Acute vs Chronic Inflammation
Inflammation is the tissue reaction to injurious agents, and it may be acute or chronic. Acute inflammation has an immediate phase and a delayed phase. Chronic inflammation is a sequel of acute inflammation. The article will discuss the acute and chronic inflammation in detail, highlighting the difference between them.
Acute inflammation occurs in two phases; the immediate phase and the delayed phase. Immediate phase of acute inflammation is almost completely due to histamine release. Serotonin also plays a tiny part in the mechanism. Delayed phase of acute inflammation features release of other more potent inflammatory mediators. Acute inflammation can also be divided into two steps; fluid exudate and cellular exudate. Fluid exudate and cellular exudate overlap with each other and with immediate and delayed phases. However, fluid exudate starts early.
The injurious agents damage tissues. They trigger release of histamine from mast cells, blood vessel lining cells, and platelets. There is an initial reflex contraction of the capillary bed to limit entry of injurious agents into the blood stream. Histamine and serotonin relax capillaries and increase permeability of capillaries. This marks the onset of fluid exudation, and water and electrolytes leak into the inflamed tissues. Therefore, osmotic pressures inside and outside capillaries equalize. Through enlarged gaps in the blood vessel wall lining, proteins leak out. These proteins draw water out into the tissues. Protein breakdown due to tissue damage increases this water movement further. At the venous end of the capillary bed, water does not enter the circulation because water gets held by in tissue by electrolytes and proteins. Thus, swelling occurs. Usually the blood vessel wall lining and cell membranes of the blood cells are negatively charged, keeping them apart. In inflammation, these charges change. Loss of fluid from the blood stream at inflamed sites disturbs the laminar blood flow. Inflammatory mediators promote roulaux formation. All these changes drag cells towards the vessel wall. White blood cells bind to integrin receptors on the vessel wall, roll along the wall, and exit into the inflamed tissue. Red blood cells spurt out through the gap (diapedesis). This is called cellular exudate. Once outside, white blood cells migrate towards the injurious agent along the concentration gradient of chemicals released by the agent. This is called chemotaxis. After reaching the agent white cells engulf and destroy the agents. The assault of white cells is so severe that surrounding healthy tissue also gets damaged. According to the type of the injurious agent, the type of white cells entering the site varies. Resolution, chronic inflammation, and abscess formation are known sequels of acute inflammation.
Chronic inflammation is one of the consequences of acute inflammation. Acute inflammation, demolition, healing, and immune reaction occur all at once in chronic inflammation. Demolition phase features removal of damaged tissues from the inflamed site. White blood cells and scavenger cells are active here. Demolition makes way for new healthy tissue. Damage can heal by regeneration of healthy tissue or by scarring. Immune reaction features ongoing fluid and cellular exudate in response to the effects of the injurious agent. Examples of chronic inflammatory diseases are chronic osteomyelitis, chronic tuberculosis, and chronic bowel inflammation.
What is the difference between Acute and Chronic Inflammation?
• Acute inflammation runs a short course while chronic inflammation can last a long time.
• Acute inflammation occurs as a stand-alone process as well as a part of chronic inflammation.
You may also be interested in reading: