1. Repair Dr. Gehan Mohamed Dr. Abdelaty Shawky

2. Intended Learning outcomes  Understanding the classification of human cells according to their ability for proliferation.  Identifying the types of repair.  Discussing the mechanism of wound healing.  Recognizing the complications of wound healing.  Understanding the process of healing of bone fracture.  Being oriented with the factors affecting the process of repair.

3. Types of cells according to the ability of cell proliferation: 1. Labile cells: 1. Labile cells: are Contentiously dividing cells and renew themselves: e.g skin epithelium,mucosal lining of the GIT, haematopoietic cells (blood cells ). 2. Quiescent cells (Stable): 2. Quiescent cells (Stable): cells divide when there is a need e.g hepatic, kidney and pancreas. 3. Permanent cells: 3. Permanent cells: Non-dividing cells so when injured heal by fibrous tissue e.g : nerve cells and skeletal, cardiac muscle cells

4. Repair (Healing) * Definition: Replacement of damaged tissue with new healthy living tissue. * Types: A. Regeneration: healing by the same type of tissue cells from surrounding healthy living cells, this occurs with small damages of labile cells and stable cells for examples liver cirrhosis and bone fractures B. Fibrosis (scar tissue): B. Fibrosis (scar tissue): healing by granulation tissue (fibroblast with new capillaries) which mature to hypovascular fibrous tissue (scar), this occurs in the healing process of permanent cells or in stable cells with high damage. for example myocardial infraction and wounds

5. Wound Healing Cutaneous wound healing is generally divided into 4 phases: 1.Homeostasis. 2.Inflammation. 3.Granulation tissue formation and Re- epithelialization 4.Remodeling. - Wound healing is a fibroproliferative response that is mediated through growth factors and cytokines.

6. 1. Homeostasis Immediately after injury the cut vessels bleed inside the wound defect to form a blood clot that unit the two cut ends temporarily. Vasoconstriction of the injured vessels at the edges of the wound followed by platelets aggregation and adherence to the damaged endothelium. Stimulation of coagulation system will form fibrin. Fibrin network is formed over the aggregated platelets to form a 1ry homeostatic plug that stops bleeding inside the wound.

7. 2. Inflammation Mediated by polymorphs and macrophages. Within the first 6-8 hours, the polymorphonuclear leukocytes (PMNs) kill any organism in the wound and liquefy any necrotic debris. As the process continues, monocytes also exude from the blood vessels. These are termed macrophages. The macrophages continue and engulf the necrotic debris and also manufacture various growth factors during days 3-4.

8. 3. Granulation tissue formation and re- epithelization In days 5-7, fibroblasts migrate into the wound, laying down new collagen of the subtypes I and III Angiogenesis is the formation of new capillaries from the healthy blood vessels at the edge of the wound. These new capillaries fill the wound defect and surrounded by fibroblasts. The newly formed capillaries + fibroblasts = granulation tissue. Re-epithelization occurs by proliferation and migration of the healthy epidermal cells from the edges of the wound inwards.

9. Granulation tissue

10. Epithelization capillary fibroblast

11. 4. Remodeling - After the third week, the wound undergoes constant alterations, known as remodeling. Collagen is deposited from fibroblasts and degraded by collagenase enzyme which secreted from macrophages in a controlled manner. Wound contraction is a process occurs by the action of myofibroblasts (modified fibrobalsts), which resemble contractile smooth muscle cells. This occurs to give the healing wound more strength.

12. Types of wound healing 1. Healing by primary union (first intention): - Occurs with clean, non-gaping wounds (stitched surgical incision). 2. Healing by secondary union (secondary intention): - Occurs with extensive tissue loss as in: large wounds, infected wounds, abscess, ulcers….etc.

14. * Complications of the healing process: A. Complications from deficient granulation tissue formation : 1. Ulcers: discontinuity of the covering epithelium or mucous membrane. 2. Sinus: is blind end track of septic granulation tissue connecting a cavity to the outside e.g. pilonidal sinus 3. Fistula: is a tract of septic granulation tissue connecting 2 epithelial surfaces e.g. perianal fistula. 4. Weak atrophic scar: this may lead to hernia.

15. B. Complications due to excessive granulation tissue formation : 1. Hypertrophied scar. 2. Keloid formation: if the formed scar exceeded the original size of the wound.

16. Hypertrophic scar Keloid

17. A B

18. C. Other complications: 1.Infection: leading to delayed healing 2.Squamous cell carcinoma: rarely scars may develop 3.Cicatrisation: contracture of the size of the scar 4.Implantation epidermiod cyst: is a cyst formed secondary to entrapment of part of the epithelium inside dermis. 5.Stump neuroma: following amputation causing a painful coiled mass of nerves

19. Bone Fracture * TYPES: Simple. Compound. Comminuted: fracture into pieces. Greenstick is a partial fracture involve only one side of bone, common in children.

20. Types of Fracture

21. * Mechanism of healing of bone fracture:

22. * Complications of bone fracture: 1. Delayed union (healing): due to old age, anaemia, calcium or vitamin D deficiency… 2. Non union: due to soft tissue interposition between the two fracture ends. 4. Mal union of healed bones: due to improper reduction. 5. Bone necrosis: due to injury to nutrient artery.

23. Factors affecting Repair I. Local factors : The type of the damaged cells ( labile, stable or permanent). Severity of the damage. Presence of foreign body. Presence of necrotic tissue. Infection. Irradiation. Blood supply.

24. II. General factors: Age of patient. Nutrition status. Diseases: Diabetes, malignancy, anaemia. Drugs: Corticosteroid therapy, chemotherapy..