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Inflammation and Healing (wound healing)

INFLAMMATION AND HEALING . Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cell and tissues.

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Inflammation and Healing (wound healing)

  1. 1. A COMPILATION ON INFLAMMATION AND HEALING
  2. 2. INDEX 1. INFLAMMATION A) DEFINITION B) CAUSES C) SIGNS OF INFLAMMATION D) TYPES OF INFLAMMATION E) ACUTE INFLAMMATION F) REGULATION INFLAMMATION G) CHEMICAL MEDIATORS OF INFLAMMATION H) CHRONIC INFLAMMATION 2. HEALING A) DEFINITION B) REGENERATION C) REPAIR D) WOUND HEALING E) HEALING IN SPECIALISED TISSUE
  3. 3. INFLAMMATION
  4. 4. DEFINITION Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cell and tissues.
  5. 5. CAUSES The agents causing inflammation may be as under: 1.Physical agents like heat, cold, radiation, mechanical trauma. 2.Chemical agents like organic and inorganic poisons. 3.Infective agents like bacteria, viruses , and their toxins. 4.Immunological agents like cell-mediated and antigen- antibody reactions. Thus inflammation is distinct from infection – the former is the protective response by the body while the latter is invasion into the body by harmful microbes and their resultant ill effects by toxin. Inflammation involves two processes: a) inflammatory response b) healing
  6. 6. SIGNS OF INFLAMMATION The famous 5 cardinal signs of inflammation as: 1. Redness 2. Swelling 3. Heat 4. Pain 5. Loss of function
  7. 7. TYPES OF INFLAMMATION Depending upon the defense capacity of the host and duration of response inflammation can be classified into Acute and Chronic 1. Acute inflammation is a short duration and represents the early body reaction and is usually followed by repair . The main features of acute inflammation are: a) accumulation of fluid and plasma at the affected site. b) intravascular activation of the platelets c) polymorphonuclear neutrophils as inflammatory cells. 2. Chronic inflammation is of longer duration and occurs either after the causative agent of acute inflammation persists for a long time or the stimulus is such that it induces chronic inflammation from the beginning. The characteristic feature of chronic inflammation is presence of chronic inflammatory cells such as lymphocytes plasma cells and macrophages.
  8. 8. ACUTE INFLAMMATION The changes is acute inflammation can be conveniently described under the following 2 headings: 1. Vascular events 2. Cellular events Vascular events Alteration in the microvasculature is the earliest response to tissue injury. These alterations include : a) Haemodynamic changes b) Changes in vascular permeability
  9. 9. A) Haemodynamic changes – the earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissues. The sequence of these changes is as under: 1. Irrespective of the type of injury immediate vascular response is of transient vasoconstriction of arterioles . With mild form of injury the blood flow may be re-established in 3-5 secs while with more severe injury vasoconstriction last for about 5 mins. 2. Next follows persistent progressive vasodilatation which involves mainly the arterioles . Vasodilatation results in increased blood volume in microvascular bed of the area which is responsible for redness and warmth at the site of acute inflammation. 3. Progressive vasodilatation in turn may elevate local hydrostatic pressure resulting in transudation of fluid into extracellular space . This is responsible for swelling at local site. 4. Slowing or stasis of microcirculation occurs . Slowing is attributed to increased permeability of microvasculature the results in increased concentration of red cells. 5. Stasis or slowing is followed by leucocytic margination or peripheral orientation of leucocytes along the vascular endothelium after this these move and migrate through gaps between endothelial cells into
  10. 10. the extravascular space. This process is called as emigration . The reaction elicited is known as triple response or red line response consisting of following : 1.Red line appears within a few seconds following stroking and results from local vasodilatation of capillaries and venules. 2.Flare is the bright reddish appearance or flush surrounding the red line and results in vasodilatation of adjacent arterioles . 3.Wheal is the swelling or edema of the surrounding skin occuring due to transudation of fluid into the extravascular space . B) Altered vascular permeability- PATHOGENESIS- in and around inflamed tissue compartment which comes from blood plasma by its escape through the endothelial wall of peripheral vascular bed. In the initial stage the escape of fluid is due to vasodilatation and consequent elevation in hydrostatic pressure. This is transudate in nature. The presence of edema due to increased vascular permeability of microvascular bed .
  11. 11. MECHANISM OF INCREASED VASCULAR PERMEABILITY- 1) CONTRACTION OF ENDOTHELIAL CELLS-This is most common mechanism of increased leakiness that affects venules exclusively while capillaries and arterioles remain unaffected . The endothelial cells develop temporary gaps between them due to their contraction resulting in vascular leakiness. It is mediated by histamine 2) RETRACTION OF ENDOTHELIAL CELLS- in this mechanism there is structural re-organisation of the cytoskeleton of endothelial cells that causes reversible retraction at the intercellular junctions. This change too affects the venules and is mediated by cytokines such as interleukin -1. 3) DIRECT INJURY TO ENDOTHELIAL CELLS- Direct injury to the endothelial causes cell necrosis and appearance of physical gaps at the sites of detached endothelial cells . Process of thrombosis is intiated at the site of endothelial cells . 4) ENDOTHELIAL INJURY MEDIATED BY LEUCOCYTES –Adherence of leucocytes to the endothelium at the site of inflammation may result in activation of leucocytes. The activated leucocytes release proteolytic enzymes and toxic oxygen species which may cause increased vascular leakiness and endothelial injury.
  12. 12. 5) NEOVASCULARISATION- In addition the newly formed capillaries under the influence of vascular endothelial growth factor during the process of repair and in tumors are excessively leaky. CELLULAR EVENTS The cellular phase of inflammation consists of 2 processes: 1. Exudation of leucocytes 2. Phagocytosis 1.Exudation of leucocytes- the escape of leucocytes from the lumen of microvasculature to the interstitial tissue is the most important feature of inflammatory response .the acute inflammation includes first line of body defense followed by monocytes and macrophages . The changes leading to migration of leucocytes are: a) Changes in the formed elements of blood- in the early stage of inflammation the rate of flow of blood is increased due to vasodilatation . But subsequently there is slowing of blood stream. due to slowing and stasis the central stream of cells widens and peripheral plasma zone becomes narrower because of loss of plasma by exudation. This phenomenon is known as margination.
  13. 13. b) Rolling and adhesion- Peripherally margination and pavemented neutrophils slowly roll over the endothelial cells lining the vessel walls. This is followed by transient bond between the leucocytes and endothelial cells becoming firmer. It includes 3 phases: 1)selectins 2)integrins 3)immunoglobulins superfamily adhesion molecules c)Emigration –after sticking of neutrophils to endothelium the former move along the endothelial cells is found where the neutrophils throw out cytoplasmic pseudopods. Subsequently the neutrophils lodged between the endothelial cells and basement membrane cross the basement membrane by damaging it locally with secreted collagenases and escape into the extravascular space this is known as emigration. d) Chemotaxis-The chemotactic factor ( cytokines, platelet factor etc) mediated transmigration of leucocytes after crossing several barriers ( endothelium, basement membrane , etc) to reach the interstitial tissues is called chemotaxis
  14. 14. 2.Phagocytosis-phagocytosis is defined as the process of engulfment of solid particulate material by the cells(cell-eating). The cells performing this function are called phagocytes. There are mainly two types of phagocytic cells: a) Polymorphonuclear neutrophils (PMNs) which appear early in acute inflammatory response also called as microphages. b) Circulating monocytes and fixed tissue mononuclear phagocytes called macrophages . The process of phagocytosis is similar for both polymorphs and macrophages and involves the following 4 steps: 1.Recognition and attachment stage(opsonisation) 2. Engulfment stage 3. Secretion stage 4. Digestion or degradation stage
  15. 15. CHEMICAL MEDIATORS OF INFLAMMATION Chemical factors or permeability factors are of increased vascular permeability , these are large and increasing number of endogenous compounds which can enhance vascular permeability. However, currently many chemical mediators have been identified which partake in other processes of acute inflammation as well eg: vasodilatation , chemotaxis, fever, pain etc. The substances acting as chemical mediators of inflammation may be released from the cells , the plasma, or damaged tissue itself. They are broadly classified into 2 groups: 1)Mediators released by cells 2)Mediators originating from plasma
