Tissue responses to injury
By Mrs Zayneb Makki,
Clinical University Teacher
How may cells/tissues be response to stress?
1...
Mechanisms of cellular changes to injury
a. damage to DNA
b. damage to cell membranes or other organelles
c. damage to enz...
– release of cell contents activates inflammation
– the necrotic area is often eventually replaced by a scar –
Healing
An ...
4. Eventually vascularity decreases and a fibrous scar are formed.
Healing By Primary Intention
 When wound edges are bro...
 age
 systemic disease -circulatory, diabetes
 nutrition deficiency (Vitamin C,Zinc)
 drugs taken (steroids)
Complicat...
3. Physical carcinogenesis
 ionizing radiation
- environmental: radioactive metals, uranium, radium, radioactive gases, r...
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Tissue responses to injury almuzian

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Tissue responses to injury almuzian

  1. 1. Tissue responses to injury By Mrs Zayneb Makki, Clinical University Teacher How may cells/tissues be response to stress? 1. Depending on the dose of intensity 2. cellular vulnerability Type of stress 1. infection 2. physical agents 3. mechanical (trauma) 4. thermal 5. chemicals/drugs 6. radiation 7. hypoxia 8. immunological reactions 9. nutritional imbalance 10. genetic disease Tissue response to injury 1. Atrophy 2. Hyperatrphy 3. Hyperplasia 4. Metaplasia 5. Dysplasia Cell injury 1. Reversible • Temporary structural/metabolic changes • cells adapt to changes in environment • return to normal once stimulus removed. 2. Irreversible • Permanent damage – metabolic – genetic • Cell death may occur as a consequence
  2. 2. Mechanisms of cellular changes to injury a. damage to DNA b. damage to cell membranes or other organelles c. damage to enzyme and structural protein synthesis d. disruption of ATP synthesis e. morphological changes Necrosis a form of traumatic cell death that results from acute cellular injury Apoptosis Definition: is the process of programmed cell death (PCD) that may occur in multicellular organisms. Types: It is either pathological or physiological apoptosis. Process: It can be stimulated by various stimuli or injury and not produce inflammation. The steps are nuclear changes like  loss of microvilli junction,  chromatine fragmentation  then release of apoptotic bodies  the remaining parts of the cell will be phagocytic by the other cells. There are seven distinctive morphologic patterns of necrosis The presence of the nulclie determine that the cell is alive or dead while the situation of the cytoplasm determine the cause and mechanism of necrosis) 1. Coagulative necrosis is typically seen in hypoxic (low-oxygen) environments, such as an infarction. Cell outlines remain after cell death and can be observed by light microscopy. 2. Liquefactive necrosis (or colliquative necrosis) is usually associated with cellular destruction and pus formation (e.g., pneumonia). This is typical of bacterial or, sometimes, fungal infections because of their ability to stimulate an inflammatory reaction. Ischemia (restriction of blood supply) in the brain produces liquefactive, rather than coagulative necrosis due to the lack of any substantial supportive stroma. 3. Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e.g., tuberculosis), fungi, and some foreign substances. It can be considered a combination of coagulative and liquefactive necrosis. 4. Fatty necrosis results from the action of lipases on fatty tissues (e.g., acute pancreatitis, breast tissue necrosis). 5. Fibrinoid necrosis is caused by immune-mediated vascular damage. It is marked by deposition of fibrin-like proteinaceous material in arterial walls, which appears smudgy and eosinophilic on light microscopy. Effects of Necrosis on tissue 1. Functional – depends on the tissue/organ 2. inflammation
  3. 3. – release of cell contents activates inflammation – the necrotic area is often eventually replaced by a scar – Healing An attempt to restore integrity to an injured tissue following tissue damage and overlaps with the inflammatory process. Types of healing: a. resolution : return to normal b. regeneration: lost tissue replaced by same type to restore tissue c. repair : tissue lost replaced by fibrous scar What factors determine the balance of regeneration and repair? 1. cell type involved  Labile continual cell division (stem cells)  Stable infrequent cell division, but can increase (hepatocyte)  permanent no cell division possible. Now neural stem cells (neural precurser cells) have been identified. 2. tissue architecture, • Simple tissues vs. complex tissues 3. amount of tissue lost, small or large. How is the healing process controlled? i.e. What is the controlling factors? 