Pathology Tissue Repair Methods

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Wound healing

See our Privacy Policy and User Agreement for details. Published on Sep 26, Robbins Basic Pathology - Tissue Repair. SlideShare Explore Search You. Submit Search. Successfully reported this slideshow. We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads.

You can change your ad preferences anytime. Upcoming SlideShare. Like this presentation? Why not share! Fibroblasts migrate into the damaged area and proliferate within the first few days after the tissue damage. Macrophage Derived Growth Factors MGDF's are a complex group of mediators responsible, at least in part for the activation of fibroblasts.

Alongside the fibroblastic activation, capillaries in the region of the tissue damage bud and grow towards the repair zone. Loops and arcades are formed together with anastamoses which re-establish a blood flow through the region, providing oxygen and nutrients whilst removing metabolic and repair waste products. Oxygen is critical for many of the reparative processes, but especially for collagen production Vanables , Niinikoski A wide range of growth factors and chemical mediators have been identified which exert influences on the developing capillaries.

There is growing evidence that various therapies are able to positively influence these proliferative and angiogenic events include :. Granulation tissue invasion follows the 'demolition' phase when autolytic enzymes are released from PMN's and dead cells Walter and Israel The activation of fibroblasts and capillary budding would normally occur by about the third day after the tissue insult.

The combination of capillary budding and collagen production results in a more vascular than usual repair site. The fibroblasts initially produce predominantly type III collagen which will become type I collagen as the repair matures — during remodelling Walter and Israel Fibroblasts also produce fibronectins and proteoglycans which are essential components of the ground substance Figure 5 Walter and Israel , Forrest , Hardy Myofibroblasts are derived from fibroblasts activated by a variety of chemical mediators, and are responsible for wound contraction and the early strength of the repair.

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They draw the edges of the wound together, thus reducing the size of the final scar Gabbiani ; Lorena et al ; Peacock ; Hardy ; Wipff et al, ; McAnulty, Granulation tissue matures with lymphatic development in much the same way as capillary development , nerve fibre ingrowth and mast cell invasion. Collagen fibres are oriented in response to local stress thus providing tensile strength in the required directions see Forrest and Hardy for useful collagen reviews.

As the granulation tissue matures, there is a process of devascularisation with obliteration of the lumen of the vessels. The remodelling phase primarily involves the refinement of the collagen and its associated extracellular matrix. The initial deposition of collagen produces relatively weak fibrils with random orientation With maturity, the collagen becomes more obviously oriented in line with local stresses Culav et al , Gomez et al A proportion of the original fine Type III collagen is reabsorbed due to the action of collagenases and is replaced with Type I collagen with more cross links and greater tensile strength Vanables , Forrest Collagen synthesis and lysis both occur at a greater rate in a normal wound compared with non wounded tissue as old fibrous tissue is removed and new scar tissue is laid down.

The maturing scar is therefore a dynamic system rather than a static one. There are several influential factors during this long phase, including physical stress. This remodelling process is initiated whilst the proliferative stage proceeds, therefore providing a considerable overlap between the phases. Final remodelling will continue for months, and typically at least a year from the initial damage.

The potential mechanism by which physical stress can influence cell and tissue behaviour is usefully considered by Ingber , Kahn and Scott and Killian et al provide more recent papers linking mechanical stress and tissue repair, as do Bring et al and Cyr and Ross whilst Mackey et al also provide a valuable review. Figure 8: Representation of regained tissue strength after Lin et al, Similarly, if delivering therapy during the proliferative phase, there would be no benefit in simply creating a bigger volume of scar tissue.

The advantage of appropriate intervention is that it stimulates a maximally efficient response, and therefore the required repair material is generated with best quality and minimal time. In the remodelling phase, the refinement of the scar tissue is the aim and the use of therapy can have a significant effect, especially given the growing body of evidence relating the effects of mechanical stress and collagen behaviour. Inappropriate therapy at any stage is perfectly capable of inhibiting these events and therefore results in a less good repair — therapy is not guaranteed to be beneficial — one has to be mindful of the events needed and be selective of the most appropriate evidenced therapy at each stage.

The other interesting recent development is that there is an increasing body of knowledge which supports the idea that existing therapies have an effect on the chemical environment of the repairing tissue Watson, Exercise therapy, manual therapy and various modalities in electrotherapy are now known to exert such effects - some examples having been provided earlier in this paper. The mode of action of those therapies, historically employed, is actually a lot more complex than was originally conceived and hitherto understood.