  16. 16. 1)Cell- derived mediators- a)Vasoactive amines-these have roles in early inflammatory response i.e. histamine and serotonin. The main action of histamine are vasodilatation , increased vascular permeability, itching, and pain. Stimulation of mast cells and basophils also releases products of arachidonic acid metabolism including release of slow-reacting substances of anaphylaxis. Serotonin is less potent mediator of increased vascular permeability and vasodilatation than histamine. b)Arachidonic acid metabolites-arachidonic acid is fatty acid, eicosatraenoic acid and it has two main sources i.e. from diet directly and conversion of essential fatty acids c)Lysosomal components-the inflammatory cells neutrophils and monocytes contain lysosomal granules which on release elaborate a variety of mediators of inflammmation. d)Platelet activating factor(PAF)- it is released from IgE- sensatised basophils or mast cells endothelium and platelets. They increase vascular permeability , vasodilatation in low concentration , bronchoconstriction, chemotaxis e)Cytokines
  17. 17. 2) Plasma- derived mediators- These include the various products derived from activation and interaction of 4 interlinked systems: kinin, clotting, fibrinolytic, and complement . Each of these systems has its inhibitors and accelerators in plasma with negative and positive feedback mechanisms respectively. REGULATION OF INFLAMMATION The onset of inflammatory responses outlines above may have potentially damaging influence on the host tissues as evident in hypersensitivity conditions . Such self damaging effects are kept in check by the host mechanisms so as to resolve inflammation . Mechanisms are: a)Acute phase reactants-these are released in plasma in response to tissue trauma and infection. These are mainly synthesised in liver and to some extent in macrophages. b)Corticosteroids – glucocorticoids act as anti inflammatory agents. c)Free cytokine receptors- cytokines in serum correlates with disease activity. d)Suppressor T cells- prohibition of suppressor t cells is seen which inhibits the function of T and B cells. e)Anti-inflammatory chemical mediators-it has an anti- inflammatory action.
  18. 18. INFLAMMATORY CELLS
  19. 19. MORPHOLOGY OF ACUTE INFLAMMATION 1. PSEUDOMEMBRANOUS INFLAMMATION-It is inflammatory response of mucous surface to toxins of diphtheria or irritant gases. as a result of denudation of epithelium , plasma exudes on the surface where it coagulates and together with necrosed epithelium. 2. ULCER- ulcers are local defects von the surface of an organ produced inflammation. Common sites for ulceration are the stomach, intestinal ulcers in typhoid fever , ulcers of legs. in the acute stage there is infiltration by polymorphs with vasodilatation while long standing ulcers develop infiltration by lymphocytes and macrophages. 3. SUPPURATION(ABSCESS FORMATION)-When acute bacterial infection is accompanies by intense neutrophilic infiltrate in the inflamed tissue, it results in tissue necrosis. A cavity is formed which is called abscess and contains a pus and process of abscess formation is called suppuration.
  20. 20. 4.CELLULITIS- it is a diffuse inflammation of soft tissue resulting from spreading effects of substances like hyaluronidase released by some bacteria. 5.BACTERIAL INFECTION OF BLOOD-This includes: a) bacteraemia b) Septicaemia means presence of rapidly multiplying highly pathogenic bacteria in the blood c) Pyaemia SYSTEMIC EFFECTS OF ACUTE INFLAMMATION 1.FEVER- occurs due to bacteraemia . It is thought be mediated through release of factors like prostaglandins, interleukins and tumor necrosis factor in response to infection. 2.LEUCOCYTOSIS- Commonly accompanies the acute inflammatory reactions . Typhoid fever is an acute inflammation however induces leucopenia with relative lymphocytosis. 3.LYMPHANGITIS- It is one of the important manifestations of localised inflammatory injury. The lyphatics and lymph nodes that drain the inflamed tissues show reactive inflammatory changes in the form of lymphangitis .
  21. 21. 4.SHOCK- It may occur in severe cases. Massive release of cytokine a mediator of inflammation in response to severe tissue injury results in profuse systemic vasodilatation , increased vascular permeability and intravascular volume loss. The net effect of these changes is hypotension and shock. FATE OF ACUTE INFLAMMATION The acute inflammation process can culminate in one of the 4 outcomes: 1.RESOLUTION-It means complete return to normal tissue following acute inflammation . This occur when tissue changes are slight and cellular changes are reversible. 2.HEALING-This takes place when tissue destruction in acute inflammation is extensive so that there is no tissue regeneration but there is actually healing by fibrosis. 3.SUPPURATION-When the pyogenic bacteria causing acute inflammation result in severe tissue necrosis the process proresses to suppuration. Intially there is intense neutrophillic infiltration. 4.CHRONIC INFLAMMATION-The acute inflammation may progress to chronic inflammation in which the processes of inflammation and healing proceed side by side.