1. cell to extracellular matrix interactions  correct position of cells  influence behavior  mediated via integrins and MMP (See below) Angiogenesis is the physiological process involving the growth of new blood vessels by migration of endothelial cells from pre-existing vessels. Control of angiogenesis mediated by Integrins then the matrix metalloproteinases (MMP) which degrade the extracellular matrix to allow new blood vessel to form. 2. cell to cell interactions  growth and inhibitors factors  cytokines and chemotaxis stimulus include hypoxia triggered by ROS (Reactive Oxygen Species) and then vascular endothelial growth factor (VEGF), cytokines and macrophages from hypoxic cells. Repair It is the formation of a fibrous scar via granulation tissue. The steps are (imagine trauma to the dermis with wound formation and then healing) 1. macrophages (stimulated by coagulation, complementary system and chemotaxis) remove debris with chronic inflammation is occurs simultaneously. This starts from deep layer to the superficial layer 2. Endothelial cells and fibroblasts migrate in from the edges (stimulated by fibrinctin and beta TGF), forming a loose CT (granulation tissue) under the superficial layers 3. Increase in blood vessels and collagen
  4. 4. 4. Eventually vascularity decreases and a fibrous scar are formed. Healing By Primary Intention  When wound edges are brought together so that they are adjacent to each other (re-approximated)  Minimal clot,  Mild inflammatory response,  Mild granulation,  Minimal scar  Minimal epithelial regeneration Healing By Secondary Intention  Wound edges not approximated, like in infected or burns etc  Larger clot  More inflammation  Much greater bulk of granulation tissue needed  Large scar with significant contraction  More epithelial regeneration (varies) Tertiary Intention (Delayed primary or secondary closure)  The wound is purposely left open  The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.  Examples: healing of wounds by use of tissue grafts. Healing In Oral Tissues 1. oral fibroblasts  can remodel wounds more effectively  can migrate and proliferate better 2. also less inflammatory response, 3. les granulation 4. less scarring than skin because fibroblast responses determine this 5. resembles fetal healing in some respects Factors Influencing Wound Healing 1. local  Infection  presence of foreign/necrotic material  irradiation  poor blood supply  size and location of wound  movement within wound 2. Systemic
  5. 5.  age  systemic disease -circulatory, diabetes  nutrition deficiency (Vitamin C,Zinc)  drugs taken (steroids) Complication of the healing process 1. Cosmetic changes 2. Functional changes 3. Molecular changes (if the molecular damage occurs then the consequences are:  scar maturation (vascularity reduces, scar contracts)  scar complications (excessive contraction, defective scar, excessive scar tissue – like keloid, or calcification) 4. DNA Damage which resulted in  tissue damage – functional etc  persistent genetic damage which may efeect ageing, cancer, inherited disease Keloid Scar – Prevention and Treatment 1. avoid “cosmetic procedures in high risk individuals 2. excision often results in recurrence 3. treat with pressure, dressings, corticosteroids etc 4. new therapy – intra-lesion interferon, Factors of Cancer Development 1. Genetic susceptibility to cancer a. inherited cancer syndromes– single mutant genes b. familial cancer pattern of inheritance not clear c. defective DNA repair ( due to chemicals, physical factors, viral or other factors)  oncogenes (which cause mutation, increase division, change transcription)  tumor suppressor genes (TSG) inhibit cell division and suppress growth, “anti -oncogenes”  other genes – repair genes – apoptosis genes – destructive enzymes 2. Chemical carcinogenesis  active form – direct: tumor arises at the site of carcinogen application – indirect: tumor arises at different site from carcinogen application  co-carcinogens increase the effect examples: – Smoking – Dietary hydrocarbons – Asbestos
  6. 6. 3. Physical carcinogenesis  ionizing radiation - environmental: radioactive metals, uranium, radium, radioactive gases, radon - iatrogenic: X rays: diagnostic and therapeutic, radioactive iodine  ultraviolet light - squamous cell carcinoma, basal cell, carcinoma, melanoma 4. Viral oncogenesis  Epstein Epstein— causing Burkitt’s lymphoma  Hepatitis B and C hepatocellular carcinoma  Human Papilloma Papilloma virus carcinoma oral cancer 5. Other Influences Act As Promoters  inflammation  hormones – (oestrogen) & (testosterone)  drugs, like alcohol

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