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Healing and repair by Dr. Kachinda wezi 2018
- 1. HEALING AND REPAIR Dr.kachinda Wezi LAMU
- 2. HEALING AND REPAIR •Wound healing is complex but orderly • The phenomenon involves a number of processes • One is the induction of an acute inflammatory process by an initial injury, with the aim of: - Destroying and removing the injurius irritant - Liquefied materials by autolytic and heterolytic processes - Removing the products of inflammation (dead cells and exudates) into lymph and bld vessels
- 3. • Regeneration ofparenchymal cells • Migration and proliferation of both parenchymal and connective tissue cells • Remodelling of connective and parenchyma component • Damaged tissue is then repaired and restored as near to the previous normal condition as possible
- 4. Review of thegeneral features of repair • Cells of the body divided into three groups: - Labile cells - Stable cells - Permanent cells • Division is based on their regenerative capacity, and their relationship to the cell growth cycle
- 5. Labile cells(continously dividing cells) •They continue to proliferate throughout the life of an animal with the aim of replacing those that are constantly destroyed • They include; - The surface epithelia, such as stratified squamous epithilia of the skin - Oral cavity, vaginal and cervical linning, the linning mucosa of the excretory ducts( eg salivary glands, pancrease, biliary tract e.t.c - Columnar epithelia of the GIT, uterus,UT,
- 6. Stable cells(quiescent cells) •Normally demonstrate a low level of proliferation(replication) • The cells may undergo rapid division in response to a variety of stimuli • They can reconstitute the tissue of origin e.g - Parenchymal cells of the glands, such as liver, kidney and pancrease - Mesenchymal cells such as fibroblasts, smooth muscle cells, osteoblasts,chondroblasts etc
- 7. • Liver isable to regenerate after hepatectomy, and following toxic, viral or chemical injury • For labile and stable cells to reconstitute the normal structure, it is essential that the underlying framework or the stroma of the orga or tissue must be present • The basement membrane(BM) is the main structural component necessary for organised regeneration • When the BM is disrupted, cells proliferate in a hapharzad manner and produce a disorganise mass with no resemblance to the original tissu
- 8. • This resultsinto scarring (fibrosis) • E.g hepatitis virus destroys only parenchyma cells without injuring the connective tissue framework of the liver,thus in viral hepatitis, complete regeneration of the liver cells takes place • On the other hand a large liver abscess destroys hepatocytes and connective tissue frame work, and this is followed by scarring
- 9. Permanent(non-dividing cells) • Theseare cells which have left the cell cycle, and cannot undergo mitotic division in postnatal life • E.g nerve cells, cardiac cells • The neurons destroyed in the CNS are permanently lost • They are replaced by the proliferation of the glial cells
- 10. • Except fortissues composed solely of non-diving cells, most adult tissues cells consists of a mixture of all of the three types of cells
- 11. Modes of repair (Generallycomprises of two) • Repair by regeneration - This takes place in cells that posses the capacity to proliferate - If cells have lost their capacity to proliferate, they cannot repair themselves by regeneration - The power of regeneration differs widely with different cells - For those tissues where the cells have retained the power to proliferate, healing occurs by regeneration - But in tissues where cells have lost their capacity to proliferate, the place for such cells is filled by connective tissue
- 12. Repair by connectivetissue (by granulation) • Involves four important steps - Migration and proliferation of fibroblasts - Deposition of extracellular matrix - Formation of new blood vessels (angiogenesis) - Maturation and organisation of the scar, known as remodelling
- 13. • As earlyas 24hrs after injury, fibroblasts and vascular endothelial cells begin to profliferate to the specialised type of tissue, known as granulation tissue which is the distinguishing feature(hallmark) of healing • However it is the histologic features that are characteristic - Proliferation of new blood vessels - Proliferation of fibroblasts
- 14. The role ofgrowth factors in healing • They trigger the migration of fibroblasts to the site of injury • Stimulate synthesis of collagen and other connective tissue molecules • Favours new blood vessel which originate by budding from pre-existing vessels, a process kown as angiogenesis • The new blood vessels have a leaky inter- endothelial junctions and allows the passage of proteins and rbcs into the extra-vascular space. Therefore new granulation tissue is often oedematous
- 15. WOUND HEALING • involvesboth epidermal growth and formation of connective tissue. • Use of sterile scalpel and aseptically sutured is the best example of a clean closed wound. • When wound is clean, healing takes place without interference. • • This is known as ‘healing by first intension or by primary union’
- 16. • If onthe other hand, as a result of infection or because large segments of tissues are lost, the wound remains open; repair is complicated and takes place by ‘healing by second intension or by secondary union’.