  22. 22. CHRONIC INFLAMMATION DEFINITION AND CAUSES: Chronic inflammation is defined as prolonged process in which tissue destruction and inflammation occur at same time. Causes: 1.Chronic inflammation following acute inflammation –when the tissue destruction is extensive or the bacteria survive and persist in small numbers at the site of acute inflammation. 2. Recurrent attacks of acute inflammation- when repeated bouts of acute inflammation culminate in chronicity of the process e.g. recurrent urinary tract infection . 3. Chronic inflammation starting de novo- when the infection with organism of low pathogenicity is chronic from the beginning. E.g. infection with Myobacterium tuberculosis
  23. 23. GENERAL FEATURES OF CHRONIC INFLAMMATION 1.MONONUCLEAR CELL INFILTRATION-chronic inflammatory lesions are infiltrated by mononuclear inflammatory cells like phagocytes and lymphoid cells. The blood monocytes on reaching the extravascular space transform into tissue macrophages .besides the role of macrophages in phagocytosis they may get activated in response to stimuli such as cytokines. 2. TISSUE DESTRUCTION OR NECROSIS-Tissue destruction and necrosis are central feature of most forms of chronic inflammatory lesions. This is brought by activated macrophages which release a variety of biologically active substances. E.g. protease, lipase .etc. 3. PROLIFERATIVE CHANGES –As a result of necrosis proliferation of small blood vessels and fibroblast is stimulated resulting in formation of inflammatory granulation tissue. Eventually healing by fibrosis and collagen laying takes place.
  24. 24. 2. TISSUE DESTRUCTION OR NECROSIS-Tissue destruction and necrosis are central feature of most forms of chronic inflammatory lesions. This is brought by activated macrophages which release a variety of biologically active substances. E.g. protease, lipase .etc. 3. PROLIFERATIVE CHANGES –As a result of necrosis proliferation of small blood vessels and fibroblast is stimulated resulting in formation of inflammatory granulation tissue. Eventually healing by fibrosis and collagen laying takes place. 1.FEVER-Invariably there is mild fever often with loss of weight and weakness. 2.ANAEMIA-Chronic inflammation is accompanied by anaemia of varying degree. 3.LEUCOCYTOSIS 4.ESR- It is elevated 5.AMYLOIDOSIS-Longer term cases of chronic suppurative inflammation may develop secondary systemic amyloidosis. TYPES OF CHRONIC INFLAMMATION 1.NON-SPECIFIC-When the irritant substance produces a non-specific chronic inflammatory reaction with formation of granulation tissue and healing by fibrosis , like chronic ulcer. 2.SPECIFIC-When injurious agent causes a characteristic histologic tissue response like, tuberculosis.
  25. 25. PATHOGENESIS OF INFLAMMATION
  26. 26. HEALING
  27. 27. HEALING Injury to tissue may result in cell death and tissue destruction. Healing on the other hand is the body response to injury in an attempt to restore normal structure and function. The process of healing involves 2 processes: 1. Regeneration-when healing takes place by proliferation of parenchymal cells and usually results in complete restoration of the original tissue . 2. Repair – when the healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring .
  28. 28. REGENERATION Some parenchymal cells are short lived while others have long lifespan. In order to maintain proper structure of tissues these cells are under the constant regulatory control of their cell cycle. These include growth factor such as :epidermal growth factor , fibroblast growth factor, platelet growth factor. All the cells divide at different pace , depending upon their capacity to divide so they are divided into 3 groups : 1. Labile cells :the cells continue to multiply throughout life under normal physiological condition. 2. Stable cell: these cells decrease or lose their ability to proliferate after adolescence but retain the capacity to multiply in response to stimuli throughout the adult life. 3. Permanent cells : these cells lose their ability to proliferate around the time of birth.
  29. 29. So regeneration of any type of parenchymal cells involve the following 2 processes : 1. Proliferation of original cells from the margin of injury with migration so as to cover the gap. 2. Proliferation of migrated cells with subsequent differentiation and maturation so as to reconstitute the original tissue.
