Process of Plaque Formation

• Plaque Formation Process pt1:

  1. Damaged endothelial cells release substances (cell adhesion molecules), which attract monocytes and platelets to the area
  2. These cells then bind to the affected endothelium and cross the arterial wall to enter the intima
  3. As monocytes leave the blood system to enter the tissues they change slightly and become macrophages and release Free radicals or reactive oxygen species
  4. LDLs also enter into the sub-intimal wall structure
  5. The lipid/cholesterol carried by the LDLs then become oxidized by reactive oxygen species
• Plaque Formation Process pt2:

  1. macrophages ingest the oxidised LDLs and become bloated
  2. Ingesting LDLs alters macrophage structure and function and they are now known as foam cells
  3. The process of engulfing LDLs is associated with the release of more ROS, which attracts more monocytes (which then change to macrophages/foam cells) and LDLs to the site in a positive feedback loop of recruitment
  4. And in this way the collection of foam cells and LDLs increases over time
  5. The platelet cells and the foam cells in the intima both release a number of chemical substances including growth factors
• Plaque Formation Process pt3

  1. Growth factors diffuse across the internal elastic laminae to affect smooth muscle cells (SMCs) in the tunica media
  2. As a consequence, some of these SMCs migrate and cross into the intima via the gaps between elastic fibres in the internal elastic lamina
  3. Hence there is a blurring of intimal and medial components
  4. Once in the intima, SMCs proliferate and collagen and elastin fibres are also secreted increasing the presence of these components within the intima
  5. A distinct localised mass begins to form within the wall structure – the plaque/atheroma