- 17. 1 Healing byfirst intension (Primary union). • For example: Sutured surgical wound with little loss of tissue, less bleeding and without bacterial contamination. • The incisional gap immediately fills with clotted blood, containing fibrin and blood cells
- 18. • The sequentialdevelopment is as follows: • 1. Clot formation. When the incision is closed by sutures the gap between opposed tissues become filled with blood, which coagulate to form clot ( consisting of fibrin, platelets and red blood cells and a few white blood cells) which seals the defect
- 19. 2. Inflammatory response. •Vascular congestion, oedema and infiltration of leukocytes, initially neutrophils and later monocytes(macrophages), appear at the edge of the lesion. • The phagocytes migrate into the clot and progressively digest it.
- 20. • The resultantfluid digest is absorbed into the blood stream and lymphatics. • The process is termed resolution of the exudates 3. Epithelial regeneration. • Epithelial cells migrate through the clot , actively ingesting and digesting fibrin and cell debris in their path.
- 21. • They growunder the superficial scab. • In a primary incision, the gap between the epidermal is bridged within 24 hrs. • Re-epitheliasation, and differentiation into appropriate layers is complete within approximately 7 day
- 22. • Phagocytic response. •About the same time as the phagocytes move into the clot, fibroblasts at the edges of the lesion swell up • they start to divide and migrate into the clot along the fibrin at the rate of 0.2mm per day. • When the wound margins are opposed, fibroblasts meet within the clot within 2 to 3 days
- 23. 4. Endothelial response. •Closely following the macrophages into the clot are the endothelial cells originating from blood vessels at the edge of the wound. • Endothelial cells enlarge, start to divide and solid buds of cells migrate into the clot following the same course of as fibroblasts along the fibrin meshwork ; they move at the same rate.
- 24. • These solidcords becomes canalised to permit the flow of blood. • Continuity of blood flow between the two margins may become established within 2 to 3 days. • Lymphatic channels undergo similar changes. • After 3 to 4 days , the clot becomes populated by highly vascularised , actively growing connective tissue;
- 25. • this processis termed organisation and newly-formed highly vascularised connective tissue with a component of acute inflammatory exudation known as granulation tissue
- 26. 5. Collagen formation. •With the proliferation of the fibroblasts, there is deposition of collagen fibres • Vitamin C is vital in man but not in domestic animals being required for the maturation of fibroblasts. • With the deposition of collagen, vascularisation starts to diminish which leads to contraction and shrinkage and formation of the scar tissue
- 27. 2. Healing bysecond Intension (secondary union) • This occurs in an open wound where there is excessive loss of tissue • In such cases the wounds are infected, many blood vessels are torn and the wounds contain areas of necrosis and inflammation. • Following injury, inflammatory reaction and haemorrhage occur.
- 28. • Blood clotsand neutrophils gather into the area in large numbers to destroy the irritant (usually bacteria). • Since more fibrin and more necrotic debris and exudate are required to be removed, the inflammatory reaction is intense
- 29. • Since thereis more extensive loss of tissue, and a large defect has to be repaired, much larger amounts of granulation tissue are formed than in the healing by 1st intension. • By the 2nd day, pus may be visible in the wound • In 48 – 72 hours, macrophages and lymphocytes appear in the area and gradually outnumber the neutrophils
- 30. • Macrophages involvethemselves in liquefying and removing the necrotised tissue and cellular debris. • Underneath the mass of blood covering the wound are tiny red granules, or capillary buds • Along with the newly formed capillaries there is proliferation of fibroblasts.