  30. 30. REPAIR Repair is the replacement of injured tissue by fibrous tissue. Two processes are involved in repair: 1. Granulation tissue formation ; and 2. Contraction of wounds Repair response takes place by participation of mesenchymal cells , endothelial cells , macrophages , platelets , and the parenchymal cells of the injured organ. Granulation tissue formation- The term granulation tissue derives its name from slightly granular and pink appearance of the tissue . Each granule corresponds histologically to proliferation of new blood vessels which are slightly lifted on surface by thin covering of fibroblast and young collagen . The 3 following phases :
  31. 31. 1. Phase of inflammation : following trauma , blood clots at the site of injury . There is acute inflammatory response with exudation of plasma , neutrophils and some monocytes within 24 hours. 2. Phase of clearance : combination of proteolytic enzymes liberated from neutrophils , autolytic enzymes from dead tissue cells and phagocytic activity of macrophages clear off the necrotic tissue , debris and red blood cells. 3. Phase of ingrowth of granulation tissue : the phase consists of 2 main processes : a) Angiogenesis : formation of new blood vessels at the site of injury takes place by proliferation of endothelial cells from the margins of severed blood vessels. Initially, the proliferated endothelial cells are solid buds but within few hours develop lumen and start carrying blood . Soon these blood vessels differentiate into muscular arterioles thin walled . The process of angiogenesis is stimulated by proteolytic destruction of basement membrane .
  32. 32. b) fibrogenesis : the newly formed blood vessels are present in amorphous ground substance . The new fibroblast originate from fibrocytes as well as by mitotic division of fibroblasts. Some of these fibroblasts have combination of morphologic and functional characteristics of smooth muscle cells. Collagen fibrils begin to appear by about 6th day. More and more collagen fibres are formed and new blood vessels decrease. This results in formation of inactive looking scar known as cicatrisation. Contraction Of Wound – the wound starts contracting after 2-3 days and the process by the 14th day. During this period the wound is reduced by approximately 80% of its original size. Contracted wound results in rapid healing since lesser surface of injured tissue has to be replaced. In order to explain the mechanism of wound contraction a number of factors have been proposed : 1. Dehydration as result of removal of fluid by drying of wound. 2. Contraction of collagen 3. Discovery of myofibroblasts appearing in active granulation tissue . These cells have features intermediate between fibroblasts and smooth muscle cells. Their migration into wound area and active contraction decrease their size.
  33. 33. WOUND HEALING Healing of skin wounds provides a classical example of combination of regeneration and repair. This can be accompanied by one of the two following ways : 1. Healing by first intention (primary union) 2. Healing by second intention ( secondary union) Healing by first intention This is defined as healing of wound which has following features : a) Clean and uninfected b) Surgically incised c) Without much loss of cells and tissue d) Edges of wound and approximated by surgical sutures. The events in primary union are : - Initial haemorrhage – immediately after injury the space between the approximated surface of incised wound filled with blood which then clots and seals the wound against dehydration and infection.
  34. 34. - Acute inflammatory response - this occurs within 24 hrs of appearance of polymorphs from the margins of incision . By 3rd day , polymorphs are replaced by macrophages. - Epithelial changes – the basal cells of epidermis form both the cut margins start proliferating and migrating towards incisional space in the form of epithelial spurs. The migrated epithelial cells separate the underlying viable dermis from the overlying necrotic material and clot forming scab which casts off . By 5th day multilayered new epidermis in formed which is differentiated into superficial and deeper layers. - Organisation - by the 3rd day fibroblast also invade the wound area. By the 5th day new collagen fibrils start forming which dominate till healing is completed . In 4 weeks the scar tissue with scanty cellular and vascular elements a few inflammatory cells and epithelialised surface is formed . - Surface tracks – each suture track is a separate wound and incites the same phenomena as in healing of primary wound i.e. filling the space with haemorrhage some inflammatory reactions .when sutures are removed around 7th day much of epithelialised suture track is avulsed
  35. 35. Healing by second intention This is defined as healing of wound having the following characteristics : 1. Open with large tissue defect at times infected 2. Having extensive loss of cells and tissues 3. The wound is not approximated by surgical sutures but is left open. The basic events in secondary union but differ in having larger tissue defect which has to be bridged . Hence healing takes place from the base upwards as well as from the margins inwards. This healing is slow , ugly, scar as compared rapid healing and neat scar of primary union. - Initial haemorrhage – as a result of injury the wound space is filled with blood and fibrin clot which dries. - Inflammatory phase – there is initial acute inflammatory response followed by appearance of macrophages which clear off the debris as in primary union. - Epithelial changes – epidermal cells from both margins of wounds proliferate and migrate into wound in form of epithelial spurrs till they meet in centre and re-epithelialise the gap completely. However epithelial cells do not cover completely .
