Tissue healing

Wound healing is a complex process in which the skin, and the tissues under it, repair themselves after injury. In this article, wound healing is depicted in a discrete timeline of physical attributes (phases) constituting the post-trauma repairing process. In undamaged skin, the epidermis (surface layer) and dermis (deeper layer) form a protective barrier against the external environment. When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. This process is divided into predictable phases: blood clotting (hemostasis), inflammation, tissue growth (proliferation), and tissue remodeling (maturation). Blood clotting may be considered to be part of the inflammation stage instead of a separate stage. Wound healing is a complex process in which the skin, and the tissues under it, repair themselves after injury. In this article, wound healing is depicted in a discrete timeline of physical attributes (phases) constituting the post-trauma repairing process. In undamaged skin, the epidermis (surface layer) and dermis (deeper layer) form a protective barrier against the external environment. When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. This process is divided into predictable phases: blood clotting (hemostasis), inflammation, tissue growth (proliferation), and tissue remodeling (maturation). Blood clotting may be considered to be part of the inflammation stage instead of a separate stage. The wound healing process is not only complex but also fragile, and it is susceptible to interruption or failure leading to the formation of non-healing chronic wounds. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease, infection, and metabolic deficiencies of old age. Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection. Depending on each patient's needs, it can range from the simplest first aid to entire nursing specialties such as wound, ostomy, and continence nursing and burn center care. Timing is important to wound healing. Critically, the timing of wound reepithelialization can decide the outcome of the healing. If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; If the epithelization of a wounded area is fast, the healing will result in regeneration. Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase: The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation. The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. Subdivisions of the cellular phase are: Macrophages and inflammatory components (within 1–2 days), Epithelial-mesenchymal interaction: re-epithelialization (phenotype change within hours, migration begins on day 1 or 2), Fibroblasts and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14), Endothelial cells and angiogenesis (begins on day 4), Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size). Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing. When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass.