Abnormalities In Tissue Repair.

PRESENTED BY GROUP 5.5

 GROUP MEMBERS.
S/N NAMES OF PRESENTERS REGISTRATION NUMBER
1 ANYEDE SAVIOUR ILLA 2019-08-09861
2 MWESIGE MICHAEL COLLINS 2020-08-2020
 INTRODUCTION.
 Complication s in tis s u e repair can aris e from
abnormalities in any of the following basic components
of the process:

1. Inadequate granulation tissue formation.

2. Excessive scar formation.
3. Exuberant granulation tissue formation.
4. Excessive contraction.
5. Others.
1. Inadequate granulation tissue formation.
Inadequate formation of granulation tissue or formation of
scar can lead to two types of complications:

 Wound dehiscence ;
• This refers to the rupture of a wound.
• Occurs most frequently after abdominal surgery due to
increased abdominal pressure.
• Vomiting, coughing or ileus can also generate
mechanical stress on the abdominal wound leading to
dehiscence.
 Ulceration

• Wounds can ulcerate because of inadequate

vascularization during healing as seen in lower
extremity wounds of individuals with atherosclerotic
peripheral vascular disease.

• Non-healing wounds also occur in areas devoid of

sensation thus formation of neuropathic ulcers
occasionally seen in patients with diabetic peripheral
neuropathy
2.Excessive scar formation.
Excessive formation of the components of the repair
process can give rise to hypertrophic scars and keloids.

 Hypertrophic scar
• Is defined as widened scar that does not extend beyond
the original boundaries of wound due to accumulation of
excessive amounts of collagen.

• Hypertrophic scars generally develop after thermal or

traumatic injury that involves the deep layers of the
dermis.
 Keloid

• Is defined as an abnormal scar due to accumulation of

extracellular matrix below the dermis that grows
beyond the boundaries of original site of skin injury and
doesn’t regress.

• Keloids formation seems to be an individual

predisposition, and for unknown reasons
Differences between hypertrophic and keloid scar
HYPERTROPHIC SCAR
 Limited to the area of
original tissue damage
 Occur soon after injury or
surgery
 Can regress with time
 Promote scar
contractures
 Myofibroblasts that
express alpha SMA
KELOID SCAR
Spread outside wound
margins
Develop up to or even
beyond 1 year
Do not regress with time
Do not promote scar
contractures
Absence of myofibroblasts
 Increased TGF-B1 Increased TGF-B1 and
expression in HTS TGF-B2 expression in
tissue and fibroblast Keloid fibroblast
 Increased collagen High in collagen type I
type III
 Raised, linear , firm Raised, hard dermal
lesion overgrowth
 Affect any age Common in young

 May be improved with May be worsened with

surgery surgery
3. Exuberant granulation tissue formation.
Exuberant granulation consisting of the formation of excess
amounts of granulation tissue protruding above the level of
the surrounding skin and blocks re-epithelialization (proud
flesh).

 Desmoids (aggressive fibromatoses)

• A form of fibrous tumor caused by excessive proliferation of fibroblasts
and other connective tissue elements. They lie in the interface between
benign and malignant tumors.

• Malignant because their local invasiveness & potential to recur and

Benign because they don’t metastasize
4. Excessive Contraction
An exaggeration of this process gives rise to
contractures thus deformities in the healing wound and
surrounding tissues.
 Contractures
• Abnormal & permanent shortening or tightening of
muscles , tendons, ligaments or skin.

• Contractures are commonly seen after serious burns

and can compromise the movement of joints.
5. Infection by microbes
• Delayed healing from prolonged inflammation causing
excessive tissue damage.
• Cellulitis from bacterial infection on the wound site.
• Abscess formation requiring drainage and potential
surgical intervention.
• Necrotizing fasciitis
REFERENCES.
1. Harsh Mohan textbook of pathology 6th edition.
2. Robbins and Cortran pathological basis of disease 10th edition.