Documente Academic
Documente Profesional
Documente Cultură
Types of Bone
Microscopically
Lamellar Bone (cortical and spongy)
Collagen fibers arranged in parallel layers
Normal adult bone
Woven Bone (non-lamellar)
Randomly oriented collagen fibers
In adults, seen at sites of fracture healing, tendon or ligament
attachment and in pathological conditions
Lamellar Bone
1) Cortical bone
Composed of osteons
(Haversian systems)
medullary cavity by
Volkmanns canals
Haversian System
Osteon with
osteocyte
central
haversian canal
containing
osteon
Cells
Vessels
Nerves
Volkmanns
canal
Connects
osteons
Haversian
canal
Volkmanns
canal
Lamellar Bone
2) Cancellous bone
(trabecular or spongy
bone)
Bony trabeculae that
are oriented in
direction of the
greatest stress
Woven Bone
Coarse with random
orientation
Weaker than lamellar
bone
Normally remodeled to
lamellar bone
Bone Composition
Cells
Osteocytes
Osteoblasts
Osteoclasts
Extracellular Matrix
Organic (35%)
Collagen (type I) 90%
Osteocalcin, osteonectin, proteoglycans, glycosaminoglycans, lipids
(ground substance)
Inorganic (65%)
Osteoblasts
Derived from mesenchymal
stem cells
Line the surface of the bone
and produce osteoid
Immediate precursor is
fibroblast-like preosteoblasts
Osteocytes
Osteoblasts surrounded by bone
matrix
trapped in lacunae
Osteoclasts
Derived from
stability
Blood Supply
Long bones have
(intramedullary)
Periosteal vessels
Metaphyseal vessels
Nutrient Artery
Normally the major blood supply for the diaphyseal
Periosteal Vessels
Arise from the capillary-rich periosteum
Supply outer 15 to 20% of cortex normally
Capable of supplying a much greater proportion of the
Metaphyseal Vessels
Arise from periarticular vessels
Penetrate the thin cortex in the metaphyseal region
Mechanical Stability
Early stability
promotes
revascularization
After first month,
loading and
interfragmentary
motion promotes
greater callus
formation
Formation
Endochondral Bone Formation
Cutting Cones
Primarily a
mechanism to
remodel bone
Osteoclasts at the
front of the cutting
cone remove bone
Trailing
osteoblasts lay
down new bone
Bone healing
Heals by original tissue leaving no scar
Contact Healing
Gap Healing
Stages of healing
1. Reactive Phase
i. Fracture and inflammatory phase
ii. Hematoma and Granulation tissue formation
2. Reparative Phase
iii. Cartilage Callus formation
iv. Woven then lamellar bone deposition
3. Remodeling Phase
v. Remodeling to original bone contour
Reactive Phase
After fracture, the first change is the presence of blood
Reparative
Days after fracture, the cells of the periosteum replicate
and transform.
The periosteal cells proximal to the fracture gap
develop into chondroblasts which form hyaline cartilage.
The periosteal cells distal to the fracture gap develop
into osteoblasts which form woven bone.
Remodeling Phase
The remodeling process substitutes the trabecular bone
Hormones
Estrogen
Stimulates fracture healing through receptor mediated
mechanism
Decrease the release of a specific inhibitor of IL-1 which
stimulates bone resorption
Thyroid hormones
Thyroxine and triiodothyronine stimulate osteoclastic
bone resorption
Glucocorticoids
Inhibit calcium absorption from the gut causing
Hormones
Parathyroid Hormone
Intermittent exposure stimulates
Osteoblasts
Increased bone formation
Growth Hormone
Increases callus formation and fracture strength
blood supply
Interposition of soft
tissue at fracture site
Bone death caused
by radiation, thermal
or chemical burns or
infection
osteochondral cells
Smoking
Cigarette smoke inhibits osteoblasts
Nicotine causes vasoconstriction diminishing blood flow
at fracture site
Diabetes Mellitus
Associated with collagen defects including decreased
collagen content, defective cross-linking and alterations
in collagen sub-type ratios
Problems In Healing
1- dealyed union.
2- non-union.
3- malunion.
4- avascular necrosis.
5- growth disturbance.
6- joint instability.
7- osteoarthorosis.
Delayed Union
when the time healing is prolonged.
CAUSES:
- biological or biochemical:
poor blood supply .
sever soft tissue damage
periosteal stripping (avoidable)
imperfect splintage
infection
Delayed union
Clinical features:
-fracture tenderness persists .
-acute pain if subjected to stress.
On x-ray:
-Fracture line remains visible
-bone ends are not sclerosed or atrophied
Non -Union
Nonunion is permanent failure of healing
following a broken bone.
-causes:
* separation of fragments
* soft tissue b/t bony fragments
* excessive movement at fracture site
* poor local blood supply
* sever soft tissue damage
* infection
* abnormal bone
MALUNION
-unsatisfactory position (angulation, rotation, shortening).
AVASCULAR NECROSIS
-bone death .
-certain regions more than others include:
1- head of femur
2- proximal part of scaphoid
3- body of talus
-it is an early complication
Because of ischemia but radiological
findings seen later
AVASCULAR NECROSIS
-Clinical features;
-no symptoms
-pain if fracture fail to unite or bony
collapse
-on x-ray:
increase bone density
Thank You