WOUNDS 4

Healing 4




2.2.3 PROLIFERATIVE PHASE (FIBROPLASIA) Within 10 hours, if no infection, occurs, fibroblasts begin to migrate and lay down collagen. In the Incremental phase the fibroblasts continue to produce larger quantity of collagen and the tensile strength of the healing wound increases. More fibroblasts appear perhaps from the primitive mesodermal stem cells and this further increases the quantity of collagen produced by the endoplasmic reticulum of the fibroblasts and forms cross banded fibrils; fibroblasts also manufacture mucopolysaccharide ground substance. This helps the alignment and approximation of the collagen.

Within 2 to 3 days, the inflammatory cell population begins to change to one of monocyte predominance. These mono cytes are attracted and infiltrate the wound site. These monocytes differentiate into macrophages, and in conjunction with resident macrophages, join the repair process. Macrophages not only continue to phagocytose tissue and bacterial debris, but also secrete multiple growth factors. These peptide growth factors activate and attract local endothelial cells, fibroblasts, and keratinocytes to begin their respective repair functions. More than 20 different cytokines and growth factors are known to be secreted by macrophages, the primary cells responsible for regulating repair.

Ell Proliferation (FIBROPLASIA )
*The proliferating phase starts with this deposition of febrin and fibrinogen matrix and the activation and production of local fibroblasts (fibroplasial). At the beginning fibrin fibrinogen matrix is populated with platelets and macrophages. These macrophages and the local extra cellular matrix (ECM) release growth factors that initiate fibroblast activation.

Fibroblasts migrate into the wound using the newly deposited fibrin and fibronectin matrix as a scaffold.

Local fibroblasts become activated and increase protein synthesis in preparation for cell division.

As fibroblasts proliferate, they become the prominent cell type in 3 to 5 days in clean, non infected wounds, After cell division and proliferation, fibroblast begin synthesis and secretion of extra cellular matrix products. The initial wound matrix is temporary and is composed of fibrin and the glycosaminoglycan (GAG), hyaluronic acid. Because of its large water of hydration, hyaluronic acid provides and matrix that helps cell migration.

As fibroblasts enter and populate the wound, they use hyaluronidase to digest the provisional hyaluronic acid-rich matrix, and larger, gulfated GAGs deposited in addition collagens are deposited here and there by fibroblasts onto the fibroneetin and GAG scaffold.

Collagen types I and III are the major fibrillar collagens comprising the extracellular matrix and are the major structural proteins both in unwounded and wounded skin.

There are now at least 19 different types of collagens described, each of which shares the right handed triple helix as the bias structural unit. Most collagen types are synthesized by fibroblasts, however, it is now known that some types are synthesized by epidermal cells.*

2.2.4 EPETHELIALISATION: The keratinocytes in the skin at the site of injury show activity. The epidermis thickens, the basal cells enlarge and move over to cover the wound defect. The fixed basal cell divide and the new cells cover the defect. Adhesion glycoproteins (fibronectin) provide direction and tracks for these cells till the cover is complete.

*Within hours after injury, morphological changes can be seen in karatinocytes at the wound margin.
In skin wounds the epidermis thickens, and marginal basal cells enlarge and migrate over the wound defect.
Wound closure is provided by fixed basal cells in a zone near the edge of the wound. Their daughter cells flatten and migrate over the wound matrix as a sheet. Cells adhesion glycoprotcins, such as tenascin and fibrocction provide the “railroad tracks” to facilitate epithelial cell migration over the wound matrix. Following the restablishment of the epithelial layer, jeratinocytes and fibriblasts secrete laminin and type IV collagen to form the basement membrance. The kertinocytes then become columnar and divide as the layering of the epidermis is established, thus reforming a barrier to further contamination and moisture loss of the wound.

The ultimate pattern of collagen is scar is one of densely packed fibers and not the reticular pattern found in unwounded dermis.*


2.2.5 REMODELLING: The extracellular matrix is a network of protein and polysaccharides. Collagen is the main component of this matrix.

Fibroblasts also contain myofibrilis which help to pull the wound edges together.This wound contraction further adds to the tensile strength.

*During remodeling, wounds gradually becomes stronger with time. Wound tensile strength increases rapidly form 1 to 8 weeks post wounding. Thereafter, tensile strength increases at a slower pace and has been documented to increase up to 1 year after wounding in animal studies. However, the tensile strength of wounded skin at best only reaches approximately 80% that of unwounded skin. The final result of tissue repair is scar, which is brittle, less elastic than normal skin, and does not contain any skin appendages such as hair follicles or sweat glands.*

2.2.6 CLINICAL WOUND HEALING OPEN WOUNDS: At the end of 4 weeks an uncomplicated wound has reached
• 50% of its final strength
• 75% at the end of 8 weeks and
• Nearly 95% after 6 months
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The information in large print is sufficient for your undergraduate course. The sections between astrix* knowledge is required for the higher postgraduate courses.