Repair

1. Repair DR: Gehan Mohamed

2. Types of cells Conteniously dividing cells (Labile): e.g epithelium, haematopoietic (blood). Quiescent (Stable): e.g hepatic, kidney and pancreas as their cells divide when there is need. Non-dividing (Permanent): nerve cells and skeletal muscle cells

3. Repair (healing) Definition : Tissue repairinvolves replacement of damaged tissue with new healthy living tissue. Types Usually involves two separate but coordinated components • Regeneration: healing by the same type of tissue cells from surrounding healthy living cells, this occurs with in small damages of labile cells and stable cells for examples liver cirrhosis and bone fractures B) Fibrosis (scar tissue): healing by granulation tissue (fibroblast with new capillaries formed) which mature a vascular fibrous tissue (scar), this occurs in the healing process of permanent cells and stable cells with high damage. for example myocardial infraction and wounds

4. Introduction to wond healing • The adult wound healing process can be divided into 4 distinct phases: • The homeostasis phase • the inflammatory phase • the proliferative phase • the remodeling phase.

5. Sequence of events in healing Initial phase - Hemostasis • Following vasoconstriction, platelets adhere to damaged endothelium and discharge adenosine diphosphate (ADP), promoting thrombocyte clumping, which dams the Wound • The inflammatory phase is initiated by the release of numerous cytokines by platelets. • Fibrinogen is cleaved into fibrin and the framework for completion of the coagulation process is formed. Fibrin provides the structural support for cellular constituents of inflammation. • This process starts immediately after the insult and may continue for a few days

6. Sequence of events in healing Second phase - Inflammation • Within the first 6-8 hours, the polymorphonuclear leukocytes (PMNs) or PNLs “cleanse” the wound, clearing it of debris. The PMNs attain their maximal numbers in 24-48 hours and commence their departure by hour 72 • As the process continues, monocytes also exude from the vessels. These are termed macrophages. The macrophages continue the cleansing process and manufacture various growth factors during days 3-4. • Many factors influencing the wound healing process are secreted by macrophages. These include TGFs, cytokines and interleukin-1 (IL-1), tumor necrosis factor (TNF)

7. Sequence of events in healing Third phase - Granulation This phase consists of different subphases which are: • fibroplasia • matrix deposition • angiogenesis • and re-epithelialization • In days 5-7, fibroblasts have migrated into the wound, laying down new collagen of the subtypes I and III • Angiogenesis is theThe formation of new vasculature which requires extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation of endothelial cells • Re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal structures. This process commences with the spreading of cells within 24 hours. Division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound. This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound.

8. Sequence of events in healing Fourth phase - Remodeling After the third week, the wound undergoes constant alterations, known as remodeling, • This can last for years after the initial injury occurred. Collagen is degraded and deposited in an equilibrium-producing fashion • The collagen deposition in normal wound healing reaches a peak by the third week after the wound is created. • Contraction of the wound is an ongoing process resulting in part from the proliferation of the specialized fibroblasts termed myofibroblasts, which resemble contractile smooth muscle cells.

9. Types of healing

10. Types of healing

11. Types of healing

12. Complications of the healing process • This process can go wrong and produce an increase of fibroblastic proliferation with a resultant hypertrophic scar • Further exuberance can result in keloid formation where scar production extends beyond the area of the original insult. Conversely, insufficient healing can result in atrophic scar formation.

13. Complications of the healing process • Weak scar: this may lead to hernia • Cicatrisation: contracture of the size of the scar • Implantation epidermiod cyst • Stump neuroma: following amputation causing a painful coiled mass of nerves • Sinus: is a track of septic granulation tissue connecting a cavity to the outside and has one blind end e.g. pilonidal sinus • Fistula: is a tract of septic granulation tissue connecting 2 epithelial surfaces • Infection : leading to delayed healing • Rarely scars may develop squamous cell carcinoma • Ulcers: discontinuity of the covering epithelium or muscle membrane

14. Fractures: • Definition :Break in the bone. TYPES: • Simple / Compound . • Single - Horizontal, oblique, spiral, • Comminuted – multiple. • Greenstick is a partial fracture common in children.

15. Types of Fracture:

16. Stages of wound healing Remodeling Vessel regression, Collagen remodeling Proliferation Reepithelialization, Angiogenesis, Fibrogenesis, Inflammation PMNs, Macrophages, Lymphocytes Hemostasis Fibrin clot, platelet deposition 1D 3D 1wk 6wk 8wk Time after injury

17. Healing in Bone: • 1D - Hematoma formation (fibrin mesh) • 3D - Inflammation • 1W - Soft callus – granulation, matrix. • 3-6W - Callus – ossification, woven bone • 8+W - Re-modeling – absorb/deposit, strength, lamellate.

18. Complications: • Delayed healing. • Non healing. • Joint involvement - ankylosis • Abnormal position – arthritis. • Bone necrosis – nutrient artery • Pseudoarthrosis

19. Factors affecting Healing: Local factors which delay healing: • Mobilization of the fractured ends. • Improper reduction – abnormal position. • Infection. Debris, dead tissue in wound. • Joint involvement. Poor blood supply to area of injury.

20. Factors affecting repair: General factors which delay healing : -bad nutrition • Starvation • Diabetes • Corticosteroid therapy Chronic deblitating disease as T.B,malignancy Old Age of patient.