# Inflammation

Inflammation

- - In the early inflammatory phase (days 1–2), platelet activation causes an influx of  inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of  the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). - Inflammation

- - In the early inflammatory phase (days 1–2), platelet activation causes an influx of  inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of  the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). - Inflammation

- - In the early inflammatory phase (days 1–2), platelet activation causes an influx of  inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of  the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). -