- 31. • The gapis then completely filled with a layer of fibroblasts and proliferating capillaries. • The newly formed tissue does not contain nerves and is therefore without sensation. • Eventually granulation tissue is formed • In the granulation tissue, fibroblasts and capillaries are arranged in a definite order
- 32. • Fibroblasts, inthe deeper part of the wound, are arranged at right angles to the capillaries and parallel to the surface. • Fibroblasts bring the tissues closely together to avoid any gap during healing. • Regeneration of the epidermis follows the same sequence as described for healing by primary union.
- 33. • Sweat glands,sebaceous glands, hair and hair follicles, and melanoblasts do not regenerate
- 34. • The areais therefore not pigmented, and is dry because it lacks sweat and sebaceous glands • The area gets devascularized after the completion of healing and a relatively avascular scar is left. • Following the shrinkage of collagen, the area may get considerably distorted. • The scar is therefore white.
- 35. • If irritatation,movement, or trauma this prevents the healing, granulation tissue continues getting produced and may be present in abnormally large amounts • This is called excessive granulation tissue, • Sometimes, for unknown reasons, the connective tissue under the scar continues to grow, protrudes above the skin, and blocks re-epithelialization.
- 36. • This massof proliferating connective tissue (i.e. excessive amount of collagen) may give rise to a raised tumorous scar known as a keloid • Keloids are not true tumours though they may recur after excision • The phenomenon of wound contraction differentiates the primary from the secondary healing.
- 37. • This occursin large surface wounds • Contraction is due to the presence of myofibroblasts, which are altered fibroblasts that have many structural and functional features of smooth muscle cells.
- 38. Factors affecting woundhealing • Many general (systemic) and local factors influence quality of the inflammatory-reparative response. These are: 1. General factors (Systemic) a) Nutrition plays a very important role in healing, especially proteins. Low protein levels in the diet have an adverse effect on healing
- 39. • In theabsence of the some amino acids, connective tissue of weak tensile strength is formed • Methionine increases the rate of utilization of the protein, • and its sulphur radicle may also be used for the formation of chondroitin sulphate which imparts firmness to the ground substance
- 40. • In proteindeficiency, few fibroblasts form and synthesis of collagen is inhibited and healing retarded. • Metabolic status can change wound healing. Diabtes for example is associated with delayed wound healing • Circulation status-can regulate wound healing: inadequate blood supply usually caused by arteriosclerosis or venous abnormalities that retard venous drainage also retards healing
- 41. • Vitamin C(ascorbic acid): • Its deficiency is an important cause of poor and delayed wound healing. • Deficiency of vitamin C results in impaired synthesis of normal collagen • Zinc: Many enzymes, such as the metalloenzymes and DNA and RNA polymerases, are Zinc dependent. Wound healing is delayed in patients with Zinc deficiency, and is restored to normal when Zinc is restored to normal by Zinc administration
- 42. • Age: Withadvancing age, the rate of healing may be impaired due to inadequate blood supply in the old age as result of generalized vascular disease (arteriosclerosis). • Glucocorticosteroids: Glucocorticosteroids have well documented anti-inflammatory effects, and influences various components of inflammation and fibroplasias. Steroids block or retard the process of repair. Less collagen and blood vessels are formed.
- 43. • Local factors(Local Influences) • Infection –is the single most important cause of delay • Mechanical factors –eg, early motion of wounds, can delay wound healing • Foreign bodies, such as unnecessary sutures or fragments of steel, glass or even bone, constitutes empediments to healing
- 44. • Size, location,and type of wound influences wound healing. • Wounds in richly vascularised areas , such as the face heals faster than those in poorly vascularised ones, such as the foot. • Small injuries produced intentionally heals faster than large ones caused by blunt traumas