  36. 36. - Granulation tissue – the main bulk of secondary healing is by granulation. Granulation tissue is formed by proliferation of fibroblasts and neovascularisations from adjoining viable element . The newly formed granulation tissue is deep red , granular and very fragile . With time the scar maturation becomes pale andwhite due to increase in collagen and decrease in vascularity. - Wound contraction – contraction of wound is an important feature of secondary healing not seen in primary healing . Due to action in myofibroblasts present in granulation tissue the wound contracts to one-third to one-fourth of its original size. - Presence of infection – bacterial contamination of an open wound delays the process of healing due to release of bacterial toxins that provoke necrosis , suppuration and thrombosis.
  37. 37. Complications of wound healing During the course of healing, following complications may occur : 1. Infection of wound due to entry of bacteria delays the healing. 2. Implantation cyst formation may occur due to persistance of epithelial cells in wound after healing . 3. Pigmentation – healed wound may at times have rust like colour due to staining with haemosiderin. Some coloured particulate material left in the wound may persist . 4. Deficient scar formation – this may occur due to inadequate formation of granulation tissue. 5. Incisional hernia – a weal scar, especially after laparotomy may be site of bursting open of wound or an incisional wound. 6. Hypertrophied scars and keloid formation – at time the scar formed is excessive , ugly and painful. Excessive formation of collagen in healing may result in formation of keloids. 7. Excessive contraction 8. Neoplasia
  38. 38. Factors Influencing Healing Two types of factors influence the wound healing : A. Local factors : 1. infection – most important factor which delays healing. 2. Poor blood supply to wound slows healing 3. Foreign bodies including sutures interfere healing and cause intense inflammatory reaction. 4. Movement delays wound healing 5. Exposure to ionising radiation delays granulation tissue formation . 6. Exposure to ultraviolet light facilitates healing 7. Type , size, location of injury determines whether healing takes place by resolution or organisation. B. Systemic factors : 1. age – wound healing is rapid in young and somewhat slowed in aged 2. Nutrition – deficiency of constituents like proteins, vit. C. and zinc delays wound healing
  39. 39. 3. Systemic infection delays wound healing . 4. Administration of glucocorticoids has anti-inflammatory effect. 5. Uncontrolled diabetics are more prone to develop infection 6. Haematologic abnormalities like defect of neutrophils, and bleeding disorders slow the process of wound healing. HEALING IN SPECIALISED TISSUES In some specialised tissues either repair or regeneration may predominate . Some of the examples are : 1. Fracture healing Healing of fracture by callus formation depends on some clinical considerations whether fracture is - Traumatic or pathological - Complete or incomplete - simple or compound
  40. 40. However basic events in healing of any type of fracture are similar and resemble healing of skin wound 1. Primary union of fracture occurs in few special situations when the ends of fracture are approximated as is done by application of compression clamps. In this case the bony union takes place with formation of medullary callus without periosteal callus formation. 2. Secondary union is more common process of fracture healing . Though it is continous process secondary bone union is under 3 headings : a) procallus formation b) osseous callus formation c) remodelling Complications of fracture healing : fibrous union may result instead of osseous union if immobilisation of fractured bone is done. Non-union : may result if some soft tissue is interposed between fractural end Delayed union : may occur from causes of delayed wound healing in general such as infection etc.
  41. 41. 2. Healing of nervous tissue Central nervous system : the nerve cells of brain , spinal cord , ganglia once destroyed are not replaced . Axons of CNS also does not show any regeneration. The damaged neuroglial cells may show proliferation of astrocytes called gliosis. Peripheral nervous system : the peripheral nerves shows regeneration mainly from proliferation of schwann cells and fibrils from distal end. 3. Healing of muscle Skeletal muscle :the regeneration of striated muscle is similar to peripheral nerves. On injury the cut end of muscle fibres retract but are held together by stromal connective tissue. the injured site is filled with fibrous material, polymorphs and macrophages. Smooth muscle : non-striated muscles has limited regenerative capacity e.g. appearance of smooth muscle in arteriole in granulation tissue. The smooth lesions are replaced by permanent scar tissue. Cardiac muscle : destruction of heart muscle is replaced by fibrous tissue . However the situation where endomysium of indivisual cardiac fibre is intact, regeneration of cardiac fibre may occur in young.

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