BONE HEALING

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)

Osteons communicate with

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

Function poorly understood

regulating bone metabolism in
response to stress and strain

Osteoclasts
Derived from

hematopoietic stem cells

(monocyte precursor
cells)
Multinucleated cells
whose function is bone
resorption
Reside in bone
resorption pits
(Howships lacunae)

Components of Bone Formation

Soft tissue
Periosteum
Cortex
Bone marrow

For Bone Healing we need

Adequate blood supply
Adequate mechanical

stability

Blood Supply
Long bones have

three blood supplies

Nutrient artery

(intramedullary)
Periosteal vessels
Metaphyseal vessels

Nutrient Artery
Normally the major blood supply for the diaphyseal

cortex (80 to 85%)

Enters the long bone via a nutrient foramen
Forms medullary arteries up and down the bone

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

cortex in the event of injury to the medullary blood supply

Metaphyseal Vessels
Arise from periarticular vessels
Penetrate the thin cortex in the metaphyseal region

and anastomose with the medullary blood supply

Vascular Response in Fracture Repair

Fracture stimulates the release of growth factors that

promote angiogenesis and vasodilation

Blood flow is increased substantially to the fracture site
Peaks at two weeks after fracture

Mechanical Stability
Early stability

promotes
revascularization
After first month,
loading and
interfragmentary
motion promotes
greater callus
formation

Mechanisms of Bone Formation

Cutting Cones
Intramembranous Bone

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

Intramembranous (Periosteal) Bone

Formation
Mechanism by which a long bone grows in width
Osteoblasts differentiate directly from preosteoblasts

and lay down seams of osteoid .

Endochondral Bone Formation

Mechanism by which a long bone grows in length
Osteoblasts line a cartilage precursor
The chondrocytes hypertrophy, degenerate and calcify

(area of low oxygen tension)

Vascular invasion of the cartilage occurs followed by
ossification (increasing oxygen tension)

Bone healing
Heals by original tissue leaving no scar

Contact Healing
Gap Healing

-Gaps less than 200-500 microns are primarily filled with

woven bone that is subsequently remodeled into lamellar
bone
Contact Healing:
-Direct contact between the fracture ends allows healing
to be with lamellar bone immediately

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

cells within the tissues adjacent to the injury site.

Blood vessels constrict.
Within a few hours a hematoma is formed.
Fibroblasts survive and replicate forming granulation
tissue .

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

with compact bone.

The trabecular bone is first resorbed by osteoclasts,
creating a shallow resorption pit known as a "Howship's
lacuna".
Then osteoblasts deposit compact bone within the
resorption pit.

 Eventually, the fracture callus is remodeled into a new

shape which closely duplicates the bone's original shape

and strength. The remodeling phase takes 3 to 5 years
depending on factors such as age or general condition.

Regulation of Bone Healing

Growth factors
Cytokines
Prostaglandins/Leukotrienes
Hormones
Growth factor antagonists

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

increased PTH and therefore increased osteoclastic

bone resorption

Hormones
Parathyroid Hormone
Intermittent exposure stimulates
Osteoblasts
Increased bone formation

Growth Hormone
Increases callus formation and fracture strength

Local Anatomic Factors That

Influence Fracture Healing
Soft tissue injury
Interruption of local

blood supply
Interposition of soft
tissue at fracture site
Bone death caused
by radiation, thermal
or chemical burns or
infection

Systemic Factors That Decrease

Fracture Healing
Malnutrition
Causes reduced activity and proliferation of

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