HEALING OF SPECIALISED
TISSUE
BONE
Bone healing can be described in 6
stages :
1. Stage of hematoma formation
2. Stage of liquefaction
3. Stage of neovascularisation
4. Stage of soft callus formation
5. Stage of hard callus formation
6. Stage of remodelling

Stage of hematoma formation:
 Accumulation of blood at fracture
site
 Also contains devitalized soft tissue,
dead bone, and necrotic marrow
Stage of liquefaction:
 Degradation of nonviable products at
the fracture site
Stage of neovascularisation:
 Revascularization starts from
adjacent normal bone, with new
blood vessels growing into the
fracture site
 Similar to the formation of
granulation tissue in soft tissue
 Clinically : signs and symptoms
characteristic of inflammation
Stage of soft callus formation:
 Occurs 3 to 4 days following injury
 Soft tissue is deposited where
neovascularization has taken place :
soft callus
 The soft callus :
 Forms a bridge between the
fractured bone segments
 Serves as an internal splint,
preventing damage to the newly laid
blood vessels
 Achieves a fibrocartilaginous union.
 Clinically : End of pain and
inflammatory signs.
Stage of hard callus formation:
 Mineralization of the soft callus and
conversion to bone
 May take up to 2 to 3 months and leads
to complete bony union.
 Clinically : allows weight bearing and
appears healed on x rays
Stage of remodeling :
 Excessive callus is reabsorbed
 Marrow cavity is recanalized.
 Allows correct transmission of forces
and restores the contours of the bone.
OTHER DIFFERENCES
 Bone
morphogenic proteins (BMPs)
is a type of Tumor growth Factor
 It stimulates the differentiation of
mesenchymal cells into
chondroblasts and osteoblasts,
 Directly affects bone and cartilage
repair
CARTILAGE
 Consists
of cells (chondrocytes)
surrounded by an extracellular matrix
made up of several proteoglycans,
collagen fibers, and water.
 Very avascular
 Depends on diffusion for transmission
of nutrients across the matrix.
 Perichondrium is hypervascular and
contributes to the nutrition of the
cartilage.
Therefore, injuries to cartilage may be
associated with permanent defects due to
the meager and tenuous blood supply
 Healing
depends on depth of injury
 Healing varies in :
1. Superficial injuries
2. Deeper injuries
SUPERFICIAL CARTILAGE INJURY
 Disruption
of the proteoglycan
matrix and injury to the
chondrocytes.
 No inflammatory response
 There is increase in synthesis of
proteoglycan and collagen
 But, the healing power of cartilage is
often inadequate
 Hence
i.
ii.
iii.
superficial injuries:
Have incomplete overall
regeneration
Are slow to heal
Result in persistent structural
defects
DEEP CARTILAGE INJURY
 Involves
the underlying bone and soft
tissue.
 So there is exposure of vascular
channels of the surrounding damaged
tissue
 This helps in the formation of
granulation tissue.
 Heals better than superficial injuries !!
Hemorrhage
Initial inflammatory stage
Proliferation stage
Fibrous tissue undergoes
chondrification
Hyaline cartilage formed
TENDONS AND LIGAMENTS
Tendon : links muscle and bone
Ligament : links bone and bone
 Consist of parallel bundles of collagen
interspersed with spindle cells
 Can be subjected to a variety of
injuries, such as laceration, rupture,
and contusion.
 As underlying bone or muscles are
mobile, the damaged ends usually
separate.
 Healing
progresses in a similar fashion
as in other areas of the body ie via the
3 stages
 Matrix is characterized by
accumulation of type I and III collagen
along with increased water, DNA, and
glycosaminoglycan content.
 As the collagen fibers are organized,
transmission of forces across the
damaged portion can occur.
 Restoration of the mechanical integrity
may never be equal to that of the
undamaged tendon.
.
 Healing
1.
2.
depends on following factors :
Tendon vasculature
 Hypovascular tendons tend to heal
with less motion and more scar
formation
Tenocytes
 Specialised cells that are very
metabolically active and have a
large regenerative potential
NERVE
 Nerve
injuries are very common
 There are three types of nerve injuries:
1. Neurapraxia : temporary interruption
of conduction without loss of axonal
continuity
2. Axonotemesis : loss of the relative
continuity of the axon and its covering
of myelin, but preservation of the
connective tissue framework of the
nerve
3. Neurotemesis : complete transection
Times of degeneration in nerve:
 Distal to wound
 Wallerian degeneration :
Phagocytes remove the
degenerating axons and myelin
sheath from the distal stump
 Proximal to wound
 Traumatic degeneration upto last
node of Ranvier
 Pattern
a)
b)
c)
of nerve regeneration:
survival of axonal cell bodies
regeneration of axons that grow
across the transected nerve to
reach the distal stump
migration and connection of the
regenerating nerve ends to the
appropriate nerve ends or organ
targets
FETAL TISSUE
Healing depends on age of gestation:
 Upto 3rd trimester:
 no scar formation at all
 From beginning of 3rd trimester:
 "transition wound"
 scarless healing
 loss of the ability to regenerate skin
appendages
 Later :
 scar formation
 healing continues to be faster
Biggest difference :
lack of scar formation!
 Reasons
i.
ii.
iii.
iv.
:
wound environment,
inflammatory responses,
differential growth factor profiles
wound matrix.
Wound Environment
 Sterile
 Temperature-stable
 Fluid
Growth Factors
 Absence of TGF, which may have a
significant role in scarring.
Inflammation
 Fetal wounds contain lower numbers
of PMNs and macrophages
 Neutropenia
 Due to this immaturity of the fetal
immune system there is reduced
fetal inflammation
Wound Matrix
 Has excessive hyaluronic acid
production
 Fetal fibroblasts produce more
collagen than adult fibroblasts
 Increased level of hyaluronic acid
aids in the orderly organization of
collagen.
 Hence , enhanced healing and less
postoperative adhesion formation
THANK YOU !!!