrosis (marble bones)
 acromegaly
 deposition < resorption
 osteoporosis (osteopenia)
 rickets / osteomalacia
o Epiphyseal Plates
 3 basic ways:
 increased growth
 decreased growth
 torsional growth  twisting forces causes
deformity
 others:
 Generalized
 increase in growth (gigantism)
o Marfan’s syndrome
o Pituitary gigantism
 Decrease in growth (dwarfism)
o Achondroplasia
 o Pituitary dwarfism (Lorain type)
o Rickets
 Localized
 Increase
o Chronic inflammation
o Displaced fracture of long bone’s shaft
o Congenital AVM (arteriovenous
malformation)
 Decrease
o Disuse retardation
o Injury: physical, thermal
o Ischemia
o Infection
o In Articular Cartilage
 3 ways:
 Destruction
 RA, infections, Ankylosing Spondylitis,
prolonged immobilization of a synovial joint,
continuous compression of articular
cartilage, intra-articular injections of
hydrocortisone
 Degeneration
 Premature aging of cartilage, previous
destruction of cartilage,
incongruity/irregularity of joint surfaces
 Peripheral proliferation
 Perichondrium thickening  chondrophyte
formation  osteophyte formation
o In Synovial Membrane
 3 ways:
 effusion
 hypertrophy
 forming of adhesions between itself & articular
cartilage
o In Joint Capsule & Ligaments
 Joint laxity (unduly stretched & elongated)
 Joint contracture ( tight & shortened)
o In muscles around:
 Disuse atrophy
 Work hypertrophy
 Ischemic necrosis
 Contracture
 Regeneration
b. Know the phases of bone healing.
o 3 stages:
 early inflammatory stage
 hematoma develops  during the first few hours
 inflammatory cells & fibroblasts  infiltrate bone
 mediated by prostaglandin
 formation of granulation tissue
 ingrowth vascular tissue & migration of
mesenchymal cells
 exposed cancellous bone & muscle  primary
nutrient and oxygen supply provided
 repair stage
 fibroblasts  begin to lay down a stroma  helps
support vascular ingrowth  progresses 
collagen matrix laid down  osteoid secreted 
mineralized  formation of soft callus  callus
ossifies  bridge of woven bone formation
 late remodelling stage
 healing bone is restored to its original shape,
structure and mechanical strength
c. Know the difference between metaphyseal and diaphyseal healing.
o Metaphyseal Healing / Cuboidal Healing
 Cancellous bone  rich in blood supply, hence less
necrosis
 Steps:
 External callus (periosteal)
 Internal callus (endosteal)
 Osteogenic:
 Trabeculae proliferates
 Primary woven bone formation
 Mature lamellar bone
 Consolidated
o Diaphyseal Healing / Tubular Healing
 Cortical bone
 Steps:
 Hematoma
 External callus (periosteal)
 Internal callus (endosteal)
  Fracture callus  stickier  mature
 Osteogenic differentiates into:
o Osteoblast:
 Primary woven bone
o Chondroblast:
 Cartilage
 Endochondral ossification  clinical union
 Mature lamellar bone
 Consolidated
 Cortical bone with Internal Fixation:
 Steps:
 No stimulus for callus formation
 Cortex of each fracture fragment
communicate  primary bone healing
 OC cross fracture site
 New bridging osteons
 New osteons formation
 Haversian remodelling
d. Know the reaction of growth plate.
o See answer in 3a.
e. Recognize how bone attains in adult shape.
o Peak bone mass: 20yrs old (female) & 30yrs old (male)
f. Know how cortical and cancellous bone remodel.
o Cortical:
 Remodels by osteoclastic tunneling (cutting cone)
 OC resorption  OB layering  lamellae layering
 cement line laid down
 OC  make up head of cutting cone
 Followed by capillaries , and then OB  lay down
the osteoid to fill the cutting cone
 Sclerostin  inhibits osteoblastogenesis 
decrease bone formation
 Continues to change over time
 Cortical area  decreases as age (higher fracture
risk)
 Medullary canal volume  increases as age
o Cancellous:
 Osteoclastic resoprtion
 Osteoblastic deposition of layers of lamellae
g. Explain the response of bone to stress.
o Stress fracture (fatigue fracture)
 As a result of repeated stresses  develop a small crack
or fatigue fracture
 React by:
 Healing
 Crack does not proceed to a displaced fracture
 Examples:
 March fracture: 2nd,3rd,4th metatarsals in military
recruits
  Runners: lower end of fibula
 Jumpers & Ballet: upper third of tibia
 Steps:
 Crack develops
 Insidious onset of local pain  aggravated by
activity, relieved by rest
 Local deep tenderness
 Healing process
 Subperiostal & endosteal new bone
h. Describe Wolff’s Law
o Developed by German anatomist and surgeon, Julius Wolff
(1836-1902)
o Bone in a healthy person or animal will adapt to the loads
under which it is placed
o If loading on particular area increases  bone will remodel
itself over time  become stronger so they can resist the
loading
o Trabeculae’s internal architecture  undergoes adaptive
changes  external cortical bone undergoes secondary
changes  becoming thicker
o Inverse: loading of bone decreases  bone less dense and
weaker  due to lack of stimulus required for continued
remodeling
o All of these remodellings  via MECHANOTRANSDUCTION 
forces or other mechanical signals are converted to
biochemical signals in cellular signalling
 Mechanocoupling
 Biochemical coupling
 Signal transmission
 Cell response
o Factors:
 Duration
  Magnitude
 Rate of loading (only cyclic loading can induce bone
formation)
o Short process:
 Osteocytes  most sensitive to mechanical loading
 Regulate bone remodelling  signalling other cells
 via signalling molecules / direct contact
 Osteoprogenitor  differentiate into OB or OC
 Mechanosensors
 May differentiate one way or another depending
on loading condition
o Examples:
 Tennis player  racquet-holding arm bones become
much stronger than the other arm
 Weightlifters  increases in bone density
i. Know the types of bone deformity (loss of alignment, abnormal
length, bony outgrowth.
o Loss of alignment
 Twisting (torsional) deformity & angulatory deformity
o Abnormal length
 Commonly affects long bone  shorter / gone.  could
be limb length disrepancy
o Bony outgrowth
 Eg: osteochondroma
 Permukaan tulang terdapat perubahan bentuk yang
sangat terlihat, sehingga deformitas tampak
j. Know in general common bone neoplasm.
o Cartilage tumours
  Osteochondroma, chondroma, chondroblastoma,
chondrosarcoma, chondromyxoid fibroma
o Osteogenic tumours
 Osteoid osteoma, osteoblastoma, osteosarcoma
o Fibrogenic tumours
 Desmoplastic fibroma, fibrosarcoma
o Fibrohistiocytic tumours
 Benign &malignant fibrous histiocytoma
o Ewing sarcoma / primitive neuroectodermal tumour
o Haematopoietic tumours
 Plasma cell myeloma
 Malignant lymphoma
o Giant cell tumour
o Notochordal tumours
 chordoma
o Vascular tumours
 Haemangioma, angiosarcoma
o Smooth muscle tumours
 Leiomyoma, leiomyosarcoma
o Lipogenic tumours
 Lipoma, liposarcoma
o Neural tumours
  neurilemmoma
o Miscellaenous tumours
 Adamantinoma, metastatic malignancy
o Miscellaenous lesions
 Aneurysmal bone cyst, simple cyst, fibrous dysplasia,
osteofibrous dysplasia, langerhans cell histiocytosis,
erdheim-chester disease, chest wall hamartoma
o Joint lesions
 Synovial chondromatosis
4. Muscle Physiology.
a. Describe the innervations of muscle and neuromuscular junction.
o Neuromuscular junction  meeting point of a nerve fibre and
the muscle fibre that it supplies
o Innervation  through action potential from synaptic vesicle
to muscle
b. Explain the physiology of muscle contraction.Explain the mechanism
of muscle growth (hypertrophy, atrophy, growth in length) and
contracture.
o Muscle contraction
 All or none principle
 Occurs at the muscle fiber level within a particular
motor unit
 Action potential mechanism:
 Resting membrane potential  depolarization 
repolarization  end of repolarization &
afterpotential  resting membrane potential
 Electrical transmission:
 Action potential  presynaptic terminal 
voltage-gated Ca2+ channels open  Ca2+
diffuse in  synaptic vesicles release
acetylcholine (neurotransmitter molecule)  Ach
diffuses into synaptic cleft  Ach combine with
receptor sites  ligand-gated Na+ channels open
 Na+ diffuses in  depolarization  threshold 
action potential produced in postsynaptic.
 Neuromuscular Junction Actions:
 Nerve pulse  synaptic end bulb  release Ach
from synaptic vesicles  diffuse across synaptic
cleft (between motor neuron and motor end plate)
 free Ach binds with motor end plate  ion
channels open  Na+ flow across membrane 
into muscle cell  muscle action potential 
travels along sarcolemma & T-tubules
 Ach released previously  broken down by AchE
(acetylcholinesterase) in synaptic cleft
 Stimulation (Cock Stage)
 Action potential travelling reaches sarcoplasmic
reticulum  Ca channels in SR membrane opens
 release of stored Ca2+ into cytoplasm
 Cross-Bridge Formation (Attach Stage)
 When available  Ca2+ binds to troponin
complex  troponin changes shape  displaces
the attached tropomyosin protein  exposing
active site  myosin head binds to exposed active
site on actin molecule  cross bridge formation
 * myosin: ATPase (catalyzes the ATP hydrolysis 
ADP and Pi. This causes myosin head to bend/flex
at 45 degrees into its “cocked” position. In relax,
myosin head bound to ATP in a low-energy
configuration)
 Flexion of the Cross Bridge (Flex Stage)
 ADP and Pi released from mysin head  myosin
head rotate  cross bridge flexes  actin filament
slide to myosin filament  this miniscule
movement is the essence of muscular contraction
 Release of Myosin Head (Release Stage)
 Sarcomere contracted a tiny distance  binding
and flexion process repeated to continue
contraction
  myosin head released from actin molecule
(molecule of ATP in cytoplasm binds to ATP
binding site on myosin head)  myosin head
released by active state  troponin complex back
to original shape  attached tropomyosin move
back & cover the active site  ATP molecule
bound to myosin head  myosin head back to
resting position  sequence ready to be repeated
o Mechanism of muscle growth
 Hypertrophy
 Increase in diameter of muscle fibers
 Due to very forceful, repetitive muscular activity,
increase in myofibrils, SR and mitochondria

 Atrophy
 Wasting away due to degeneration of cells
 Muscle fiber decrease in size due to a progressive
loss of myofibrils
  Disuse atrophy, denervation atrophy
 Growth in length
o Contracture
 Fibrous tissue of the muscular fascia: thicken & shorten
 bending of joint
 Elastic replaced by inelastic fiber-like tissue.
 Due to paralysis, muscular atrophy, muscular dystrophy
 Eg: Dupuytren’s, Ischemic, Organic, Volkmann’s