The repair control system and links between its various components are complex, and there is an ever increasing volume of literature which continues to identify new mediators, cytokines and variants. Whilst this knowledge base continues to expand, the links between the effects of therapy and these chemical control systems is also growing.

Current Methods for Skeletal Muscle Tissue Repair and Regeneration.

If repair is underway, then keep it moving. If it is delayed, then stimulate it in order to help get it back on track. Whilst there are myriad approaches, those that are most effective appear to follow this philosophy. Aller, M.

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Arias, et al. Azuma, Y. Ito, et al. Beck, A. Salem, et al. Bjordal, J. Lopes-Martins, et al. Bossini, P. Fangel, et al. Boursinos, L. Karachalios, et al. Bring, D. Kreicbergs, et al. Broughton, G. Janis, et al. Butterfield, T. Best, et al. Calatroni, A. Avenoso, et al. Chao, Y. Tsuang, et al. Cheung, W. Chin, et al. Culav, E. Clark, et al. Cyr, L. Ross Dierich, M. Forster, et al. Dimmen, S. Nordsletten, et al.

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Egozi, E. Ferreira, et al. Fitzsimmons, R. Gordon, et al. Forrest, L. Frick, M. Murthy Fujiwara, Y. Uesugi, et al. Gabbiani, G. Gomez, M. Woo, et al. Granger, D. Senchenkova Inflammation and the Microcirculation. San Francisco, Morgan and Claypool. Handschin, C. Spiegelman Hardy, M.

Hildebrand, K. An in vivo study. Hill, M. Wernig, et al. Hurley, J. Muir's Textbook of Pathology. Hurst, S. Wilkinson, et al. Ingber, D. Jimenez, P. Jimenez Khan, K. Scott Khanna, A. Nelmes, et al. Kido, S. Kuriwaka-Kido, et al. Killian, M. Cavinatto, et al. Kuo, Y. Wang, et al. Leung, M.

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Ng, et al. Li, J. Loose tissues contract more than tissues with poor laxity, and square wounds tend to contract more than circular wounds. Wound contraction depends on the myofibroblast located at the periphery of the wound, its connection to components of the extracellular matrix, and myofibroblast proliferation. Radiation and drugs, which inhibit cell division, have been noted to delay wound contraction. Contraction does not seem to depend on collagen synthesis.

The remodeling phase starts around the peak of the proliferation phase. The result of this phase is an organised, quality and functional scar similar to the tissue it is busy repairing. In non-central nervous system CNS tissue that undergoes primary healing, very little remodeling occurs because of the lack of extra-cellular matrix produced during repair. Secondary healing, in contrast, involves fiber alignment and contraction to reduce the wound size and to reestablish tissue strength.

Complete recovery of original tissue strength is rarely obtained in secondary healing because repaired tissue remains less organized than non-injured tissue, which results in scar formation. In CNS tissue where there is no repair or regeneration of injured neurons, there is also relatively little reestablishment of structural integrity in the region. Instead, during CNS remodeling, the glial scar around the lesion becomes denser as astrocytic processes become more intertwined and more or less isolates but does not repair the injured region.

Restoration of continuity occurs directly by fibrous adhesion, without formation of granulation tissue; it results in a thin scar. Wound healing occurs by union by adhesion of granulating surfaces, when the edges of the wound are far apart and cannot be brought together. Granulations form from the base and sides of the wound toward the surface. Wound healing occurs by the gradual filling of a wound cavity by granulations and a cicatrix. This classification is based on a treatment protocol of Clanton et al. It is possible that some phases overlap, dependable on the individual response to healing and the type of injury.

Not every patient undergoes all phases to achieve a full rehabilitation. This phase starts when signs of inflammation begin to reduce. Inflammation signs are heat, swelling, redness and pain.

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Soft tissue healing is a natural process that occurs in the body after an injury. This process happens without the need for medication and therapy, but this can play an important role in cases where problems are identified in this natural process, such as repeated trauma, inhibited response or delayed reactions. The aim would then be to facilitate and stimulate the soft tissue healing process. It is thus very important to be selective of the most appropriate therapy at each stage. The content on or accessible through Physiopedia is for informational purposes only.

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